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      Myocardial Stress in Patients with Acute Cerebrovascular Events

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          Signs of myocardial involvement are common in patients with acute cerebrovascular events. ST segment deviations, abnormal left ventricular function, increased N-terminal pro-brain natriuretic peptide (NT-proBNP), prolonged QT interval, and/or raised troponins are observed in up to one third of the patients. The huge majority of these findings are fully reversible. The changes may mimic myocardial infarction, but are not necessarily identical to coronary thrombosis. Based on the literature these signs may represent an acute catecholamine release provoked by the cerebrovascular catastrophe itself and not coronary thrombosis. However, all patients with signs of cardiac involvement during acute cerebrovascular events should receive a cardiological follow-up in order to exclude concomitant ischemic heart disease.

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          Most cited references 31

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          Cardiac-specific troponin I levels to predict the risk of mortality in patients with acute coronary syndromes.

          In patients with acute coronary syndromes, it is desirable to identify a sensitive serum marker that is closely related to the degree of myocardial damage, provides prognostic information, and can be measured rapidly. We studied the prognostic value of cardiac troponin I levels in patients with unstable angina or non-Q-wave myocardial infarction. In a multicenter study, blood specimens from 1404 symptomatic patients were analyzed for cardiac troponin I, a serum marker not detected in the blood of healthy persons. The relation between mortality at 42 days and the level of cardiac troponin I in the specimen obtained on enrollment was determined both before and after adjustment for baseline characteristics. The mortality rate at 42 days was significantly higher in the 573 patients with cardiac troponin I levels of at least 0.4 ng per milliliter (21 deaths, or 3.7 percent) than in the 831 patients with cardiac troponin I levels below 0.4 ng per milliliter (8 deaths, or 1.0 percent; P or = 65 years). In patients with acute coronary syndromes, cardiac troponin I levels provide useful prognostic information and permit the early identification of patients with an increased risk of death.
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            Catecholamines, infection, and death in acute ischemic stroke.

            Experimental studies have recently suggested that acute ischemia may facilitate the appearance of fatal infections as part of a brain-induced immunodepression syndrome. However, the mechanisms and neurological consequences of infections complicating acute ischemic stroke have received much less attention at the bedside. The incidence of infection and death after non-septic stroke was compared in this prospective study with longitudinal changes of cytokines, leukocytes, normetanephrine (NMN) and metanephrine (MN) in 75 consecutive patients. In multivariate analysis, infection, n = 13 (17%), was associated with the upper quartile of MN (OR 3.51, 95% CI 1.30-9.51), neurological impairment (NIHSS) on admission (OR 3.99, 95% CI 1.34-11.8), monocyte count (OR 1.78, 95% CI 1.13-2.79), and increased interleukin (IL)-10 (OR 1.54, 95% CI 1.00-2.38). Mortality at 3 months, n = 16 (21%), was associated with increased levels of NMN on admission (OR 2.34 95% CI 1.15-4.76), NIHSS score (OR 2.57, 95% CI 1.29-5.11), and higher IL-6 levels (OR 1.29, 95% 1.00-1.67). These findings suggest that acute ischemic stroke is associated with an early activation of the sympathetic adrenomedullar pathway that lowers the threshold of infection and increases the risk of death. Moreover, these findings are independent of the blood borne effects of pro- and anti-inflammatory cytokines, and circulating leukocytes.
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              Left ventricular wall motion abnormalities in patients with subarachnoid hemorrhage: neurogenic stunned myocardium.

              The purpose of this study was to determine whether a relation exists between electrocardiographic (ECG) abnormalities and left ventricular wall motion in patients with subarachnoid hemorrhage. Although ECG changes simulating acute myocardial infarction are frequently seen in patients with subarachnoid hemorrhage, their relation to left ventricular wall motion has not been established. Twelve patients with subarachnoid hemorrhage were classified according to the presence of ST segment elevation in at least two consecutive leads on admission: seven patients with ST segment elevation (group I) and five patients without ST segment elevation (group II). No patients had a previous history of heart disease. Left ventricular regional wall motion was evaluated by the centerline method. The mean (+/- SEM) duration from onset of subarachnoid hemorrhage to left ventriculography was 9 +/- 3 h in group I and 10 +/- 1 h in group II. Coronary angiography was performed to rule out wall motion abnormalities due to coronary artery disease while the ST segment was still elevated. Two-dimensional echocardiography was used to evaluate wall motion thereafter. All patients in group I showed ST segment elevation in ECG leads V4 to V6. Wall motion of the left ventricular apex was significantly reduced in group I compared with group II (-2.48 +/- 0.41 vs. -0.45 +/- 0.72, p < 0.02). No patients showed organic stenosis or vasospasm, or both, of epicardial coronary arteries. Wall motion abnormalities decreased echocardiographically in all patients, but one patient in group I died in hospital at 2 or 3 weeks after the onset of subarachnoid hemorrhage, when the T wave was inverted in leads V4 to V6. These findings suggest that patients with subarachnoid hemorrhage and ST segment elevation may demonstrate transient corresponding regional wall motion abnormalities. The mechanism of neurogenic stunned myocardium was not clearly elucidated in the present study.

                Author and article information

                S. Karger AG
                April 2008
                31 October 2007
                : 110
                : 2
                : 123-128
                aGlobal Development, Novo Nordisk, Bagsværd, and bDepartment of Cardiology Y, Bispebjerg Hospital, Copenhagen, Denmark
                110491 Cardiology 2008;110:123–128
                © 2007 S. Karger AG, Basel

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                Page count
                Tables: 3, References: 51, Pages: 6


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