Systolic Time Intervals in Heart Failure in Man

Systolic Time Intervals in Heart Failure in Man

February 1968 | ARNOLD M. WEISSLER, M.D., WILLARD S. HARRIS, M.D., AND CLYDE D. SCHOENFELD, M.D.
The systolic time intervals in patients with heart failure were analyzed using simultaneous recordings of the electrocardiogram, phonocardiogram, and carotid arterial pulsation. These intervals were compared to those in 211 normal subjects. In patients with heart failure, the pre-ejection period was prolonged, and the left ventricular ejection time was shortened, while total electromechanical systole remained relatively unchanged. Both components of the pre-ejection period, the Q-1 interval and isovolumic contraction time, were prolonged. These changes occurred without a measurable change in ventricular depolarization time. The prolongation of the pre-ejection period was well correlated with reduced stroke volume and cardiac output in heart failure and was independently augmented by high arterial pressure. The shortening of the left ventricular ejection time was also correlated with stroke volume and cardiac output. It is postulated that a defect in the mechanical performance of the heart is responsible for the abnormal systolic time intervals in human heart failure. The systolic time intervals in normal individuals were found to be inversely related to heart rate. The duration of electromechanical systole (QS2), left ventricular ejection time (LVET), and pre-ejection period (PEP) decreased with increasing heart rate. The QS2 was longer in females than in males. The PEP and LVET were not significantly affected by sex. The QRS duration was slightly shorter in females than in males. In patients with heart failure, the PEP was prolonged, and the LVET was shortened, while QS2 remained normal. The prolongation of the PEP was due to an increase in both the Q-1 interval and isovolumic contraction time. The deviation in PEP was well correlated with the cardiac index and stroke index, and was independently augmented by high levels of arterial pressure. The deviation in LVET was correlated with the cardiac index and stroke index but to a lesser extent. The deviation in PEP was related to stroke index by the equation ΔPEP = -1.7 SI + 85.9. The deviation in PEP was also related to arterial pressure. The deviation in LVET was not significantly related to arterial pressure. The results of these correlations are consistent with previous experimental studies. The findings suggest that the prolonged pre-ejection period in heart failure is due to a diminished rate of isovolumic left ventricular pressure rise. The prolonged pre-ejection period and shortened ejection time correlate well with reduced stroke volume and cardiac output. This suggests that both abnormalities may be caused by the same underlying defect in the mechanical performance of the heart. The findings also indicate that the duration of total electromechanical systole is essentially unaltered in patients with heart failure. This may encroach on the subsequent systolic ejection period. The reduced velocity of myocardial fiber shortening during the ejection period would diminish the stroke volume, especially if theThe systolic time intervals in patients with heart failure were analyzed using simultaneous recordings of the electrocardiogram, phonocardiogram, and carotid arterial pulsation. These intervals were compared to those in 211 normal subjects. In patients with heart failure, the pre-ejection period was prolonged, and the left ventricular ejection time was shortened, while total electromechanical systole remained relatively unchanged. Both components of the pre-ejection period, the Q-1 interval and isovolumic contraction time, were prolonged. These changes occurred without a measurable change in ventricular depolarization time. The prolongation of the pre-ejection period was well correlated with reduced stroke volume and cardiac output in heart failure and was independently augmented by high arterial pressure. The shortening of the left ventricular ejection time was also correlated with stroke volume and cardiac output. It is postulated that a defect in the mechanical performance of the heart is responsible for the abnormal systolic time intervals in human heart failure. The systolic time intervals in normal individuals were found to be inversely related to heart rate. The duration of electromechanical systole (QS2), left ventricular ejection time (LVET), and pre-ejection period (PEP) decreased with increasing heart rate. The QS2 was longer in females than in males. The PEP and LVET were not significantly affected by sex. The QRS duration was slightly shorter in females than in males. In patients with heart failure, the PEP was prolonged, and the LVET was shortened, while QS2 remained normal. The prolongation of the PEP was due to an increase in both the Q-1 interval and isovolumic contraction time. The deviation in PEP was well correlated with the cardiac index and stroke index, and was independently augmented by high levels of arterial pressure. The deviation in LVET was correlated with the cardiac index and stroke index but to a lesser extent. The deviation in PEP was related to stroke index by the equation ΔPEP = -1.7 SI + 85.9. The deviation in PEP was also related to arterial pressure. The deviation in LVET was not significantly related to arterial pressure. The results of these correlations are consistent with previous experimental studies. The findings suggest that the prolonged pre-ejection period in heart failure is due to a diminished rate of isovolumic left ventricular pressure rise. The prolonged pre-ejection period and shortened ejection time correlate well with reduced stroke volume and cardiac output. This suggests that both abnormalities may be caused by the same underlying defect in the mechanical performance of the heart. The findings also indicate that the duration of total electromechanical systole is essentially unaltered in patients with heart failure. This may encroach on the subsequent systolic ejection period. The reduced velocity of myocardial fiber shortening during the ejection period would diminish the stroke volume, especially if the
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