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Managing Patients With Critical Cardiac Conditions

As this effective preventive tool is widely used, oral health professionals need to remain up-to-date regarding product innovations and the most current evidence-based approaches.

This course was published in the October 2017 issue and expires October 2020. The authors have no commercial conflicts of interest to disclose. This 2 credit hour self-study activity is electronically mediated. 

After reading this course, the participant should be able to:

  1. Discuss the prevalence of cardiovascular diseases (CVD) in the United States and worldwide.
  2. Identify the indications for antithrombotic therapies.
  3. Explain the treatments used in treating CVD and their impact on the provision of oral health care services.

Cardiovascular disease (CVD) is the leading cause of morbidity and mortality in the United States, claiming about 2,200 deaths daily or one death every 40 seconds.1 Globally, CVDs accounted for more than 17 million deaths, representing over 30% of all causes worldwide in 2015.CVD encompasses a broad group of diseases and conditions, including coronary artery disease, cerebrovascular disease and stroke, heart failure, high blood pressure, disorders of the heart rhythm, peripheral artery disease, venous thromboembolism, valvular disorders, and congenital heart defects. An estimated 92.1 million US adults have at least one type of CVD,1 with coronary artery disease being the most common.3 CVD and stroke are the most costly diseases, accounting for 14% of total health expenditures in 2012 and projected to nearly triple to $918 billion by 2030, when it is estimated that 43.9% of the US population will have some form of CVD.1 However, the mortality attributable to CVD, which was steadily increasing until the 1980s, has since declined.1

Better awareness of the disease signs and symptoms and risk and prevention factors, as well as advances in interventional cardiology, pharmacotherapies, and patient-centered care strategies contribute to improving patient outcomes.1,4,5 Pharmacotherapeutic approaches for management of several CVDs and prevention of adverse events and complications following interventional cardiology procedures incorporate anticoagulant,6antiplatelet,7 and combination antithrombotic therapies,4,8 including dual antiplatelet therapy (DAPT) and triple antithrombotic therapy (TATT).


The medical history intake process requires careful consideration of the implications of conditions reported and medications taken. This analysis is complicated by the fact that many cardiovascular medications are taken for more than one indication. Additionally, cardiovascular conditions may be managed by several medications working synergistically to achieve the therapeutic effect. Even patients who dutifully take all medications according to their prescribed schedule and dosage may be variable in their knowledge of their conditions and the possible impact on dental treatment. Medication compliance, even following discharge for acute coronary events, has been historically disappointing, and sometimes deficient.9,10 Oral health professionals need to remain familiar with continuously updated CVD treatment guidelines, as they can have life-altering impact on patient health and can help to ensure safe treatment.


Acute coronary syndrome is not a single disease, but rather describes a group of related higher risk conditions characterized by myocardial ischemia, which is a reduced flow of blood to the heart muscle caused by partial to full blockage of the coronary arteries.11 Although chronic heart conditions have similar and often co-occurring etiologies, acute coronary syndrome is distinguished by its acute nature and must be efficiently diagnosed by a medical professional as a potentially fatal risk. Symptoms include burning with radiation to jaw and left arm, but research suggests that, especially in older women, these signs may be more subtle, and include nausea, vomiting, and breathlessness.8 Getting a patient into emergency care is suggested when there is any suspicion of acute cardiac events.

Diagnosis is made definitively through electrocardiography (ECG or EKG) and intravascular angiography. Patients with chronic heart disease commonly have stable angina, or episodic bouts of chest pain associated with exertion or stress that are relieved by medications, such as nitrates (nitroglycerin). Those with unstable angina, non-ST-elevated myocardial infarction, or ST-elevated myocardial infarction present with symptoms associated with acute myocardial ischemia, often at rest. All categories are associated with atherosclerotic plaques and resulting thrombi, obstructing the lumen, or diameter of the coronary arteries. Progression to ST-elevated myocardial infarction, with resulting tissue damage and necrosis (cell death) results in a clinically detectable biomarker in the blood, troponin, which may take several hours to appear, signifying the occurrence of myocardial infarction, and underlining the need to access emergency services as soon as possible.8,12

Acute coronary syndrome most often does not occur in isolation from other CVDs, and may be complicated by comorbidities such as atrial fibrillation.13 The medical interventions, discussed below, are based on a large body of evidence from clinical trials and continuously updated professional medical guidelines. They are prescribed and timed according to diagnosed risk level and individual patient characteristics. Noninvasive therapies include various drug regimens that combine antithrombotic agents, antihyperlipidemics (cholesterol- and triglyceride-lowering drugs, such as statins) and others. More invasive approaches, such as percutaneous coronary intervention (PCI) may be deemed appropriate at any point along the continuum of disease.


Atrial fibrillation is the most common form of all cardiac arrhythmias, affecting more than 33 million people worldwide, with the highest concentration in North America.14 Individuals with atrial fibrillation are five times more likely to experience stroke, the second leading cause of death after heart disease worldwide.2,3 It is associated with risk for other CVDs, such as hypertension, heart failure, and acute coronary syndrome. Several categories of advancing disease states, which reflect the frequency and degree of aberration from normal heart rhythm and function, contribute to the level of morbidity and mortality risk for patients, the most serious of which is stroke.15

Atrial fibrillation may be caused by structural or electrophysical abnormalities in the atrial chambers of the heart, causing rapid and irregular heart contractions, which makes the heart less effective in moving the blood out of the atria to the ventricles and to circulation. The subsequent pooling or stasis of blood in the atria can cause abnormal coagulation, and resulting thrombi may travel to the brain, initiating an ischemic stroke. Subsequently, atrial fibrillation is the most frequent indication for long-term anticoagulation therapy, and patients with atrial fibrillation are commonly prescribed combination antithrombotic agents.14,16 Among all patients undergoing PCI, 5% to 8% have atrial fibrillation.17


PCI, first introduced in the 1990s, has revolutionized the treatment of coronary artery disease4,18 and is now among the most commonly performed medical procedures. An estimated 492,000 patients underwent PCI in the US in 2010.1 The goal of this intervention is to widen the lumen of a coronary artery that is occluded by intravascular deposits to some degree and to restore the blood flow to the cardiac tissue. Initially, this was accomplished by balloon angioplasty—a technique that uses a balloon catheter compressing the intravascular deposits and thus re-opening the vessel. Unfortunately, up to 50% of patients experienced restenosis, prompting the development of new techniques to improve patient outcomes.4,19 Introduction of bare metal stents, followed by the first and second-generation drug-eluting stents (DES), have progressively reduced complication rates and dramatically improved outcomes associated with percutaneous coronary angioplasty.4 The two types of complications associated with stents are stent thrombosis—development of a thrombus in the stented segment of the artery, and stent restenosis—narrowing of the vessel wall due to proliferation of the vascular tissue overgrowing the stent frame.18 While bare metal stents lowered the rate of stent thrombosis compared to balloon angioplasty,19 they also caused vessel injury and inflammation, leading to stent restenosis.4,18 DES were developed to overcome this complication by using anti-proliferative drugs.18 However, anti-proliferative drugs released by DES naturally slow the healing of the vascular wall post-PCI, and the incomplete endothelialization contributes to early (within 30 days post-PCI) or late (beyond 30 days post-PCI) stent thrombosis.18 The most important method of preventing this life-threatening complication is DAPT of appropriate duration.5,18,20,21


DAPT is standard in management of acute coronary syndromes (ST-elevated myocardial infarction and non-ST-elevated myocardial infarction) and post-PCI to prevent thromboembolic events that can lead to repeat myocardial infarction, stroke, and stent thrombosis with possible fatal outcomes.8,22 Use of aspirin (75 mg to 162 mg) and another antiplatelet agent (most frequently P2Y12 inhibitor such as clopidogrel 75 mg, prasugrel 10 mg, or ticagrelor 80 mg)8,23 that target different pathways of platelet activation, provides additive antiplatelet effect.Combination with clopidogrel is used most frequently, unless the patient has genetic polymorphisms for the hepatic cytochrome P450 enzymes that metabolize this drug to its active form and may derive less antiplatelet effect from clopidogrel as a result.7,8 Both prasugrel and ticagrelor are more potent than clopidogrel and provide a more intensive platelet inhibition,7 resulting in reduced risk of ischemic events; however, this is balanced by increased bleeding risk.8 Prasugrel is preferred in DAPT for the first year following acute coronary syndrome or stent implantation, but due to the high risk of intracranial bleeding, subsequent DAPT may be best provided with clopidogrel.23 A recent review of clinical trials regarding DAPT evaluating various drug combinations and duration of treatment found that dual therapy with aspirin and clopidogrel was shown to reduce myocardial infarction, stroke and death post-PCI at 1 year. At the same time, the risk of severe bleeding in clopidogrel+aspirin group was not significantly higher than in aspirin+placebo group.23 This indicates that long-term less-intense antiplatelet therapy with clopidogrel may provide adequate protection with less risk for bleeding events. Moreover, in addition to preventing thrombosis, DAPT may protect against atherosclerosis progression and future plaque rupture events.23

One question about DAPT still remains unclear: how long should the therapy continue? This depends on a multitude of factors, including the indication for which DAPT was prescribed, the type of stent used in PCI, and patient characteristics, such as the degree of advanced coronary artery disease, number of previous coronary events, and atherothrombotic and bleeding risks.20,21,23 To determine the optimal duration of DAPT in patients with coronary artery disease, the American College of Cardiology and the American Heart Association convened a task force on clinical practice guidelines and published a systematic review in 2016.21 This comprehensive report compared the incidence of death, major hemorrhage, myocardial infarction, stent thrombosis, and major adverse cardiac events in patients randomized to prolonged or shorter-duration DAPT after newer generation stent implantation or after myocardial infarction. For some patients with advanced coronary artery disease or multiple coronary events, the recommended dual therapy may be extended beyond 12 months at the risk of increased bleeding, while for others who benefit from latest generation, safer DES, it may be as short as 3 months to 6 months.21 Clinical decision making regarding the duration of DAPT requires careful evaluation of risks and benefits, and the report emphasizes that the “net benefit of extending DAPT is not static but dynamic” depending on the bleeding and thrombotic tendency for each patient.21

Regardless of the indications or the recommended duration of DAPT, there is a consensus that adherence to the prescribed regimen is critical for successful outcomes in management of acute coronary syndrome, and post-PCI.5,18,22,24 However, a 2014 systematic review evaluated patient adherence to DAPT rates and reasons for discontinuation and found that while adherence was generally high at 1 month after PCI, it declined by 12 months after stent implantation.5 Lack of clear communication with physicians and lack of understanding of the importance of DAPT were factors associated with nonadherence to prescribed therapy. On the bright side, the same study showed that rates of adherence following DES implantation increased from 54% in 2004-2006 to 83% in 2007-2009.5This improvement followed publishing of the science advisory by the American Dental Association, American Heart Association, and several other American medical boards in 2007 warning against premature discontinuation of DAPT in patients with coronary artery stents.22 The advisory recognized that antiplatelet therapy is often stopped at the instruction of the health care providers, including dentists, based on the misguided concerns of the excessive bleeding despite no evidence of clinically significant bleeding following dental procedures, availability of effective local measures for controlling oral bleeding, and the fact that most dental and periodontal procedures can be safely performed with only minor risk of bleeding or can be postponed until antiplatelet therapy is completed. The advisory warned that premature discontinuation of antiplatelet therapy can have life-threatening consequences and that patients should consult with their cardiologists or prescribing physicians even if the DAPT discontinuation is advised by another health care provider. Likewise, providers concerned about bleeding associated with medical or dental procedure, should contact the patient’s treating physician to discuss optimal patient management strategy.22

Unfortunately, despite these recommendations, a 2012 analysis of the reasons for the interruption or suspension of the antiplatelet therapy found that more than one-fifth of patients who temporarily discontinued aspirin, clopidogrel, or both agents, reported dental procedures as their reason for interruption of DAPT.24 This underscores the need for ongoing patient and provider education about the importance of adherence to DAPT for a full, uninterrupted prescribed duration to ensure patient safety and successful treatment outcomes.


Patients with atrial fibrillation, or another condition, such as prosthetic heart valves, deep vein thrombosis, or pulmonary embolism, that requires long-term oral anticoagulation are at high risk for stroke and ischemic events.25,26 About 30% of them also have a diagnosis of acute coronary syndrome or undergo PCI, which necessitates DAPT.20 These patients can be prescribed TATT, which combines an oral anticoagulant (most frequently warfarin) with DAPT (aspirin in combination with clopidogrel, or seldom with prasugrel or ticagrelor).25,27,28 However, the therapeutic benefits of the TATT vs a double therapy of oral anticoagulant and clopidogrel, are not clear, as rates of thrombotic and thromboembolic events in patients on oral anticoagulant+clopidogrel alone did not differ from the group on TATT, showing no benefit of adding aspirin.20,29 At the same time, patients on TATT are at significantly higher risk for major bleeding, fatal in approximately one out of 10 bleeding events.25,28,29

The anticoagulation effect of warfarin must be monitored by the International Normalized Ratio (INR)6 and the required INR range for patients on TATT is more narrow (2.0-2.5)28 than the typical recommendation of 2-4.The optimal duration of TATT is also unclear: most guidelines recommend 3 months to 6 months of therapy depending on the stent types and patients’ bleeding risks, but shorter duration may also be effective with a newer generation of stents.20,28 Balancing the risk of thrombotic events and bleeding is challenging but strict adherence to the prescribed regimen is critical and must be communicated to the patient.25


Considering the small number of patients who are managed with TATT, the seriousness of their medical situation, and the short duration of triple therapy, it is unlikely that dental professionals will encounter these patients presenting for routine oral health care. However, knowledge of the cardiovascular conditions that require these complex multi-drug therapies, as well as familiarity with commonly prescribed agents and regimens, contributes to the understanding of disease progression and the recovery process, and ensures patient safety in the dental environment. For patients on long-term dual therapies presenting for oral health care, evaluation of the invasiveness of treatment and potential bleeding risk will guide the development of an appropriate treatment plan and optimal patient management. When peri- or post-procedural bleeding is anticipated, elective treatments should be postponed until prescribed therapy is completed, and urgent care, when necessary, should be provided under the guidance of the patient’s treating physician.22Reviewing patients’ medical histories and all prescribed and over-the-counter medications and supplements at each recare visit, as well as collaborating closely with their treating physicians, will ensure a safe experience and help in anticipating and preventing medical emergencies.


  1. Benjamin EJ, Blaha MJ, Chiuve SE, et al. Heart disease and stroke statistics—2017 update: a report from the American Heart Association. Circulation. 2017;135:e146–e603.
  2. World Health Organization. Cardiovascular Diseases. Available at: factsheets/fs317/en/. Accessed September 27, 2017.
  3. Centers for Disease and Prevention. Heart Disease Facts & Statistics. Available at: Accessed September 27, 2017.
  4. Ellis SG, Riaz H. Bioresorbable stents: the future of interventional cardiology? Cleve Clin J Med. 2016;83(11 Suppl 2):S18–S23.
  5. Czarny MJ, Nathan AS, Yeh RW, Mauri L. Adherence to dual-antiplatelet therapy after coronary stenting: a systematic review. Clin Cardiol. 2014;37:505–513.
  6. Stramoski S, Matthews A. The new generation of blood thinners. Dimensions of Dental Hygiene. 2016;14(10):36–39.
  7. Stramoski S, Matthews A. Treating patients on antiplatelet therapy. Dimensions of Dental Hygiene. 2017;15:34–37.
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  9. Newby LK, LaPointe NMA, Chen AY, et al. Long-term adherence to evidence-based secondary prevention therapies in coronary artery disease. Circulation. 2006;113:203–212.
  10. Baroletti S, Dell’Orfano H. Medication adherence in cardiovascular disease. Circulation. 2010;121:1455–1458.
  11. de Lemos J, O’Rourke R, Harrington, R. Unstable angina and non-ST-segment myocadial infarction. In: Fuster V, Walsh RA, Harrington RA. eds. Hurst’s The Heart. 13th ed. New York: McGraw-Hill Education; 2011.
  12. Kim MC, Kini AS, Fuster V. Definitions of acute coronary syndromes. In: Fuster V, Walsh RA, Harrington RA. eds. Hurst’s The Heart. 13th ed. New York: McGraw-Hill Education; 2011.
  13. January CT, Wann LS, Alpert JS, et al. 2014 AHA/ACC/HRS guideline for the management of patients with atrial fibrillation: executive summary. Circulation. 2014;130:2071–2104.
  14. Chugh SS, Havmoeller R, Narayanan K, et al. Worldwide epidemiology of atrial fibrillation. Circulation. 2014;129:837–847.
  15. Prystowsky EN, Halperin J, Kowey P. Atrial fibrillation, atrial flutter, and atrial tachycardia. In: Fuster V, Walsh RA, Harrington RA. eds. Hurst’s The Heart. 13th ed. New York: McGraw-Hill Education; 2011.
  16. Michaud GF, Stevenson WG. Supraventricular tachyarrhythmias. In: Kasper D, Fauci A, Hauser S, Longo D, Jameson JL, Loscalzo J, eds. Harrison’s Principles of Internal Medicine. 19th ed. New York: McGraw-Hill Education; 2015.
  17. Gibson CM, Mehran R, Bode C, et al. Prevention of bleeding in patients with atrial fibrillation undergoing PCI. N Engl J Med. 2016;375:2423–2434.
  18. Bonaventura A, Montecucco F, Liberale L. Coronary stenting: a matter of revascularization. World J Cardiol. 2017;9:207.
  19. Fischman DL, Leon MB, Baim DS, et al. A randomized comparison of coronary-stent placement and balloon angioplasty in the treatment of coronary artery disease. N Engl J Med. 1994;331:496–501.
  20. Gao X, Chen Y, Fan Z, et al. Antithrombotic regimens for patients taking oral anticoagulation after coronary intervention: a meta-analysis of 16 clinical trials and 9185 patients. Clin Cardiol. 2015;38:499–509.
  21. Bittl JA, Baber U, Bradley SM, Wijeysundera DN. Duration of dual antiplatelet therapy: a systematic review for the 2016 ACC/AHA guideline focused update on duration of dual antiplatelet therapy in patients with coronary artery disease: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. J Am Coll Cardiol. 2016;68:1116–1139.
  22. Grines CL, Bonow RO, Casey Jr DE, et al. Prevention of premature discontinuation of dual antiplatelet therapy in patients with coronary artery stents: a science advisory from the American Heart Association, American College of Cardiology, Society for Cardiovascular Angiography and Interventions, American College of Surgeons, and American Dental Association, with representation from the American College of Physicians. J Am Dent Assoc. 2007;138:652–655.
  23. Halkar M, Lincoff AM. Dual antiplatelet therapy for acute coronary syndromes: how long to continue? Cleve Clin J Med.2016;83:675–688.
  24. Kovacic JC, Lee P, Karajgikar R, et al. Safety of temporary and permanent suspension of antiplatelet therapy After drug eluting stent implantation in contemporary “real-world” practice: Antiplatelet cessation after DES. J Intervent Cardiol. 2012;25:482–492.
  25. Shmyr D, Merwe VV der, Yakiwchuk E, Barry A, Kosar L. Triple antithrombotic therapy for atrial fibrillation and coronary stents. Can Fam Physician. 2017;63:375.
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  27. Mega J, Carreras ET. Antithrombotic therapy: triple therapy or triple threat? ASH Educ Program Book. 2012;2012:547–552.
  28. Lopes RD, Rao M, Simon DN, et al. Triple vs dual antithrombotic therapy in patients with atrial fibrillation and coronary artery disease. Am J Med. 2016;129:592–599.
  29. Dewilde WJM, Oirbans T, Verheugt FWA, et al. Use of clopidogrel with or without aspirin in patients taking oral anticoagulant therapy and undergoing percutaneous coronary intervention: an open-label, randomised, controlled trial. Lancet Lond Engl. 2013;381:1107–1115.



From Dimensions of Dental Hygiene. October 2017;15(10):45-48.


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