What Causes a Heart Attack and How a Heart Attack is Treated

Each year at least 5 million people in the United States visit emergency rooms due to chest pain. Chest pain may be due to partial blockage of blood circulation or complete obstruction of blood supply to the heart muscle resulting in extensive heart muscle damage. High cholesterol is one of the most important predictive risk factors of coronary artery disease. It leads to plaque formation in heart blood vessels that blocks circulation. This is known as a heart attack.

The main cause for a heart attack is plaque rupture with clot formation, restricting the blood flow to the heart. Some of the known factors leading to plaque rupture include thin fibrous cap, large lipid-rich core, and inflammatory cells. Two-thirds of those with acute heart attack have blockage of less than 50 percent. There is less than 75 percent blockage in more than 90 percent of heart attack cases, suggesting plaque rupture leads to heart attacks.

Recent studies have shown that inflammation of the inner layer of blood vessels leads to vessel injury and plaque vulnerability. During autopsies multiple layers of atherosclerotic plaque is observed frequently, suggesting an ongoing process of rupturing and healing as one mechanism of atherosclerosis progression. As these plaques age, calcification forms over like multiple eggshell layers which are resistant to rupture. Cardiovascular events usually occur as a consequence of disruption of a vulnerable plaque. High cholesterol and cigarette smoking have been shown to be directly associated with plaque instability and disruption. Lowering cholesterol stabilizes plaque.

Several medical therapies have proven to be beneficial. Aspirin, in doses ranging from 162 – 325 mg, reduces the incidence of death or heart attack by 30-50 percent. Another important class of drugs called thrombolytic agents-or clot busters–plays an important role in treating blocked vessels. Giving clot busters within six hours of an acute heart attack is very crucial and has revolutionized the medical management of patients. However, despite the important beneficial effects, there are many deficiencies. Only 33 percent of acute heart attack patients receive this therapy and only 60 percent of patients have full restoration of coronary blood flow, whereas 20-30 percent still have reduced flow.

Interventions in acute heart attack are an alternative to clot busting therapy. Balloon angioplasty has been introduced in addition to clot busting therapy or as a stand-alone procedure. Full restoration of normal coronary blood flow is achieved in 85-95 percent after angioplasty and in only 65-75 percent after clot busting therapy. Angioplasty has changed cardiac treatment by restoring blood flow in narrowed or blocked coronary vessels, improving heart function and survival.

Stents have become a regular addition to angioplasty to treat unfavorable angioplasty results and to reduce re-narrowing rates. The coronary artery after placement of a stent is much smoother and larger than after angioplasty alone, due to stretching and expansion of the coronary artery wall. Stent placement may lead to enhanced squeezing of plaque material. Newer techniques such as hydrodynamic clot busting devices (example angiojet) rely on aspiration of clot and debris in coronary circulation and improve the success of angioplasty even more.

Coronary artery disease includes both the narrowing and dysfunction of the blood vessel inner layer lining, leading to chest pains. These events can be ongoing, repetitive or periodical. Aggressive risk factor modification, including smoking cessation, cholesterol control and exercise, play an important role in stabilization of the plaque and in preventing acute heart attacks.

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