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Right ventricular contractility in myocardial infarctionimplications concerning the measurement of left ventricular filling pressure
ABSTRACTS
HIS BUNDLE UECTRUGRANOFTHE DCG: ATRUF, RBPRESmATIUNCFTHRINTRACELLULkR~ P. Jacob Varghese, MD; M. V. Elisari, MD; R. Parameswaran, MD; Anthony N. Damato, ND; Sun Ii.Lau, MD, U. S. Public Health Service Hospital, Staten Island, New York, Albert Einstein Medical Center, Philadelphia, Pa. In 5 dogs the A-V conduction system consisting of the A-V node, entire bundle of His and left and right bundle branches was isolated using the dissection technique of Elieari et al., and perfused with oxygenated Tyrode at constant temperature. Transmembrane action potentials (TAP) using standard microelectrode techniques were simultaneously recorded from the penetrating and branching portions of the His bundle (H) along with a bipolar surface electrogram @SE) from the same area. Interelectrode conduction times (IECT) and duration of BSE were measured during antegrade, retrograde and premature activation of H. During antegrade and retrograde activation of H the duration of the BSE was equal to the IECT. Polarity of the BSE changed with direction of activation. Conduction delay within Iiwas manifested as an increase in IECT and a decrease in rate of rise of TAP and was reflected In BSE as change in duration, morphology and amplitude. Decremental conduction and block within the H resulted in disappearance of both the BSE and TAP recorded distal to the site of block. 'Conduction delay and block distal to the His i.e., between His and right bundle (RB) did not affect the characteristics of the BSE. When the BSE included the RB the duration of it was greater than the IRCT and the RB was seen as a separate sharp deflection. These studies demonstrate that the BSE represents total activity of the H and faithfully reflects electrical events occurring within the entire H. They also fortify the basis of clinical His bundle electrography.
RIGHT VENTRICULAR CONTRACTILITY IN MYOCARDIAL INFARCTION-IMPLICATIONS CONCERNING THE MEASDREMSNT OF LEFT VENTRICULAR FILLING PRESSURE Louis Vismara, MD; Dean T. Mason, MD, FACC; Ezra A. Amsterdam, MD, FACC and Robert Zelis, MD, FACC, Dept. Med., Univ. Calif. Sch. Med., Davis, Ca. Although the left ventricle (LV) has been extensively studied in myocardial infarction (MI), the right ventricle (RV) has been relatively ignored. To gain insight into the variable pathophysioloqy of MI, RV pressure (RVP) and its first derivative (dp/dt) were measured in six patients (pt) with diaphraqmatic MI (DMI) and ten pt Instantaneous RV contractile with anterior MI &MI). element velocity (VCE) was calculated as the ratio of (dp/dt)/32* (developed RVP). Vmax extrapolated from developed RVP-VCE curves was considerably reduced in DMI (DMI, 1.61; AMI, 3.16 muscle lengths/set, pc.01) sugqestinq that the right coronary disease seen in DMI leads to RV ischemia. Cardiac indices were similar (DMI, 1.97; AMI, 2.17 L/min, NS) but AM1 had increased LV filling pressure (pulmonary capillary wedge pressure: DMI, 6.8; AMI, 16.3 mm Hq, p<.Ol). Although RV end diastolic pressures were similar (DMI, 6.1; AMI, 7.1, NS) the slight elevation in AM1 is a reflection of LV failure (RV systolic pressure: DMI, 25.7; AMI, 36.5, pc.01) whereas in DMI it is a reflection of RV failure. The increased RV preload elevates submaximal VCE leading to less striking differences in RV VCE at 5 mm Hq (DMI, 1.26; AMI, 2.02, pc.021. The depressed RV contractility seen in DMI as a consequence of RV ischemia is another factor affecting indices of RV filling. Thus, central venous pressure would be expected to have limited usefulness in reflecting absolute or relative changes in LV filling pressure in DMI.
LONG TERM PROGNOSIS FOR PATIENTS WITH THIl'ASCICULAB BLOCK COMPLICATING ACUTE MYOCARDIAL INFARCTION David D. Waters, MD; Henry F. Mizgala, MD, FRCP(C), Division of Cardiology, Montreal General Hospital, Montreal, Canada. Trifascicular block complicating acute myocardial infarction (AMI) often precedes complete heart block (CHB) and is associated with a high mortality. To evaluate the long term prognosis of these patients, 109 consecutive patients treated with temporary transvenous pacemakers for bradyarrhythmias and conduction disturbances complicating AM1 were examined. Twenty eight had trifascicular block i.e. incomplete bilateral bundle branch block (IBBBB). Twelve of these (43X) died while in hospital, 7 primarily of pump failure, 4 primarily of arrhythmias, and 1 of pneumonia and septic shock. Two of the 16 discharged alive were lost to follow-up but the remaining have been followed for 9 to 31 months (average 15.5 received permanent pacemakers before dismonths). TWO charge and one developed asymptomatic CHB 29 months after discharge for which he was treated with a pacemaker. One of these 13 patients died suddenly; all others remain well. Of the 12 patients who died in hospital, 8 had a documented period of CHB, while only 5 of the 13 who left hospital alive had CHB while in hospital. These results suggest that 1) patients with AMI causing IBBBB do not require permanent pacemakers unless CHB persists beyond the acute stage of AMI 2) progression from IBBBB to CHB during the hospital phase of AM1 seems to increase the in-hospital mortality 3) these patients appear to have a good prognosis if they survive the acute phase of their illness.
A GEOMETRIC SIUDY OF THE PROTECTIVE ZONE FOR VENTRICULAR FIBRILLATION Ira W. Weiss, MD; Eduardo R. Seroppian, MD; Bernard Lown, MD, FACC; John V. Temte, MD, PM, Harvard School of Public Health, Boston, Massachusetts A relatively low energy (0.5-1.0 Wsec) electrical discharge (S ) can initiate ventricular fibrillation (VF) when appl&ed to the endocardial or epicardial surface of the heart within the vulnerable period (VP), a 20-40 msec interval during ventricular repolarisation. We have previously documented that a second 0.5-1.0 Wsec discharge (S2), delivered to the same site as Sl, can prevent VF if S2 occurs during the protective mm (PZ), a 25-90 msec interval beginning lo-40 msec after the end of the VP. In this investigation we have studied whether protection is preserved when S2 is delivered to sites other than that of s . In all seven mongrel dogs studied we were able to rapeatedly demonstrate a PZ when S was delivered to geometrically arrayed epicardial eleczrodes within 1 cm of s also delivered to the epicardium. In three of the dogs'brotection was preserved even when S2 was delivered 2 cm from the Sl site. However, protection could not be found when S2 was delivered more than 2 cm from the,Sl site. Epicardial-endocardial transmural protection was found across the right ventricular wall (Sl and S electrodes less than 5 mm apart), but not across the 1eft ventricular wall (Sl and S electrodes more than 1 cm old energy for protection apart). The minimum thresi: against VF and the temporal boundaries of the PZ did not change significantly when protective impulses were delivered to sites other than that of Sl. These findings suggest that protection against VF is the result of local, rather than widespread, myocardial changes induced by S2. The protective impulse probably inhibits local impulse re-entry, a prerequisite of ventricular fibrillation.
January 1973
The American Journal of CARDIOLOGY
Volume 31
163
HIS BUNDLE UECTRUGRANOFTHE DCG: ATRUF, RBPRESmATIUNCFTHRINTRACELLULkR~ P. Jacob Varghese, MD; M. V. Elisari, MD; R. Parameswaran, MD; Anthony N. Damato, ND; Sun Ii.Lau, MD, U. S. Public Health Service Hospital, Staten Island, New York, Albert Einstein Medical Center, Philadelphia, Pa. In 5 dogs the A-V conduction system consisting of the A-V node, entire bundle of His and left and right bundle branches was isolated using the dissection technique of Elieari et al., and perfused with oxygenated Tyrode at constant temperature. Transmembrane action potentials (TAP) using standard microelectrode techniques were simultaneously recorded from the penetrating and branching portions of the His bundle (H) along with a bipolar surface electrogram @SE) from the same area. Interelectrode conduction times (IECT) and duration of BSE were measured during antegrade, retrograde and premature activation of H. During antegrade and retrograde activation of H the duration of the BSE was equal to the IECT. Polarity of the BSE changed with direction of activation. Conduction delay within Iiwas manifested as an increase in IECT and a decrease in rate of rise of TAP and was reflected In BSE as change in duration, morphology and amplitude. Decremental conduction and block within the H resulted in disappearance of both the BSE and TAP recorded distal to the site of block. 'Conduction delay and block distal to the His i.e., between His and right bundle (RB) did not affect the characteristics of the BSE. When the BSE included the RB the duration of it was greater than the IRCT and the RB was seen as a separate sharp deflection. These studies demonstrate that the BSE represents total activity of the H and faithfully reflects electrical events occurring within the entire H. They also fortify the basis of clinical His bundle electrography.
RIGHT VENTRICULAR CONTRACTILITY IN MYOCARDIAL INFARCTION-IMPLICATIONS CONCERNING THE MEASDREMSNT OF LEFT VENTRICULAR FILLING PRESSURE Louis Vismara, MD; Dean T. Mason, MD, FACC; Ezra A. Amsterdam, MD, FACC and Robert Zelis, MD, FACC, Dept. Med., Univ. Calif. Sch. Med., Davis, Ca. Although the left ventricle (LV) has been extensively studied in myocardial infarction (MI), the right ventricle (RV) has been relatively ignored. To gain insight into the variable pathophysioloqy of MI, RV pressure (RVP) and its first derivative (dp/dt) were measured in six patients (pt) with diaphraqmatic MI (DMI) and ten pt Instantaneous RV contractile with anterior MI &MI). element velocity (VCE) was calculated as the ratio of (dp/dt)/32* (developed RVP). Vmax extrapolated from developed RVP-VCE curves was considerably reduced in DMI (DMI, 1.61; AMI, 3.16 muscle lengths/set, pc.01) sugqestinq that the right coronary disease seen in DMI leads to RV ischemia. Cardiac indices were similar (DMI, 1.97; AMI, 2.17 L/min, NS) but AM1 had increased LV filling pressure (pulmonary capillary wedge pressure: DMI, 6.8; AMI, 16.3 mm Hq, p<.Ol). Although RV end diastolic pressures were similar (DMI, 6.1; AMI, 7.1, NS) the slight elevation in AM1 is a reflection of LV failure (RV systolic pressure: DMI, 25.7; AMI, 36.5, pc.01) whereas in DMI it is a reflection of RV failure. The increased RV preload elevates submaximal VCE leading to less striking differences in RV VCE at 5 mm Hq (DMI, 1.26; AMI, 2.02, pc.021. The depressed RV contractility seen in DMI as a consequence of RV ischemia is another factor affecting indices of RV filling. Thus, central venous pressure would be expected to have limited usefulness in reflecting absolute or relative changes in LV filling pressure in DMI.
LONG TERM PROGNOSIS FOR PATIENTS WITH THIl'ASCICULAB BLOCK COMPLICATING ACUTE MYOCARDIAL INFARCTION David D. Waters, MD; Henry F. Mizgala, MD, FRCP(C), Division of Cardiology, Montreal General Hospital, Montreal, Canada. Trifascicular block complicating acute myocardial infarction (AMI) often precedes complete heart block (CHB) and is associated with a high mortality. To evaluate the long term prognosis of these patients, 109 consecutive patients treated with temporary transvenous pacemakers for bradyarrhythmias and conduction disturbances complicating AM1 were examined. Twenty eight had trifascicular block i.e. incomplete bilateral bundle branch block (IBBBB). Twelve of these (43X) died while in hospital, 7 primarily of pump failure, 4 primarily of arrhythmias, and 1 of pneumonia and septic shock. Two of the 16 discharged alive were lost to follow-up but the remaining have been followed for 9 to 31 months (average 15.5 received permanent pacemakers before dismonths). TWO charge and one developed asymptomatic CHB 29 months after discharge for which he was treated with a pacemaker. One of these 13 patients died suddenly; all others remain well. Of the 12 patients who died in hospital, 8 had a documented period of CHB, while only 5 of the 13 who left hospital alive had CHB while in hospital. These results suggest that 1) patients with AMI causing IBBBB do not require permanent pacemakers unless CHB persists beyond the acute stage of AMI 2) progression from IBBBB to CHB during the hospital phase of AM1 seems to increase the in-hospital mortality 3) these patients appear to have a good prognosis if they survive the acute phase of their illness.
A GEOMETRIC SIUDY OF THE PROTECTIVE ZONE FOR VENTRICULAR FIBRILLATION Ira W. Weiss, MD; Eduardo R. Seroppian, MD; Bernard Lown, MD, FACC; John V. Temte, MD, PM, Harvard School of Public Health, Boston, Massachusetts A relatively low energy (0.5-1.0 Wsec) electrical discharge (S ) can initiate ventricular fibrillation (VF) when appl&ed to the endocardial or epicardial surface of the heart within the vulnerable period (VP), a 20-40 msec interval during ventricular repolarisation. We have previously documented that a second 0.5-1.0 Wsec discharge (S2), delivered to the same site as Sl, can prevent VF if S2 occurs during the protective mm (PZ), a 25-90 msec interval beginning lo-40 msec after the end of the VP. In this investigation we have studied whether protection is preserved when S2 is delivered to sites other than that of s . In all seven mongrel dogs studied we were able to rapeatedly demonstrate a PZ when S was delivered to geometrically arrayed epicardial eleczrodes within 1 cm of s also delivered to the epicardium. In three of the dogs'brotection was preserved even when S2 was delivered 2 cm from the Sl site. However, protection could not be found when S2 was delivered more than 2 cm from the,Sl site. Epicardial-endocardial transmural protection was found across the right ventricular wall (Sl and S electrodes less than 5 mm apart), but not across the 1eft ventricular wall (Sl and S electrodes more than 1 cm old energy for protection apart). The minimum thresi: against VF and the temporal boundaries of the PZ did not change significantly when protective impulses were delivered to sites other than that of Sl. These findings suggest that protection against VF is the result of local, rather than widespread, myocardial changes induced by S2. The protective impulse probably inhibits local impulse re-entry, a prerequisite of ventricular fibrillation.
January 1973
The American Journal of CARDIOLOGY
Volume 31
163