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Ischemic heartdisease


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Ischemic heartdisease

  1. 1. Ischemic Heart Disease Vincent Steniger
  2. 2. Contents Overview <ul><li>Coronary Artery Disease </li></ul><ul><li>Heart Anatomy </li></ul><ul><li>Atherosclerotic Plaque/Atheroma </li></ul><ul><li>Angina Pectoris </li></ul><ul><li>Myocardial Infarction </li></ul><ul><li>Sudden Death </li></ul><ul><li>Overall Management </li></ul><ul><li>Ischemic Heart Disease and Dentistry </li></ul>
  3. 3. Coronary Artery Disease
  4. 4. CAD: Statistics <ul><li>CAD is the largest killer of American males and females </li></ul><ul><li>13 million Americans have CAD </li></ul><ul><li>1.1 million MI’s per year </li></ul><ul><li>Every 26 seconds  an American will suffer from a coronary event </li></ul><ul><li>Every 60 seconds  an American will die because of a coronary event </li></ul><ul><li>@ 42% of those having a coronary event will die from it </li></ul><ul><li>@350K people die per year because of a coronary event in the Emergency Department before even being admitted to the hospital </li></ul><ul><li>Death Rate in 2001: </li></ul><ul><ul><li>177 in 100,000 </li></ul></ul>
  5. 5. CAD: Demographics and Statistics <ul><li>84% of those who die from CAD are 65 or older </li></ul><ul><li>If under the age of 65, 80% mortality rate with the first myocardial infarction </li></ul><ul><li>Within 1 year of initial MI: </li></ul><ul><ul><li>25% of men and 38% of women will die </li></ul></ul><ul><li>Within 8 years of initial MI: </li></ul><ul><ul><ul><li>50% of men and women under 65 will die </li></ul></ul></ul><ul><li>An average of 11.5 years of life are lost due to an MI </li></ul><ul><li>IMPORTANT: </li></ul><ul><ul><li>50% of men and 64% of women who have died suddenly via CAD DID NOT HAVE ANY PREVIOUS SYMPTOMS </li></ul></ul><ul><li>Sudden Death: </li></ul><ul><ul><li>Those with a previous history of MI have a 5-6 times Sudden Death rate compared to the general population </li></ul></ul>
  6. 7. Manifestations of Coronary Artery Disease/Ischemic Heart Disease <ul><li>Sudden death </li></ul><ul><li>Heart Attack/Myocardial infarction </li></ul><ul><li>Acute coronary syndrome </li></ul><ul><li>Stable/Unstable angina pectoris </li></ul><ul><li>Heart failure or Arrhythmia </li></ul>
  7. 8. Exactly what is Coronary Artery Disease (Ischemic Heart Disease) and how/why does it occur? <ul><li>Start with anatomy… </li></ul>
  8. 9. Heart Anatomy <ul><li>Facts: </li></ul><ul><ul><li>The heart is about the size of a fist and weighs less than 1 pound </li></ul></ul><ul><ul><li>The average bpm is 72 </li></ul></ul><ul><ul><li>The heart pumps 2,500 to 5,000 quarts of blood through vasculature stretching 75,000 miles </li></ul></ul><ul><ul><li>Blood Supply to the heart: </li></ul></ul><ul><ul><ul><li>Right Coronary Artery  Right Atrium and Right Ventricle </li></ul></ul></ul><ul><ul><ul><ul><li>Posterior Descending Artery  bottom of Left Ventricle </li></ul></ul></ul></ul><ul><ul><ul><li>Left Main Coronary Artery: </li></ul></ul></ul><ul><ul><ul><ul><li>Circumflex Artery  Left Atrium and Side and Back of Left Ventricle </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Left Anterior Descending Artery  Front and bottom of Left Ventricle </li></ul></ul></ul></ul>
  9. 11. Definition <ul><li>&quot; Ischaemia &quot; refers to an insufficient amount of  blood. The coronary arteries are the only source of  blood for the heart muscle. If this coronary arteries are blocked, the blood supply will reduce. </li></ul>
  10. 12. Risk Factors for Ischemic Heart Disease <ul><li>Obesity </li></ul><ul><li>Genetics </li></ul><ul><li>Diabetes Mellitus </li></ul><ul><li>Tobacco Use </li></ul><ul><li>Latent Life Style (lack of exercise) </li></ul><ul><li>Hypertension </li></ul><ul><li>Hypercholesterolemia </li></ul><ul><li>Age </li></ul>
  11. 13. <ul><li>Why would there be an insufficient blood supply to the heart? </li></ul><ul><ul><li>Remember that the coronary arteries are the only source of fuel to the heart </li></ul></ul><ul><ul><li>The coronary arteries may become partially/completely occluded: </li></ul></ul><ul><ul><ul><li>Atherosclerotic Plaques </li></ul></ul></ul>
  12. 14. Atherosclerotic Plaque: Definition and Formation <ul><li>Focal accumulation of smooth muscle cells, foam cells, cholesterol crystals and lipid under the endothelium of the artery (within the Tunica Intima) </li></ul><ul><li>Given time, this plaque can protrude into the lumen of the vessel reducing blood flow </li></ul><ul><li>Often develops at branch points or curves within the vasculature  blood is slowed and/or turbulent </li></ul>
  13. 15. Atheroma/ Atherosclerotic Plaque <ul><li>Where does the plaque begin?  within the Tunica Intima, the innermost wall of the artery </li></ul><ul><li>What is a plaque made of? </li></ul><ul><ul><li>Superficial fibrous cap made of smooth muscle cells, collagen, elastin and proteins </li></ul></ul><ul><ul><ul><li>Also contains Macrophages, Foam Cells, T Cells </li></ul></ul></ul><ul><ul><li>Necrotic Center of cholesterol crystals, lipids, Apolipoprotein B  LDL </li></ul></ul>
  14. 18. Atheroma Formation: The Hypothesized Process <ul><li>(1) Via damage to the arterial endothelium via turbulent blood flow, toxins such as those from tobacco, hypertension, high concentration of fats or genetic factors there is now a “hole” within the endothelium </li></ul><ul><ul><li>Remember that the endothelium is only 1 cell layer thick </li></ul></ul><ul><li>(2) Blood and whatever the blood contains (LDL, toxins…) can leak into this hole irritating the vessel </li></ul><ul><li>(3) Because of this irritation, there is a stimulated increase in smooth muscle cells and collagen matrix </li></ul><ul><li>(4) Platelets and monocytes adhere to the injured area of the endothelium and release cytokines creating a wave of chemotaxis. These cells also cause an upregulation of adhesion factors for inflammatory cells on the endothelial cell surface </li></ul><ul><li>(5) More monocytes and T cell are able to enter the endothelial hole via these receptors </li></ul><ul><li>(6) Once monocytes have entered the vascular wall they can differentiate into macrophages </li></ul><ul><li>(7) Via lipid receptors on the Macrophages, lipids are phagocytized creating foam cells </li></ul><ul><li>(8) This process continues and the atheroma enlarges </li></ul><ul><li>(9) Foam cells can eventually act to disrupt the fibrous cap of the atheroma via proteolytic degradation resulting in ulceration of the plaque and adherence of platelets (thrombus) and emboli formation </li></ul><ul><li>(10) A plaque, thrombus or emboli can cause partial or full occlusion of a blood vessel </li></ul>
  15. 19. Atheroma: Continued <ul><li>As the atheroma within the coronary arteries enlarges, the blood flow to the heart decreases and therefore so does the O2 supply </li></ul><ul><li>The heart is not in danger of hypoxia until 50% of the vessel is occluded </li></ul><ul><li>As the heart senses a decrease in O2, there is attempted compensation: </li></ul><ul><ul><li>Increase Heart Rate </li></ul></ul><ul><ul><li>Increase Blood Pressure </li></ul></ul><ul><ul><li>Aggravation/Worsening of the atheroma </li></ul></ul><ul><li>When 70% of the artery is occluded, Angina Pectoris will occur </li></ul>
  16. 20. Angina Pectoris <ul><li>At least 70% occlusion of coronary artery resulting in pain. What kind of pain? </li></ul><ul><ul><li>Chest pain </li></ul></ul><ul><ul><li>Radiating pain to: </li></ul></ul><ul><ul><ul><li>Left shoulder </li></ul></ul></ul><ul><ul><ul><li>Jaw </li></ul></ul></ul><ul><ul><ul><li>Left or Right arm </li></ul></ul></ul><ul><li>Usually brought on by physical exertion as the heart is trying to pump blood to the muscles, it requires more blood that is not available due to the blockage of the coronary artery(ies) </li></ul><ul><li>Is self limiting  usually stops when exertion is ceased </li></ul>
  17. 21. Angina Pectoris Continued <ul><li>Angina Pectoris can be Stable or Unstable: </li></ul><ul><li>Stable: </li></ul><ul><ul><li>The pain and pattern of events is unchanged over a period of time (months  years) </li></ul></ul><ul><li>Unstable: </li></ul><ul><ul><li>The pain and pattern is changing, be it in duration, intensity or frequency </li></ul></ul><ul><ul><li>A Myocardial Infarction waiting to happen </li></ul></ul>
  18. 22. Myocardial Infarction <ul><li>Partial or total occlusion of one or more of the coronary arteries due to an atheroma, thrombus or emboli resulting in cell death (infarction) of the heart muscle </li></ul><ul><li>When an MI occurs, there is usually involvement of 3 or 4 occluded coronary vessels </li></ul>
  19. 23. Myocardial Infarctions: Statistics <ul><li>250,000 deaths per year. </li></ul><ul><li>30% mortality within the first 2 hours </li></ul><ul><li>45 Minutes of Ischemia: </li></ul><ul><ul><li>Cardiac muscle death occurs </li></ul></ul><ul><li>How is the Diagnosis Made? </li></ul><ul><ul><li>Electrocardiographic changes </li></ul></ul><ul><ul><ul><li>ST elevation </li></ul></ul></ul><ul><ul><li>Myocardial enzyme elevation </li></ul></ul><ul><ul><ul><li>Creatine kinase </li></ul></ul></ul><ul><ul><ul><li>Troponin </li></ul></ul></ul><ul><ul><ul><li>C Reactive Protein </li></ul></ul></ul>
  20. 24. MI, Atheroma, Other Sequelae <ul><li>When there is an atheroma, as mentioned before there can be rupture resulting in thrombus formation because of the build up of platelets </li></ul><ul><li>When there is breakage of the thrombus there is emboli formation </li></ul><ul><li>An emboli can travel to the brain (cerebral infarct) can remain in the heart (myocardial infarct) or even travel to the extremities cutting off blood supply </li></ul><ul><li>As the area beneath the is disrupted atheroma hemorrhages, there can is increased risk of abscess formation and infection </li></ul>
  21. 25. Complications of Myocardial Infarctions <ul><li>Infarction leading to inability of the heart to function properly leading to Heart Failure </li></ul><ul><li>Angina/Pain </li></ul><ul><li>Cardiogenic shock </li></ul><ul><li>Ventricular aneurysm and rupture </li></ul><ul><li>Embolism Formation </li></ul><ul><li>Arrhythmias  Myocardial Infarctions can lead to Ventricular Fibrillation (shockable!) </li></ul>
  22. 26. Sudden Death <ul><li>Sudden Death : </li></ul><ul><ul><li>250,000 deaths in the US per year are caused by what is referred to as “sudden” cardiac death </li></ul></ul><ul><ul><li>Sudden Cardiac Death is also known as a “Massive Heart Attack” in which the heart converts from sinus rhythm to ventricular fibrillation </li></ul></ul><ul><ul><li>In V-Fib, the heart is unable to contract fully resulting in lack of blood being pumped to the vital organs </li></ul></ul><ul><ul><li>V-Fib requires shock from defibrillator “SHOCKABLE RHYTHM” </li></ul></ul>
  23. 27. Management of Ischemic Heart Disease: <ul><li>Pharmaceuticals: </li></ul><ul><ul><li>Beta Blockers </li></ul></ul><ul><ul><ul><li>Act either selectively or non-selectively on Beta receptors: </li></ul></ul></ul><ul><ul><ul><ul><li>Beta 1  cardiac muscle  increase rate and contraction </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Beta 2  dilates bronchial smooth muscle </li></ul></ul></ul></ul><ul><ul><li>Ca ++ Channel Blockers </li></ul></ul><ul><ul><ul><li>Acts on vasculature blocking Ca++ and causing vasodilation </li></ul></ul></ul><ul><ul><li>Nitrates </li></ul></ul><ul><ul><ul><li>Vasculature vasodilation </li></ul></ul></ul><ul><ul><li>Anti-Hypercholesterolemia </li></ul></ul><ul><ul><ul><li>HMG CoA Reductase Inhibitors  reduction in “manmade” cholesterol thus helping to reduce atheroma formation </li></ul></ul></ul><ul><ul><li>Antiplatelet Medication: </li></ul></ul><ul><ul><ul><li>Clopidogrel (Plavix) </li></ul></ul></ul><ul><ul><ul><li>Aspirin </li></ul></ul></ul>
  24. 28. Management of Ischemic Heart Disease: <ul><li>Lifestyle: </li></ul><ul><ul><li>Diet </li></ul></ul><ul><ul><li>Exercise Preventive treatment </li></ul></ul><ul><ul><li>Low fat, low cholesterol diet </li></ul></ul><ul><ul><li>Cessation of smoking </li></ul></ul><ul><ul><li>R ed wine (in moderation) </li></ul></ul>
  25. 29. Dental Considerations <ul><li>Assessment and Overall Management </li></ul><ul><li>Pharmaceuticals </li></ul><ul><li>Emergency Situations </li></ul><ul><li>Oral Effects of Pharmaceuticals </li></ul><ul><li>Antibiotic Prophylaxis </li></ul><ul><li>Post MI: when to treat </li></ul>
  26. 30. Assessment <ul><li>Consider three areas: </li></ul><ul><ul><li>How severe or stable the ischemic heart disease is </li></ul></ul><ul><ul><li>The emotional state of the patient </li></ul></ul><ul><ul><li>The type of dental procedure </li></ul></ul>
  27. 31. RISK <ul><li>Major Risk for Perioperative Procedures: </li></ul><ul><ul><li>Unstable Angina (getting worse) </li></ul></ul><ul><ul><li>Recent MI </li></ul></ul><ul><li>Intermediate Risk for Perioperative Procedures: </li></ul><ul><ul><li>Stable Angina </li></ul></ul><ul><ul><li>History of MI </li></ul></ul><ul><li>Most dental procedures, even surgical procedures fall within the risk of less than 1% </li></ul><ul><li>Some OMFS procedures fall within an intermediate risk of less than 5% </li></ul><ul><li>Highest risk procedures  those done under general anesthesia </li></ul>
  28. 32. Management for Low-Intermediate Risk <ul><li>Short appointments </li></ul><ul><li>AM appointments </li></ul><ul><li>Comfort </li></ul><ul><li>Vital Signs Taken </li></ul><ul><li>Avoidance of Epinephrine within Local Anesthetic or Retraction Cord </li></ul><ul><li>O2 Availability </li></ul>
  29. 33. Dental Considerations for Ischemic Heart Disease <ul><li>Pharmaceutical Considerations: </li></ul><ul><ul><li>Interaction of NSAIDS with Beta Blockers </li></ul></ul><ul><ul><li>If patient is taking a non-selective Beta Blockers  limit local anesthetic use to 2 carpules with 1:100K epinephrine (increase in receptors for epinephrine) </li></ul></ul><ul><ul><li>In uncontrolled hypertensive patients use judgment when giving epinephrine  Carbocaine use encouraged </li></ul></ul><ul><ul><li>Statins (HMG CoA Reductase Inhibitors) when combined with Erythromycin and Clarithromycin can lead to renal failure and muscle pathology </li></ul></ul>
  30. 34. Dental Considerations for Ischemic Heart Disease <ul><li>Pharmaceuticals and Oral Manifestations: </li></ul><ul><ul><li>Of Note: </li></ul></ul><ul><ul><ul><li>Ca ++ Channel Blockers, mainly (nifedipine, verapamil, diltiazem, amlodipine) may cause gingival hyperplasia in some patients </li></ul></ul></ul><ul><ul><ul><li>Consider: </li></ul></ul></ul><ul><ul><ul><ul><li>Meticulous Oral Hygiene for the patient </li></ul></ul></ul></ul><ul><ul><ul><ul><li>3 month recall of scaling, possible SRP </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Gingivectomy if needed </li></ul></ul></ul></ul>
  31. 35. <ul><li>Common Situations: </li></ul><ul><ul><li>Orthostatic Hypotension due to use of anti-hypertensives (beta blockers, nitroglycerin…) </li></ul></ul><ul><ul><ul><li>Raise chair slowly </li></ul></ul></ul><ul><ul><ul><li>Allow patient to take his/her time </li></ul></ul></ul><ul><ul><ul><li>Assist patient in standing </li></ul></ul></ul><ul><ul><li>Post-Op Bleeding: </li></ul></ul><ul><ul><ul><li>When patients on Plavix or Aspirin, expect increased bleeding because of decreased platelet aggregation </li></ul></ul></ul>Dental Considerations for Ischemic Heart Disease
  32. 36. Dental Considerations for Ischemic Heart Disease <ul><li>Emergent Situations: </li></ul><ul><ul><li>Possible MI: </li></ul></ul><ul><ul><ul><li>Remember that pain in the jaw may be referred pain from the myocardium  assess the situation, have good patient history, follow ABC’s </li></ul></ul></ul><ul><ul><li>Angina: </li></ul></ul><ul><ul><ul><li>In situations of angina pectoris, all operatories should have nitroglycerin to be placed sublingually </li></ul></ul></ul>
  33. 37. Dental Considerations for Ischemic Heart Disease <ul><li>Emergent Situations: </li></ul><ul><ul><li>Chest Pain-MI: </li></ul></ul><ul><ul><ul><li>STOP PROCEDURE </li></ul></ul></ul><ul><ul><ul><li>Remove everything from patient’s mouth </li></ul></ul></ul><ul><ul><ul><li>Give sublingual nitroglycerin </li></ul></ul></ul><ul><ul><ul><li>Wait 5 minutes  if pain persists, give more nitroglycerin, assume MI </li></ul></ul></ul><ul><ul><ul><li>911 </li></ul></ul></ul><ul><ul><ul><li>Give chewable aspirin  ABC’s </li></ul></ul></ul>
  34. 38. Post MI: When to Treat <ul><li>Why delay treatment? </li></ul><ul><ul><li>Remember that with an MI there is damage to the heart, be it severe or minimal that may effect the patient’s daily life </li></ul></ul><ul><li>MI within 1 month  Major Cardiac Risk (ASA IV) </li></ul><ul><li>MI within longer then 1 month: </li></ul><ul><ul><li>Stable  routine dental care ok </li></ul></ul><ul><ul><li>Unstable  treat as Major Cardiac Risk </li></ul></ul><ul><li>Older studies suggest high re-infarction rates when surgery performed within 3 months, 3-6 months… however, this was abdominal and thoracic surgery under general anesthesia </li></ul><ul><li>New research suggests delaying elective tx for 1 month is advisable. Emergent care should be done with local anesthetic without epinephrine and monitoring of vital signs </li></ul><ul><li>When in doubt: </li></ul><ul><ul><li>CONSULT THE PCP OR CARDIOLOGIST </li></ul></ul>
  35. 39. Conclusion: <ul><li>When treating patients with Ischemic Heart Disease or recent MI… </li></ul><ul><ul><li>Use caution and common sense </li></ul></ul><ul><ul><li>When in doubt: </li></ul></ul><ul><ul><ul><li>CONSULT THE PCP OR CARDIOLOGIST </li></ul></ul></ul>