In transient ischemic attack, the blood vessel is blocked. The blockage can be caused by a blood clot that forms in the blood vessel (thrombosis) or it can be caused by a clot or debris that floats downstream (embolus).
Atherosclerosis, or "hardening of the arteries" can cause fatty plaque formations in he blood vessel wall. The plaque can rupture and causes a small blood clot to form and occlude the blood vessel. Blockage can also occur when debris from narrowing of a carotid artery breaks off, and floats downstream to cause the occlusion. Sometimes, in people with an irregular heart beat called atrial fibrillation, small blood clots can be formed and travel to the brain to cause the obstruction.
A blood thinner, also called an anti-coagulant, is used to stop plateleTs, or heavy cells, present in blood plasma from forming clots. They are most used in those who are at risk for heart attack, stroke, or aneurisms. A blood thinner can be composed of several different chemical formations. The most common blood thinner, and most often used is aspirin, taken in doses of 81mg per day, essentially one baby aspirin.
Blood thinners — such as aspirin, warfarin (Coumadin) and heparin derivatives — decrease your risk of blood clotting. But these medications must be taken precisely as directed to work safely and effectively. Taking too little of these drugs may not be effective, and taking too much can lead to serious bleeding. Regular blood tests may be required to assure proper dosing.
Also, in some cases, blood thinners may not be able to counter the strong clotting tendency of an underlying disease, such as cancer. So, clots may still form.
If you take a blood thinner, be sure to follow your doctor's advice on dosing and ask about foods and other medications — including over-the-counter drugs and herbal supplements — that may interfere with the action of the blood thinner.
Thursday, February 12, 2009
MAKE IDEAL LIST OF EACH MODIFIABLE RISK FACTOR
HYPERTENSION
Elevated blood pressure (above 140/90 mm Hg) is the most important treatable risk factor for TIA and stroke. Antihypertensive drugs reduce the risk of strokes, regardless of whether patients have hypertension.2 Currently, however, the American Heart Association (AHA) does not have any recommendations for antihypertensive drug therapy in "nonhypertensive" patients after a TIA or stroke.3
Hypertension occurs more frequently and more severely in blacks; therefore, this patient group merits special attention. Patients with diabetes mellitus or chronic renal disease also are at increased risk for hypertension and, thus, TIA or stroke. In patients with diabetes mellitus or chronic renal disease, the treatment goal is to keep blood pressure below 130/80 mm Hg.
Important new guidelines from the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7) require lifestyle modifications (weight reduction, sodium restriction, regular aerobic activity, limited alcohol intake) to prevent cardiovascular disease in prehypertensive patients with a systolic blood pressure of 120 to 139 mm Hg or a diastolic blood pressure of 80 to 89 mm Hg.4 [SOR C, consensus opinion]
Starting Antihypertensive Drug Therapy After a TIA or Stroke. Typically, blood pressure lowers without treatment in the first two weeks after a stroke. Therefore, it is rational to wait two weeks before continuing or beginning antihypertensive drug therapy.
In the patient found to have high blood pressure after a stroke or TIA, evidence of end-organ damage should be sought, because such damage suggests a chronic disorder rather than an acute condition. In some patients with chronically elevated blood pressure, the brain may depend on abnormally higher perfusion pressures because of derangement of the normal cerebral autoregulation of intracranial blood vessels. In this setting, abrupt lowering of blood pressure could promote cerebral ischemia or even extend an evolving infarction. Rarely, TIA is a manifestation of hemodynamically significant critical stenosis of an extracranial or intracranial vessel. In this condition, the brain requires increased cerebral perfusion pressure, and overtreatment of blood pressure may promote cerebral ischemia. The physician may note that TIAs occur when the patient's blood pressure drops or when the patient stands up or sits up.
In most patients, blood pressure should not be treated aggressively immediately (i.e., within the first 24 hours) after a stroke or TIA unless the systolic blood pressure is higher than 220 mm Hg or the diastolic blood pressure is above 120 mm Hg.5 Important exceptions include patients with acute myocardial infarction (especially with left ventricular failure), hypertensive crisis or hypertensive encephalopathy, renal failure, aortic dissection, or retinal hemorrhages.
If, in the absence of the previously mentioned conditions, treatment is necessary, blood pressure should be reduced slowly over days to prevent worsening ischemia.
Angiotensin-Converting Enzyme (ACE) Inhibitors. Increased attention is being directed at ACE inhibitors because of the results of the recent Heart Outcomes Prevention Evaluation (HOPE) study.6 In this large, randomized trial, inpatients considered to be at "high cardiovascular risk" were treated with ramipril or placebo. Over four years, the relative reduction in the risk of stroke was 32 percent (within a composite outcome) in the patients who received ramipril. Debate currently centers on whether the HOPE study findings were unique to ACE inhibitors as a class or occurred because of a more general blood pressure-lowering effect that also could be obtained with other antihypertensive drug classes.
In the Perindopril Protection Against Recurrent Stroke Study (PROGRESS),7 patients with stroke or TIA within the previous five years were given placebo or combination therapy consisting of perindopril (an ACE inhibitor) and indapamide (a diuretic). In both hypertensive and "non-hypertensive" patients, the drug combination resulted in a 43 percent reduction in the relative risk of recurrent stroke (four-year follow-up). In PROGRESS, hypertension was defined as a systolic blood pressure of 160 mm Hg or higher or a diastolic blood pressure of 90 mm Hg or higher.
To date, however, no consensus statements indicate a preference for one antihypertensive drug or drug class over another for use in secondary (or primary) stroke prevention.2,8,9 In particular, the use of ACE inhibitors after acute stroke remains controversial.
DIABETES
Diabetes mellitus, independent of its association with hypertension, increases the overall risk of stroke by approximately 25 to 50 percent.19 There is no conclusive evidence that "tight" glucose control results in a reduction of ischemic stroke or other macrovascular events.20,21
Recent data from the Microalbuminuria, Cardiovascular, and Renal Outcomes in HOPE (MICRO-HOPE) substudy22,23 indicate that ramipril therapy reduces cardiovascular and cerebrovascular events in patients with diabetes mellitus and one cardiac risk factor. In MICRO-HOPE, stroke events were reduced by 33 percent, and stroke-related deaths were reduced by 37 percent.
HEART DISEASE AND ATRIAL FIBRILLATION
Cardiac disease (i.e., rheumatic heart disease, mitral valve stenosis, atrial fibrillation with or without valvular disease) is a predisposing factor for TIA and stroke. In addition, the electrocardiographic finding of left ventricular hypertrophy resulting from prolonged hypertension is associated with a fourfold increased risk of stroke.
Patients with atrial fibrillation who also have other risk factors are at particularly high risk for TIA or stroke. These additional risk factors include a history of hypertension, poor left ventricular function, rheumatic mitral valve disease, prosthetic heart valves, previous stroke, systemic embolism, and age greater than 75 years. Patients with atrial fibrillation who have already had a TIA are considered to be at high risk for stroke. The results of one study11 of patients with atrial fibrillation and TIA or minor stroke indicate that anticoagulant therapy is significantly more effective than aspirin in preventing recurrent stroke.
In addition, short-term cardiac morbidity is substantial after a TIA. One recent study12 suggested that among patients who have a TIA, the 90-day risk for a cardiac event is higher in those who have any abnormal finding on an electrocardiogram (ECG). In this study, the ECG findings of left ventricular hypertrophy, atrial fibrillation, and atrioventricular conduction abnormalities in patients with TIA were independently associated with more than a doubling of the risk of a cardiac event.
HYPERCHOLESTEROLEMIA
Convincing evidence from observational studies shows that elevated blood lipid levels are a risk factor for ischemic stroke.13 High cholesterol levels are a risk factor for coronary heart disease (CHD) and, thus, a substantial secondary risk factor for stroke.
Recent data indicate that in patients with CHD, treatment with statins (3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors) results in a 30 to 32 percent reduction of the stroke risk.2,14,15 [Reference 2: SOR A, beneficial] Because statins have multiple vascular effects, as well as cholesterol-lowering properties, the exact mechanism of stroke prophylaxis is unknown.
Current guidelines16,17 recommend consideration of statin therapy in patients with known CHD, many of whom could present with TIA or stroke. According to a recent Cochrane review,18 it is not clear whether statin therapy is as effective in the prevention of recurrent stroke or TIA as it is in the primary prevention of stroke in patients with CHD.
Elevated blood pressure (above 140/90 mm Hg) is the most important treatable risk factor for TIA and stroke. Antihypertensive drugs reduce the risk of strokes, regardless of whether patients have hypertension.2 Currently, however, the American Heart Association (AHA) does not have any recommendations for antihypertensive drug therapy in "nonhypertensive" patients after a TIA or stroke.3
Hypertension occurs more frequently and more severely in blacks; therefore, this patient group merits special attention. Patients with diabetes mellitus or chronic renal disease also are at increased risk for hypertension and, thus, TIA or stroke. In patients with diabetes mellitus or chronic renal disease, the treatment goal is to keep blood pressure below 130/80 mm Hg.
Important new guidelines from the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7) require lifestyle modifications (weight reduction, sodium restriction, regular aerobic activity, limited alcohol intake) to prevent cardiovascular disease in prehypertensive patients with a systolic blood pressure of 120 to 139 mm Hg or a diastolic blood pressure of 80 to 89 mm Hg.4 [SOR C, consensus opinion]
Starting Antihypertensive Drug Therapy After a TIA or Stroke. Typically, blood pressure lowers without treatment in the first two weeks after a stroke. Therefore, it is rational to wait two weeks before continuing or beginning antihypertensive drug therapy.
In the patient found to have high blood pressure after a stroke or TIA, evidence of end-organ damage should be sought, because such damage suggests a chronic disorder rather than an acute condition. In some patients with chronically elevated blood pressure, the brain may depend on abnormally higher perfusion pressures because of derangement of the normal cerebral autoregulation of intracranial blood vessels. In this setting, abrupt lowering of blood pressure could promote cerebral ischemia or even extend an evolving infarction. Rarely, TIA is a manifestation of hemodynamically significant critical stenosis of an extracranial or intracranial vessel. In this condition, the brain requires increased cerebral perfusion pressure, and overtreatment of blood pressure may promote cerebral ischemia. The physician may note that TIAs occur when the patient's blood pressure drops or when the patient stands up or sits up.
In most patients, blood pressure should not be treated aggressively immediately (i.e., within the first 24 hours) after a stroke or TIA unless the systolic blood pressure is higher than 220 mm Hg or the diastolic blood pressure is above 120 mm Hg.5 Important exceptions include patients with acute myocardial infarction (especially with left ventricular failure), hypertensive crisis or hypertensive encephalopathy, renal failure, aortic dissection, or retinal hemorrhages.
If, in the absence of the previously mentioned conditions, treatment is necessary, blood pressure should be reduced slowly over days to prevent worsening ischemia.
Angiotensin-Converting Enzyme (ACE) Inhibitors. Increased attention is being directed at ACE inhibitors because of the results of the recent Heart Outcomes Prevention Evaluation (HOPE) study.6 In this large, randomized trial, inpatients considered to be at "high cardiovascular risk" were treated with ramipril or placebo. Over four years, the relative reduction in the risk of stroke was 32 percent (within a composite outcome) in the patients who received ramipril. Debate currently centers on whether the HOPE study findings were unique to ACE inhibitors as a class or occurred because of a more general blood pressure-lowering effect that also could be obtained with other antihypertensive drug classes.
In the Perindopril Protection Against Recurrent Stroke Study (PROGRESS),7 patients with stroke or TIA within the previous five years were given placebo or combination therapy consisting of perindopril (an ACE inhibitor) and indapamide (a diuretic). In both hypertensive and "non-hypertensive" patients, the drug combination resulted in a 43 percent reduction in the relative risk of recurrent stroke (four-year follow-up). In PROGRESS, hypertension was defined as a systolic blood pressure of 160 mm Hg or higher or a diastolic blood pressure of 90 mm Hg or higher.
To date, however, no consensus statements indicate a preference for one antihypertensive drug or drug class over another for use in secondary (or primary) stroke prevention.2,8,9 In particular, the use of ACE inhibitors after acute stroke remains controversial.
DIABETES
Diabetes mellitus, independent of its association with hypertension, increases the overall risk of stroke by approximately 25 to 50 percent.19 There is no conclusive evidence that "tight" glucose control results in a reduction of ischemic stroke or other macrovascular events.20,21
Recent data from the Microalbuminuria, Cardiovascular, and Renal Outcomes in HOPE (MICRO-HOPE) substudy22,23 indicate that ramipril therapy reduces cardiovascular and cerebrovascular events in patients with diabetes mellitus and one cardiac risk factor. In MICRO-HOPE, stroke events were reduced by 33 percent, and stroke-related deaths were reduced by 37 percent.
HEART DISEASE AND ATRIAL FIBRILLATION
Cardiac disease (i.e., rheumatic heart disease, mitral valve stenosis, atrial fibrillation with or without valvular disease) is a predisposing factor for TIA and stroke. In addition, the electrocardiographic finding of left ventricular hypertrophy resulting from prolonged hypertension is associated with a fourfold increased risk of stroke.
Patients with atrial fibrillation who also have other risk factors are at particularly high risk for TIA or stroke. These additional risk factors include a history of hypertension, poor left ventricular function, rheumatic mitral valve disease, prosthetic heart valves, previous stroke, systemic embolism, and age greater than 75 years. Patients with atrial fibrillation who have already had a TIA are considered to be at high risk for stroke. The results of one study11 of patients with atrial fibrillation and TIA or minor stroke indicate that anticoagulant therapy is significantly more effective than aspirin in preventing recurrent stroke.
In addition, short-term cardiac morbidity is substantial after a TIA. One recent study12 suggested that among patients who have a TIA, the 90-day risk for a cardiac event is higher in those who have any abnormal finding on an electrocardiogram (ECG). In this study, the ECG findings of left ventricular hypertrophy, atrial fibrillation, and atrioventricular conduction abnormalities in patients with TIA were independently associated with more than a doubling of the risk of a cardiac event.
HYPERCHOLESTEROLEMIA
Convincing evidence from observational studies shows that elevated blood lipid levels are a risk factor for ischemic stroke.13 High cholesterol levels are a risk factor for coronary heart disease (CHD) and, thus, a substantial secondary risk factor for stroke.
Recent data indicate that in patients with CHD, treatment with statins (3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors) results in a 30 to 32 percent reduction of the stroke risk.2,14,15 [Reference 2: SOR A, beneficial] Because statins have multiple vascular effects, as well as cholesterol-lowering properties, the exact mechanism of stroke prophylaxis is unknown.
Current guidelines16,17 recommend consideration of statin therapy in patients with known CHD, many of whom could present with TIA or stroke. According to a recent Cochrane review,18 it is not clear whether statin therapy is as effective in the prevention of recurrent stroke or TIA as it is in the primary prevention of stroke in patients with CHD.
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