Serum cardiac enzymes in stroke.

Abstract

SUMMARY Serum cardiac enzyme levels (CK, LDH, SCOT) were estimated and the ECG recorded for 4 days following admission of 288 patients (Group I) to a stroke intensive care unit. Sixty-four of these patients, subsequently found not to have strokes, served as controls. Mean serum levels of all 3 cardiac enzymes were elevated in 8% of the 224 patients with stroke. The mean serum enzyme levels in patients with transient ischemic attacks (TIA) did not differ from controls.In a second group of 230 patients with stroke (Group II) serum CK levels were measured and the isoenzymes were fractionated to determine the tissue source of the enzymes. One hundred and one patients had raised total CK values and 25 of these (11%) had raised CK-MB (heart) iso-enzyme, the remainder having CK-MM (skeletal muscle) fraction. No serum CK-BB (brain) iso-enzyme was detected in any patient. Patients with positive serum levels of CK-MB had more evidence of acute myocardial ischemia on ECG (p < 0.05), and more cardiac arrhythmias (p < 0.001) than those with normal CK levels. Scattered areas of myocytolysis were found in the myocardium at autopsy in one patient.The acute rise in serum cardiac enzymes which we have recorded in the initial stages of stroke suggest that acute myocardial involvement is a commoner complication than is generally recognized. Also, since the CK-MB rises were modest and progressive, it is more likely that this acute myocardial dysfunction is a consequence, rather than a cause, of the acute cerebrovascular lesion.

Serum Cardiac Troponin T Levels as an Indicator of Myocardial Injury in Ischemic and Hemorrhagic Stroke Patients

“…It's now common knowledge that either ischemic or hemorrhagic cerebrovascular disorders have a negative effect on cardiac functions (Norris et al 1979;Ay et al 2002;Butcher and Parsons 2002). Cardiac abnormalities, as judged by release of cardiac enzymes, changes in electrocardiography (ECG), or clinical or echocardiographic evidence of left ventricular dysfunction usually develop just after intracerebral disorders (i.e., stroke, subarachnoid hemorrhage) (Bhagat et al 1997;James et al 2000).…”

“…In myocardial damage, serum levels of different cardiac enzymes and proteins (i.e., creatine kinase-myocardial subfraction [CK-MB] and cardiac troponin T [cTnT]) increase dramatically (Norris et al 1979). Although CK-MB is a commonly used marker of myocardial necrosis, it may also be released as a result of damage to non-cardiac muscle which decreases its specificity (Norris et al 1979).…”

“…Although CK-MB is a commonly used marker of myocardial necrosis, it may also be released as a result of damage to non-cardiac muscle which decreases its specificity (Norris et al 1979). Furthermore some patients may develop clinically important myocardial dysfunction due to sublethal injury that does not result in CK-MB release.…”

“…Many studies in the literature clearly depicted the increase in CK-MB levels and changes in ECG after stroke (Norris et al 1979;Rudehill et al 1982;Brouwers et al 1989;Kuroiwa et al 1995). However the studies searching for cTnT which is more sensitive and specific to myocardium after stroke, is relatively scarce (James et al 2000;Parekh et al 2000).…”

Assessment of relationship between acute ischemic stroke and heart disease - protocol of a prospective observational trial

“…Likewise, in patients surviving cerebrovascular diseases, other manifestations of cardiovascular disease, particularly coronary artery disease, are the main causes of long-term mortality 6,7 . There is currently no clear link between acute coronary syndrome and stroke, although it has been repeatedly described [8][9][10][11][12][13] . Due to the acute stroke, clinical symptoms of acute coronary syndrome may be blurred and, cause of the association between acute stroke and acute coronary syndrome has not yet been completely verified.…”