ISCHEMIC HEART DISEASESBY

DR. SUMAIRA IQBAL

LEARNING OBJECTIVES

• By the end of lecture students should be able to

• Enlist causes of ischemic heart diseases

• Explain role of collateral circulation

• Summarize complication of MI

• Explain angina and its pathophysiology

• Outline the treatment of ischemic heart diseases

INTRODUCTION

• 35% people age above 65 years suffer from IHD in US

• Ends up at acute coronary occlusion and fibrillation

• Atherosclerosis is the cause– altered lipid metabolism

• Overweight

• Sedentary lifestyle

• Arteries become calcified

CAUSES

A. Not Reversible

1. Aging

2. Male Sex

3. Genetic Predisposition

B. Reversible

1. Cigarette smoking (↓HDL) → doubles chances of dying from heart attack)

2. ↑BP → ↑ vascular damage

3. Obesity - doubles mortality

C. Partially reversible

1. Cholesterol or triglycerides

2. Hyperglycemia or diabetes mellitus

3. Low levels of HDL

D. Others

1. Physical inactivity

2. Personality type

3. C-reactive protein

ACUTE CORONARY OCCLUSION

1. Thrombus– local atherosclerotic plaque

• Plaque formation due to rough surface , platelets aggregate and fibrin adhere

2. Embolus

3. Local coronary artery spasm—direct stimulation of vascular smooth muscles by edges of atherosclerotic plaque

• Collateral circulation anastomosis – life saving in IHD to restore blood supply of the ischemia area

COLLATERAL CIRCULATION

• After occlusion blood supply ceases little or no blood flow leads to ischemia leading to infarction

• After infarction blood from collaterals and local occluded vessel dilatation leads to stagnation of blood in the infarcted area

SUB ENDOCARDIAL INFARCTION

• Sub endocardial muscle frequently becomes infarcted

• No evidence of infarction in the outer surface portions of the heart.

• Reason: sub endocardial muscle has a higher oxygen consumption and extra difficulty obtaining adequate blood flow because the blood vessels in the sub endocardium are intensely compressed by systolic contraction of the heart

• Compromised blood flow to any area of the heart causes damage first in the subendocardial regions then spreads outward toward the epicardium.

CAUSES OF DEATH AFTER ACUTE CORONARY OCCLUSION

1. Decreased cardiac output

2. Damming of blood in the pulmonary blood vessels and then death resulting from pulmonary edema

3. Fibrillation of the heart

4. Rupture of the heart.

DECREASED CARDIAC OUTPUT

• Non functional ischemic and weak fiber fail to contract with full strength

• Systolic stretch– bulging of ischemic tissue while contraction

• Pumping ability is reduced– cardiac output is decreased

• Cardiac failure, peripheral ischemia and cardiogenic shock occurs

DAMMING OF BLOOD IN THE BODY– PULMONARY EDEMA

• Blood not forced forward stays in atria and pulmonary circulation

• Backpressure stasis

• Decreased blood flow to kidney lead to decreased urinary output

• Congestive symptoms

FIBRILLATION OF VENTRICLES AFTER MYOCARDIAL INFARCTION

1. Elevated ECF K+ conc.

2. Injury current.

3. Powerful sympathetic reflexes.

4. Dilatation of the ventricles – circus movement.

RUPTURE OF INFARCTED AREA

• After few days of infarction the dead tissue degenerate become thin prone to rupture

• During contraction systolic stretch

• Due to rupture—cardiac tamponade occurs

STAGES OF RECOVERY FROM ACUTE M.I

STAGES OF RECOVERY FROM ACUTE M.I

• In ischemia central tissue non functional

• Large infarct—tissue dies

• Replaced by fibrous tissue

• Collateral develops

• Tissue become functional or undergo fibrosis

• Fibrous tissue contract and degenerates

`CORONARY STEAL’ SYNDROME

• On vascular dilatation, most of the blood flowing into the coronary vessels to flow through the normal muscle tissue, thus leaving little blood to flow through the small anastomotic channels into the ischemic area, so the condition worsens.

• Function of the Heart after recovery

Role of cardiac reserve-

• Pain in Coronary disease-

Release of acidic substances that stimulate pain endings in the cardiac muscle.

ANGINA PECTORIS

• Definition- sustain progressive constriction of coronary arteries leading to cardiac pain

• Site of pain- beneath sternum migrates to left arm, shoulder, neck or even side of face

• Type– hot, compressing pressure

• Reason for this distribution of pain- same spinal cord segment

ANGINA PECTORIS

• Chronic Angina Pectoris-

• Emotional events leads to increase metabolism and strong sympathetic stimulation

• Also exacerbates by cold temperature and full stomach

• Treatment

- Rest ( by reducing workload on heart)

- Nitroglycerin

- Beta Blockers

SURGICAL TREATMENT OF CORONARY DISEASE

• Aortic- Coronary Bypass Surgery.

• Coronary Angioplasty.

THANK YOU