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Heart failure has become a leading health problem worldwide. Its prevalence is also increasing as people are living longer. Poorly controlled hypertension is a primary cause of heart failure, which occurs when the heart is unable to pump blood efficiently to meet the metabolic needs of the body.

Prevention of heart failure should be a major focus of antihypertensive therapy. Each year, about 1.1 million American suffer a heart attack and about 460,000 are fatal. Half of the deaths occur within an hour of the start of symptoms and before the person reaches the hospital. The medical name for heart attack, or coronary, is myocardial infarction wherein the primary physiologic organ and system involved are the coronary circulatory and myocardium.

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Myocardium is the cardiac muscle layer of the wall of the heart, which receives its blood supply, thus its oxygen and other nutrients, from the coronary arteries. If an artery is blocked by an occlusion, or spasm, the myocardial cells do not obtain the sufficient oxygen, the portion of myocardium undergoes processes of degenerations.

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Although, such an attack may seem sudden, usually it has been building for years, particularly if the person has ignored risk factors and early warning signs. The condition of heart attack is one of the most deceiving conditions since, the warning signs and symptoms do not exacerbate in some cases.

Furthermore, the risk factors often accumulate n the body but the reaction of the heart towards it remain tolerable, which usually are ignored. However, the effect suddenly implicates a devastating manifestation that occurs in a very quick period; hence, the term, “heart attack – silent killer” has been identified in this condition. Heart attack remains as one of the most fatal conditions as the human civilization progress its current lifestyle and practices.

Chapter I: What is Heart Attack

“When the supply of blood to the heart is sharply reduced or cut off, the heart is deprived of needed oxygen. If blood flow is not restored within minutes, portions of the heart muscle begin to die, permanently damaging the heart muscle” (1, 465). Heart attack occurs when heart muscle tissue dies because its blood supply is severely reduced or stopped.

A heart attack is also called coronary thrombosis, coronary occlusion, or myocardial infarction. It may occur when one of the coronary arteries supplying blood to the heart is blocked; moreover, if the heart attack is severe, the victim may conjure death. “Atheromatous plaque blocks 30% to 60% of a blood vessel and rupture, exposing its contents into the bloodstream and triggering a blood clot that completely shuts off the artery. If the heart stops beating, cardiopulmonary resuscitation (CPR) must be initiated” (4, 432).

The deprivation of blood in the heart causes heart tissues to undergo necrosis or tissue death especially if blood is not restored within minutes. Upon the occurrence of oxygen deprivation, there is a rise in cardiac enzymes signifying tissue damage and echocardiographic changes, in addition to classical clinical symptoms (6, 97).

The amount of muscle that depended on the involved coronary artery for its blood supply and whether any other coronary arteries can provide the involved region of heart muscles with an alternative blood supply. If heart muscles die, it cannot grow back; hence, instituting the damage as permanent and irreversible unless cardiac surgical interventions are applied (4, 432-433).

Systolic heart failure or left ventricular dysfunction is often the consequence of poorly controlled hypertension or coronary artery disease. This may result in a low cardiac output state and pulmonary congestion. Not all patients with heart failure have a congestive state. Lowering the patient’s systolic and diastolic BP should be the goal of therapy. Diastolic heart failure is responsible for up to 74% of all cases of heart failure in hypertensive patients and is often undiagnosed in clinical practice.

Diastolic heart failure occurs when the left ventricle has normal contractility, but is unable to adequately relax and fill during diastole due to thickened walls and stiffness.

This is usually seen in the elderly. Especially women, and is most commonly associated with years of hypertension that progressed to left ventricular hypertrophy. Unlike systolic dysfunction, there is no definitive pharmacologic therapy for diastolic dysfunction. The basis of therapy includes prevention or treatment of ischemia, reduction in filling pressures, and most important, controlling systolic and diastolic hypertension in accordance with published guidelines.

If the infracted area is small or subendocardial, ECG often cannot detect any changes in heart rhythms. If the infarction is transendocadial (full thickness), regional wall abnormalities can be detected, the region involved corresponding to the occluded coronary artery. In most cases, the amount of muscle that appears to be affected on ECG will be greater than the actual amount infracted. There will be reduced contraction in the afflicted site of infarction. Hypokinesia refers to contraction that is decreased but still in the same direction as normal.

The myocardium will also show reduced thickening in systole, while Akinesia is when the myocardium or heart muscles are static. Dyskinesia occurs when most damage to myocardial tissue has occurred and the muscle moves out of synchronization with the rest of the ventricle, often, paradoxical movement will result (6, 97).

Chapter II: What Are Causes of Heart Attack

There are three basic scenarios that can produce a heart attack. The first, and by far the most common, is partial or complete blockage of one of the arteries that supply the heart with oxygen, most often by a blood clot. Usually the arteries have been narrowed by years of coronary artery disease in which plaque, which is composed of cholesterol-rich fatty deposits, proteins, calcium, and excess smooth muscle cells, builds up on the arterial walls.

The arterial walls thicken, inhibiting the flow of blood to the heart muscle. “The roughening of arterial walls by deposits of plaque not only narrows the arteries, but also makes it easier for blood clots to form along their inner surfaces.

When a clot grows, or detaches from its place of origin and travels through the blood vessels, it may block a coronary artery completely, resulting in a heart attack (1, 465).” The ruptured plaque, by direct release of tissue factor and exposure of the subintima, is highly thrombogenic, which exemplifies further risk for thrombosis.

Exposed collagen further provokes platelet aggregation. Some plaques, particularly those that have a high lipid content and a thin fibrous cap, are prone to rupture. “Considerable research has been done during the past decade on the complexity and the instability of vulnerable plaques” (2, 398).

Heart attacks occur if a blood clot develops rapidly at the site of a blood-vessel injury. Blood clots more readily under the influence of the stress hormones adrenocorticotropic hormone (ACTH) and epinephrine, and the inflammation-causing hormone serotonin. However, these chemicals can cause only limited clotting unless another chemical, thromboxane, is produced. Thromboxane causes a protein “net” to be spun on which a clot can grow to an artery-clogging size (1, 292).

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