ASSOCIATION OF SILENT-MYOCARDIAL-ISCHEMIA WITH NEW ATHEROTHROMBOTIC BRAIN INFARCTION IN OLDER PATIENTS WITH EXTRACRANIAL INTERNAL OR COMMONCAROTID ARTERIAL-DISEASE WITH AND WITHOUT PREVIOUS ATHEROTHROMBOTIC BRAIN INFARCTION
Ws. Aronow et al., ASSOCIATION OF SILENT-MYOCARDIAL-ISCHEMIA WITH NEW ATHEROTHROMBOTIC BRAIN INFARCTION IN OLDER PATIENTS WITH EXTRACRANIAL INTERNAL OR COMMONCAROTID ARTERIAL-DISEASE WITH AND WITHOUT PREVIOUS ATHEROTHROMBOTIC BRAIN INFARCTION, Journal of the American Geriatrics Society, 43(11), 1995, pp. 1272-1274
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 witho
ut prior ABI. DESIGN: In a prospective study of 208 older patients wit
h 40 to 100% ECAD diagnosed by carotid duplex ultrasonography, 24-hour
ambulatory electrocardiograms were obtained to detect silent myocardi
al ischemia. At 42-month mean follow-up, silent myocardial ischemia wa
s correlated with the incidence of new ABI in patients with and withou
t 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 wome
n, mean age 81 +/- 8 years (range 60 to 100). One-hundred three (50%)
of the patients had prior ABI. MEASUREMENTS AND MAIN RESULTS: Sixy-nin
e (33%) of the 208 patients had silent myocardial ischemia. Mean follo
w-up was 42 +/- 25 months (range 3 to 101 months). At follow-up, the i
ncidence of new ABI was 64% in patients with prior ABI and 32% in pati
ents 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 oth
er prognostic variables. Patients with silent ischemia have a 2.1 time
s higher probability of developing new ABI than those without silent i
schemia after controlling other prognostic variables. CONCLUSIONS: Pri
or ABI and silent ischemia are independent risk factors for the develo
pment of new ABI in patients with 40 to 100% ECAD. This probably refle
cts that silent ischemia is a marker for more advanced or more signifi
cant atherosclerotic disease rather than a causal factor for ABI.