Remix education

Ischemic Heart Disease

Ischemic Heart Disease

Ischemic heart disease results from imbalance between the myocardial need for oxygen and the adequacy of the blood supply.
The cause of reduction in coronary blood flow is atherosclerotic narrowing of the coronary vessel in 85-95% of cases. Ischemic heart disease can be classified depending upon the rate of development of arterial narrowing
• Myocardial Infarction (MI, AMI)
• Angina pectoris
• Ischemic cardiomyopathy

Myocardial infarction

Myocardial infarction is frequent fatal form of IHD (ischemic heart disease), it usually result from sudden reduction or arrest of a significant portion of coronary flow. In this case thrombotic occlusion is almost always present in one or more coronary arterial trunk.

Angina Pectoris

√ Angina pectoris is a symptom complex consisting of severe chest pain resulting from transient ischemia. Most often it is precipitated by exercise or exertion and relieved by rest or sublingual nitroglycerin.
√ The underline cause of such episodic pain is coronary atherosclerosis and sometimes thrombotic occlusion of smaller coronary branches.
√ Ischemia Cardio Myopathy
It is generally seen in the later decades of life in patients who had slow progressive impairment of the coronary blood flow leading eventually to myocardial, ischemic and diffuse fibrotic changes
Pathogenesis of IHD
Pathogenesis of all forms of IHD is an imbalance between myocardial oxygen supply and demand. Three factors are involved
• The adequacy of coronary arterial flow
• The level of myocardial metabolic demand
• Oxygen transport capacity of blood

Morphological Types

There are 4 types of IHD, two of them are mentioned below:
Transmural infarcts mostly occur in left ventricle and occasionally they may extend into the left atrium or immediate adjacent portion of the right ventricle.
The thicker walls of left ventricle carrying most of the cardinal work load, is more vulnerable to hypoxia than the thinner walled, light ventricle and atria.

The classical intramural infract extend from the endocardium to the Beta Blockerseipicardium They may be as small as 2.5cm in transverse diameter or may be massive in size and may involve the entire circumference of the left ventricle. Usually infarct ranges from 4-10cm in longest dimension.
If there is blockade of left anterior ascending coronary artery, which is in 40-50% of cases, infarct is seen in the anterior wall of left ventricle near apex and anterior 2/3rd of the intraventricular septum.
Blockade right coronary artery seen in 30-40% of cases and its result in the infarction of posterior wall of left ventricle and posterior 1/3rd of intraventicular septum.
Blockage of left circumflex coronary artery seen in 15-20% of cases and results in infarct of lateral wall of left ventricle.

Histo-pathological Pattern of Myocardial Infarction

The histo-pathological changes occur in more or less orderly progression.
Under the light microscope the cellular coagulative necrosis is not detectable for first 4-6 hours However at this time, stretching and waviness of myocardial fibers at the bottom of infarct may appear within and after an hour of ischemia.
Usually within 24 hours, the myocardial fibers undergo sufficient enzyme changes to yield classic coagulative necrosis. The coagulative changes are almost always accompany by some interstitial edema,
fresh hemorrhage, and scant marginal neutrophilic exudation. On electron microscopy, within 10-15 minutes of coronary occlusion, depletion of glycogen occur, along with slight dilatation of mitochondria, slight margination of nuclear chromatin. These changes are reversible but after 20-60mins of ischemia, mitochondrial swelling increases and amorphous densities appear in the mitochondrial matrix. These changes are the early signs of irreversible injuries.
At the same time clamping of chromatin becomes evident at the periphery of the nuclei.

Clinical course of the Myocardial Infarct

The diagnosis of acute MI is based upon
• Clinical history
• ECG changes
• Alteration of serum enzymes

Clinical history

Typical the cardinal pain in sudden onset with sever constricting, crushing or burning sub-sternal or pericardial pain. That afterwards radiates to the left shoulder, arm or jaw. It is often accompanied by sweating, nausea, vomiting or breathlessness.
Occasionally, the clinical features are much less specific with burning, sub-sternal or epigastria discomfort which is interpreted as indigestion or heart burn.

ECG Changes

These consist of new Q-wave along with ST wave changes in the case of transmural infarct.
Only ST waves changes in sub-endocardial infarct.

Alteration in the Serum Enzyme

Elevated level of lactic dehydrogenase (LDH) are usually apparent after 12 hours of onset and reaches peak in 48-72 hours after the coronary inclusion.


• Exercise Stress Test
o Used to confirm diagnosis of angina
• Other Diagnostic Test
o Echocardiography
o Coronary angiography

Pharmacological Therapy

To restore balance between myocardial oxygen supply and demand:
• Nitrates
• Beta Blocker
• Ca+ Channel Blockers


(Causes vasodilation)
▪ Reduce Myocardial Oxygen Demand
▪ Relax vascular smooth muscles
▪ Reduce venous return to heart
▪ Arteriolar dilator decrease resistance against which left ventricle contracts and reduces wall tension and oxygen demand
▪ Dilate coronary arteries with augmentation of coronary blood flow
▪ Side effects – generalized warmth, transient, throbbing headache or light headedness, hypotension
▪ ER if no relief after X2 nitro unstable angina or MI

Beta Blockers

▪ Prevent effort induced angina
▪ Decrease mortality after myocardial infarction
▪ Reduce myocardial oxygen demand by slowing heart rate, force of ventricular contraction and decrease blood pressure.
▪ Contra-Indication
Symptomatic CHF, history of bronchospasm, bradycardia or AV block, Peripheral vascular disease with s/s of claudication.

Abrupt Ceassation
Tachycardia, angina or MI
Inhibit vasodilator beta 2 receptors
Should be avoided in patients with predominant coronary artery vasoperin

Ca+ Channel Blockers

▪ Anti-anginal agents prevent angina
▪ Helpful episodes of coronary vasospasm
▪ Decreases myocardial oxygen requirement and increase myocardial oxygen supply
▪ Portent arterial vasodilators, decreases systemic vascular resistance, blood pressure, left ventricular wall stress with decrease myocardia oxygen consumption.

Drug Selection

▪ Chronic Stable angina beta blockers and long acting nitrate or calcium channel blockers (not verapamil = bradycardia) or both
▪ If contraindicated to BB, a CCB is recommended (bronchospasm, IDDM or claudication)

Other Methods

Patients with 1-2 vessels disease with normal left ventricular function are referred for catheter based procedure.
Patients with 2 and 3 vessels diseases with widespread ischemia, left ventricular dysfunction or DM and those with lesion are procedures and are referred for CABG (coronary artery bypass graft)

Cardiac Care Control

▪ Decrease amount of myocardial necrosis
▪ Preserve LV function
▪ Prevent Major adverse cardiac events
▪ Treats life threatening complications