Angina and heart attack (myocardial infarction)
The concern for most patients and health care professionals is that any chest pain may originate from the heart. Angina is the term given to pain that occurs because the coronary arteries (blood vessels to the heart muscle) narrow and decrease the amount of oxygen that can be delivered to the heart itself. This can cause the classic symptoms of chest pressure or tightness with radiation to the arm or jaw associated with shortness of breath and sweating.
Unfortunately, many people don’t present with classic symptoms, and the pain may be difficult to describe — or in some people may not even be present. Instead of angina or typical chest pressure, their anginal equivalent (symptom they get instead of chest pain) may be indigestion, shortness of breath, weakness, dizziness, and malaise. Women and the elderly are at higher risk for having an atypical presentation of heart pain.
The narrowing of blood vessels or atherosclerosis is due to plaque buildup. Plaque is a soft amalgam of cholesterol and calcium that forms along the inside lining of the blood vessel and gradually decreases the diameter of the blood vessel and restricts the flow of blood. If the plaque ruptures, it can cause a blood clot to form and completely block the vessel.
When a coronary artery completely occludes (becomes blocked), the muscle it supplies blood to is at risk of dying. This is a heart attack or myocardial infarction. In most circumstances, this pain is more intense than routine angina, but again, there are many variations in signs and symptoms.
The diagnosis of angina is a clinical one. After the health care professional takes a careful history and assesses the potential risk factors, the diagnosis is either reasonably pursued or else it is considered not to be present. If angina is the potential diagnosis, further evaluation may include electrocardiograms (EKG or ECG) and blood tests.
Treatment of angina
The purpose of making the diagnosis of angina is to restore normal blood supply to the heart muscle before a heart attack occurs and permanent muscle damage results. Aside from minimizing risk factors by controlling blood pressure, cholesterol, and diabetes, and stopping smoking, medications can be used to make the heartbeat more efficiently (for example, beta-blockers), dilate blood vessels (for example, nitroglycerin), and make blood less likely to clot (aspirin).
Treatment of heart attack
An acute heart attack (myocardial infarction) is a true emergency since complete blockage of blood supply will cause part of the heart muscle to die and be replaced by scar tissue. This lessens the ability of the heart to pump blood to meet the body’s needs. As well, the injured heart muscle is irritable and can cause electrical disturbances like ventricular fibrillation, a condition in which the heart jiggles like Jell-O and cannot beat in a coordinated fashion. This is the cause of sudden death in a heart attack. The cause of an acute heart attack is the rupture of cholesterol plaque in a coronary artery. This causes a blood clot to form and occlude the artery.
The treatment for heart attack is an emergent restoration of blood supply. Two options include the use of a drug like TPA or TNK to dissolve the blood clot (thrombolytic therapy) or emergency heart catheterization and using a balloon to open up the blocked area (angioplasty) and keeping it open with a mesh cage called a stent. Emergent angioplasty is preferred if the patient lives close to a hospital with that capability but many people do not. Staged treatment with initial thrombolytic therapy followed by angioplasty is also reasonable.
Coronary artery bypass surgery is considered when there is diffuse artery disease that is not amenable to angioplasty and stenting.