Journal of the American Geriatrics Society · 1995
Association of silent myocardial ischemia with new atherothrombotic brain infarction in older patients with extracranial internal or common carotid arterial disease with and without previous atherothrombotic brain infarction.
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Aronow W S, Ahn C, Mercando A D, Epstein S, Gutstein H, Schoenfeld M R
Аннотация
OBJECTIVE: To correlate silent myocardial ischemia with the incidence of new atherothrombotic brain infarction (ABI) in older patients with 40 to 100% extracranial carotid arterial disease (ECAD) with and without prior ABI.
DESIGN: In a prospective study of 208 older patients with 40 to 100% ECAD diagnosed by carotid duplex ultrasonography, 24-hour ambulatory electrocardiograms were obtained to detect silent myocardial ischemia. At 42-month mean follow-up, silent myocardial ischemia was correlated with the incidence of new ABI in patients with and without prior ABI.
SETTING: A large long-term health care facility where 208 older patients with 40 to 100% ECAD and technically adequate 24-hour ambulatory electrocardiograms for detecting silent myocardial ischemia were studied.
PATIENTS: The 208 patients included 68 men and 140 women, mean age 81 +/- 8 years (range 60 to 100). One-hundred three (50%) of the patients had prior ABI.
MEASUREMENTS AND MAIN RESULTS: Sixty-nine (33%) of the 208 patients had silent myocardial ischemia. Mean follow-up was 42 +/- 25 months (range 3 to 101 months). At follow-up, the incidence of new ABI was 64% in patients with prior ABI and 32% in patients with no prior ABI (P < .0001). At follow-up, the incidence of new ABI was 65% in patients with silent ischemia and 40% in patients with no silent ischemia (P = .0005). The multivariate Cox regression model showed that patients with prior ABI have a 2.5 times higher chance of developing new ABI than those without prior ABI after controlling other prognostic variables. Patients with silent ischemia have a 2.1 times higher probability of developing new ABI than those without silent ischemia after controlling other prognostic variables.
CONCLUSIONS: Prior ABI and silent ischemia are independent risk factors for the development of new ABI in patients with 40 to 100% ECAD. This probably reflects that silent ischemia is a marker for more advanced or more significant atherosclerotic disease rather than a causal factor for ABI.
DESIGN: In a prospective study of 208 older patients with 40 to 100% ECAD diagnosed by carotid duplex ultrasonography, 24-hour ambulatory electrocardiograms were obtained to detect silent myocardial ischemia. At 42-month mean follow-up, silent myocardial ischemia was correlated with the incidence of new ABI in patients with and without prior ABI.
SETTING: A large long-term health care facility where 208 older patients with 40 to 100% ECAD and technically adequate 24-hour ambulatory electrocardiograms for detecting silent myocardial ischemia were studied.
PATIENTS: The 208 patients included 68 men and 140 women, mean age 81 +/- 8 years (range 60 to 100). One-hundred three (50%) of the patients had prior ABI.
MEASUREMENTS AND MAIN RESULTS: Sixty-nine (33%) of the 208 patients had silent myocardial ischemia. Mean follow-up was 42 +/- 25 months (range 3 to 101 months). At follow-up, the incidence of new ABI was 64% in patients with prior ABI and 32% in patients with no prior ABI (P < .0001). At follow-up, the incidence of new ABI was 65% in patients with silent ischemia and 40% in patients with no silent ischemia (P = .0005). The multivariate Cox regression model showed that patients with prior ABI have a 2.5 times higher chance of developing new ABI than those without prior ABI after controlling other prognostic variables. Patients with silent ischemia have a 2.1 times higher probability of developing new ABI than those without silent ischemia after controlling other prognostic variables.
CONCLUSIONS: Prior ABI and silent ischemia are independent risk factors for the development of new ABI in patients with 40 to 100% ECAD. This probably reflects that silent ischemia is a marker for more advanced or more significant atherosclerotic disease rather than a causal factor for ABI.