Ischemic Heart Disease : Symptoms, Pathophysiology, Diagnosis, And Treatment

Monday, February 3rd 2014. | Disease

Ischemic Heart Disease : Symptoms, Pathophysiology, Diagnosis, And Treatment

Ischemic heart disease (IHD), also known as coronary artery disease (CAD), is defined as a lack of oxygen and decreased or no blood flow to the myocardium resulting from coronary artery narrowing or obstruction.

Pathophysiology of Ischemic Heart Disease :

The major determinants of myocardial oxygen demand (MVo2) are heart rate, contractility, and intramyocardial wall tension during systole. Wall tension is thought to be the most important factor. Because the consequences of IHD usually result from increased demand in the face of a fixed oxygen supply, alterations in MVo2 are important in producing ischemia and for interventions intended to alleviate it.

A clinically useful indirect estimate of MVo2 is the double product (DP), which is heart rate (HR) multiplied by systolic blood pressure (SBP) (DP = HR × SBP). The DP does not consider changes in contractility (an independent variable), and because only changes in pressure are considered, volume loading of the left ventricle and increased MVo2 related to ventricular dilation are underestimated.

The caliber of the resistance vessels delivering blood to the myocardium and MVo2 are the prime determinants in the occurrence of ischemia.

The normal coronary system consists of large epicardial or surface vessels (R1) that offer little resistance to myocardial flow and intramyocardial arteries and arterioles (R2) that branch into a dense capillary network to supply basal blood flow (Figure 11-1). Under normal circumstances, the resistance in R2 is much greater than that in R1. Myocardial blood flow is inversely related to arteriolar resistance and directly related to the coronary driving pressure.

Atherosclerotic lesions occluding R1 increase arteriolar resistance, and R2 can vasodilate to maintain coronary blood flow. With greater degrees of obstruction, this response is inadequate, and the coronary flow reserve afforded by R2 vasodilation is insufficient to meet oxygen demand. Relatively severe stenosis (greater than 70%) may provoke ischemia and symptoms at rest, whereas less severe stenosis may allow a reserve of coronary blood flow for exertion.

The diameter and length of obstructing lesions and the influence of pressure drop across an area of stenosis also affect coronary blood flow and function of the collateral circulation. Dynamic coronary obstruction can occur in normal vessels and vessels with stenosis in which vasomotion or spasm may be superimposed on a fixed stenosis. Persisting ischemia may promote growth of developed collateral blood flow.
Critical stenosis occurs when the obstructing lesion encroaches on the luminal diameter and exceeds 70%. Lesions creating obstruction of 50% to 70% may reduce blood flow, but these obstructions are not consistent, and vasospasm and thrombosis superimposed on a “noncritical” lesion may lead to clinical events such as AMI. If the lesion enlarges from 80% to 90%, resistance in that vessel is tripled. Coronary reserve is diminished at about 85% obstruction due to vasoconstriction.

Diagnosis of Ischemic Heart Disease :

Important aspects of the clinical history include the nature or quality of the chest pain, precipitating factors, duration, pain radiation, and the response to nitroglycerin or rest. There appears to be little relationship between the historical features of angina and the severity or extent of coronary artery vessel involvement. Ischemic chest pain may resemble pain arising from a variety of noncardiac sources, and the differential diagnosis of anginal pain from other etiologies may be difficult based on history alone.

The patient should be asked about existing personal risk factors for coronary heart disease (CHD) including smoking, hypertension, and diabetes mellitus.

Treatment of Ischemic Heart Disease

Risk factors for IHD are additive and can be classified as alterable or unalterable. Unalterable risk factors include gender, age, family history or genetic composition, environmental influences, and, to some extent, diabetes mellitus. Alterable risk factors include smoking, hypertension, hyperlipidemia, obesity, sedentary lifestyle, hyperuricemia, psychosocial factors such as stress and type A behavior patterns, and the use of drugs that may be detrimental (e.g., progestins, corticosteroids, and cyclosporine). Although thiazide diuretics and β blockers (nonselective without intrinsic sympathomimetic activity) may elevate both cholesterol and triglycerides by 10% to 20%, and these effects may be detrimental, no objective evidence exists from prospective well-controlled studies to support avoiding these drugs.

The Drugs Could be used : Adrenergic Blocking Agents, Nitrates, Calcium Channel Antagonists.

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