Cardiac causes of stroke
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At least 20% of all ischemic strokes are cardioembolic.
Cardiac conditions that cause cerebral embolism are classified as major or minor depending on whether the causal link has or has not been fully established between the underlying cardiac condition and the stroke.
Atrial fibrillation, acute myocardial infarction, valvular heart disease, infective endocarditis, nonbacterial thrombotic endocarditis, and atrial myxoma are the main cardiac causes of cerebral embolism.
Patent foramen ovale, atrial septal aneurysm, mitral valve prolapse, mitral annular calcification, calcific aortic stenosis, and mitral valve strands are cardiac conditions with a potential causal link to cerebral embolism, but until now, either they have been found to be poor predictors of recurrent stroke or their risk of recurrent stroke is unknown.
The management of patients with a stroke of cardiac source is twofold: 1) treatment of the acute phase of stroke and 2) prophylactic treatment of recurrent thromboembolism. When possible, primary prevention of cerebral embolism should be recommended, particularly in cardiac conditions with known high risk of stroke (eg, atrial fibrillation, mitral stenosis, or presence of mechanical prosthetic heart valves).
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References and Recommended Reading
- 1.Cerebral Embolism Task Force: Cardiogenic brain embolism. Arch Neurol 1989, 46:727–743.Google Scholar
- 3.EAFT (European Atrial Fibrillation Trial) Study Group: Secondary prevention in non-rheumatic atrial fibrillation after transient ischaemic attack or minor stroke. Lancet 1993, 342:1255–1262.Google Scholar
- 4.The Stroke Prevention in Atrial Fibrillation Investigators Committee on Echocardiography: Transesophageal echocardiographic correlates of thromboembolism in high-risk patients with nonvalvular atrial fibrillation. Ann Intern Med 1998, 128:639–647. In this study of patients with AF, those with spontaneous echo contrast or thrombus in the left atrium had a risk of recurrent stroke of 7.5% per year; those with plaques of larger than 4 mm in the thoracic aorta had a risk of 12% per year; those who had both aortic plaques and left atrial echo contrast or thrombus had a risk of 20.5% per year; and those who had none of these abnormalities had a risk of 1.2% per year.Google Scholar
- 5.Stein PD, Alpert JS, Dalen JE, et al.: Antithrombotic therapy in patients with mechanical and biological prosthetic heart valves. Chest 1998, 114:602S-610S. This is the report of the fifth American College of Chest Physicians consensus conference on recommendations for antithrombotic therapy in patients with mechanical and biologic prosthetic heart valves.PubMedGoogle Scholar
- 23.The SCATI (Studio sulla Calciparina nell’Angina e nella Trombosi Ventricolare nell’Infarto) group: Randomised controlled trial of subcutaneous calcium-heparin in acute myocardial infarction. Lancet 1989, 2:182–186.Google Scholar
- 24.Kontny F, Dale J, Abildgaard U, Pedersen TR: Randomized trial of low molecular weight heparin (dalteparin) in prevention of left ventricular thrombus formation and arterial embolism after acute anterior myocardial infarction: the Fragmin in Acute Myocardial Infarction (FRAMI) Study. J Am Coll Cardiol 1997, 30(4):962–969.PubMedCrossRefGoogle Scholar
- 26.Stroke Prevention in Atrial Fibrillation Investigators: Adjusted-dose warfarin versus low-intensity, fixeddose warfarin plus aspirin for high-risk patients with atrial fibrillation: Stroke Prevention in Atrial Fibrillation III randomised clinical trial. Lancet 1996, 348:633–638.CrossRefGoogle Scholar
- 32.Collaborative overview of randomized trials of antiplatelet therapy: I. Prevention of death, myocardial infarction, and stroke by prolonged antiplatelet therapy in various categories of patients. Antiplatelet Trialists’ Collaboration. BMJ 1994, 308:81–106. The Antiplatelet Trialists’ Collaboration has shown by metaanalysis that in high-risk patients (with previous vascular occlusive disease), antiplatelet agents reduce by one third the risk of nonfatal stroke.Google Scholar
- 33.Stroke Prevention in Atrial Fibrillation Investigators: Warfarin versus aspirin for prevention of thromboembolism in atrial fibrillation: stroke prevention in atrial fibrillation II study. Lancet 1994, 343:687–691.Google Scholar
- 34.Petty GW, Brown RD, Whisnant JP, et al.: Frequency of major complications of aspirin, warfarin, and intravenous heparin for secondary stroke prevention. A population-based study. Ann Intern Med 1999, 130:14–22. This is a population-based study demonstrating that the complication rate with warfarin therapy is much higher than in randomized clinical trials (7.9 per 100 person-years).PubMedGoogle Scholar
- 35.Hirsh J, Dalen JE, Anderson DR, et al.: Oral anticoagulants. Mechanism of action, clinical effectiveness, and optimal therapeutic range. Chest 1998, 114:445S-469S. This article lists the recommendations of the fifth American College of Chest Physicians consensus conference on the use of oral anticoagulants.PubMedGoogle Scholar
- 37.Patrono C, Coller BS, Dalen JE, et al.: Platelet active drugs: the relationships among dose, effectiveness, and side effects. Chest 1998, 114:470S-488S. This article lists the recommendations of the fifth American College of Chest Physicians consensus conference on the use of platelet active drugs.PubMedGoogle Scholar
- 39.Hung J, Landzberg MJ, Jenkins KJ, et al.: Transcatheter closure of patent foramen ovale for presumed paradoxical emboli: low incidence of recurrent neurologic events at intermediate term follow-up [abstract]. Circulation 1998, 98:I100.Google Scholar
- 40.Ugurlu BS, Dearani JA, Daly RC, et al.: Surgical patent foramen ovale closure for prevention of paradoxical embolism induced cerebrovascular events [abstract]. Circulation 1998, 98:I100.Google Scholar
- 42.Amarenco P, Duyckaerts C, Tzourio C, et al.: The prevalence of ulcerated plaques in the aortic arch in patients with stroke. N Engl J Med 1992, 326:221–225. This case-control study showed that plaques greater than 4 mm in thickness, ulcerated plaques, and those with mobile components are more likely to be associated with stroke.PubMedCrossRefGoogle Scholar
- 44.Mittusch R, Doherty C, Wucherpfennig H, et al.: Vascular events during follow-up in patients with aortic arch atherosclerosis. Stroke 1997, 28:36–39.Google Scholar
- 46.Cohen A, Tzourio C, Bertrand B, et al.: Aortic plaque morphology and vascular events. A follow-up study in patients with ischemic stroke. Circulation 1997, 96:3838–3841. This case-control study has shown that plaques greater than 4 mm in thickness, when hypoechoic and noncalcified, are more likely to be associated with stroke.PubMedGoogle Scholar