Stroke is a type of cardiovascular disease. It affects the arteries leading to and within the brain. A stroke occurs when a blood vessel that carries oxygen and nutrients to the brain is either blocked by a clot or bursts. When that happens, part of the brain cannot get the blood (and oxygen) it needs, so it starts to die.
Ischemic stroke accounts for about 83 percent of all cases. Ischemic strokes occur as a result of an obstruction within a blood vessel supplying blood to the brain. The underlying condition for this type of obstruction is the development of fatty deposits lining the vessel walls. This condition is called atherosclerosis.
Hemorrhagic stroke results from a weakened vessel that ruptures and bleeds into the surrounding brain. The blood accumulates and compresses the surrounding brain tissue. The two types of hemorrhagic strokes are intracerebral hemorrhage or subarachnoid hemorrhage.
Two types of weakened blood vessels usually cause hemorrhagic stroke: aneurysms and arteriovenous malformations (AVMs). An aneurysm is a ballooning of a weakened region of a blood vessel. If left untreated, the aneurysm continues to weaken until it ruptures and bleeds into the brain. An arteriovenous malformation (AVM) is a cluster of abnormally formed blood vessels. Any one of these vessels can rupture, also causing bleeding into the brain.
Several types of heart disease are risk factors for stroke. Likewise, stroke is a risk factor for coronary heart disease. Coronary heart disease and stroke share many of the same risk factors such as high LDL (“bad”) cholesterol levels, low HDL (“good”) cholesterol levels, high blood pressure, smoking, diabetes, physical inactivity, and being overweight or obese. Individuals with coronary heart disease, angina, or who have had a heart attack due to atherosclerosis, have more than twice the risk of stroke than those who haven’t. If you have atherosclerosis in the coronary arteries you are very likely to have atherosclerosis in other parts of your body.
Heart Attack, or (acute) myocardial infarction, occurs when blood flow to a section of heart muscle becomes blocked. If the flow of blood isn’t restored quickly, the section of heart muscle becomes damaged from lack of oxygen and begins to die. Heart attack is a leading killer of both men and women in the United States. But fortunately, today there are excellent treatments for heart attack that can save lives and prevent disabilities. Treatment is most effective when started within 1 hour of the beginning of symptoms. If you think you or someone you’re with is having a heart attack, call 9–1–1 right away.
Classical symptoms of acute myocardial infarction include sudden chest pain (typically radiating to the left arm or left side of the neck), shortness of breath, nausea, vomiting, palpitations, sweating, and anxiety (often described as a sense of impending doom). Women may experience less typical symptoms than men, most commonly shortness of breath, weakness, a feeling of indigestion, and fatigue. Approximately one quarter of all myocardial infarctions are silent, without chest pain or other symptoms. A heart attack is a medical emergency, and people experiencing chest pain are advised to alert their emergency medical services, because prompt treatment is beneficial.
Heart attack rates are higher in association with intense exertion, be it psychological stress or physical exertion, especially if the exertion is more intense than the individual usually performs. Quantitatively, the period of intense exercise and subsequent recovery is associated with about a 6-fold higher myocardial infarction rate (compared with other more relaxed time frames) for people who are physically very fit. For those in poor physical condition, the rate differential is over 35-fold higher.
One observed mechanism for this phenomenon is the increased arterial pulse pressure stretching and relaxation of arteries with each heart beat which, as has been observed with intravascular ultrasound, increases mechanical "shear stress" on atheromas and the likelihood of plaque rupture. Acute severe infection, such as pneumonia, can trigger myocardial infarction. A more controversial link is that between Chlamydophila pneumoniae infection and atherosclerosis. While this intracellular organism has been demonstrated in atherosclerotic plaques, evidence is inconclusive as to whether it can be considered a causative factor.
Treatment with antibiotics in patients with proven atherosclerosis has not demonstrated a decreased risk of heart attacks or other coronary vascular diseases. There is an association of an increased incidence of MI in the morning hours. Some investigators have noticed that the ability of platelets to aggregate varies according to a circadian rhythm, although they have not proven causation. Some investigators theorize that this increased incidence may be related to the circadian variation in cortisol production affecting the concentrations of various cytokines and other mediators of inflammation.
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