Related Experiment Videos
Insights
Elevated cardiac enzymes, particularly CK-MB (heart) iso-enzyme, are common in stroke patients, indicating acute myocardial involvement. This cardiac dysfunction appears to be a consequence, not a cause, of the cerebrovascular event.
Area of Science:
- Neurology
- Cardiology
- Biochemistry
Background:
- Stroke patients admitted to intensive care units often present with elevated cardiac enzyme levels.
- The relationship between acute cerebrovascular events and myocardial involvement requires further investigation.
Purpose of the Study:
- To investigate the incidence and significance of elevated serum cardiac enzyme levels in patients following acute stroke.
- To determine the tissue source of elevated creatine kinase (CK) using isoenzyme fractionation.
Main Methods:
- Serum cardiac enzymes (CK, LDH, SGOT) and ECG were monitored in stroke patients and controls.
- Creatine kinase (CK) isoenzymes (CK-MB, CK-MM, CK-BB) were analyzed in a subset of stroke patients.
Main Results:
- 8% of stroke patients showed elevated mean serum cardiac enzyme levels; TIA patients did not differ from controls.
- 11% of stroke patients had elevated CK-MB (heart) iso-enzyme, associated with increased evidence of myocardial ischemia and arrhythmias.
- No significant elevation of CK-BB (brain) iso-enzyme was detected in any patient.
Conclusions:
- Acute myocardial involvement is a common complication in the early stages of stroke, potentially more so than previously recognized.
- Elevated CK-MB levels in stroke patients suggest myocardial dysfunction as a consequence, rather than a cause, of the cerebrovascular lesion.
Abstract:
Serum cardiac enzyme levels (CK, LDH, SGOT) 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 isoenzyems 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 has more evidence of acute myocardial ischemia on ECG (p less than 0.05), and more cardiac arrhythmias (p less than 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.