AIM: The aim of this study was to investigate the role of sympathovagal imbalance in patients with ''ischemic'' sudden death (arrhythmic death preceded by ST segment shift). Although heart rate variability is a powerful tool for risk stratification after myocardial infarction, the mechanism precipitating sudden death is poorly known. METHODS: We analyzed the records of 10 patients who had ischemic sudden death during ECG Holter monitoring. Thirty patients with angina and transient myocardial ischemia during Holter monitoring served as control subjects. Arrhythmias, ST segment changes and heart rate variability were analyzed by a computed interactive Holter system. RESULTS: In 8 patients the sudden death was induced by ventricular fibrillation; in 2 by atrioventricular block followed by sinus arrest. All 10 patients showed ST segment shift. ST depression (maximal change 0.54+/-0.16 mV) occurred in 6 patients and ST elevation (maximal change 0.65+/-0.24 mV) in 4. The standard deviation of normal RR intervals (SDNN) was 92+/-30 ms during total Holter monitoring period vs 70+/-10 ms and 46+/-8 ms in epoch 1 and epoch 2 respectively. The SDNN was lower before the occurrence of ischemic sudden death: 54+/-12 ms (P< 0.005) in epoch 3 and 26+/-5 (P<0.005) in epoch 4 (i.e. 5 min before the onset of fatal ST segment shift). In controls the SDNN was 108+/-30 ms during total Holter monitoring period, whereas is measured 58+/-28 ms 5 min before the most significant episode of ST shift vs 26+/-5 in the group with sudden death (P<0.001). CONCLUSION: Sympathovagal imbalance, as detected by a marked decrease in heart rate variability, is present in the period (5 min) immediately preceding the onset of the ST shift precipitating ischemic sudden death. These findings suggest that transient autonomic dysfunction may facilitate, during acute myocardial ischemia, fatal arrhythmias precipitating in sudden death.
AIM: The aim of this study was to investigate the role of sympathovagal imbalance in patients with ''ischemic'' sudden death (arrhythmic death preceded by ST segment shift). Although heart rate variability is a powerful tool for risk stratification after myocardial infarction, the mechanism precipitating sudden death is poorly known. METHODS: We analyzed the records of 10 patients who had ischemic sudden death during ECG Holter monitoring. Thirty patients with angina and transient myocardial ischemia during Holter monitoring served as control subjects. Arrhythmias, ST segment changes and heart rate variability were analyzed by a computed interactive Holter system. RESULTS: In 8 patients the sudden death was induced by ventricular fibrillation; in 2 by atrioventricular block followed by sinus arrest. All 10 patients showed ST segment shift. ST depression (maximal change 0.54+/-0.16 mV) occurred in 6 patients and ST elevation (maximal change 0.65+/-0.24 mV) in 4. The standard deviation of normal RR intervals (SDNN) was 92+/-30 ms during total Holter monitoring period vs 70+/-10 ms and 46+/-8 ms in epoch 1 and epoch 2 respectively. The SDNN was lower before the occurrence of ischemic sudden death: 54+/-12 ms (P< 0.005) in epoch 3 and 26+/-5 (P<0.005) in epoch 4 (i.e. 5 min before the onset of fatal ST segment shift). In controls the SDNN was 108+/-30 ms during total Holter monitoring period, whereas is measured 58+/-28 ms 5 min before the most significant episode of ST shift vs 26+/-5 in the group with sudden death (P<0.001). CONCLUSION: Sympathovagal imbalance, as detected by a marked decrease in heart rate variability, is present in the period (5 min) immediately preceding the onset of the ST shift precipitating ischemic sudden death. These findings suggest that transient autonomic dysfunction may facilitate, during acute myocardial ischemia, fatal arrhythmias precipitating in sudden death.