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

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 • Angina • Myocardial infarction • Silent Ischemia – Asymptomatic episodes of myocardial ischemia in those with CAD Dx

• Syndrome X

2

– 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 • 65 – 80 percent sensitive • 65 – 75 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 (http://brighamrad.harvard.edu/education/online/Cardiac/SS/SS.html) – 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

• 90% of MIs are due to thrombus formation that obstructs an atherosclerotic coronary artery 25 26 27

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 120 – 130 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

• 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 • • • • •

37

Hypertension: Medical Management • • • •

38

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

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

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

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

41 42

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 (VO2R or HRR) • Can expect the following outcomes – 10 – 15 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