CAD and Coronary Syndromes

Question 1

Cardiac Risk Factors

Answer 1

• A. Prior coronary event
• B. Non-cardiac atherosclerosis
• C. Diabetes mellitus
• D. Dyslipidemia
• E. Hypertension
• F. Family History
• G. Cigarette smoking
  
  • The risk factors are as if you’ve already had an MI
• H. Sedentary lifestyle
• I. Obesity
• J. Age – if youre over 70, your age is a bigger risk factor than smoking
• All of these risk factors result in endothelial dysfunction!

Question 2

Clinical syndromes of coronary artery disease

Answer 2

• A. Stable angina – angina that is brought on by external factor (walking, cold, etc.)
• B. Acute coronary syndromes
  
  • ST elevation M.I.
  • Non ST elevation M.I.
  • Unstable angina
  • Noncardiac chest pain – acute coronary syndromes are atypical chest pain that isn’t precipitated like stable angina is
  • These are what a lot of current treatments focus on
• Noncardiac chest pain – coronary vasospasm, tachyarrhymthmias, hypertensive crisis, valvular heart disease; these are ischemic chest pain conditions related to MI

Question 3

mechanism of stable angina

Answer 3

• Fixed coronary artery blockage limits the ability of blood flow to increase with increased demand of the heart muscle for oxygen.
• Study of coronary artery disease is the study of ischemic heart disease

Question 4

Stable angina precipitated angina

Answer 4

• Exercise – particularly upstairs or uphill
• Eating
• Anxiety or other emotional stress
• Cold environment
• Chest pain brought on by myocardium not receiving enough oxygen to meet demands
• Patients are referred to as stable when symptoms, if present, are manageable with either medical or revascularization therapy. Stable angina pectoris, or stable angina, refers to chest discomfort that occurs predictably and reproducibly at a certain level of exertion and is relieved with rest or nitroglycerin. Most patients with ischemic heart disease will experience angina as part of the clinical manifestations of the disease.

Question 5

Treatment of stable angina

Answer 5

• ANGIOPLASTY AND STENTING DOES NOT PROLONG LIFE IN STABLE ANGINA!!!
• A. Aspirin
• B. Beta blockers
• C. Statins & lipid management
  
  • If you take atorvastatin, and you go from 10-20mg, you get a 6% reduction in cholesterol
• D. ACE inhibitors & BP management
• E. Nitroglycerin
• F. Calcium channel blockers
• There is a new group of drugs (PCKS9) that are very potent in reducing cholesterol
• The principal goals in the care of patients with stable ischemic heart disease are to secure the diagnosis, relieve symptoms, and to prevent future cardiac events
• Patients w/ suspected ischemic heart dz - complete history, physical exam, 12 lead ECG.
• Most patients - stress testing to either secure the diagnosis or evaluate its severity.
• Beta blockers - preferred for initial tx of sxs.
• Calcium channel blockers and nitrates - relieve sxs when initial tx with beta blockers not successful or if beta blockers are contraindicated
• Aspirin, statin, smoking cessation, control of BP and excess weight, and optimal management of diabetes.

Question 6

Acute coronary syndrome

Answer 6

• Someone with an angina that won’t go away
• Abrupt onset of severe persisting chest pain
• New onset of resting or nocturnal chest pain
• Abrupt marked increase in frequency and/or severity of stable angina
• New onset chest pain within 2 weeks
• Unstable angina is an acute coronary syndrome that is defined by the absence of biochemical evidence of myocardial damage. It is characterized by specific clinical findings of prolonged (>20 mins) angina at rest, new onset of severe angina, angina that is increasing in frequency, longer in duration or lower in threshold, or angina that occurs after a recent episode of MI.
• When there’s thrombus, the angioplasty is a life prolonging treatment

Question 7

Mechanism of . unstable angina

Answer 7

• (Acute Coronary Syndrome)
  
  • Abrupt decrease in coronary blood flow without increase in myocardial oxygen demand.
  • THIS RESULTS FROM CORONARY THROMBUS

Question 8

Mechanism of coronary thrombus

Answer 8

• Endothelial dysfunction results in lipid (cholesterol) deposition between the INTIMA and the MEDIA
• Endothelial dysfunction secondary to:
  
  • High Cholesterol (LDL cholesterol)
  • High Blood Pressure
  • Tobacco Use
  • Diabetes Mellitus
  • Local factors such as Stress
  • Sedentary Lifestyle
• Monocytes release factors that dissolve a portion of the fibrous cap so that more white cells can come in to clean up
  
  • The fibrous cap can now rupture which exposes a huge mess of macrophages, white blood cells, and lipids
  • There is an immediate clumping of platelets at the surface so the clotting factors are activated – this is when a thrombus forms which may occlude the coronary artery

Question 9

mechanism of coronary thrombus

Answer 9

• Certain focal areas under Intima become sites of LIPID POOLS
• Lipid Pools injure the endothelium (intima) resulting in formulation of fibrous cap over intima (& lipid pool). Initially this is stable.
• BUT, the body wishes to “CLEAN UP” the lipid pools.
• White blood cells leave the circulation and enter the pool “eating” the lipids.
• These white blood cells produce enzymes (“proteases” ) which dissolve the edges of the fibrous cap
• The thinned fibrous cap RUPTURES exposing the thrombogenic lipid pool to the circulation
• Circulating platelets aggregate and a platelet thrombus is formed (“White Thrombus”)
• Fibrin thrombus then forms trapping red cells in the large fibrin clot (“Red Thrombus”) and partially or totally occludes the coronary artery

Question 10

Clinical events from coronary thrombus

Answer 10

• ACUTE CORONARY SYNDROMES
• Acute ST elevation myocardial infarction (STEMI): TOTAL OCCLUSION
• Acute Non-ST elevation myocardial infarction (NSTEMI): PARTIAL OCCLUSION
  
  • They are lysing their thrombus so it stabilizes and then the thrombus reoccurs and it destabilizing
  • ST segment depression is classic
  • Unstable angina
• What is the one thing that distinguishes STEMI or NSTEMI from people who have an angina but no infarction
  
  • TROPONIN!!! – positive troponin = acute MI
  • There are growing sensitivities to troponin
• Resting or Accelerating Angina (Unstable Angina): TRANSIENT OCCLUSION

Question 11

Hospital treatment of acute coronary syndromes

Answer 11

• STEMI: Emergency Angioplasty
• NSTEMI: Urgent Angioplasty (1-3 days after admission)
• UNSTABLE ANGINA: Stress Test and/or Cardiac Catheterization – Angioplasty if indicated
• Getting to the emergency room is a major factor
• Minutes save muscle!! The outcome is greatly improved by the speed with which the patient is seen and treated
• Stress echo will tell you if this is ischemic or not

Question 12

Long term treatment of acute coronary syndromes

Answer 12

• Aspirin
  
  • Can increase bleeding risk without reducing thrombotic risk
  • There is a right dose = 70-100mg
• Clopidogrel (Plavix) for one year
• Beta-Blocker (atenolol, metoprolol, carvedilol) – we still put people on them if they need it for blood pressure
  
  • He only likes carvedilol – its an alpha and beta blocker and doesn’t cause insulin resistance or elevate cholesterol and doesn’t cause as much bronchospasm as the other ones
  • The other two raise cholesterol and precipitate asthma sometimes
• High dose statin
  
  • He doesn’t care what their cholesterol is – they have already demonstrated that they have abnormal lipid metabolism
• ACE inhibitor (lisinopril) or ARB
• Weight reduction – low fat diet
• DAILY aerobic exercise
• NO TOBACCO