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Effects of atrial systole on the systolic time intervals in man
122
Abstracts
dependent information must be used as a yardstick. The described procedures have been programmed for on-line analysis where data are recorded at the bedside and results are transmitted by teletypewriter in less than 2 minutes. Effects of Atria1 Systole on the Systolic Time Intervals in Man. D. H. KRAMER, M.D. and P. M. SHAH, M.D., Rochester, N. Y. The effects of the timing of atria1 systole on ventricular function were studied by simultaneous recording of the ECG, phonocardiogram and carotid pulse in 10 patients with complete heart block. In beats preceded by effective atria1 systole (P-R > 50 msec. with transthoracic and >lOO msec. with transvenous pacers) the exact timing of P had no effect on the pre-ejection period (PEP) or left ventricular ejection time (LVET). In 7 patients with a fixed paced rate (65-82/min.), beats with preceding atria1 systole had shorter PEP (average A 18 msec.) and longer LVET (average A 49 msec.) than those without. In 2 patients with acute left heart failure, diastolic atria1 systole had no effect on PEP or LVET. In 1 patient the atria1 rate was considerably faster than the ventricular rate, resulting in a P wave in each diastole. The PEP and LVET remained unchanged for all such beats. Thus, in compensated patients, beats preceded by atria1 contraction, irrespective of the exact timing in diastole, produced a more rapid rate of development of ventricular tension and an increased stroke volume, as indicated by a shorter PEP and prolonged LVET. For those beats without a preceding atria1 contraction PEP was consistently longer and LVET shorter, thus suggesting either a loss of atria1 transport function or mitral regurgitation due to ineffective valve closure. The contribution by atria1 systole was also influenced by the functional state of the myocardium. On the Mechanism of Overdrive Suppression of Ventricular Pacemakers. D. J. KRELLENSTEIN,M.D. and M. VASSALLE,M.D., Brooklyn, N. Y. Cessation of electrical pacing is followed by a period of ventricular asystole (overdrive suppression). It has been proposed that an increase in K, plays a role in the mechanism of this phenomenon. In anesthetized dogs an idioventricular rhythm was obtained by His bundle ligation or vagal nerve stimulation. One minute periods of overdrive were imposed, and the overdrive suppression and coronary sinus potassium concentration (K,,) measured. The animals were then cooled
and the experiments repeated. The results showed that hypothermia increased overdrive suppression and K,,. Also, ventricular pacemakers were found more sensitive to increased K, when cooled. In isolated perfused canine hearts, the coronary sinus eflluent was collected before, during and after overdriving. Purkinje fibers from the same hearts were excised and exposed to the re-oxygenated effluent collected previously. The Purkinje fiber rate fell consistently when the K,, was higher in the perfusate. During long periods of overdrive, the K,, returned to control values but the suppression remained, thus demonstrating that an increased K, is not the only inhibitory factor. Accordingly, the coronary sinus effluent collected during the tenth minute of overdrive did not slow Purkinje fibers. In conclusion, for short periods of overdrive, an increase in K, contributes to the ensuing suppression. For longer periods of overdrive, a modified intracellular ionic concentration may play an inhibitory role. Ventricular Cellular Dimensions in Dogs with Banded Pulmonary Arteries. M. LAKS, M.D. and H. J. C. SWAN, ~\I.D., F.A.c.c., Los Angeles, Calif. Previously reported quantitative determinations have been based on the estimation of cell diameter. In our opinion, the best estimate of myocardial cell size would be the determination of myocardial cell volume (length and width). The purpose of this study was to measure in dogs cell length and width at the base and apex of the right (RV) and left (LV) ventricles in the normal heart (N) and in the heart with pulmonary arterial banding (PAB). After 3-9 months of PAB with RV systolic pressure greater than 50 mm. Hg, all of the RV and 2 of the 5 LV weights were greater than normal. Tissues were taken from the trabeculae carneae at the ventricular right base (RB), right apex (RA), left base (LB) and left apex (LA). They were placed in osmium tetroxide, embedded in Epon 812 stained with Azure II methylene blue and sectioned at 0.5~. The mean cell lengths in the hearts with PAB were greatest at the RB 105 -+ 5 (S.E.M.) and LB 103 f 5.7, followed by LA 95 -c 4 and RA 9.2 f 5; all were greater (fi < 0.01) than normal (RB 67 -+ 2.5, LB 67 f 3.3, LA 70 & 2.8 and RA 70 f 3.4). The mean cell widths of the hearts with PAB (RB 24 & 0.7, RA 16 2 0.6 and LB 16 -C 0.4) were greater (p < 0.01) than normal (RB 16 + 0.4, RA 13 & 0.5 and LB 14 f 0.4); however, they were the same at the LA (PAB 14 f 0.4; N 13 -I0.5; 0 > 0.1). The mean cell widths of the PAB THE
AMERICAN
JOURNAL
OF CARDIOLOGY
Abstracts
dependent information must be used as a yardstick. The described procedures have been programmed for on-line analysis where data are recorded at the bedside and results are transmitted by teletypewriter in less than 2 minutes. Effects of Atria1 Systole on the Systolic Time Intervals in Man. D. H. KRAMER, M.D. and P. M. SHAH, M.D., Rochester, N. Y. The effects of the timing of atria1 systole on ventricular function were studied by simultaneous recording of the ECG, phonocardiogram and carotid pulse in 10 patients with complete heart block. In beats preceded by effective atria1 systole (P-R > 50 msec. with transthoracic and >lOO msec. with transvenous pacers) the exact timing of P had no effect on the pre-ejection period (PEP) or left ventricular ejection time (LVET). In 7 patients with a fixed paced rate (65-82/min.), beats with preceding atria1 systole had shorter PEP (average A 18 msec.) and longer LVET (average A 49 msec.) than those without. In 2 patients with acute left heart failure, diastolic atria1 systole had no effect on PEP or LVET. In 1 patient the atria1 rate was considerably faster than the ventricular rate, resulting in a P wave in each diastole. The PEP and LVET remained unchanged for all such beats. Thus, in compensated patients, beats preceded by atria1 contraction, irrespective of the exact timing in diastole, produced a more rapid rate of development of ventricular tension and an increased stroke volume, as indicated by a shorter PEP and prolonged LVET. For those beats without a preceding atria1 contraction PEP was consistently longer and LVET shorter, thus suggesting either a loss of atria1 transport function or mitral regurgitation due to ineffective valve closure. The contribution by atria1 systole was also influenced by the functional state of the myocardium. On the Mechanism of Overdrive Suppression of Ventricular Pacemakers. D. J. KRELLENSTEIN,M.D. and M. VASSALLE,M.D., Brooklyn, N. Y. Cessation of electrical pacing is followed by a period of ventricular asystole (overdrive suppression). It has been proposed that an increase in K, plays a role in the mechanism of this phenomenon. In anesthetized dogs an idioventricular rhythm was obtained by His bundle ligation or vagal nerve stimulation. One minute periods of overdrive were imposed, and the overdrive suppression and coronary sinus potassium concentration (K,,) measured. The animals were then cooled
and the experiments repeated. The results showed that hypothermia increased overdrive suppression and K,,. Also, ventricular pacemakers were found more sensitive to increased K, when cooled. In isolated perfused canine hearts, the coronary sinus eflluent was collected before, during and after overdriving. Purkinje fibers from the same hearts were excised and exposed to the re-oxygenated effluent collected previously. The Purkinje fiber rate fell consistently when the K,, was higher in the perfusate. During long periods of overdrive, the K,, returned to control values but the suppression remained, thus demonstrating that an increased K, is not the only inhibitory factor. Accordingly, the coronary sinus effluent collected during the tenth minute of overdrive did not slow Purkinje fibers. In conclusion, for short periods of overdrive, an increase in K, contributes to the ensuing suppression. For longer periods of overdrive, a modified intracellular ionic concentration may play an inhibitory role. Ventricular Cellular Dimensions in Dogs with Banded Pulmonary Arteries. M. LAKS, M.D. and H. J. C. SWAN, ~\I.D., F.A.c.c., Los Angeles, Calif. Previously reported quantitative determinations have been based on the estimation of cell diameter. In our opinion, the best estimate of myocardial cell size would be the determination of myocardial cell volume (length and width). The purpose of this study was to measure in dogs cell length and width at the base and apex of the right (RV) and left (LV) ventricles in the normal heart (N) and in the heart with pulmonary arterial banding (PAB). After 3-9 months of PAB with RV systolic pressure greater than 50 mm. Hg, all of the RV and 2 of the 5 LV weights were greater than normal. Tissues were taken from the trabeculae carneae at the ventricular right base (RB), right apex (RA), left base (LB) and left apex (LA). They were placed in osmium tetroxide, embedded in Epon 812 stained with Azure II methylene blue and sectioned at 0.5~. The mean cell lengths in the hearts with PAB were greatest at the RB 105 -+ 5 (S.E.M.) and LB 103 f 5.7, followed by LA 95 -c 4 and RA 9.2 f 5; all were greater (fi < 0.01) than normal (RB 67 -+ 2.5, LB 67 f 3.3, LA 70 & 2.8 and RA 70 f 3.4). The mean cell widths of the hearts with PAB (RB 24 & 0.7, RA 16 2 0.6 and LB 16 -C 0.4) were greater (p < 0.01) than normal (RB 16 + 0.4, RA 13 & 0.5 and LB 14 f 0.4); however, they were the same at the LA (PAB 14 f 0.4; N 13 -I0.5; 0 > 0.1). The mean cell widths of the PAB THE
AMERICAN
JOURNAL
OF CARDIOLOGY