Pathophysiology of Ischemic Heart Disease

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1 1 Pathophysiology of Ischemic Heart Disease 2 Ischemic Heart Disease Coronary artery disease leading cause of death in industrialized countries Leads to angina, myocardial infarction, sudden cardiac death, and chronic heart failure Causes Modifiable and non-modifiable risk factors Arteriosclerosis natural changes in the intima, connective tissue, and diameter of artery Atherosclerosis pathologic phenomenon occurring in the coronary, carotid, iliac, and femoral arteries as well as the aorta 3 Coronary Artery Anatomy 4 Normal Coronary Artery 5 The atherosclerotic process Response to Injury hypothesis - inflammatory response resulting in proliferation of tissue within the arterial wall which may result in obstruction of blood flow Causes: -elevated levels of cholesterol and triglyceride in the blood, -high blood pressure turbulent blood flow -tobacco smoke. -glycolated substances 6 Response to Injury Hypothesis (pg. 230) 1. Injury to endothelium with release of growth factors 2. Monocytes attach to endothelium 3. Monocytes mirgrate to the intima, take up cholesterol, form fatty streaks 4. Platelets adhere to the endothelium and release growth factors 5. Migration of smooth muscle cells from the media to the intima 6. Fibromuscular plaque 7 Atherosclerotic Plaque 8 Treatment Mainly through aggressive risk factor modification Smoking cessation High cholesterol reduce LDL, increase HDL Weight reduction Blood pressure management Hypertension Increase physical activity Blood Glucose modification Primary vs. Secondary risk reduction 9 Regression??? Even with aggressive medical management, may only see 1-2% reduction in stenosis 1

2 severity (Resource Manual, 2000) Lipid lowering may Reduce risk of MI and early death Stabilize plaques Exercise shown to reduce plaques by as much as 25% (Hambrecht, 1993) 10 Ischemic Heart Disease A result of CAD Imbalance between supply and demand Narrowing and hardening of the arteries leads to imbalance between the supply and demand of blood for cardiac muscle 11 Etiology of Ischemic Heart Disease 12 Etiology of Ischemic Heart Disease Myocardial Oxygen Supply O2 carrying capacity Diastolic perfusion pressure Venturi effect Coronary vascular resistance External compression Intrinsic Control of Coronary Tone Dilation Vs. contraction Nitric Oxide and Endothelin 13 Vascular Control Nitric Oxide Formally discovered (Nobel Prize) in1998. Implicated in many physiological processes In the intact, coronary artery wall, regulates vascular tone by relaxing neighboring arterial smooth muscle in response to many different substances and conditions Find reduce amounts of nitric oxide in those with significant CAD, thus less dilation and less blood supply Endothelin Powerful vasoconstrictor Elevated in those with damage endothelial wall 14 Etiology of Ischemic Heart Disease Myocardial oxygen demand Wall tension Wall stress = P(ventricular) r (vent.) 2 (h; wall thickness) Heart Rate ATP consumption Contractility Force of contraction 15 IHD: Demand > Supply IHD: Demand > Supply Angina Myocardial infarction Silent Ischemia Asymptomatic episodes of myocardial ischemia in those with CAD Dx Syndrome X 2

3 Symptoms of angina pectoris with no evidence of significant atherosclerosis. May be due to problems in smallest of coronary arteries that are not visualized by angiographic techniques 16 Diagnosis of CAD/IHD All methods of Dx are compared to angiography, 2 Electrocardiogram Exercise stress testing percent sensitive percent specificity 17 Gold Standard in Dx of IHD Coronary Angiography Before STENT Placement 18 Angiography (con t) 19 Diagnosis of IHD Nuclear Exercise Studies ( A radionucleotide is injected intravenously at peak exercise and nuclear imaging is then performed Looking for cold spots in images 90 percent sensitive; 80 percent specific Exercise Echocardiography Pharmacologic Stress Tests For patients unable to exercise 20 Medical Management Pharmacologic treatment Acute Recurrent Percutaneous transluminal coronary angioplasty (PTCA) Coronary Artery Bypass Graft (CABG) Saphenous vein graft Internal mammary artery Beating Heart CABG 21 PTCA 22 CABG 23 Angina Demand > Supply Diagnosis (DX) stress testing, angiography Treatment Pharmacologic Secondary Risk Reduction Exercise based on symptomology 24 Myocardial Infarction (MI) Condition of irreversible necrosis of heart muscle that results from prolonged ischemia Approximately 1.5 million occur each year with 30% of these resulting in death 3

4 90% of MIs are due to thrombus formation that obstructs an atherosclerotic coronary artery MI: Causes of thrombus formation Atherosclerotic plaque rupture is considered to be the major trigger of coronary thrombosis formation Dysfunctional endothelium May occur in the setting of certain triggers Physical activity or emotional stress 28 Pathology of MI Transmural Infarct Subendocardial Infarct Functional Changes Impaired contractility Stunning Vs. Hibernation Ventricular Remodeling 29 Dx and Rx of MI Dx ECG abnormalities Serum Markers of Infarction Rx Acute usually involves thrombolytic therapy PTCA Hospital Management 30 Potential Triggering Mechanisms of Acute Myocardial Infarction 31 Exercise Responses End-points for testing Heart rate bts/min 70 % pred max HR 5 METs Mild angina or dyspnea 2 mm ST-segment depression Hypotension Non-sustained VTach 32 Exercise Prescription 33 Hypertension 4

5 Epidemiology 50 million Americans Cause as many as 800,000 deaths per year Essential 95% of causes are of unknown origin Secondary Hypertension Definable cause such as age, severity, onset, SxS, Family history 34 Hemodynamic progression of essential hypertension (EH) 35 Etiology of Hypertension BP = Q x TPR Heart Blood vessel tone Kidney Hyperinsulimia 36 Hypertension: End Organ Damage Heart left ventricular hypertrophy, CHF, myocardial ischemia, infarction Cerebrovascular stroke Aorta and pulmonary vascular aneurysm; atherosclerosis Kidney nephrosclerosis, renal failure Retina arterial narrowing, hemorrhages, papilledemia 37 Hypertension: Medical Management Mild hypertension - weight control and proper diet should be initiated along with exercise Pharmacologic treatment should be considered Moderate to severe should always be exercise tested first using similar modes as those with CAD Mode for training cardiovascular; can do light circuit training but no static resistance or heavy weight lifting 38 Hypertension: Medical Management Nonpharmacologic treatment Weight reduction Exercise sedentary have a 20 50% higher risk of developing hypertension than their more active peers. Diet Sodium Potassium Alcohol Other Relaxation Therapy 39 Behavioral Strategies and hypertension 5

6 40 Pharmacologic Diuretics reduce circulatory volume, Q, and mean arterial pressure Sympatholytic agents block peripheral vasoconstriction and reduce heart rate and contractility Vasodilators reduce peripheral resistance in capetence vessels Renin-angiotensin system antagonists Hypertension: Exercise Testing Standard Protocols Medications should be taken at usual time relative to the exercise bout Paying special attention to exaggerated pressor response (SBP > 260 mmhg; DBP > 115 mmhg) 43 Hypertension: Prescription Cardiorespiratory start around 55 to 70% exercise intensity (VO 2 R or HRR) Can expect the following outcomes mmhg decrease in systolic BP in a 4 to 6 week period 5 10 mmhg decrease in diastolic BP Resistance 8 to 10 exercises, 10 to 15 repetitions each 6