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Electrocardiographic changes and myocardial damage in patients with acute cerebrovascular accidents
Insights
Patients with acute cerebrovascular accident frequently develop electrocardiographic abnormalities and elevated cardiac enzymes, particularly creatine phosphokinase (CPK). Elevated CPK is a strong predictor of cardiac damage and mortality in these patients.
Area of Science:
- Cardiology
- Neurology
Background:
- Acute cerebrovascular accident (CVA) can lead to cardiac complications.
- Electrocardiographic (ECG) abnormalities and elevated cardiac enzymes are common in CVA patients.
Purpose of the Study:
- To investigate the incidence of ECG abnormalities and cardiac enzyme elevation in CVA patients.
- To determine the correlation between these findings, cardiac damage, and mortality.
Main Methods:
- Prospective study of 100 consecutive CVA patients.
- Serial ECG monitoring and measurement of serum cardiac enzymes (CPK, HBDH, GOT, LDH) within the first three days of admission.
- Comparison with a control group and correlation with mortality.
Main Results:
- 90% of CVA patients exhibited ECG abnormalities, significantly higher than controls.
- Elevated serum creatine phosphokinase (CPK) was observed in 29% of patients, with a 6-fold increase.
- Elevated CPK correlated with increased incidence of ST depression, T wave inversion, conduction defects, atrial fibrillation, and significantly higher mortality (66% vs. 30%).
- Serum CPK was more effective than ECG in assessing cardiac damage and predicting mortality.
Conclusions:
- Acute cerebrovascular accident is associated with a high incidence of cardiac complications, including ECG abnormalities and elevated cardiac enzymes.
- Serum CPK is a valuable biomarker for evaluating cardiac damage and predicting mortality in CVA patients.
- Repeated evaluation of serum CPK and ECG, along with arrhythmia monitoring, is recommended for CVA patients.
Abstract:
In 100 consecutive patients with acute cerebrovascular accident, due to cerebral thrombosis in 72, cerebral hemorrhage in 12, embolus in 6, and subarachnoid hemorrhage in 10, there were 90 who had electrocardiographic abnormalities during the first three days after admission, compared to 50% in a control group. The patients with cerebrovascular accident had a 7- to 10-fold higher incidence of ST segment depression, prolonged Q-Tc interval and atrial fibrillation, and a 2- to 4-fold higher incidence of T wave inversion, conduction defects, premature ventricular beats and left ventricular hypetrophy. Patients who died had a 2-, 3- and 5-fold higher incidence of electrocardiographic evidence of recent myocardial infarction, atrial fibrillation and conduction defects than those who survived, but these changes occurred in only 5, 21 and 14% of all patients, and other electrocardiographic changes could not be correlated with mortality. During the first three days after admission 29 patients had elevation of serum enzymes which may be derived from cardiac muscle, particularly CPK, which was increased 6-fold, compared to 2-fold increases in HBDH, GOT, and LDH. Only 5 of these patients had electrocardiographic evidence of recent myocardial infarction. Patients with elevated serum CPK had a 2-fold higher incidence of ST segment depression, T wave inversion, conduction defects and atrial fibrillation than those with normal CPK, and a mortality of 66%, compared to 30%. Of 41 patients who died, 49% had elevated serum CPK, compared to 15% of 59 patients who survived. These differences were significant (P less than 0.01). Serum CPK was more frequently helpful than the electrocardiogram in evaluating the extent of cardiac damage and in predicting mortality. Patients with acute cerebrovascular accident should have repeated evaluation of serum CPK and the ECG, and be monitored for arrhythmias.