Supplement to the Guidelines for the Management of Transient Ischemic Attacks (Excerpt)
January 1, 2000 8 minutes read
Supplement to the Guidelines for the Management of Transient Ischemic Attacks (Excerpt)
A Statement From the Ad Hoc Committee on Guidelines for the Management of Transient Ischemic Attacks, Stroke Council, American Heart Association
Gregory W. Albers, MD, Chair; Robert G. Hart, MD; Helmi L. Lutsep, MD; David W. Newell, MD; Ralph L. Sacco, MD
In 1994, a panel of the American Heart Association Stroke Council published guidelines for the management of transient ischemic attacks (TIAs).1
Over the last five years, many significant advances in medical and surgical therapy for patients with TIAs have occurred. In addition, new data regarding risk factors for cerebral ischemic events have become available. These scientific advances have prompted this supplement to the 1994 guidelines, which provides updated recommendations for management of patients with TIAs.
Specific stroke-prevention strategies after a TIA are tailored to the most likely cause of the event and the patient’s underlying risk factors as determined by a focused, expedient diagnostic evaluation. For more information about epidemiology, etiology, and diagnostic evaluation of TIAs, see the original guidelines.1
For the current report, panel members followed the rules of evidence used by the 1998 American College of Chest Physicians Conference on Antithrombotic Therapy.2
Risk Factor Modification
The approach to stroke prevention among patients who have already had their first TIA includes identification and modification of stroke risk factors. Nonmodifiable risk markers for stroke include age, sex, race-ethnicity, and heredity.3 Although those risk markers cannot be changed, they nonetheless serve as important identifiers of patients at risk for stroke, for whom an aggressive search for other modifiable risk factors might be particularly important. Modifiable stroke risk factors include hypertension, cardiac disease (particularly atrial fibrillation), diabetes, hypercholesterolemia, cigarette smoking, excessive use of alcohol, and physical inactivity. Numerous prospective studies and clinical trials have consistently shown a decreased risk of stroke with control of most of those conditions, although a few of these studies were conducted in TIA cohorts.1
Reduction of both systolic and diastolic pressure in hypertensive subjects substantially reduces stroke risk.4,5 Reduction of isolated systolic hypertension to <140 mm Hg in the elderly, for example, in the recently completed Syst-Eur trial demonstrated that treatment of older patients with isolated systolic hypertension led to a 42% reduction in stroke risk with no significant decline in overall mortality.6 Current guidelines for the treatment of hypertension have been published by the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure.7
Diabetes mellitus is a well-established stroke risk factor.8,9 Death due to cerebrovascular disease is substantially increased in patients with two-hour blood glucose values above the 97.5 percentile, compared to those with values below the 80th percentile.10
Intensive treatment of both Type 1 and Type 2 diabetes, aimed at obtaining near-normal levels of blood glucose, can substantially reduce the risk of microvascular complications such as retinopathy, nephropathy, and neuropathy, but has not been conclusively shown to reduce macrovascular complications, including stroke.11-14
One recent study demonstrated that aggressive treatment of blood pressure in persons with Type 2 diabetes reduced the risk of stroke by 44% (P-0.01).13 Recent guidelines for management of diabetes have been published by the American Diabetes Association.15
Lifestyle factors, including cigarette smoking, heavy use of alcohol, and physical inactivity, have all been associated with an increased risk of stroke.16-19 Modification of those behaviors can lead to a decrease in risk of stroke, which may be mediated by reductions in other stroke risk factors, such as hypertension, diabetes, hypercholesterolemia, and coronary artery disease.
Clinical trials analyzing the relationship of lipid-lowering strategies and stroke have yet to confirm a reduction in risk for patients who have already had a TIA or stroke. Data addressing the impact of treatment with statins on the incidence of stroke are derived exclusively from trials of primary and secondary prevention of coronary disease. In those studies, stroke was either a secondary end point or a nonspecified end point determined on the basis of post hoc analyses. Meta-analyses of the lipid-lowering trials with the new statin agents have found significant reductions in stroke risk.20 A 29% reduced risk of stroke and a 22% reduction in overall mortality were found.
Secondary prevention trials showed a 32% reduction in stroke risk, and primary trials demonstrated a 20% reduction. Two large trials in which stroke was prespecified as a secondary end point have also shown significant reductions with pravastatin among subjects with coronary artery disease and normal to only modest elevations of cholesterol.21,22 Some clinical trials have also demonstrated carotid plaque regression with statins.23,24
Although statins have not been tested in patients with stroke or TIA, clinical trials in patients with cerebrovascular disease are under way. TIA patients with cardiovascular risk factors and cholesterol levels >200 mg/dL should have a complete lipid analysis (total cholesterol, LDL, HDL, and triglycerides), and most likely will benefit from cholesterol-lowering regimens that include statins.
There are no data available from randomized clinical trials to address the risks or benefits of postmenopausal hormone replacement therapy after a TIA. Ongoing trials, such as the Women’s Estrogen Stroke Trial and the Postmenopausal Estrogen and Progestin Intervention Trial, may help provide more evidence-based recommendations regarding the use of postmenopausal hormone replacement therapy. Data from observational studies suggest that hormone replacement therapy may be associated with a reduction in myocardial infarction and death. Data suggesting an increased risk of stroke from oral contraceptive use cannot be extrapolated to postmenopausal hormone replacement therapy (for which the goal is to obtain physiological levels of estrogen).
Studies are continuing regarding the importance of other risk factors, including elevation of homocysteine, lipoprotein fractions [including lipoprotein (a)], and hypercoagulable states from antiphospholipid antibodies, factor V, protein C, and protein S deficiencies.25,26
Despite the wealth of data on the importance of stroke risk factors, control of those conditions is still inadequate because of poor patient compliance and adherence to behavior modifications, as well as decreased detection and treatment by health care providers.27,28 Further reductions in the risk of stroke among patients with TIA will require enhancements in our ability to detect, modify, and treat cerebrovascular risk factors.
References
1. Feinberg WM, Albers GW, Barnett HJM, et al. Guidelines for the management of transient ischemic attacks. From the Ad Hoc Committee on Guidelines for the Management of Transient Ischemic Attacks of the Stroke Council of the American Heart Association. AHA medical/scientific statement; special report. Circulation 1994; 89:2,950-2,965.
2. Guyatt GH, Cook DJ, Sackett DL, et al. Grades of recommendation for antithrombotic agents. Chest 1998; 114:441S-444S.
3. Sacco RL, Benjamin EJ, Broderick JP, et al. Risk Factors Panel: American Heart Association Prevention Conference IV: Prevention and rehabilitation of stroke: Risk factors. Stroke 1997; 28:1,507-1,517.
4. Collins R, Peto R, MacMahon S, et al. Blood pressure, stroke, and coronary heart disease, Part 2. Short-term reductions in blood pressure: Overview of randomised drug trials in their epidemiological context. Lancet 1990; 335:827-838.
5. SHEP Cooperative Research Group. Prevention of stroke by anti-hypertensive drug treatment in older persons with isolated systolic hypertension: Final results of the Systolic Hypertension in the Elderly Program (SHEP). JAMA 1991; 265:3,255-3,264.
6. Staessen JA, Fagard R, Thijs L, et al. Randomised double-blind comparison of placebo and active treatment for older patients with isolated systolic hypertension: The Systolic Hypertension in Europe (Syst-Eur) Trial Investigators. Lancet 1997; 350:757-764.
7. The sixth report of the Joint National Committee on prevention, detection, evaluation, and treatment of high blood pressure. Arch Intern Med 1997; 157:2,413-2,446.
8. Wolf PA, D’Agostino RB, Belanger AJ, et al. Probability of stroke: A risk profile from the Framingham Study. Stroke 1991; 22:312-318.
9. Kuller LH, Dorman JS, Wolf PA. Cerebrovascular diseases and diabetes. In: National Diabetes Data Group, Department of Health and Human Services, National Institutes of Health. Diabetes in America: Diabetes Data Complied for 1984. Bethesda, MD: National Institutes of Health; 1985.
10. Balkau B, Shipley M, Jarrett RJ, et al. High blood glucose concentration is a risk factor for mortality in middle-aged nondiabetic men: 20-year follow-up in the Whitehall Study, the Paris Prospective Study, and the Helsinki Policemen Study. Diabetes Care 1998; 21:360-367.
11. Effect of intensive diabetes management on macrovascular events and risk factors in the Diabetes Control and Complications Trial. Am J Cardiol 1995; 75: 894-903.
12. UK Prospective Diabetes Study Group. Intensive blood- glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes: UKPDS 33. Lancet 1998; 352:837-853.
13. UK Prospective Diabetes Study Group. Tight blood pressure control and risk of macrovascular and microvascular complications in Type 2 diabetes: UKPDS 38. BMJJ 1998; 317:703-713.
14. The Diabetes Control and Complications Trial Research Group. The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus. N Engl J Med 1998; 329:977-986.
15. American Diabetes Association. Clinical practice recommendations 1998. Diabetes Care 198; 21(suppl 1):1-89.
16. Sacco RL, Gan R, Boden-Albala B, et al. Leisure-time physical activity and ischemic stroke risk: The Northern Manhattan Stroke Study. Stroke 1998; 29:380-387.
17. Lee IM, Hennekens CH, Berger K, et al, Exercise and risk of stroke in male physician. Stroke 1999; 30:1-6.
18. Truelsen T, GronbaekM, Schnohr P, et al. Intake of beer, wine, and spirits and risk of stroke: The Copenhagen City Heart Study. Stroke 1998; 29:2,467-2,472.
19. Sacco RL, Elkind M, Boden-Albala B, et al. The protective effect of moderate alcohol consumption on ischemic stroke. JAMA 1999; 281:53-60.
20. Hebert PR, Gaziano JM, Chan KS, et al. Cholesterol lowering with statin drugs, risk of stroke, and total mortality: An overview of randomized trials. JAMA 1997; 278:313-321.
21. Sacks FM, Pfeffer MA, Moye LA, et al. The effect of pravastatin on coronary events after myocardial infarction in patients with average cholesterol levels: Cholesterol and Recurrent Events Trial investigators. N Engl J Med 1996; 335:1,001-1,009.
22. The Long-Term Intervention with Pravastatin in Ischemic Disease (LIPID) Study Group. Prevention of cardiovascular events and death with pravastatin in patients with coronary heart disease and a broad range of initial cholesterol levels. N Engl J Med 1998; 339:1,349-1,357.
23. Furberg CD, Adams HP, Applegate WB, et al. for the Asymptomatic Carotid Artery Progression Study (ACAPS) Research Group. Effect of lovastatin on early carotid atherosclerosis and cardiovascular events. Circulation 1994; 90:1,679-1,687.
24. Crouse JR III, Byington RP, Bond MG, et al. Pravastatin,
lipids, and atherosclerosis in the carotid arteries. Am J Cardiol 1995; 75:455-459.
25. Giles WH, Croft JB, Greenlund KJ, et al. Total homocysteine concentration and the likelihood of nonfatal stroke: Results from the third National Health and Nutrition Examination Survey, 1988-1994. Stroke 1998; 29:2,473-2,477.
26. Sacco RL, Roberts JK, Jacobs BS. Homocysteine as a risk factor for ischemic stroke: an epidemiological story in evolution. Neuroepidemiology 1998; 17:167-173.
27. Joseph LN, Babikian VL, Allen NC, et al. Risk factor modification in stroke prevention: The experience of a stroke clinic. Stroke 1999; 30:16-20.
28. Gorelick PB. Stroke prevention: Windows of opportunity and failed expectations. A discussion of modifiable cardiovascular risk factors and a prevention proposal. Neuroepidemiology 1997; 16:163-173.
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