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Effect of additional warmup on standard treadmill response
ABSTRACTS
CONTINUOUS UNIPOLAR STRENGTH-INTERVAL CURVES AND CONDUCTION TIMES DURING PNOCARDIAL ISCHEMIA AND REPERFUSION Herbert J. Levine, MD, FACC; Boas Avitall, PM; Stephen G. Pauker, MD, FACC; Shapur Naimi, MD, FACC, Tufts New England Medical Center, Boston, Massachusetts
RELATIONSHIPS BETWEEN ELECTRICAL LOSS AND MUSCLE MASS LOSS IN MYOCARDIAL INFARCTION Nancy C. Flowers, MD, FACC; R. Chris Hand; Leo G. Horan, MD, FACC; M.R. Sridharan, MD, University of Louisville, Louisville, Kentucky
A computer program was developed to generate alternating anodal and cathodal or continuous anodal strength-interval curves (SIC) during and following 15 min. coronary ligations in 14 anesthetized dogs atrially paced at 2.5 Hz. SIC's were generated every 45-120 sec. and simultaneous conduction times (CT) determined. Within 1-2 min. of ligation, anodal mid-curve and late diastolic thresholds (TH) fell sharply, while cathodal TH fell slightly or changed little. After 5 min. of ligation, anodal TH remained low, cathodal TH rose and CT's prolonged markedly. At lo-15 min. of ligation, if ischemic zone was small, anodal TH were low, often approaching cathodal, and CT returned towards control. If ischemic zone was large, unipolar TH's and CT's rose in late ligation. Throughout ligation, the falling limb of the SIC shifted progressively to the left, indicating shorter refractory periods. Following abrupt roper-fusion, anodal phase 3 dips, often wider and deeper than control, promptly reappeared (l-2 min.); refractory periods approached control, and superconductivity was noted. By 3-5 min. of reperfusion, refractory periods were longer than control and CT's were prolonged. Thus, vulnerability to arrhythmias of early (5 min.) ligation is characterized by low anodal mid-curve and late diastolic TH's, short refractory periods, and long CT's, favoring re-entry. Vulnerability to arrhythmias of early reperfusion is characterized by low dip TH's and short CT's. Finally, directional changes in anodal excitability correlate better than cathodal with vulnerability to arrhythmias of ligation and reperfusion.
Much attention has been directed toward enzymatic and electrical means of estimating the size of myocardial inno previous comparisons have been refarction. However, ported on simultaneously acquired data from multiple lead 3 vectorcarbody surface maps, the more simply obtained diographic orthogonal leads (VCG) and precordial electrocardiographic (ECG) grid systems. Experimental myocardial infarctions have been produced in ten dogs utilizing a technique of coronary occlusion by a catheter-implanted bead in a completely closed chest (thus avoiding changes in the electrical properties of the thoSimultaneously acquired body surface map data, VCG rax) . data and ECG grid data were obtained before and 7 days The post infarction electrical data following infarction. The resulting were subtracted from the preinfarction. difference data for all three graphic systems were examined both for instantaneous and cumulative values during Infarct volume was measured by ventricular activation. The best correlaserial section of the ventricular mass. tion between instantaneous potential at msec 17 (r = .88) for difference map data dropped as the cumulative difference potential between I and 31 msec wasobtained (r = .85). But the VCG correlation for msec 18 (r = .7D) improved with cumulative spread (r = .8O). Precordial grid data ran a poor third (maximum r = .48). We concluded that the difference map was superior in both localizing and estimating size of myocardial infarction though the VCG did well Cauticn must be exercised with any of in estimating size. the techniques to avoid inclusion of late activation data, which may contain variable effects of delayed conduction or block.
THURSDAV, MARCH 9, 1978 AM EXERCISE TESTING AND CARDIAC 8:30 to 12:OO RELATIOESHIP OF REGIOEAL MIOCARDIAL BLOOD FLOW TO THE ElECTRICAL STABILITY OF TPAESMUPAL AED SUBEEDOCARDIAL ISCBENIC MIOCARDIUM Michael Clemen, P. Jacob Varghese and Bertram Pitt, Johns Hopkins Hospital, Baltimore, Maryland.
EFFECT OF ADDITIONAL WARMUP ON STANDARD TREADMILL RESPONSE. Jack Ernst, BSc; David Sheps, MD, FACC; F.W. Briese, PhD; and R.J. Myerburg, MD, FACC. University of Miami, Miami, Florida
This study was performed to determine the role of regional myocardiel blood flow (MBF) (ml/min/lOO gm) in predicting electrical stability, as measured by ventricular fibrillation threshold (VFT), of subendocardial (SI) and transmural (TI) ischemic myocardium. In 12 open chested dogs VFI and MBF, as measured by 1Ou radioactive microspheres, were determined in the subendocardium (En) and subepicardium (Ep) of the region supplied by the left anterior descending (LAD) end left circumflex (LCX) coronary arteries during control conditions (C), folloving,SI created by partial stenosis, and TI produced by occlusion of the LAD. VFT vas determined by delivering a train of impulses after every 12th paced beat through bipolar hook electrodes placed in each region. Using a constant current source, the intensity of the train was increased by lma until ventricular fibrillation occurred. LAD-En LCX-En LCX-Ep LAD-Ep VFT MBF VFTMSF VFT !4BF VFT MBF C 16 80 16 81 19 80 16 78 SI
TI 9C.05
5* 5*+
44* 1.5*+
12 5*
80 7.5*+
20 8*+
80 78
20 8*+
REHABILITATION
85 82
compared to C, +p~.05 compared to SI During SI a decline in MBF predicts regional electrical instability while with regional TI the entire heart becomes electrically unstable.
Eleven normal males, mean age = 32 years, underwent treadmill exercise testing (TT) using standard (S) and modified (M) Bruce treadmill protocols on separate days. All subjects had at least 1 TT prior to this study. M Bruce protocol is identical to the S protocol except for an additional 3 minute warmup (1.7 mph, 5% grade). A randomized testing sequence was used to test the hypothesis that, excluding the warmup, the response to both protocols are similar. Care was taken to assure that subjects were exercised to the same level of maximal fatigue on both M and S TT. The mean duration for M (excluding the 3 minute warmup stage) was greater than S (M = 651 + 115 seconds, S = 6312 121 seconds, pc.03). Increased dzration for M occurred regardless of testing sequence. Peak heart rate (HR) for M WAS 187 + 11 Vs. 183 + 14 for S. Peak pressurerate product (PRP) (HR x systolic pressure x 10-a) was 378 + 47 for M vs. 357 + 58 for S, pc.01. Four minutes of exercise were required during M to approach a PRP similar to that attained with S in one minute (M = 154 + 25 at minute 4, S = 157 k 29 at minute 1). To test th< hypothesis that these differences are due to greater oxygen debt created by S compared to M peripheral venous lactate levels were obtained at the end of stage II in 3 subjects. comparing rest vs. stage II values there was a marked increase with S (10.7 vs. 28.7mg/lOGml). During M protocol there was no difference between rest VS. stage II values (19.5 VS. 17.9mg/lOGml). We conclude that the responses to the 2 protocols, corrected for the longer warmup period of the M protocol are different. The differences (>TT duration, hemodynamic responses, and lower lactates) are likely attributable to a longer warmup period and less anaerobic metabolism with M compared to S.
February 1078
The American Journal of CARDIOLOGY
Volume 41
429
CONTINUOUS UNIPOLAR STRENGTH-INTERVAL CURVES AND CONDUCTION TIMES DURING PNOCARDIAL ISCHEMIA AND REPERFUSION Herbert J. Levine, MD, FACC; Boas Avitall, PM; Stephen G. Pauker, MD, FACC; Shapur Naimi, MD, FACC, Tufts New England Medical Center, Boston, Massachusetts
RELATIONSHIPS BETWEEN ELECTRICAL LOSS AND MUSCLE MASS LOSS IN MYOCARDIAL INFARCTION Nancy C. Flowers, MD, FACC; R. Chris Hand; Leo G. Horan, MD, FACC; M.R. Sridharan, MD, University of Louisville, Louisville, Kentucky
A computer program was developed to generate alternating anodal and cathodal or continuous anodal strength-interval curves (SIC) during and following 15 min. coronary ligations in 14 anesthetized dogs atrially paced at 2.5 Hz. SIC's were generated every 45-120 sec. and simultaneous conduction times (CT) determined. Within 1-2 min. of ligation, anodal mid-curve and late diastolic thresholds (TH) fell sharply, while cathodal TH fell slightly or changed little. After 5 min. of ligation, anodal TH remained low, cathodal TH rose and CT's prolonged markedly. At lo-15 min. of ligation, if ischemic zone was small, anodal TH were low, often approaching cathodal, and CT returned towards control. If ischemic zone was large, unipolar TH's and CT's rose in late ligation. Throughout ligation, the falling limb of the SIC shifted progressively to the left, indicating shorter refractory periods. Following abrupt roper-fusion, anodal phase 3 dips, often wider and deeper than control, promptly reappeared (l-2 min.); refractory periods approached control, and superconductivity was noted. By 3-5 min. of reperfusion, refractory periods were longer than control and CT's were prolonged. Thus, vulnerability to arrhythmias of early (5 min.) ligation is characterized by low anodal mid-curve and late diastolic TH's, short refractory periods, and long CT's, favoring re-entry. Vulnerability to arrhythmias of early reperfusion is characterized by low dip TH's and short CT's. Finally, directional changes in anodal excitability correlate better than cathodal with vulnerability to arrhythmias of ligation and reperfusion.
Much attention has been directed toward enzymatic and electrical means of estimating the size of myocardial inno previous comparisons have been refarction. However, ported on simultaneously acquired data from multiple lead 3 vectorcarbody surface maps, the more simply obtained diographic orthogonal leads (VCG) and precordial electrocardiographic (ECG) grid systems. Experimental myocardial infarctions have been produced in ten dogs utilizing a technique of coronary occlusion by a catheter-implanted bead in a completely closed chest (thus avoiding changes in the electrical properties of the thoSimultaneously acquired body surface map data, VCG rax) . data and ECG grid data were obtained before and 7 days The post infarction electrical data following infarction. The resulting were subtracted from the preinfarction. difference data for all three graphic systems were examined both for instantaneous and cumulative values during Infarct volume was measured by ventricular activation. The best correlaserial section of the ventricular mass. tion between instantaneous potential at msec 17 (r = .88) for difference map data dropped as the cumulative difference potential between I and 31 msec wasobtained (r = .85). But the VCG correlation for msec 18 (r = .7D) improved with cumulative spread (r = .8O). Precordial grid data ran a poor third (maximum r = .48). We concluded that the difference map was superior in both localizing and estimating size of myocardial infarction though the VCG did well Cauticn must be exercised with any of in estimating size. the techniques to avoid inclusion of late activation data, which may contain variable effects of delayed conduction or block.
THURSDAV, MARCH 9, 1978 AM EXERCISE TESTING AND CARDIAC 8:30 to 12:OO RELATIOESHIP OF REGIOEAL MIOCARDIAL BLOOD FLOW TO THE ElECTRICAL STABILITY OF TPAESMUPAL AED SUBEEDOCARDIAL ISCBENIC MIOCARDIUM Michael Clemen, P. Jacob Varghese and Bertram Pitt, Johns Hopkins Hospital, Baltimore, Maryland.
EFFECT OF ADDITIONAL WARMUP ON STANDARD TREADMILL RESPONSE. Jack Ernst, BSc; David Sheps, MD, FACC; F.W. Briese, PhD; and R.J. Myerburg, MD, FACC. University of Miami, Miami, Florida
This study was performed to determine the role of regional myocardiel blood flow (MBF) (ml/min/lOO gm) in predicting electrical stability, as measured by ventricular fibrillation threshold (VFT), of subendocardial (SI) and transmural (TI) ischemic myocardium. In 12 open chested dogs VFI and MBF, as measured by 1Ou radioactive microspheres, were determined in the subendocardium (En) and subepicardium (Ep) of the region supplied by the left anterior descending (LAD) end left circumflex (LCX) coronary arteries during control conditions (C), folloving,SI created by partial stenosis, and TI produced by occlusion of the LAD. VFT vas determined by delivering a train of impulses after every 12th paced beat through bipolar hook electrodes placed in each region. Using a constant current source, the intensity of the train was increased by lma until ventricular fibrillation occurred. LAD-En LCX-En LCX-Ep LAD-Ep VFT MBF VFTMSF VFT !4BF VFT MBF C 16 80 16 81 19 80 16 78 SI
TI 9C.05
5* 5*+
44* 1.5*+
12 5*
80 7.5*+
20 8*+
80 78
20 8*+
REHABILITATION
85 82
compared to C, +p~.05 compared to SI During SI a decline in MBF predicts regional electrical instability while with regional TI the entire heart becomes electrically unstable.
Eleven normal males, mean age = 32 years, underwent treadmill exercise testing (TT) using standard (S) and modified (M) Bruce treadmill protocols on separate days. All subjects had at least 1 TT prior to this study. M Bruce protocol is identical to the S protocol except for an additional 3 minute warmup (1.7 mph, 5% grade). A randomized testing sequence was used to test the hypothesis that, excluding the warmup, the response to both protocols are similar. Care was taken to assure that subjects were exercised to the same level of maximal fatigue on both M and S TT. The mean duration for M (excluding the 3 minute warmup stage) was greater than S (M = 651 + 115 seconds, S = 6312 121 seconds, pc.03). Increased dzration for M occurred regardless of testing sequence. Peak heart rate (HR) for M WAS 187 + 11 Vs. 183 + 14 for S. Peak pressurerate product (PRP) (HR x systolic pressure x 10-a) was 378 + 47 for M vs. 357 + 58 for S, pc.01. Four minutes of exercise were required during M to approach a PRP similar to that attained with S in one minute (M = 154 + 25 at minute 4, S = 157 k 29 at minute 1). To test th< hypothesis that these differences are due to greater oxygen debt created by S compared to M peripheral venous lactate levels were obtained at the end of stage II in 3 subjects. comparing rest vs. stage II values there was a marked increase with S (10.7 vs. 28.7mg/lOGml). During M protocol there was no difference between rest VS. stage II values (19.5 VS. 17.9mg/lOGml). We conclude that the responses to the 2 protocols, corrected for the longer warmup period of the M protocol are different. The differences (>TT duration, hemodynamic responses, and lower lactates) are likely attributable to a longer warmup period and less anaerobic metabolism with M compared to S.
February 1078
The American Journal of CARDIOLOGY
Volume 41
429