Alexander E Merkler1, Traci M Bartz2, Hooman Kamel2, Elsayed Z Soliman2, Virginia Howard2, Bruce M Psaty2, Peter M Okin2, Monika M Safford2, Mitchell S V Elkind2, W T Longstreth2. 1. From the Clinical and Translational Neuroscience Unit (A.E.M., H.K.), Feil Family Brain and Mind Research Institute (A.E.M., H.K.), and Departments of Neurology (A.E.M., H.K.) and Medicine (P.M.O., M.M.S.), Weill Cornell Medical College, New York, NY; Department of Biostatistics (T.M.B.), Cardiovascular Health Research Unit (B.M.P.), and Departments of Medicine (B.M.P.), Epidemiology (B.M.P., W.T.L.), Health Services (B.M.P.), and Neurology (W.T.L.), University of Washington, Seattle; Epidemiological Cardiology Research Center (E.Z.S.), Wake Forest University School of Medicine, Winston-Salem, NC; Department of Epidemiology (V.H.), School of Public Health, University of Alabama at Birmingham; Kaiser Permanente Washington Health Research Institute (B.M.P.), Seattle; and Department of Neurology, Vagelos College of Physicians and Surgeons (M.S.V.E.), and Department of Epidemiology (M.S.V.E.), Mailman School of Public Health, Columbia University, New York, NY. alm9097@med.cornell.edu. 2. From the Clinical and Translational Neuroscience Unit (A.E.M., H.K.), Feil Family Brain and Mind Research Institute (A.E.M., H.K.), and Departments of Neurology (A.E.M., H.K.) and Medicine (P.M.O., M.M.S.), Weill Cornell Medical College, New York, NY; Department of Biostatistics (T.M.B.), Cardiovascular Health Research Unit (B.M.P.), and Departments of Medicine (B.M.P.), Epidemiology (B.M.P., W.T.L.), Health Services (B.M.P.), and Neurology (W.T.L.), University of Washington, Seattle; Epidemiological Cardiology Research Center (E.Z.S.), Wake Forest University School of Medicine, Winston-Salem, NC; Department of Epidemiology (V.H.), School of Public Health, University of Alabama at Birmingham; Kaiser Permanente Washington Health Research Institute (B.M.P.), Seattle; and Department of Neurology, Vagelos College of Physicians and Surgeons (M.S.V.E.), and Department of Epidemiology (M.S.V.E.), Mailman School of Public Health, Columbia University, New York, NY.
Abstract
OBJECTIVE: To test the hypothesis that silent myocardial infarction (MI) is a risk factor for ischemic stroke, we evaluated the association between silent MI and subsequent ischemic stroke in the Cardiovascular Health Study. METHODS: The Cardiovascular Health Study prospectively enrolled community-dwelling individuals ≥65 years of age. We included participants without prevalent stroke or baseline evidence of MI. Our exposures were silent and clinically apparent, overt MI. Silent MI was defined as new evidence of Q-wave MI, without clinical symptoms of MI, on ECGs performed during annual study visits from 1989 to 1999. The primary outcome was incident ischemic stroke. Secondary outcomes were ischemic stroke subtypes: nonlacunar, lacunar, and other/unknown. Cox proportional hazards analysis was used to model the association between time-varying MI status (silent, overt, or no MI) and stroke after adjustment for baseline demographics and vascular risk factors. RESULTS: Among 4,224 participants, 362 (8.6%) had an incident silent MI, 421 (10.0%) an incident overt MI, and 377 (8.9%) an incident ischemic stroke during a median follow-up of 9.8 years. After adjustment for demographics and comorbidities, silent MI was independently associated with subsequent ischemic stroke (hazard ratio [HR], 1.51; 95% confidence interval [CI], 1.03-2.21). Overt MI was associated with ischemic stroke both in the short term (HR, 80; 95% CI, 53-119) and long term (HR, 1.60; 95% CI, 1.04-2.44). In secondary analyses, the association between silent MI and stroke was limited to nonlacunar ischemic stroke (HR, 2.40; 95% CI, 1.36-4.22). CONCLUSION: In a community-based sample, we found an association between silent MI and ischemic stroke.
OBJECTIVE: To test the hypothesis that silent myocardial infarction (MI) is a risk factor for ischemic stroke, we evaluated the association between silent MI and subsequent ischemic stroke in the Cardiovascular Health Study. METHODS: The Cardiovascular Health Study prospectively enrolled community-dwelling individuals ≥65 years of age. We included participants without prevalent stroke or baseline evidence of MI. Our exposures were silent and clinically apparent, overt MI. Silent MI was defined as new evidence of Q-wave MI, without clinical symptoms of MI, on ECGs performed during annual study visits from 1989 to 1999. The primary outcome was incident ischemic stroke. Secondary outcomes were ischemic stroke subtypes: nonlacunar, lacunar, and other/unknown. Cox proportional hazards analysis was used to model the association between time-varying MI status (silent, overt, or no MI) and stroke after adjustment for baseline demographics and vascular risk factors. RESULTS: Among 4,224 participants, 362 (8.6%) had an incident silent MI, 421 (10.0%) an incident overt MI, and 377 (8.9%) an incident ischemic stroke during a median follow-up of 9.8 years. After adjustment for demographics and comorbidities, silent MI was independently associated with subsequent ischemic stroke (hazard ratio [HR], 1.51; 95% confidence interval [CI], 1.03-2.21). Overt MI was associated with ischemic stroke both in the short term (HR, 80; 95% CI, 53-119) and long term (HR, 1.60; 95% CI, 1.04-2.44). In secondary analyses, the association between silent MI and stroke was limited to nonlacunar ischemic stroke (HR, 2.40; 95% CI, 1.36-4.22). CONCLUSION: In a community-based sample, we found an association between silent MI and ischemic stroke.
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