. 2022 Jul 20;23(8):261. doi: 10.31083/j.rcm2308261

Dental Management Considerations for Patients with Cardiovascular Disease—A Narrative Review

Kanishk Gupta ^1,^†Santhosh Kumar ^2,^†Meena Anand Kukkamalla ^3,^†Vani Taneja ^4,^*,^†Gufaran Ali Syed ⁵Fawaz Pullishery ⁶Mohammad A Zarbah ⁷Saeed M Alqahtani ⁸Mohammed A Alobaoid ⁹Saurabh Chaturvedi ¹⁰

Editor: Giuseppe Biondi Zoccai

¹Department of PeriodontologyDentistry ProgramBatterjee Medical College21442 JeddahSaudi Arabia

²Department of PeriodontologyManipal College of Dental SciencesManipalManipal Academy of Higher Education576104 ManipalKarnatakaIndia

³Department of PeriodontologyFaculty of DentistryManipal University College Malaysia (MUCM)75150 MelakaMalaysia

⁴Department of Pediatric DentistryDentistry ProgramBatterjee Medical College21442 JeddahSaudi Arabia

⁵Department of EndodonticsDentistry ProgramBatterjee Medical College21442 JeddahSaudi Arabia

⁶Division of Dental Public HealthDentistry ProgramBatterjee Medical College21442 JeddahSaudi Arabia

⁷Department of Prosthetic Dental ScienceCollege of DentistryKing Khalid University62529 AbhaSaudi Arabia

⁸Department of Prosthetic DentistryCollege of DentistryKing Khalid University62529 AbhaSaudi Arabia

⁹Department of Restorative Dental Sciences and Department of Dental EducationKing Khalid University College of Dentistry61471 AbhaSaudi Arabia

¹⁰Department of Prosthetic Dental ScienceCollege of DentistryKing Khalid University62529 AbhaSaudi Arabia

Correspondence: [email protected] (Vani Taneja)

^†These authors contributed equally.

Roles

Giuseppe Biondi Zoccai: Academic Editor

Received 2022 Feb 18; Revised 2022 Jun 8; Accepted 2022 Jun 13; Collection date 2022 Aug.

This is an open access article under the CC BY 4.0 license.

PMC Copyright notice

PMCID: PMC11266964 PMID: 39076626

Abstract

Dental therapists encounter patients with various systemic diseases of which cardiovascular disease (CVD) patients form a significant segment. Relation between oral health and cardiac diseases has been well established. Common cardiac disorders encountered in a dental practice include arterial hypertension heart failureischemic heart diseasecardiac arrhythmiasinfective endocarditisstrokeand cardiac pacemaker. Patients with CVDs pose a significant challenge to dental therapy. These patients need special considerations and an adequate understanding of the underlying cardiovascular condition to provide safe and effective dental treatment. Based on the cardiac conditionan appropriate modification in dental care is crucial. A multidisciplinary approach including the patient’s cardiologist can potentially reduce complications and improve dental treatment results. This review aims at unfolding the risks associated with the dental management of a cardiac patient and outlines the measures to be undertaken for optimum dental treatment.

Keywords: anticoagulantscardiac arrhythmiasdental carehypertensionmyocardial ischemiavasoconstrictor

1. Introduction

Assessing a patient’s medical history is the first step of any dental treatment. A compromised medical status can alter the dental treatment plan andif ignored can lead to severe and sometimes fatal consequences. Cardiovascular diseases are the leading global cause of death [1 2 3]. In 2019an estimated 17.9 million deaths occurred due to cardiovascular diseases constituting 32% of all the deaths worldwide [2]. With extensive improvement in healthcare facilities and an increase in life expectancydentists are encountering more and more elderly and medically compromised patients. In a dental practicethough syncope is the most common medical emergency reported [4]cardiovascular events are not very infrequent [5 6]. Thusit is very critical for dental practitioners to possess adequate knowledgeskillsand resources to counter such emergencies effectively. Howeversince a patient’s medical status plays a pivotal role in formulating the treatment plana dentist should not hesitate to contact the patient’s physician to enquire about the medical details and discuss the dental treatment plan.

This article discusses the potential cardiovascular problems a dental practitioner encounters and dentists’ management strategies in a dental clinic.

2. Hypertension

Arterial hypertension is one of the most common chronic medical conditions affecting the population and a significant cause of death globally. Around 10.4 million people die every year due to raised blood pressure [7]. More than 200 million people in India suffer from hypertension [8]. Hypertension can be classified as primary hypertension and secondary hypertension. Primary or ‘essential’ hypertension does not have an apparent underlying causewhile secondary hypertension has specific reasons like hyperthyroidismvascular diseasesand adrenal medullary dysfunction [9]. 90–95% of the patients with high blood pressure in the United States fall into ‘Essential hypertension’ category [10]. Generallyhypertension is diagnosed based on an average of two or more elevated measurements taken on two or more instances [11 12].

In 2018the European Society of Cardiology/European Society of Hypertension (ESC/ESH) updated the arterial hypertension management guidelines and included blood pressure classification for all ages from 16 years [13]. According to this classificationhypertension is described as office systolic BP $\geq$ 140 mm Hg and/or diastolic BP $\geq$ 90 mm Hg. This categorization is different from the one recommended in the 2017 ACC/AHA High Blood Pressure Clinical Practice Guidelineswhich defined hypertension as systolic blood pressure (SBP) $\geq$ 130 mm Hg or a DBP $\geq$ 80 mm Hg [14].

Hypertension can be treated by non-pharmacological or pharmacological therapy. Non-pharmacological means include diet modificationregular exerciseweight controlsmoking cessationand limiting alcoholsaltand caffeine intake [15 16]. Pharmacologicallyantihypertensive drugs are given as monotherapy or combination therapy to control blood pressure [17]. Despite the advancement in diagnostic and therapeutic modalitiesmost cases of hypertension are either undiagnosed or uncontrolled. Such cases pose a significant public health problem for developing and developed nations. With increased blood pressurethe risk of myocardial infarctionheart failurestrokeand kidney disease increases significantly.

Undetected or insufficiently controlled hypertension can be a reason for complications in a dental setup. Thereforea thorough evaluation of a hypertensive patient visiting a dental clinic is imperative for the delivery of efficient and safe dental care. In additiondentists can play a pivotal role in detecting and timely referring hypertensive patients to medical practitioners. For thisoral health care providers should be well versed with the recent guidelinesmeasurementdiagnosisand management of hypertensive dental patients.

Before undertaking any dental procedureit is recommended to do a patient’s complete risk assessment. Proper patient evaluation with detailed medical and family history will help assess the chances of any adverse cardiovascular event occurring during the dental treatment. In a dental officevital signs including pulse and blood pressure should be measured for all the patients at every visit [18]. In additionblood pressure monitoring for hypertensive patients with systemic complications must be carried out even during the procedure [19].

According to the American Dental Associationthe guidelines for outpatient dental care for adult hypertensive patients are as follows [20]:

• Hypertensive patients with blood pressure less than 160/100 mmHg need no elective or emergency treatment modification.

• For patients with $>$ 160/100 mmHg of blood pressureB.P. measurements must be repeated.

• If B.P. is reduced or is within the permitted limit according to the physicianthen the emergency or elective dental care can be continued.

• Howeverif B.P. is confirmed to be more than 160/100 mmHgthen no elective dental treatment should be providedand the patient should be referred to a physician.

• Emergency care can be initiated if SBP is 160–180 mmHg and/or diastolic pressure 100–109 mmHgand blood pressure must be measured every 10–15 minutes during the procedure.

• If confirmed SBP $>$ 180 and/or DBP $>$ 109the dentist should consult the physician before any procedure.

• Patients with SBP $>$ 180 mmHg and/or DBP $>$ 110 mmHg must undergo physician consultation immediatelyor the patient must be sent for urgent medical evaluation if symptomatic.

Short morning appointments are preferable with adequate stress and anxiety management. Anxiolytic agents like diazepam (5–10 mg) the night before and one hour before the dental appointment may be helpful. Sudden positional changes during or at the end of the dental procedure should be avoidedespecially in older patients to prevent orthostatic hypotension. Pain during a dental procedure can cause endogenous catecholamine releaseleading to undesirable hemodynamic alterations in cardiac patients [21]. To prevent this complicationpain is controlled by using local anesthetics with vasoconstrictors like epinephrine which prolong the anesthetic effect and improve hemostasis. Howeverepinephrine due to its non-selective adrenergic profile causes an increase in heart rate (HR) and blood pressure (BP) making its use controversial in cardiac patients. Nevertheless1 or 2 cartridges of local anesthetic with 1:80,0001:100,000or 1:200,000 of epinephrine are considered safe in patients with controlled hypertension and/or coronary disease [22]. Thusa limited dose of vasoconstrictor (0.018 to 0.036 mg) [23]proper aspirationand slow injection technique can prevent systemic absorption of vasoconstrictor and prevent cardiovascular stimulation in hypertensive patients [24].

Excessive intraoperative bleeding in hypertensive patients may be of concern especially during an extensive surgical procedure or in patients taking anticoagulants like aspirin or warfarin. Thereforeassessing proper coagulation and limiting the surgical area should be considered [15]. Dental practitioners should be well acquainted with antihypertensive drugs used commonly like alpha-blockersbeta-blockersdiureticsangiotensin-converting enzyme (ACE) inhibitorsand calcium channel blockers. Knowledge of oral adverse effects [15 25] of these drugs like xerostomiagingival hyperplasialichenoid reaction orthostatic hypotensiongingival bleedingand loss of taste aids in better patient management.

Drug-drug interactions may be encountered with antihypertensive drugs and drugs commonly prescribed by dental professionals such as NSAIDs (causing decreased antihypertensive effect) [15 26]epinephrine (causing a transient increase in BP) [15 26]local anesthetics (causing decreased rate of amide metabolism) [15]sedatives (causing increased sedation) [15]systemic antifungalsand opioids. Understanding drug interactions and managing the side effects of these drugs can lead to a more holistic and effective dental management of hypertensive patients [15].

2.1 Hypertensive Crisis

According to the 2003 Joint National Committee (JNC-7) reporta significant increase in systolic blood pressure (SBP $>$ 180 mmHg) or diastolic blood pressure (DBP $>$ 120 mmHg) is described as a ‘Hypertensive Crisis’ [27]. It is further divided into hypertensive urgency (situations without progressive target organ dysfunction) and hypertensive emergency (situations with impending or progressive target organ dysfunction) [27]. About 1–2% of hypertensive patients can ultimately develop a hypertensive crisis [28]. A dental patient manifesting the symptoms of hypertensive emergency must be immediately admitted to the intensive care unit for rapid blood pressure control using parenteral antihypertensives to prevent or limit the target organ damage [27 28]. In case of hypertensive urgencylow-dose oral antihypertensives are used to decrease the BP gradually over hours to days.

2.2 Whitecoat Hypertension (WCH) and Whitecoat Effect (WCE)

Whitecoat hypertension can affect 15–30% of the people with more prevalence in the older population [29]. WCH describes persistently elevated office blood pressure with normal out-of-office BP in untreated patients [30]. The whitecoat effect is different from white coat hypertension. A transient increase in blood pressure in a medical environment due to the alerting response to a doctor or nurse is whitecoat effect [31 32]. It can occur in both hypertensive patients and normotensive people.

The risk of cardiovascular events and hypertension-mediated organ damage (HMOD) is less associated with white coat hypertension. Stillit can be related to increased chances of long-term cardiovascular problemsas reported by recent studies [33 34]. Thereforepatients with whitecoat hypertension are encouraged to make necessary life modifications to reduce cardiovascular risk and undergo regular follow-up appointments with consistent out-of-office blood pressure monitoring. In additionantihypertensive drug treatment can be considered for the whitecoat hypertensive patients with a high cardiovascular risk profile [13].

3. Ischemic Heart Disease

Ischemic heart disease (IHD) or coronary heart disease (CHD) is a pathological condition characterized by a discrepancy between myocardial oxygen demand and supply due to reduced cardiac blood flow [35]. Blockage of coronary arteries due to the atherosclerotic plaque is the most common cause of IHD. Other causes include coronary artery spasmcoronary arteritisembolism or shock secondary to hypotensionetc. Due to its pathophysiologyIHD is also known as coronary artery disease (CAD).

According to WHO Global Health EstimatesIHD is the leading cause of mortality globallycausing 16% of deaths alone [36]. In additionmore than half of all the cardiovascular events in patients less than 75 years of age are due to IHD. After the age of 40the risk for developing the IHD is 49% in males and 32% in females [37]. IHD can be categorized as chronic coronary syndromes or acute coronary syndromes. Acute coronary syndromes (ACS) include unstable angina pectoris and acute myocardial infarction. Stable angina is one of the types of Chronic Coronary Syndromes (CCS).

Dental practitioners must be well aware of the significant risk factors associated with IHD and their level of control to estimate the likelihood of the dental procedure concluding uneventfully. Some non-modifiable risk factors for IHD are agemale genderfamily historyand co-morbidities like kidney disease thyroid diseaseand type I and II diabetes along with others. Howeverthe most common and modifiable risk factors include lipid disordershigh blood pressure smokingalcoholdiabetesobesityand stress [38]. In the early stagesthe disease is generally asymptomatic. Neverthelessas atherosclerosis worsens symptoms appearespecially during emotional or physical stress when oxygen demand increases. Symptoms may include fatigueshortness of breathchest pain (angina)and ankle edema.

Angina pectoris is a sudden onsetsubsternal pain in the chest due to myocardial ischemia without infarction or necrosis. The pain may radiate to the left armleft jawneckteethor back. Anginal pain radiating to the mandible can mimic the pain of dental origin. Alsothe probability of an anginal attack in a dental environment rises due to anxietyfearand pain [39]. Thusa dental practitioner must be well aware of the clinical manifestations of angina and its management in the dental clinic.

Angina is categorized as stableunstableor Prinzmetal angina.

• Stable angina is precipitated by physical exertion or emotional stress and lasts for less than 15 minutes.

• Unstable angina represents a more severe and longer-lasting form of angina that occurs at rest without evidence of necrosis.

• Prinzmetal/variant angina occurs at rest and is most likely due to coronary artery spasm.

Complete blockage of one or more coronary arteries leads to persistent ischemia and irreversible necrosis of myocardial tissueswhich eventually lead to heart attack or myocardial infarction.

Diagnosis of IHD includes assessment of symptomsresting electrocardiogram (ECG)stress ECGcoronary computed tomography angiography (CTA)stress cardiac magnetic resonance (CMR) perfusion imagingpositron emission tomography (PET) or single-photon emission computed tomography (SPECT) perfusion imaging. In additioninvasive coronary angiography (ICA) is recommended to diagnose and manage patients with a high likelihood of IHD.

Treatment of IHD comprises the following:

(1) Antithrombotic/antiplatelet therapy- low dose aspirin [40 41]clopidogrel [42]ticagrelor [43];

(2) Antianginal medication- sublingual nitroglycerin;

(3) Modification of cardiovascular risk factors [44] — reducing low-density lipoproteins (LDL)healthy dietsmoking cessationand exercise;

(4) Revascularization- percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG).

There is a high risk of recurrence of cardiovascular events in patients with myocardial infarction (MI). Previous AHA guidelines recommended that any dental surgery within six months of MI should be avoided due to the high risk of complications during this duration [45]. The emerging evidence in cardiovascular disease management advocates that no elective dental care should be given within 30 days of MI. Any emergency care during this period should be given after the physician’s consultation and in a hospital-based setup. After one monthif the patient is symptom-freeelective dental care can be provided with caution [18].

Patients with angina or a history of myocardial infarction are managed similarly in a dental setup. Though patients with unstable angina must be immediately referred to a physicianstable angina patients can be safely provided with elective dental care. Short morning appointments are preferred. This view has been rebuttedand early morning or late afternoon appointments are advised to be avoided in IHD patients [46]. Fearpainanxietyand stress can precipitate angina and must be kept to a minimum during the dental visit of an IHD patient. Administration of oral anxiolyticsnitrous oxide or intravenous sedationand maintaining profound local anesthesia with long-acting anesthetics like bupivacaine minimize the release of endogenous catecholamines. Vasoconstrictors should be used sparingly as their absorption can increase the heart rate. Using 1:100,000 or lesser concentrations of vasoconstrictor and avoiding intravascular injection with proper aspiration are advisable. It is recommended not to use more than one (2 mL) or two cartridges (4 mL) of 2% lidocaine with 1:100,000 epinephrine (0.018 to 0.036 mg of adrenaline) for dental procedures in patients with cardiovascular disease [23 47].

If an IHD patient develops chest pain during the dental procedure and angina is suspectedthe procedure should be discontinuedand short-acting nitrates along with oxygen should be administered immediately. 0.3–0.6 mg nitroglycerine tablet can be given sublingually and repeated every 5 minutes until the patient is relieved [48]. Emergency medical assistance must be summoned after three doses (in 15 minutes) if the anginal pain continues.

IHD patients are generally on antiplatelets or anticoagulantsand therefore care must be taken in case of excessive bleeding during the dental procedure by local hemostatic techniques. Discontinuation of these medications to perform minor surgical procedures is not recommended [49 50]. If the patient is on anticoagulantsthe International Normalized Ratio (INR) should be measured preferably within 24 hours before the procedure. A minor dental surgical procedure can be done safely with INR values in the range of 2.0–4.0 when local measures to control the bleeding are used [51 52 53 54 55 56 57]. If INR is more than 4.0 no surgical intervention should be performed without the cardiologist’s consultation.

4. Valvular Heart Diseases

Valvular heart disease (VHD) is a cardiovascular disease caused due to damage or disease of heart valves. 2.5% of the US population has moderate to severe VHD and its prevalence increases with age [58]. Various forms of VHD include Degenerative valve diseaseRheumatic heart disease (RHD)and Congenital valve disease [59]. RHD is a common form of heart disease in developing nations while degenerative valve disease is more common in developed countries [60]. Common valvular disorders are aortic stenosisaortic regurgitationmitral stenosis and mitral regurgitation. 2020 ACC/AHA Guidelines for the management of patients with VHD classified the progression of VHD into 4 stages (Table 1) [58].

Table 1.

Classification of Progression of VHD [58].

Stage	Definition
A	At-risk
B	Progressive
C	Asymptomatic severe
D	Symptomatic severe

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Advanced valvular damage causes cardiac dysfunction leading to an increased risk of arrhythmiainfective endocarditisstrokeand heart failure [61]. Due to the increased number of VHD patients visiting dental care centersit has become imperative for dentists to have adequate knowledge of this disease for the safe and effective management of these patients. It is important to identify VHD before performing any dental procedure to avoid the risk of infective endocarditis (IE)risk of excessive bleeding due to anticoagulantsand worsening of the coexisting heart failure [62].

Dentists can play a vital role in the management of VHD and reducing the risk of complications like IEstrokeand heart failure which can be fatal for affected patients [63 64]. This can be done through regular dental checkupspatient educationand proper oral hygiene maintenance for these patients which minimize the risk of bacteremia caused by daily activities such as brushing and flossing [65]. In factmaintaining good oral hygiene remains the most important element in preventing IE in VHD patients [58].

4.1 Prosthetic Valves

Most patients with severe VHD need intervention for the valve which includes valve repair or valve replacement (prosthetic valve) of the diseased valve. Prosthetic valves can be mechanical or biological (also called bio-prosthetic valves). Mechanical valves are more durable than bio-prosthetic valves but need lifelong anticoagulants such as warfarin and aspirin. Though all prosthetic valves come along with a risk of thromboembolismbio-prosthetic valves are less thrombogenic than mechanical valves. The optimum INR range of anticoagulation for mitral mechanical valves is 2.5–3.5 while for aortic valves is 2–3 [66]. Thrombogenicity of older prosthetic valves is known to be higher and needs INR of up to 4 [66]. The main clinical implications for patients having prosthetic valves during dental treatment are (a) the need for antibiotic prophylaxis against infective endocarditis and (b) perioperative anticoagulation management [62].

Patients with prosthetic valves need proper dental care with appropriate antibiotic prophylaxis to prevent infective endocarditis. Patients with mechanical valves or high-risk patients with bio-prosthetic valves need appropriate anticoagulation with warfarin and aspirin. Anticoagulation in low-risk patients with bio-prosthetic valves can be managed by aspirin alone [67]. Most dental procedures involve minor bleeding which can be controlled easily and do not require cessation of anticoagulation therapy. They can be performed with an INR of up to 4.0. When anticoagulation cessation is necessary for patients with a high risk of thromboembolism like patients with the mechanical valve but no risk factorswarfarin can be stopped 48–72 hours prior to the procedure (so INR falls below 1.5) and reinitiated within 24 hours of the procedure after control of active bleeding [68 69 70]. In mechanical valve patients with the presence of risk factorswarfarin can be stopped 72 hours prior to the procedure and when INR falls below 2.0heparin can be started which can be stopped 4–6 hours before the procedure [71]. Anticoagulants are restarted immediately after active bleeding control till therapeutic INR is reached again. Irrespective of the discontinuation of anticoagulation or notINR must be recorded before any dental procedure involving significant bleeding [62]. The risk of reducing INR must be weighed against the risk of thromboembolism in consultation with the patient’s physician. Every attempt must be made to control the bleeding even after procedures like extraction or periodontal surgeries using local measures such as suturingoxidized cellulosegelatin spongethrombin and tranexamic acid mouthwashes [62].

4.2 Infective Endocarditis

Infective endocarditis (IE) is an infection of the endocardial surface of the heartwhich may involve one or more than one heart valve [72]. It can affect both native and prosthetic valves. The infection is usually seen in previously damaged heart valves or tissues. This disease has a low incidence but a high overall mortality rate. Thusprimary prevention and proper diagnosis are the main management strategies for this life-threatening disease. In industrialized countriesthe estimated annual incidence of IE is 3 to 9 cases per 100,000 individuals [73 74 75 76]. In-hospital mortality of this disease is 15–22% [77 78] and the 5-year mortality rate is around 40% [79].

Infective endocarditis is predominantly a bacterial infection with 80% of the cases caused due to streptococci and staphylococci. Formerlyaround 60% of native infective endocarditis cases were caused by streptococci. Now staphylococci are more commonly associated with several forms of IE [78 80]. IE is more commonly observed among patients with prosthetic valvesmitral valve prolapsecongenital heart diseasesintracardiac devicesrheumatic heart diseaseinfective endocarditis historyor a history of cardiac valve surgery [81]. Prosthetic valve patients with Staphylococcus aureus IE have a high mortality rate of 40% or more [73].

The healthy valvular endothelium is resistant to microbial colonization but damaged valvular endothelium gets colonized by the circulating bacteria in the bloodstream forming infective vegetation and causing infection. The presence of valvular vegetation is a major criterion in the diagnosis of IE. Severe complications of IE include sepsisparavalvular extensionembolic events strokeand heart failure. Management includes prolonged intravenous antibiotics and valvular surgery [82].

Various dental therapies and other invasive procedures have been commonly and controversially linked to implanting of bacteria in the heart valves leading to IE. Although IE does not pose an emergency in dental clinicsit is generally associated with significant morbidity and mortality. Any dental procedure that aggravates the bleeding and transfers oral bacteria to the bloodstream is an invasive dental procedurefor example scalingperiodontal therapyexodontia or any soft tissue surgery. The prevalence of transient bacteremia widely varies for different dental procedures: scaling and root planing (8%–80%)dental extraction (10%–100%)periodontal surgical procedure (36%–88%)and endodontic procedures (up to 20%) [83 84 85 86 87 88 89]. Even non-invasive dental procedures such as local anesthesiaband placementand regular practices like tooth brushing and flossing (20–68%)toothpick use (20–40%)and chewing food (7–51%) can cause transient bacteremia [87 88 89 90 91 92 93]. Thusthe degree of cumulative bacteremia due to routine daily activities is far greater than the infrequent episodes of bacteremia caused by dental procedures.

Since 1955several recommendations have been made by various expert committees and societies for antibiotic prophylaxis in preventing IE secondary to dental procedures [94]. These guidelines were based on the viewpoint that antibiotic prophylaxis can reduce or eliminate the bacteremia caused by dental or other invasive procedures and prevent IE. Howeverthese recommendations were based on expert opinions and clinical experiences rather than double-blinded randomized controlled clinical trials. No controlled studies have revealed that antibiotic prophylaxis has decreased the incidence of IE. In factfor many patientsthe adverse effects of antibiotic prophylaxis outweigh its benefits. Injudicious antibiotic use can lead to the development of resistant organismsdrug toxicity and excessive treatment cost [58].

A Cochrane Database systematic review in 2013 concluded that there is no evidence to ascertain that antibiotic prophylaxis is effective or ineffective in the prevention of IE following dental procedures [95]. In 2017 an extensive systematic review and meta-analysis was conducted by Cahill TJ et al. [96] which could not definitely conclude the effectiveness of antibiotic prophylaxis due to limited evidence. The lack of a strong evidence base in favor of antibiotic prophylaxis to prevent IE led to a major revision of AHA guidelines in 2007 wherein the writing committee recommended antibiotic prophylaxis only for the small subcategory of patients who are at the highest risk of developing IE [81]. UK National Institute for Health and Care Excellence (NICE) in 2008 also updated its guidelines and no longer recommended the use of antibiotic prophylaxis in the prevention of IE [97]. Howeverin 2016 NICE changed its guidelines which do not recommend antibiotic prophylaxis routinely for patients undergoing dental treatment [98]. According to this update antibiotic prophylaxis may be appropriate for selected cases where the dentist perceives the risk of IE to be high or the patient prefers to have the prophylaxis.

According to the American Heart Association guidelines 2007cardiac conditions which have the highest risk of adverse outcome from IE include those with prosthetic cardiac valve or prosthetic material used for cardiac valve repair history of IEcongenital heart disease (CHD)and cardiac transplant recipients developing cardiac valvulopathy [81 99]. For patients with the aforementioned cardiac conditionsantibiotic prophylaxis is rational for all dental procedures that involve gingival or periapical tissue manipulation or oral mucosal perforation. Prophylaxis is not required for dental procedures such as anesthetic injection through non-infected tissuesdental radiographssuture removal biopsiesplacement or adjustment of orthodontic or removable prosthodontic appliancesand putting orthodontic brackets [81 99].

Antibiotic prophylaxis is usually given in a single dose 30 to 60 minutes before the dental procedure but can be given up to 2 hours after the procedure. Amoxicillin is the drug of choice for adults (2 grams) and children (50 mg/kg) [81 99]. For adult patients with amoxicillin allergyazithromycin (500 mg)/clindamycin (600 mg)/clarithromycin (500 mg) or first or second-generation oral cephalosporin like cephalexin (2 grams) can be administered [81 99]. Patients who are unable to take oral medications can be given ampicillin ceftriaxoneor cefazolin intramuscularly (IM) or intravenously (IV). For patients who are allergic to ampicillin and cannot take oral medications - parenteral ceftriaxonecefazolinor clindamycin are recommended [81 99]. The latest American Heart Association scientific statement (2021) recommends that in individuals with allergies to amoxicillin or ampicillin drugsclindamycin must no longer be used as an oral or parenteral alternative as it may cause more frequent and severe drug reactions [99].

There is still a dearth of substantial scientific evidence to prove that dental procedures cause IE in patients with underlying cardiac conditions and antibiotic prophylaxis is worthwhile in preventing IE [81 99]. Even 100% effective antibiotic prophylaxis can prevent only a small number of IE cases. The majority of the IE cases are caused due to bacteremia from routine daily activities including brushingflossingand chewing. There must be a fundamental change in the management of patients at high risk of IE by shifting the focus from antibiotic prophylaxis and dental procedures towards access to proper dental care and maintenance of optimal oral health.

5. Anticoagulants

Anticoagulant therapy or antithrombotic therapy has been used widely to manage various cardiovascular conditions including myocardial infarctionstrokeand deep vein thrombosis [100]. The patients on anticoagulant therapy should be handled with proper care and in consultation with the patient’s physician. The patients on anticoagulant medication and undergoing a dental procedure that involves low to medium risk of bleeding can be effectively managed by local hemostatic measures. AHA/ACC/ADA/ESC/SCAI/ACCP guidelines do not suggest the cessation of antiplatelet therapy for procedures involving a low risk of bleeding [101 102 103].

The ratio of the patient prothrombin time to the mean prothrombin time raised to the power of international sensitivity index (ISI) value is the INR of the patient. It determines the anticoagulation status of a patient [104].

INR=\left(\frac{\text{ Patient }PT}{MeanPT}\right)^{ISI}

It is warranted to know the INR value of a patient on anticoagulation therapy before a dental procedure. It is recommended to check the INR 72 hours prior to an invasive dental procedure in a patient taking long-term anticoagulant therapy and stably anticoagulated on warfarin [105]. A physiologically normal patient has an INR value of 1and a therapeutic range of 2.0 to 3.0 is considered safe for most indications due to the reduced risk of thromboembolic events [106]. In the case of prosthetic heart valvesa higher INR range of 2.5–3.5 is required [107]. Guidelines on the management of patients on oral anticoagulant therapy (2007) recommend not to discontinue the anticoagulants in patients with stable INR in the range of 2.0–4.0 as the risk of significant bleeding is low for most outpatient dental procedures [105]. American Academy of Oral Medicine (AAOM) Clinical Practice Statement 2016 stated that an INR value of 3.5 (up to 4.0 by some experts) is safe for moderately invasive dental surgical procedures like simple tooth extractions [108]. For non-invasive dental proceduresthere is no need to maintain this safety margin [109].

If INR is above 3.5then the dental procedures should be done with a medical professional consultation weighing the risk of thromboembolism [66]. In the case of novel non-VKA (non-vitamin K antagonists) and natural/direct anticoagulant therapy (NOAC/DOAC)no discontinuation of the anticoagulant is recommended for low bleeding risk procedures. These procedures can be effectively performed 18–24 hrs after the last dose and anticoagulant can be restarted after 6 hrs of treatment. The medication discontinuation during the medium-risk procedure should be in close communication with the patient’s physician [66 103]. In cases of combined anticoagulant and antiplatelet therapy or triple therapy with 2 antiplatelets and one anticoagulantconsult the patient’s physician for individualized management [66]. The risk of thrombosis on temporary discontinuation of anticoagulants is small but life-threatening. Thusthe benefits of discontinuing anticoagulants must always be weighed against the risk of fatal thromboembolic events in consultation with the responsible medical professional.

5.1 Warfarin Therapy

Warfarina vitamin K antagonistis one of the most common oral anticoagulants used for the prevention and treatment of thromboembolism for more than 50 years. In terms of INRwarfarin has a therapeutic index of 2.0–3.0 [110]. Factors like narrow therapeutic range along with drug-drug and drug-food interactions limit its use. Over the yearsdentists have practiced various perioperative bleeding management strategies for patients on anticoagulant therapy which ranged from continuing the regular dose of anticoagulant to reducing the dose to complete halting or using a bridging anticoagulant like heparin [111]. Dental procedures are generally categorized as low bleeding risk procedures and studies have concluded that anticoagulation therapy can be safely continued for most of these procedures including dental extractions [112]. The risk for embolic events after dental surgery appears to vary from 0.02 to 1%. According to a systematic review and meta-analysis (2009) while performing minor dental procedurescontinuing the regular warfarin dose does not cause increased bleeding when compared with adjusting or discontinuing its dose [113]. A 2015 systematic review concluded that for patients undergoing dental extractions a regular dose of warfarin can be continued if INR is within the therapeutic range [114]. The benefits of warfarin therapy discontinuation must be weighed carefully against the risk of thromboembolism. If deemed essential warfarin must be discontinued five days before major surgery and restarted 12–24 hours postoperatively [115]. INR must be measured a day before surgery to monitor adequate reversal of anticoagulation [116]. When warfarin therapy is discontinued in patients with an initial INR of 2.0–3.0 for about 4 to 5 days the INR falls to the normal range (less than 1.5) on the day of surgery which is considered safe for dental procedures and associated with acceptable risk of perioperative bleeding [117]. The INR reaches the therapeutic range (2.0) after around 3 days of restarting the warfarin therapy [116 118 119] (Fig. 1). These patients have a subtherapeutic INR for approximately 2–3 days preoperatively and 2 days after surgery during which they are at risk of a thromboembolic event [116 120].

Fig. 1. — **Perioperative Warfarin therapy management**. Discontinuing warfarin for 4–5 days reduces the INR below 1.5 which is safe for dental surgical intervention. After restarting warfarinit takes around 3 days for INR to reach a therapeutic level of 2 before which there is an increased risk of thromboembolism.

There have been reports of patients experiencing fatal or non-fatal thromboembolic events due to the stoppage of oral anticoagulation for dental treatment [56]. Howeverthe majority of the patients had no severe effects. According to Todd et al. (2005) [121]an individualized approach to patients’ systemic conditions by acquiring proper history would be a rational approach in treating patients on warfarin therapy.

5.2 Direct Oral Anticoagulants (DOACS)

The classically used anticoagulant agents are the dicumarinic agents such as Warfarin (Coumadin®) and the acenocoumarol. The disadvantage of these agents is the need of dose adjustment for each patienttheir interaction with the consumed foodsand a need to monitor the international normalized ratio (INR) regularly. To overcome these drawbacksdirect oral anticoagulants (DOACs) are being used nowadays [122]. DOACs are also known as New Oral Anticoagulants (NOACs) and common examples are apixabanrivaroxabandabigatran etexilateand edoxaban [122].

The newer agents do not require regular monitoring of anticoagulation and dose adjustment. Studies have also shown no need for NAOC therapy interruption for most dental treatments due to a low incidence of bleeding complications with NAOCs [123 124]. Howeverthe disadvantages of newer agents are higher cost absence of proper reversal protocolsand lack of post-marketing clinical trials [125].

The risk of bleeding and adjustment of anticoagulant therapy with newer drugs depend on the type of dental procedure. Low-risk procedures have lesser chances of bleeding and include simple restorationslocal anesthetic administration supragingival scalingand single-tooth extraction. Moderate risk procedures include extraction of 2 to 4 teeth and gingival surgery of up to 5 teeth. High-risk procedures are associated with a higher risk of bleeding and comprise extracting $\geq$ 6 teethgeneralized gingival surgery of $\geq$ 6 teethand multiple dental implant placement [126]. According to the available evidenceDOAC therapy can be continued safely for low-to-medium risk dental procedures as the involved risk of bleeding is low. In case bleeding occurs local hemostatic measures can be used to manage it [125]. It is recommended not to perform these dental procedures during the peak concentrations of DOAC therapy but close to the end of the dosing cycle. Another alternative is to administer the DOAC after the procedure instead of before or perform the procedure 12–24 hours after the DOAC administration. In case of invasive or surgical dental procedure involving moderate to high risk of bleedingit is recommended by manufacturers to discontinue edoxaban and rivaroxaban 24 hours prior and apixaban 48 hours before the procedure [127 128 129]. If discontinuation of DOAC is necessaryit should be reinitiated on the same day of the dental procedure. Overallthere is limited evidence at hand on the dental management of patients taking NAOCs and further studies are strongly recommended.

5.3 Bleeding Complications

The commonly used anticoagulants or the antiplatelets are the clopidogrel (Plavix®)ticlopidine (Ticlid®)prasugrel (Effient®)ticagrelor (Brilinta®)and/or asprin.The antiplatelet or anticoagulant therapy during the dental treatment increases the risk of bleeding which can be significant but generally not serious. Anticoagulants or antiplatelet drugs need not be stopped for procedures that induce minor bleedingsuch as bridge placementthree teeth removaland scaling procedures [54 130]. If multiple extractions are plannedit has to be performed three teeth at a time in multiple visits choosing the most affected at the first visit [130 131]. Most cases of perioperative or postoperative bleeding can be managed by minimizing the surgical traumalimiting the area of surgery primary closure of the surgical wound with suturesapplying pressure with gauze for 15–30 minutesor using local hemostats such as tranexamic acid-soaked bite swabsgelatin spongeEACA (Epsilon amino caproic acid)4.8% tranexamic acid mouthwash (4 times a day for 2 minutes1–2 days postsurgery)calcium sulfate (CaS)fibrin spongeautologous fibrin glueresorbable oxycellulose dressing and N-butyl-2-cyanoacrylate glue (NBCA) [132 133 134 135]. The incidence of bleeding that local hemostatic methods could not manage ranges from 0 to 3.5% [57 136].

Postoperative measures for the patients on oral anticoagulants to prevent bleeding include adequate restingno vigorous rinsing or sucking; avoiding hot or hard foodstuffs that can disturb the socket with the tongue or any foreign object [137]. NSAIDs and COX-2 inhibitors should not be prescribed for analgesia to patients taking antithrombotic medications [135].

6. Arrhythmias

Cardiac arrhythmia or dysrhythmia can be described as a disturbance in the generation or conduction of cardiac electrical impulses which causes improper heart functioning [18]. Common heart rhythm abnormalities include premature atrial or ventricular beatssinus bradycardiaand sinus tachycardia [138 139]. The most common sustained cardiac arrhythmia found clinically is atrial fibrillation (AF) with approximately 46.3 million patients suffering from it globally [140]. Its incidence increases with obesity [140] and agewith 9% of the patients above 80 years having AF [141].

Dysrhythmia can be present in healthy peoplepatients on certain medications with cardiovascular problemsor other systemic diseases. Many individuals with arrhythmia are asymptomaticand the abnormality is generally found during a routine examination. Howeverothers can present a variety of symptoms like dizzinessshortness of breathweaknesssyncopeand chest pain (angina). Elderly patients with compromised cardiac conditions can even develop myocardial ischemiashockor congestive heart failure due to arrhythmia [142 143 144 145].

Patients with certain cardiac arrhythmias like atrial fibrillation have more chances of having ischemic events during stressful dental treatment or when excessive local anesthesia with a vasoconstrictor is administered. In addition the association of arrhythmias with various systemic diseases and their potentially life-threatening nature make it imperative for dentists to identify and adopt appropriate measures to manage this cardiac problem promptly and effectively.

Arrhythmias are generally managed by antiarrhythmic drugscardiac pacemakers cardioversionor surgical intervention. Beta-blockers and calcium channel blockers are the most frequently prescribed medications. Howeverthese drugs are associated with oral side effects like xerostomia and gingival overgrowth. These patients may seek attention from the dentist due to abnormal gingiva appearance (gingival enlargement)bleedingpain in the gumsor dryness of mouthand must be treated with caution. Cardiac pacemakers and automatic implantable cardioverter defibrillators (AICD) detect abnormal heart rhythm and help to restore the normal rhythm [146]. Cardioversion is the restoration of the sinus rhythm of the heart using medications or electric shock [147].

Identification of the patients with arrhythmia or those susceptible to developing arrhythmiaobtaining a detailed medical historyassessing vital signsand consultation with the patient’s physician are vital steps to prevent the development of any severe complication during or after dental treatment. High-risk patients must be referred to a well-equipped hospital facility. In a dental officestress and anxiety must be minimized to prevent the precipitation of arrhythmia. This can be achieved by premedication like short-acting benzodiazepines the night before or one hour before the appointment or by using nitrous oxide-oxygen inhalation.

Short morning dental appointments with a simple treatment plan are preferred. Local anesthetics with vasoconstrictors must be used judiciously as excessive epinephrine can precipitate arrhythmia or other unwanted cardiovascular complications [139 148 149]. The amount of vasoconstrictor should not exceed 0.04–0.054 mg per appointment [45]. In additionvasoconstrictors like epinephrine are contraindicated in patients with refractory arrhythmias and must be used carefully in patients having implanted defibrillators or pacemakers [150].

There has been conflicting evidence in the literature regarding potential electromagnetic interference by electronic dental instruments like ultrasonic scalersapex locatorsand electrosurgical units in the functioning of cardiovascular implantable electronic devices (CIEDs) like pacemakers or implantable defibrillators. Many earlier in-vitro studies have found that dental electronic devices interfere with the functioning of CIEDs. Miller et al. [151] reported significant electromagnetic interference by electrosurgery unitsultrasonic bath cleanersand ultrasonic scaling devices with pacemakers in a dental setup. Older pacemakers were unipolar and unshielded or poorly shielded. The newer ones are bipolar with better shielding which lowers the risk of malfunction due to electromagnetic interference [146].

Electric pulp testersdental handpiecesamalgamatorscuring lightsand sonic scalers have been reported to be safer [151]. Alsopiezoelectric scalers are safer to use than magnetostrictive devices in patients with CIEDs [152 153 154]. Antibiotic coverage is not advocated by American Heart Association (AHA) for patients using devices like pacemakers and automatic defibrillators during invasive dental treatment [155]. Studies mention that an increased likelihood of electromagnetic interferences is seen if the device comes within 37.5 cm of the CIED or lead wire [151].

Arrhythmia patients may receive anticoagulant therapyand therefore it becomes crucial for the dentist to determine the level of anticoagulation prior to any invasive procedure. Most dental procedures (including minor oral surgical procedures) can be performed if the International Normalized Ratio (INR) is 3.5 or less on the day of the procedure [156]. If the patient develops arrhythmia during dental treatmentthe procedure should be deferredand the patient must be urgently referred for medical evaluation. Oxygen should be providedand the patient’s vital signs like body temperaturepulserespiratory frequencyand blood pressure should be assessed. Loss of consciousness or collapse may indicate life-threatening arrhythmia or cardiac arrestand emergency medical services must be activated immediately. Performing vagal maneuvers and placing the patient in Trendelenburg’s position can be helpful [146]. If no pulse is detected cardiopulmonary resuscitation must be initiated using an automated external defibrillator without any delay.

7. Use of Local Anaesthetics with Vasoconstrictor

Dental treatment is often associated with painfearand anxiety. Stress and anxiety may lead to exaggerated endogenous catecholamine release from the adrenal medullacausing hemodynamic disturbances [157 158]. In patients with underlying cardiovascular pathologies like hypertensive heart diseaseischemic heart diseasearrhythmiasor heart transplantation patientsinadequate local anesthesia may cause massive endogenous adrenaline release provoking cardiovascular complications. Sopain control and stress reduction are essential for patients undergoing dental treatmentparticularly those with underlying cardiac disease.

Local anesthetics with vasoconstrictors (like epinephrine) in dentistry impart prolonged anesthesiareduced systemic toxicityand optimal bleeding control [159 160]. Though the use of epinephrine in local anesthetics is common for healthy patientsits use is still debatable for cardiac patients due to its potential risk of causing unwanted cardiovascular effects. Howevermany authors have reported no clinically significant hemodynamic changes during dental treatment in healthy people or patients with mild to moderate coronary disease [22 161 162 163 164 165].

The dose of vasoconstrictor used in dental treatment is significantly less than the dose used during the treatment of anaphylaxis for cardiac arrest. For exampleone cartridge of local anesthetic of 1.8 mL in volume with 1:100,000 epinephrine contains only 0.018 mg of vasoconstrictor [166]. This small amount of vasoconstrictor used in dentistry poses little risk than the more significant risk from the massive endogenous epinephrine release due to improper control of pain and anxiety during dental treatment in cardiac patients. Thusif administered carefully with aspirationthe concentration and amount of vasoconstrictor used in dentistry are generally not contraindicated for cardiac patients. Howeverit is better to use the lowest possible dose of vasoconstrictor to achieve adequate local anesthesia while treating patients with “stable” cardiac problems. Thereforeup to 0.04 mg or 40 $\mu$ g of epinephrinei.e.one or two carpules of 1.8 mL anesthetic solution with epinephrine 1:100,000 concentration is safe for controlled hypertensives and/or coronary disease patients [22 167].

Heart conditions that contraindicate the use of vasoconstrictors in dentistry include [168]:

(a) Unstable angina

(b) Recent myocardial infarction

(d) Refractory arrhythmias

(e) Untreated or uncontrolled severe hypertension

(f) Untreated or uncontrolled congestive heart failure

Alsoit is contraindicated to use epinephrine impregnated retraction cords intraligamentaryand intrabony injections in these patients due to adverse hydrodynamic effects similar to I.V. epinephrine injection [168]. Though local anesthetics can lead to a decrease in the rate of amide metabolism in hypertensive patients taking beta-blockers [15]generally non-epinephrine-containing local anesthetics do not have significant drug interactions [169]. Drug interactions mostly stem from the incorporated vasoconstrictor [169]. For exampleepinephrine can interact with commonly used antihypertensives like non-selective beta-blockers causing significant hypertensive episodes [170] and reflex bradycardia [15]. Though the response is dose-dependent and rarely seen in dental clinicsthe dentist must be careful in using vasoconstrictors in patients with significant cardiac disease due to the serious sequelae of this drug combination. Agents like clonidine [171] and dexmedetomidine [172] can be used as safer alternatives to epinephrine with the local anesthetic solution in hypertensive patients. In such patientsit can also be prudent to use lidocaineprilocaineand mepivacaine solutions without vasoconstrictor [173].

8. Conclusions

Dental treatmentalthough considered safecan be life-threatening if medical problems of the patientespecially cardiac disorders are ignored. A thorough medical and drug history from each patient at every appointment and extensive knowledge of the risk factors and clinical manifestations of various cardiac diseases can prevent many medical adversities in the dental clinic. A comprehensive treatment plan formulated in collaboration with the patient’s cardiologist can help avoid potential hazards during dental treatment for a cardiac patient. All drug prescriptionssurgical interventionsand overall management strategies should conform to the latest guidelines and protocols available.

Dentists should also identify and judiciously manage any medical emergency that can occur while the patient is on the dental chair. Stress before and during dental treatment is normal for any patientbut it can cause medical complications in cardiac patients. So pharmacologic agents can be prescribed to induce relaxation and reduce stress in these patients. Alsomorning appointments should be preferred as mornings are more relaxingand in case of any unforeseen situationthere is sufficient time to manage it.

Comprehensive knowledge of the dentist about cardiac conditions with multidisciplinary planning supported by an evidence-based approach is indispensable in imparting quality and safe dental care to this vulnerable cohort of dental patients.

Acknowledgment

We acknowledge the support of Rahul Taneja for their guidance throughout this project.

Footnotes

Publisher’s Note: IMR Press stays neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Author Contributions

KGVT and SK conceptualized the research. KGVTSKMAKGASand FP helped in data acquisitioninterpretationand manuscript preparation. KGVTSKMAK GASFPMAZSMAMAAand SC helped in drafting the manuscriptrevised their part criticallytake public responsibility for their part and agreed to be accountable for all aspects of the work. All authors contributed to editorial changes in the manuscript and approved the final manuscript to be published.

Ethics Approval and Consent to Participate

Not applicable.

Funding

This research received no external funding.

Conflict of Interest

The authors declare no conflict of interest.

References

[1].Mozaffarian DBenjamin EJGo ASArnett DKBlaha MJCushman Met al. Heart Disease and Stroke Statistics-2016 Update: A Report From the American Heart Association. Circulation . 2016;133:e38–e360. doi: 10.1161/CIR.0000000000000350. [DOI] [PubMed] [Google Scholar]
[2].The World Health Organization Cardiovascular diseases (CVDs) 2021. [(Accessed: 20 March 2022)]. Available at: https://www.who.int/news-room/fact-sheets/detail/cardiovascular-diseases-(cvds)
[3].Anderson LThompson DROldridge NZwisler ADRees KMartin Net al. Exercise-based cardiac rehabilitation for coronary heart disease. Cochrane Database of Systematic Reviews . 2016;2016:CD001800. doi: 10.1002/14651858.CD001800.pub3. [DOI] [PMC free article] [PubMed] [Google Scholar]
[4].Al-Turki OAl-Hussyeen AAl-Hammad NAlhowaish LAlmaflehi N. Medical Emergencies In Dental Practice. Journal of Dental and Medical Sciences . 2017;16:1–9. [Google Scholar]
[5].Kufta KSaraghi MGiannakopoulos H. Cardiovascular considerations for the dental practitioner. 2. Management of cardiac emergencies. General Dentistry . 2018;66:49–53. [PubMed] [Google Scholar]
[6].Anders PLComeau RLHatton MNeiders ME. The Nature and Frequency of Medical Emergencies among Patients in a Dental School Setting. Journal of Dental Education . 2010;74:392–396. [PubMed] [Google Scholar]
[7].Stanaway JDAfshin AGakidou ELim SSAbate DAbate KHet al. Globalregionaland national comparative risk assessment of 84 behaviouralenvironmental and occupationaland metabolic risks or clusters of risks for 195 countries and territories1990–2017: a systematic analysis for the Global Burden of Disease Study 2017. The Lancet . 2018;392:1923–1994. doi: 10.1016/S0140-6736(18)32225-6. [DOI] [PMC free article] [PubMed] [Google Scholar]
[8].Gupta RGaur KSRam CV. Emerging trends in hypertension epidemiology in India. Journal of Human Hypertension . 2019;33:575–587. doi: 10.1038/s41371-018-0117-3. [DOI] [PubMed] [Google Scholar]
[9].Hogan JRadhakrishnan J. The Assessment and Importance of Hypertension in the Dental Setting. Dental Clinics of North America . 2012;56:731–745. doi: 10.1016/j.cden.2012.07.003. [DOI] [PubMed] [Google Scholar]
[10].Southerland JHGill DGGangula PRHalpern LRCardona CYMouton CP. Dental management in patients with hypertension: challenges and solutions. ClinicalCosmetic and Investigational Dentistry . 2016;8:111–120. doi: 10.2147/CCIDE.S99446. [DOI] [PMC free article] [PubMed] [Google Scholar]
[11].Whelton PKCarey RMAronow WSCasey DECollins KJDennison Himmelfarb Cet al. 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/ PCNA Guideline for the PreventionDetectionEvaluationand Management of High Blood Pressure in Adults: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Circulation . 2018;138:e426–e483. doi: 10.1161/CIR.0000000000000597. [DOI] [PubMed] [Google Scholar]
[12].Whelton PKCarey RMAronow WSCasey DECollins KJDennison Himmelfarb Cet al. 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/ PCNA Guideline for the PreventionDetectionEvaluationand Management of High Blood Pressure in Adults: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Circulation . 2018;138:e484–e594. doi: 10.1161/CIR.0000000000000596. [DOI] [PubMed] [Google Scholar]
[13].Williams BMancia GSpiering WAgabiti Rosei EAzizi MBurnier Met al. 2018 ESC/ESH Guidelines for the management of arterial hypertension. European Heart Journal . 2018;39:3021–3104. doi: 10.1093/eurheartj/ehy339. [DOI] [PubMed] [Google Scholar]
[14].Whelton PKCarey RMAronow WSCasey DECollins KJDennison Himmelfarb Cet al. 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/ PCNA Guideline for the PreventionDetectionEvaluationand Management of High Blood Pressure in Adults: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Hypertension . 2018;71:e13–e115. doi: 10.1161/HYP.0000000000000065. [DOI] [PubMed] [Google Scholar]
[15].Bavitz JB. Dental Management of Patients with Hypertension. Dental Clinics of North America . 2006;50:547–562. doi: 10.1016/j.cden.2006.06.003. [DOI] [PubMed] [Google Scholar]
[16].National Heart Lung and Blood Institute . In Brief: Your Guide To Lowering Your Blood Pressure With DASH . National HeartLung and Blood Institute; 2015. pp. 1–6. [Google Scholar]
[17].Popescu SMScrieciu MMercuţ VŢuculina MDascălu I. Hypertensive Patients and their Management in Dentistry. ISRN Hypertension . 2013;2013:1–8. [Google Scholar]
[18].Patton LLGlick M. The ADA Practical Guide to Patients with Medical Conditions. 2nd edn . Wiley & Sons; New Jersey: 2015. [Google Scholar]
[19].Little JW. The impact on dentistry of recent advances in the management of hypertension. Oral SurgeryOral MedicineOral PathologyOral Radiologyand Endodontology . 2000;90:591–599. doi: 10.1067/moe.2000.109517. [DOI] [PubMed] [Google Scholar]
[20].Hupp WS. Cardiovascular Diseases. In: Patton LLGlick Meditors. The ADA Practical Guide to Patients with Medical Conditions. 2nd edn . John Wiley & Sons; New Jersey: 2015. pp. 25–42. [Google Scholar]
[21].Rose LFMealey BMinsk LCohen DW. Oral care for patients with cardiovascular disease and stroke. The Journal of the American Dental Association . 2002;133:37S–44S. doi: 10.14219/jada.archive.2002.0378. [DOI] [PubMed] [Google Scholar]
[22].Seminario-Amez MGonzález-Navarro BAyuso-Montero RJané-Salas ELópez-López J. Use of local anesthetics with a vasoconstrictor agent during dental treatment in hypertensive and coronary disease patients. a systematic review. Journal of Evidence Based Dental Practice . 2021;21:101569. doi: 10.1016/j.jebdp.2021.101569. [DOI] [PubMed] [Google Scholar]
[23].Moodley DS. Local anaesthetics in dentistry-Part 3: Vasoconstrictors in local anaesthetics. South African Dental Journal . 2017;72:176–178. [Google Scholar]
[24].Moore PAHersh EV. Local Anesthetics for Dentistry. In: American Dental Associationeditor. ADA Dental Drug Handbook: A Quick Reference . American Dental Association; Chicago: 2019. pp. 65–76. [Google Scholar]
[25].Whalen KFinkel RPanavelil TA. Lippincott Illustrated Reviews: Pharmacology. 6th edn . Wolters Kluwer; Philadelphia: 2015. [Google Scholar]
[26].Little JMiller CRhodus N. Dental Management of the Medically Compromised Patient. 6th edn . Mosby; St. Louis: 2002. [Google Scholar]
[27].Chobanian AVBakris GLBlack HRCushman WCGreen LAIzzo JLet al. Seventh Report of the Joint National Committee on PreventionDetectionEvaluationand Treatment of High Blood Pressure. Hypertension . 2003;42:1206–1252. doi: 10.1161/01.HYP.0000107251.49515.c2. [DOI] [PubMed] [Google Scholar]
[28].Varounis CKatsi VNihoyannopoulos PLekakis JTousoulis D. Cardiovascular Hypertensive Crisis: Recent Evidence and Review of the Literature. Frontiers in Cardiovascular Medicine . 2017;3:51. doi: 10.3389/fcvm.2016.00051. [DOI] [PMC free article] [PubMed] [Google Scholar]
[29].O’Brien EParati GStergiou GAsmar RBeilin LBilo Get al. European Society of Hypertension Position Paper on Ambulatory Blood Pressure Monitoring. Journal of Hypertension . 2013;31:1731–1768. doi: 10.1097/HJH.0b013e328363e964. [DOI] [PubMed] [Google Scholar]
[30].Nuredini GSaunders ARajkumar COkorie M. Current status of white coat hypertension: where are we. Therapeutic Advances in Cardiovascular Disease . 2020;14:175394472093163. doi: 10.1177/1753944720931637. [DOI] [PMC free article] [PubMed] [Google Scholar]
[31].Celis HFagard RH. White-coat hypertension: a clinical review. European Journal of Internal Medicine . 2004;15:348–357. doi: 10.1016/j.ejim.2004.08.001. [DOI] [PubMed] [Google Scholar]
[32].Mancia GDe Backer GDominiczak ACifkova RFagard RGermano Get al. 2007 Guidelines for the Management of Arterial Hypertension. Journal of Hypertension . 2007;25:1105–1187. doi: 10.1097/HJH.0b013e3281fc975a. [DOI] [PubMed] [Google Scholar]
[33].Huang YHuang WMai WCai XAn DLiu Zet al. White-coat hypertension is a risk factor for cardiovascular diseases and total mortality. Journal of Hypertension . 2017;35:677–688. doi: 10.1097/HJH.0000000000001226. [DOI] [PMC free article] [PubMed] [Google Scholar]
[34].Briasoulis AAndroulakis EPalla MPapageorgiou NTousoulis D. White-coat hypertension and cardiovascular events. Journal of Hypertension . 2016;34:593–599. doi: 10.1097/HJH.0000000000000832. [DOI] [PubMed] [Google Scholar]
[35].Jensen RVHjortbak MVBøtker HE. Ischemic Heart Disease: An Update. Seminars in Nuclear Medicine . 2020;50:195–207. doi: 10.1053/j.semnuclmed.2020.02.007. [DOI] [PubMed] [Google Scholar]
[36].WHO The top 10 causes of death. 2020. [(Accessed: 29 April 2022)]. Available at: https://www.who.int/news-room/fact-sheets/detail/the-top-10-causes-of-death.
[37].Lloyd-Jones DAdams RJBrown TMCarnethon MDai SDe Simone Get al. Heart Disease and Stroke Statistics—2010 Update. Circulation . 2010;121:e46–e215. doi: 10.1161/CIRCULATIONAHA.109.192667. [DOI] [PubMed] [Google Scholar]
[38].Kasprzyk MWudarczyk BCzyz RSzarpak LJankowska-Polanska B. Ischemic heart disease–definitionepidemiologypathogenesisrisk factors and treatment. Postępy Nauk Medycznych . 2018;31:358–360. [Google Scholar]
[39].Jowett NCabot L. Patients with cardiac disease: considerations for the dental practitioner. British Dental Journal . 2000;189:297–302. doi: 10.1038/sj.bdj.4800750. [DOI] [PubMed] [Google Scholar]
[40].Knuuti JWijns WSaraste ACapodanno DBarbato EFunck-Brentano Cet al. 2019 ESC Guidelines for the diagnosis and management of chronic coronary syndromes. European Heart Journal . 2020;41:407–477. doi: 10.1093/eurheartj/ehz425. [DOI] [PubMed] [Google Scholar]
[41].Fihn SDBlankenship JCAlexander KPBittl JAByrne JGFletcher BJet al. 2014 ACC/AHA/AATS/PCNA/SCAI/STS Focused Update of the Guideline for the Diagnosis and Management of Patients with Stable Ischemic Heart Disease. Circulation . 2014;130:1749–1767. doi: 10.1161/CIR.0000000000000095. [DOI] [PubMed] [Google Scholar]
[42].Akkaif MASha’aban ADaud NAYunusa INg MLSK Abdul Kader MAet al. Coronary Heart Disease (CHD) in Elderly Patients: Which Drug to ChooseTicagrelor and Clopidogrel? A Systematic Review and Meta-Analysis of Randomized Controlled Trials. Journal of Cardiovascular Development and Disease . 2021;8:123. doi: 10.3390/jcdd8100123. [DOI] [PMC free article] [PubMed] [Google Scholar]
[43].Wallentin LBecker RCBudaj ACannon CPEmanuelsson HHeld Cet al. Ticagrelor versus Clopidogrel in Patients with Acute Coronary Syndromes. New England Journal of Medicine . 2009;361:1045–1057. doi: 10.1056/NEJMoa0904327. [DOI] [PubMed] [Google Scholar]
[44].Chow CKJolly SRao-Melacini PFox KAAAnand SSYusuf S. Association of DietExerciseand Smoking Modification with Risk of Early Cardiovascular Events after Acute Coronary Syndromes. Circulation . 2010;121:750–758. doi: 10.1161/CIRCULATIONAHA.109.891523. [DOI] [PubMed] [Google Scholar]
[45].Research S and TCAA of Periodontology Periodontal management of patients with cardiovascular diseases. Journal of Periodontology . 2002;73:954–968. doi: 10.1902/jop.2002.73.8.954. [DOI] [PubMed] [Google Scholar]
[46].Freymiller EGAghaloo T. Dental management of patients with coronary artery disease. Journal of the California Dental Association . 1995;23:41–46. [PubMed] [Google Scholar]
[47].Hansson GK. InflammationAtherosclerosisand Coronary Artery Disease. New England Journal of Medicine . 2005;352:1685–1695. doi: 10.1056/NEJMra043430. [DOI] [PubMed] [Google Scholar]
[48].Kim KHKerndt CCAdnan GSchaller DJ. Nitroglycerin . StatPearls Publishing; Treasure Island (FL): 2022. [PubMed] [Google Scholar]
[49].Pototski MAmenábar JM. Dental management of patients receiving anticoagulation or antiplatelet treatment. Journal of Oral Science . 2007;49:253–258. doi: 10.2334/josnusd.49.253. [DOI] [PubMed] [Google Scholar]
[50].Brennan MTWynn RLMiller CS. Aspirin and bleeding in dentistry: an update and recommendations. Oral SurgeryOral MedicineOral PathologyOral Radiologyand Endodontology . 2007;104:316–323. doi: 10.1016/j.tripleo.2007.03.003. [DOI] [PubMed] [Google Scholar]
[51].Evans ILSayers MSGibbons AJPrice GSnooks HSugar AWet al. Can warfarin be continued during dental extraction? Results of a randomized controlled trial. British Journal of Oral and Maxillofacial Surgery . 2002;40:248–252. doi: 10.1054/bjom.2001.0773. [DOI] [PubMed] [Google Scholar]
[52].Zanon EMartinelli FBacci CCordioli GGirolami A. Safety of dental extraction among consecutive patients on oral anticoagulant treatment managed using a specific dental management protocol. Blood Coagulation & Fibrinolysis . 2003;14:27–30. doi: 10.1097/00001721-200301000-00006. [DOI] [PubMed] [Google Scholar]
[53].Scully CWolff A. Oral surgery in patients on anticoagulant therapy. Oral SurgeryOral MedicineOral PathologyOral Radiologyand Endodontology . 2002;94:57–64. doi: 10.1067/moe.2002.123828. [DOI] [PubMed] [Google Scholar]
[54].Lockhart PBGibson JPond SHLeitch J. Dental management considerations for the patient with an acquired coagulopathy. Part 1: Coagulopathies from systemic disease. British Dental Journal . 2003;195:439–445. doi: 10.1038/sj.bdj.4810593. [DOI] [PubMed] [Google Scholar]
[55].Little JWMiller CSHenry RGMcIntosh BA. Antithrombotic agents: Implications in dentistry. Oral SurgeryOral MedicineOral PathologyOral Radiologyand Endodontology . 2002;93:544–551. doi: 10.1067/moe.2002.121391. [DOI] [PubMed] [Google Scholar]
[56].Wahl MJ. Dental Surgery in Anticoagulated Patients. Archives of Internal Medicine . 1998;158:1610. doi: 10.1001/archinte.158.15.1610. [DOI] [PubMed] [Google Scholar]
[57].Beirne OR. Evidence to continue oral anticoagulant therapy for ambulatory oral surgery. Journal of Oral and Maxillofacial Surgery . 2005;63:540–545. doi: 10.1016/j.joms.2004.12.009. [DOI] [PubMed] [Google Scholar]
[58].Otto CMNishimura RABonow ROCarabello BAErwin JPGentile Fet al. 2020 ACC/AHA Guideline for the Management of Patients with Valvular Heart Disease: a Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation . 2021;143:e35–e71. doi: 10.1161/CIR.0000000000000932. [DOI] [PubMed] [Google Scholar]
[59].Libby PZipes DPLibby PBonow ROMann DLTomaselli GF. Braunwald’s heart disease: a textbook of cardiovascular medicine. 4th edn . Elsevier/Saunders; PhiladelphiaPA: 2018. [Google Scholar]
[60].Stoodley LKeller E. Valvular Heart Disease. The Journal for Nurse Practitioners . 2017;13:e195–e198. [Google Scholar]
[61].Flemming KDBrown RDPetty GWHuston JKallmes DFPiepgras DG. Evaluation and Management of Transient Ischemic Attack and Minor Cerebral Infarction. Mayo Clinic Proceedings . 2004;79:1071–1086. doi: 10.4065/79.8.1071. [DOI] [PubMed] [Google Scholar]
[62].Warburton GCaccamese JF. Valvular Heart Disease and Heart Failure: Dental Management Considerations. Dental Clinics of North America . 2006;50:493–512. doi: 10.1016/j.cden.2006.06.010. [DOI] [PubMed] [Google Scholar]
[63].Parnaby MGCarpetis JR. Rheumatic fever in Indigenous Australian children. Journal of Paediatrics and Child Health . 2010;46:527–533. doi: 10.1111/j.1440-1754.2010.01841.x. [DOI] [PubMed] [Google Scholar]
[64].Health Policy Analysis 2017 . Evaluation of the commonwealth Rheumatic Fever Strategy – final report . Primary Healthcare BranchCommonwealth Department of Health; Canberra: 2017. [Google Scholar]
[65].Katzenellenbogen JMRalph APWyber RCarapetis JR. Rheumatic heart disease: infectious disease originchronic care approach. BMC Health Services Research . 2017;17:793. doi: 10.1186/s12913-017-2747-5. [DOI] [PMC free article] [PubMed] [Google Scholar]
[66].Sanz MMarco del Castillo AJepsen SGonzalez‐Juanatey JRD’Aiuto FBouchard Pet al. Periodontitis and cardiovascular diseases: Consensus report. Journal of Clinical Periodontology . 2020;47:268–288. doi: 10.1111/jcpe.13189. [DOI] [PMC free article] [PubMed] [Google Scholar]
[67].Task Force on Practice Guidelines (Committee on Management of Patients with Valvular Heart Disease) ACC/AHA guidelines for the management of patients with valvular heart disease. A report of the American College of Cardiology/American Heart Association. Journal of the American College of Cardiology . 1998;32:1486–1588. doi: 10.1016/s0735-1097(98)00454-9. [DOI] [PubMed] [Google Scholar]
[68].Bonow ROCarabello BAKanu Cde Leon ACJrFaxon DPFreed MDet al. ACC/AHA2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation . 2006;114:e84–e231. doi: 10.1161/CIRCULATIONAHA.106.176857. [DOI] [PubMed] [Google Scholar]
[69].Vahanian ABaumgartner HBax JButchart EDion RFilippatos Get al. Guidelines on the management of valvular heart disease: the Task Force on the Management of Valvular Heart Disease of the European Society of Cardiology. European Heart Journal . 2007;28:230–268. doi: 10.1093/eurheartj/ehl428. [DOI] [PubMed] [Google Scholar]
[70].Butchart EGGohlke-Bärwolf CAntunes MJTornos PDe Caterina RCormier Bet al. Recommendations for the management of patients after heart valve surgery. European Heart Journal . 2005;26:2463–2471. doi: 10.1093/eurheartj/ehi426. [DOI] [PubMed] [Google Scholar]
[71].Pibarot PDumesnil JG. Prosthetic Heart Valves. Circulation . 2009;119:1034–1048. doi: 10.1161/CIRCULATIONAHA.108.778886. [DOI] [PubMed] [Google Scholar]
[72].Chen TYeh YChien KLai MTu Y. Risk of Infective Endocarditis after Invasive Dental Treatments. Circulation . 2018;138:356–363. doi: 10.1161/CIRCULATIONAHA.117.033131. [DOI] [PubMed] [Google Scholar]
[73].Hoen BDuval X. Infective Endocarditis. New England Journal of Medicine . 2013;368:1425–1433. doi: 10.1056/NEJMcp1206782. [DOI] [PubMed] [Google Scholar]
[74].de Sa DDCTleyjeh IMAnavekar NSSchultz JCThomas JMLahr BDet al. Epidemiological Trends of Infective Endocarditis: a Population-Based Study in Olmsted CountyMinnesota. Mayo Clinic Proceedings . 2010;85:422–426. doi: 10.4065/mcp.2009.0585. [DOI] [PMC free article] [PubMed] [Google Scholar]
[75].Duval XDelahaye FAlla FTattevin PObadia JFLe Moing Vet al. Temporal trends in infective endocarditis in the context of prophylaxis guideline modifications: three successive population-based surveys. Journal of the American College of Cardiology . 2012;59:1968–1976. doi: 10.1016/j.jacc.2012.02.029. [DOI] [PubMed] [Google Scholar]
[76].Fedeli USchievano EBuonfrate DPellizzer GSpolaore P. Increasing incidence and mortality of infective endocarditis: a population-based study through a record-linkage system. BMC Infectious Diseases . 2011;11:48. doi: 10.1186/1471-2334-11-48. [DOI] [PMC free article] [PubMed] [Google Scholar]
[77].Sy RWKritharides L. Health care exposure and age in infective endocarditis: results of a contemporary population-based profile of 1536 patients in Australia. European Heart Journal . 2010;31:1890–1897. doi: 10.1093/eurheartj/ehq110. [DOI] [PubMed] [Google Scholar]
[78].Selton-Suty CCélard MLe Moing VDoco-Lecompte TChirouze CIung Bet al. Preeminence of Staphylococcus aureus in Infective Endocarditis: a 1-Year Population-Based Survey. Clinical Infectious Diseases . 2012;54:1230–1239. doi: 10.1093/cid/cis199. [DOI] [PubMed] [Google Scholar]
[79].Bannay AHoen BDuval XObadia JFSelton-Suty CLe Moing Vet al. The impact of valve surgery on short- and long-term mortality in left-sided infective endocarditis: do differences in methodological approaches explain previous conflicting results. European Heart Journal . 2011;32:2003–2015. doi: 10.1093/eurheartj/ehp008. [DOI] [PubMed] [Google Scholar]
[80].Tleyjeh IMAbdel-Latif ARahbi HScott CGBailey KRSteckelberg JMet al. A Systematic Review of Population-Based Studies of Infective Endocarditis. Chest . 2007;132:1025–1035. doi: 10.1378/chest.06-2048. [DOI] [PubMed] [Google Scholar]
[81].Wilson WTaubert KAGewitz MLockhart PBBaddour LMLevison Met al. Prevention of infective endocarditis: guidelines from the American Heart Association: a guideline from the American Heart Association Rheumatic FeverEndocarditisand Kawasaki Disease CommitteeCouncil on Cardiovascular Disease in the Youngand the Council on Clinical CardiologyCouncil on Cardiovascular Surgery and Anesthesiaand the Quality of Care and Outcomes Research Interdisciplinary Working Group. Circulation . 2007;116:1736–1754. doi: 10.1161/CIRCULATIONAHA.106.183095. [DOI] [PubMed] [Google Scholar]
[82].Robinson ANTambyah PA. Infective endocarditis - an update for dental surgeons. Singapore Dental Journal . 2017;38:2–7. doi: 10.1016/j.sdj.2017.09.001. [DOI] [PubMed] [Google Scholar]
[83].Lockhart PBDurack DT. Oral microflora as a cause of endocarditis and other distant site infections. Infectious Disease Clinics of North America . 1999;13:833–850vi. doi: 10.1016/s0891-5520(05)70111-2. [DOI] [PubMed] [Google Scholar]
[84].Roberts GJHolzel HSSury MRJSimmons NAGardner PLonghurst P. Dental Bacteremia in Children. Pediatric Cardiology . 1997;18:24–27. doi: 10.1007/s002469900103. [DOI] [PubMed] [Google Scholar]
[85].Pallasch TJSlots J. Antibiotic prophylaxis and the medically compromised patient. Periodontology. 2000 . 1996;10:107–138. doi: 10.1111/j.1600-0757.1996.tb00071.x. [DOI] [PubMed] [Google Scholar]
[86].LOCKHART PB. The risk for endocarditis in dental practice. Periodontology. 2000 . 2000;23:127–135. doi: 10.1034/j.1600-0757.2000.2230113.x. [DOI] [PubMed] [Google Scholar]
[87].Cobe HM. Transitory bacteremia. Oral SurgeryOral MedicineOral Pathology . 1954;7:609–615. doi: 10.1016/0030-4220(54)90071-7. [DOI] [PubMed] [Google Scholar]
[88].Sconyers JRCrawford JJMoriarty JD. Relationship of Bacteremia to Toothbrushing in Patients with Periodontitis. The Journal of the American Dental Association . 1973;87:616–622. doi: 10.14219/jada.archive.1973.0453. [DOI] [PubMed] [Google Scholar]
[89].Forner LLarsen TKilian MHolmstrup P. Incidence of bacteremia after chewingtooth brushing and scaling in individuals with periodontal inflammation. Journal of Clinical Periodontology . 2006;33:401–407. doi: 10.1111/j.1600-051X.2006.00924.x. [DOI] [PubMed] [Google Scholar]
[90].Rise ESmith JFBell J. Reduction of Bacteremia after Oral Manipulations. Archives of Otolaryngology - Head and Neck Surgery . 1969;90:198–201. doi: 10.1001/archotol.1969.00770030200022. [DOI] [PubMed] [Google Scholar]
[91].Schlein RAKudlick EMReindorf CAGregory JRoyal GC. Toothbrushing and transient bacteremia in patients undergoing orthodontic treatment. American Journal of Orthodontics and Dentofacial Orthopedics . 1991;99:466–472. doi: 10.1016/S0889-5406(05)81580-X. [DOI] [PubMed] [Google Scholar]
[92].Felix JERosen SApp GR. Detection of Bacteremia after the Use of an Oral Irrigation Device in Subjects with Periodontitis. Journal of Periodontology . 1971;42:785–787. doi: 10.1902/jop.1971.42.12.785. [DOI] [PubMed] [Google Scholar]
[93].O’Leary TJShafer WGSwenson HMNesler DCVan Dorn PR. Possible Penetration of Crevicular Tissue from Oral Hygiene Procedures: i. Use of Oral Irrigating Devices. Journal of Periodontology . 1970;41:158–162. doi: 10.1902/jop.1970.41.41.158. [DOI] [PubMed] [Google Scholar]
[94].Jones TDBaumgartner LBellows MTBreese BBKuttner AGMcCarty Met al. Prevention of rheumatic fever and bacterial endocarditis through control of streptococcal infections. Circulation . 1955;11:317–320. [Google Scholar]
[95].Glenny AMOliver RRoberts GJHooper LWorthington HV. Antibiotics for the prophylaxis of bacterial endocarditis in dentistry. Cochrane Database of Systematic Reviews . 2013:CD003813. doi: 10.1002/14651858.CD003813.pub4. [DOI] [PubMed] [Google Scholar]
[96].Cahill TJHarrison JLJewell POnakpoya IChambers JBDayer Met al. Antibiotic prophylaxis for infective endocarditis: a systematic review and meta-analysis. Heart . 2017;103:937–944. doi: 10.1136/heartjnl-2015-309102. [DOI] [PubMed] [Google Scholar]
[97].Richey RWray DStokes T. Prophylaxis against infective endocarditis: summary of NICE guidance. BMJ . 2008;336:770–771. doi: 10.1136/bmj.39510.423148.AD. [DOI] [PMC free article] [PubMed] [Google Scholar]
[98].Thornhill MHDayer MLockhart PBMcGurk MShanson DPrendergast Bet al. A change in the NICE guidelines on antibiotic prophylaxis. British Dental Journal . 2016;221:112–114. doi: 10.1038/sj.bdj.2016.554. [DOI] [PubMed] [Google Scholar]
[99].Wilson WRGewitz MLockhart PBBolger AFDeSimone DCKazi DSet al. Prevention of viridans group streptococcal infective endocarditis: a scientific statement from the American Heart Association. Circulation . 2021;143:e963–e978. doi: 10.1161/CIR.0000000000000969. [DOI] [PubMed] [Google Scholar]
[100].Dentali F. Combined Aspirin–Oral Anticoagulant Therapy Compared with Oral Anticoagulant Therapy alone among Patients at Risk for Cardiovascular Disease. Archives of Internal Medicine . 2007;167:117–124. doi: 10.1001/archinte.167.2.117. [DOI] [PubMed] [Google Scholar]
[101].Douketis JDSpyropoulos ACSpencer FAMayr MJaffer AKEckman MHet al. Perioperative Management of Antithrombotic Therapy. Chest . 2012;141:e326S–e350S. doi: 10.1378/chest.11-2298. [DOI] [PMC free article] [PubMed] [Google Scholar]
[102].Grines CLBonow ROCasey DEJrGardner TJLockhart PBMoliterno DJet al. Prevention of premature discontinuation of dual antiplatelet therapy in patients with coronary artery stents: a science advisory from the American Heart AssociationAmerican College of CardiologySociety for Cardiovascular Angiography and InterventionsAmerican College of Surgeonsand American Dental Associationwith representation from the American College of Physicians. The Journal of the American Dental Association . 2007;138:652–655. doi: 10.14219/jada.archive.2007.0237. [DOI] [PubMed] [Google Scholar]
[103].Kristensen SDKnuuti JSaraste AAnker SBøtker HEHert SDet al. 2014 ESC/ESA Guidelines on non‐cardiac surgery: Cardiovascular assessment and management: The Joint Task Force on non‐cardiac surgery: Cardiovascular assessment and management of the European Society of Cardiology (ESC) and the European Society of Anaesthesiology (ESA) European Heart Journal . 2014;35:2383–2431. doi: 10.1093/eurheartj/ehu282. [DOI] [PubMed] [Google Scholar]
[104].Hirsh J. The International Normalized Ratio. Archives of Internal Medicine . 1994;154:282–288. doi: 10.1001/archinte.154.3.282. [DOI] [PubMed] [Google Scholar]
[105].Perry DJNoakes TJCHelliwell PS. Guidelines for the management of patients on oral anticoagulants requiring dental surgery. British Dental Journal . 2007;203:389–393. doi: 10.1038/bdj.2007.892. [DOI] [PubMed] [Google Scholar]
[106].Hirsh JDalen JEAnderson DRPoller LBussey HAnsell Jet al. Oral Anticoagulants: Mechanism of ActionClinical Effectivenessand Optimal Therapeutic Range. Chest . 2001;119:8S–21S. doi: 10.1378/chest.119.1_suppl.8s. [DOI] [PubMed] [Google Scholar]
[107].Dalen JEHirsh J. Antithrombotic therapy. introduction. Chest . 1992;102:303S–304S. [PubMed] [Google Scholar]
[108].AAOM Clinical Practice Statement: Subject: Management of Patients on Warfarin Therapy. Oral SurgeryOral MedicineOral Pathology and Oral Radiology . 2016;122:702–704. doi: 10.1016/j.oooo.2016.06.015. [DOI] [PubMed] [Google Scholar]
[109].Chaudhry SJaiswal RSachdeva S. Dental considerations in cardiovascular patients: a practical perspective. Indian Heart Journal . 2016;68:572–575. doi: 10.1016/j.ihj.2015.11.034. [DOI] [PMC free article] [PubMed] [Google Scholar]
[110].Ansell JHirsh JHylek EJacobson ACrowther MPalareti G. Pharmacology and Management of the Vitamin K Antagonists. Chest . 2008;133:160S–198S. doi: 10.1378/chest.08-0670. [DOI] [PubMed] [Google Scholar]
[111].Douketis JD. Perioperative anticoagulation management in patients who are receiving oral anticoagulant therapy: a practical guide for clinicians. Thrombosis Research . 2002;108:3–13. doi: 10.1016/s0049-3848(02)00387-0. [DOI] [PubMed] [Google Scholar]
[112].Chahine JKhoudary MNNasr S. Anticoagulation Use prior to Common Dental Procedures: a Systematic Review. Cardiology Research and Practice . 2019;2019:9308631. doi: 10.1155/2019/9308631. [DOI] [PMC free article] [PubMed] [Google Scholar]
[113].Nematullah AAlabousi ABlanas NDouketis JDSutherland SE. Dental surgery for patients on anticoagulant therapy with warfarin: a systematic review and meta-analysis. Journal of the Canadian Dental Association . 2009;75:41. [PubMed] [Google Scholar]
[114].Weltman NJAl-Attar YCheung JDuncan DPKatchky AAzarpazhooh Aet al. Management of dental extractions in patients taking warfarin as anticoagulant treatment: a systematic review. Journal of the Canadian Dental Association . 2015;81:f20. [PubMed] [Google Scholar]
[115].Polania Gutierrez JJRocuts KR. Perioperative Anticoagulation Management . StatPearls Publishing; Treasure Island (FL): 2022. [PubMed] [Google Scholar]
[116].Kearon CHirsh J. Management of Anticoagulation before and after Elective Surgery. New England Journal of Medicine . 1997;336:1506–1511. doi: 10.1056/NEJM199705223362107. [DOI] [PubMed] [Google Scholar]
[117].White RH. Temporary Discontinuation of Warfarin Therapy: Changes in the International Normalized Ratio. Annals of Internal Medicine . 1995;122:40–42. doi: 10.7326/0003-4819-122-1-199501010-00006. [DOI] [PubMed] [Google Scholar]
[118].Douketis JDLip G. Perioperative management of patients receiving anticoagulants. UpToDate . 2019:1–28. [Google Scholar]
[119].Harrison L. Comparison of 5-mg and 10-mg Loading Doses in Initiation of Warfarin Therapy. Annals of Internal Medicine . 1997;126:133–136. doi: 10.7326/0003-4819-126-2-199701150-00006. [DOI] [PubMed] [Google Scholar]
[120].Hirsh JFuster VAnsell JHalperin JL. American Heart Association/American College of Cardiology Foundation Guide to Warfarin Therapy. Circulation . 2003;107:1692–1711. doi: 10.1161/01.CIR.0000063575.17904.4E. [DOI] [PubMed] [Google Scholar]
[121].Todd DW. Evidence to support an individualized approach to modification of oral anticoagulant therapy for ambulatory oral surgery. Journal of Oral and Maxillofacial Surgery . 2005;63:536–539. doi: 10.1016/j.joms.2004.12.008. [DOI] [PubMed] [Google Scholar]
[122].Gurbel PAMyat AKubica JTantry US. State of the art: Oral antiplatelet therapy. JRSM Cardiovascular Disease . 2016;5:2048004016652514. doi: 10.1177/2048004016652514. [DOI] [PMC free article] [PubMed] [Google Scholar]
[123].Kwak ENam SPark KKim SHuh JPark W. Bleeding related to dental treatment in patients taking novel oral anticoagulants (NOACs): a retrospective study. Clinical Oral Investigations . 2019;23:477–484. doi: 10.1007/s00784-018-2458-2. [DOI] [PubMed] [Google Scholar]
[124].Lababidi EBreik OSavage JEngelbrecht HKumar RCrossley CW. Assessing an oral surgery specific protocol for patients on direct oral anticoagulants: a retrospective controlled cohort study. International Journal of Oral and Maxillofacial Surgery . 2018;47:940–946. doi: 10.1016/j.ijom.2018.03.009. [DOI] [PubMed] [Google Scholar]
[125].Lusk KASnoga JLBenitez RMSarbacker GB. Management of Direct-Acting Oral Anticoagulants Surrounding Dental Procedures with Low-to-Moderate Risk of Bleeding. Journal of Pharmacy Practice . 2018;31:202–207. doi: 10.1177/0897190017707126. [DOI] [PubMed] [Google Scholar]
[126].Randall C. Surgical Management of the Primary Care Dental Patient on Warfarin. Dental Update . 2005;32:414–426. doi: 10.12968/denu.2005.32.7.414. [DOI] [PubMed] [Google Scholar]
[127].Savaysa Accessdata.fda.gov. 2022. [(Accessed: 25 April 2022)]. Available at: https://www.accessdata.fda.gov/drugsatfda_docs/label/2015/206316lbl.pdf.
[128].Xarelto Accessdata.fda.gov. 2022. [(Accessed: 25 April 2022)]. Available at: https://www.accessdata.fda.gov/drugsatfda_docs/label/2016/202439s017lbl.pdf.
[129].Eliquis Accessdata.fda.gov. 2022. [(Accessed: 25 April 2022)]. Available at: https://www.accessdata.fda.gov/drugsatfda_docs/label/2012/202155s000lbl.pdf.
[130].Madan GAMadan SGMadan GMadan AD. Minor Oral Surgery without Stopping Daily Low-Dose Aspirin Therapy: a Study of 51 Patients. Journal of Oral and Maxillofacial Surgery . 2005;63:1262–1265. doi: 10.1016/j.joms.2005.05.164. [DOI] [PubMed] [Google Scholar]
[131].Dodson TB. Strategies for managing anticoagulated patients requiring dental extractions: an exercise in evidence-based clinical practice. Journal of the Massachusetts Dental Society . 2002;50:44–50. [PubMed] [Google Scholar]
[132].Buchbender MSchlee NKesting MRGrimm JFehlhofer JRau A. A prospective comparative study to assess the risk of postoperative bleeding after dental surgery while on medication with direct oral anticoagulantsantiplatelet agentsor vitamin K antagonists. BMC Oral Health . 2021;21:504. doi: 10.1186/s12903-021-01868-7. [DOI] [PMC free article] [PubMed] [Google Scholar]
[133].Ker KBeecher DRoberts I. Topical application of tranexamic acid for the reduction of bleeding. Cochrane Database of Systematic Reviews . 2013:CD010562. doi: 10.1002/14651858.CD010562.pub2. [DOI] [PMC free article] [PubMed] [Google Scholar]
[134].Manfredini MPoli PPCreminelli LPorro AMaiorana CBeretta M. Comparative Risk of Bleeding of Anticoagulant Therapy with Vitamin K Antagonists (VKAs) and with Non-Vitamin K Antagonists in Patients Undergoing Dental Surgery. Journal of Clinical Medicine . 2021;10:5526. doi: 10.3390/jcm10235526. [DOI] [PMC free article] [PubMed] [Google Scholar]
[135].van Diermen DEvan der Waal IHoogstraten J. Management recommendations for invasive dental treatment in patients using oral antithrombotic medicationincluding novel oral anticoagulants. Oral SurgeryOral MedicineOral Pathology and Oral Radiology . 2013;116:709–716. doi: 10.1016/j.oooo.2013.07.026. [DOI] [PubMed] [Google Scholar]
[136].Wahl MJ. Myths of dental surgery in patients. The Journal of the American Dental Association . 2000;131:77–81. doi: 10.14219/jada.archive.2000.0024. [DOI] [PubMed] [Google Scholar]
[137].Scully CCawson RA. Medical problems in dentistry. 4th edn . Wright Butterworth-Heinemann; Oxford: 1998. pp. 49–100. [Google Scholar]
[138].Gallagher JJ. Cardiac arrhythmias. 20th edn . W. B. Saunders; Philadelphia: 1996. [Google Scholar]
[139].Little JWFalace DAMiller CSRhodus NL. Cardiac arrhythmias. In: Little JWFalace DAMiller CSeditors. Dental management of the medically compromised patient. 6th edn . Mosby; St. Louis: 2002. pp. 94–114. [Google Scholar]
[140].Benjamin EJMuntner PAlonso ABittencourt MSCallaway CWCarson APet al. Heart Disease and Stroke Statistics-2019 Update: A Report From the American Heart Association. Circulation . 2019;139:e56–e528. doi: 10.1161/CIR.0000000000000659. [DOI] [PubMed] [Google Scholar]
[141].Go ASHylek EMPhillips KAChang YHenault LESelby JVet al. Prevalence of Diagnosed Atrial Fibrillation in Adults. JAMA . 2001;285:2370–2375. doi: 10.1001/jama.285.18.2370. [DOI] [PubMed] [Google Scholar]
[142].Myerberg RJKessler KMCastellanos A. RecognitionClinical assessment and management of arrhythmias and conduction disturbances. In: Alexander RESchlant RCFuster Veditors. Hurst’s the heartarteriesand veins. 9th edn . McGraw-Hill; New York: 1998. pp. 873–942. [Google Scholar]
[143].Mitrani RDMyeburg RJCastellanos A. Cardiac pacemakers. In: Hurst JWeditor. The heartarteriesand veins. 9th edn . McGraw-Hill; New York: 1998. pp. 1023–1059. [Google Scholar]
[144].O’Callaghan PARuskin JN. The implantable cardioverter. In: Hurst JWeditor. The heartarteriesand veins. 9th edn . McGraw-Hill; New York: 1998. pp. 1007–1023. [Google Scholar]
[145].Stevenson WGEllison KESweeney MOEpstein LMMaisel WH. Management of Arrhythmias in Heart Failure. Cardiology in Review . 2002;10:8–14. doi: 10.1097/00045415-200201000-00004. [DOI] [PubMed] [Google Scholar]
[146].Rhodus NLLittle JW. Dental management of the patient with cardiac arrhythmias: an update. Oral SurgeryOral MedicineOral PathologyOral Radiologyand Endodontology . 2003;96:659–668. doi: 10.1016/s1079-2104(03)00380-9. [DOI] [PubMed] [Google Scholar]
[147].Friedlander AHYoshikawa TTChang DSFeliciano ZScully C. Atrial fibrillation. The Journal of the American Dental Association . 2009;140:167–177. doi: 10.14219/jada.archive.2009.0130. [DOI] [PubMed] [Google Scholar]
[148].Little JWFalace DAMiller CSRhodus NL. Ischemic heart disease. In: Little JWFalace DAMiller CSeditors. Dental management of the medically compromised patient. 6th edn . Mosby; St Louis: 2002. pp. 79–94. [Google Scholar]
[149].Little JWFalace DAMiller CSRhodus NL. Congestive heart failure. In: Little JWFalace DAMiller CSeditors. Dental management of the medically compromised patient. 6th edn . Mosby; St Louis: 2002. pp. 114–125. [Google Scholar]
[150].MASK AG. Medical management of the patient with cardiovascular disease. Periodontology . 2000;23:136–141. doi: 10.1034/j.1600-0757.2000.2230114.x. [DOI] [PubMed] [Google Scholar]
[151].Miller CSLeonelli FMLatham E. Selective interference with pacemaker activity by electrical dental devices. Oral SurgeryOral MedicineOral PathologyOral Radiologyand Endodontology . 1998;85:33–36. doi: 10.1016/s1079-2104(98)90394-8. [DOI] [PubMed] [Google Scholar]
[152].Maiorana CGrossi GBGarramone RAManfredini RSantoro F. Do ultrasonic dental scalers interfere with implantable cardioverter defibrillators? An in vivo investigation. Journal of Dentistry . 2013;41:955–959. doi: 10.1016/j.jdent.2013.08.006. [DOI] [PubMed] [Google Scholar]
[153].Gomez GJara FSánchez BRoig MDuran-Sindreu F. Effects of Piezoelectric Units on Pacemaker Function: an in Vitro Study. Journal of Endodontics . 2013;39:1296–1299. doi: 10.1016/j.joen.2013.06.025. [DOI] [PubMed] [Google Scholar]
[154].Trenter SCWalmsley AD. Ultrasonic dental scaler: associated hazards. Journal of Clinical Periodontology . 2003;30:95–101. doi: 10.1034/j.1600-051x.2003.00276.x. [DOI] [PubMed] [Google Scholar]
[155].Dajani AS. Prevention of Bacterial Endocarditis. JAMA . 1997;277:1794–1801. [PubMed] [Google Scholar]
[156].Little JW. Bleeding disorders. In: Little JWFalace DAMiller CSeditors. Dental management of the medically compromised patient. 6th edn . Mosby; St. Louis: 2002. pp. 362–395. [Google Scholar]
[157].Uzeda MJMoura BLouro RSda Silva LECalasans-Maia MD. A Randomized Controlled Clinical Trial to Evaluate Blood Pressure Changes in Patients Undergoing Extraction under Local Anesthesia with Vasopressor Use. Journal of Craniofacial Surgery . 2014;25:1108–1110. doi: 10.1097/SCS.0000000000000736. [DOI] [PubMed] [Google Scholar]
[158].dos Santos-Paul MANeves ILINeves RSRamires JAF. Local anesthesia with epinephrine is safe and effective for oral surgery in patients with type 2 diabetes mellitus and coronary disease: a prospective randomized study. Clinics . 2015;70:185–189. doi: 10.6061/clinics/2015(03)06. [DOI] [PMC free article] [PubMed] [Google Scholar]
[159].Haas DA. An update on local anesthetics in dentistry. Journal of The Canadian Dental Association . 2002;68:546–551. [PubMed] [Google Scholar]
[160].Fencl JL. Guideline Implementation: Local Anesthesia. AORN Journal . 2015;101:682–692. doi: 10.1016/j.aorn.2015.04.014. [DOI] [PubMed] [Google Scholar]
[161].Silvestre FJVerdú MJSanchís JMGrau DPeñarrocha M. Effects of vasoconstrictors in dentistry upon systolic and diastolic arterial pressure. Medicina Oral . 2001;6:57–63. [PubMed] [Google Scholar]
[162].Laragnoit ABNeves RSNeves ILIVieira JE. Locoregional Anesthesia for Dental Treatment in Cardiac Patients: a Comparative Study of 2% Plain Lidocaine and 2% Lidocaine with Epinephrine (1:100,000) Clinics . 2009;64:177–182. doi: 10.1590/S1807-59322009000300005. [DOI] [PMC free article] [PubMed] [Google Scholar]
[163].Conrado VCLSde Andrade Jde Angelis GAMCde Andrade ACPTimerman LAndrade MMet al. Cardiovascular effects of local anesthesia with vasoconstrictor during dental extraction in coronary patients. Arquivos Brasileiros de Cardiologia . 2007;88:507–513. doi: 10.1590/s0066-782x2007000500002. [DOI] [PubMed] [Google Scholar]
[164].Bader JDBonito AJShugars DA. A systematic review of cardiovascular effects of epinephrine on hypertensive dental patients. Oral SurgeryOral MedicineOral PathologyOral Radiologyand Endodontology . 2002;93:647–653. doi: 10.1067/moe.2002.123866. [DOI] [PubMed] [Google Scholar]
[165].Ketabi MShamami MSAlaie MShamami MS. Influence of local anesthetics with or without epinephrine 1/80000 on blood pressure and heart rate: A randomized double-blind experimental clinical trial. Dental Research Journal . 2012;9:437. [PMC free article] [PubMed] [Google Scholar]
[166].Malamed SF. Medical emergencies in the dental office-E-Book . Elsevier Health Sciences; 2014. [Google Scholar]
[167].Margaix Muñoz MJiménez Soriano YPoveda Roda RSarrión G. Cardiovascular diseases in dental practice. Practical considerations. Medicina oralpatologia oral y cirugia bucal . 2008;13:E296–E302. [PubMed] [Google Scholar]
[168].Pe´russe RGoulet JTurcotte J. Contraindications to vasoconstrictors in dentistry: Part i. Oral SurgeryOral MedicineOral Pathology . 1992;74:679–686. doi: 10.1016/0030-4220(92)90365-w. [DOI] [PubMed] [Google Scholar]
[169].Decloux DOuanounou A. Local Anaesthesia in Dentistry: a Review. International Dental Journal . 2021;71:87–95. doi: 10.1111/idj.12615. [DOI] [PMC free article] [PubMed] [Google Scholar]
[170].Hersh EVGiannakopoulos H. Beta-adrenergic Blocking Agents and Dental Vasoconstrictors. Dental Clinics of North America . 2010;54:687–696. doi: 10.1016/j.cden.2010.06.009. [DOI] [PubMed] [Google Scholar]
[171].Patil PMPatil SP. Is Clonidine an Adequate Alternative to Epinephrine as a Vasoconstrictor in Patients with Hypertension. Journal of Oral and Maxillofacial Surgery . 2012;70:257–262. doi: 10.1016/j.joms.2011.07.011. [DOI] [PubMed] [Google Scholar]
[172].Ouchi KSugiyama K. Dexmedetomidine Dose Dependently Enhances the Local Anesthetic Action of Lidocaine in Inferior Alveolar Nerve Block: A Randomized Double-Blind Study. Regional Anesthesia & Pain Medicine . 2016;41:348–355. doi: 10.1097/AAP.0000000000000380. [DOI] [PubMed] [Google Scholar]
[173].Ezmek BArslan ADelilbasi CSencift K. Comparison of hemodynamic effects of lidocaineprilocaine and mepivacaine solutions without vasoconstrictor in hypertensive patients. Journal of Applied Oral Science . 2010;18:354–359. doi: 10.1590/S1678-77572010000400006. [DOI] [PMC free article] [PubMed] [Google Scholar]

PERMALINK

Dental Management Considerations for Patients with Cardiovascular Disease—A Narrative Review

Kanishk Gupta

Santhosh Kumar

Meena Anand Kukkamalla

Vani Taneja

Gufaran Ali Syed

Fawaz Pullishery

Mohammad A Zarbah

Saeed M Alqahtani

Mohammed A Alobaoid

Saurabh Chaturvedi