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Abbreviated rapid onset exercise stress testing for the exposure of ventricular arrhythmia
ABSTRACTS
RAPID ONSET EXERCISE STRESS TESTING FOR THE EXPOSURE OF VENTRICULAR ARRHYTHMIA Thomas B. Graboys, MD, FACC; Arno Schoeneberger, MD; ABBREVIATED
Regis A. DeSilva, MD; Virginia Towne; Bernard Lawn, MD, FACC, Cardiovascular Laboratory, Harvard School of Public Health, Boston, Massachusetts Exercise stress testing is a" important method for exposing advanced grades of ventricular premature beats (VPBs). Deletion of the "warn-up" phase produces a physical stress akin to sudden "start-stop" activity and more closely approximates demands of daily life. The provocatjon of VPBs was compared in a standard Bruce protocol (ETT) and a "mini-stress" during which patients (PTs) advanced through each of the eight Bruce protocol stages every 15 seconds. The study involved 52 PTS, 43 males and 9 females average age 49 years. Hemodynamic and ST segment changes were similar during Thirty-eight PTS (73%) both exercise forms of testing. undergoing the Bruce ETT exhibited VPBs while 33 (64%) did so during "mini-stress." In 10 PTS ETT yielded more advanced grades of VPBs than mini-stress while 7 PTS, including 3 with VT, had a greater yield with the mini-stress. Hence, a" abbreviated exercise test may be a valuable adjunct in management of PTS with known or suspect ventricular arrhythmia.
HEMODYNAMIC RESPONSES TO STATIC EXERCISE ARE DEPENDENT ON THE MASS dF MUSCLE ACTIVATED. F. Andrew Gaffney, M.D., Bente Danneskiold-Samsde, M.D., Ula Halskov, M.D., and Gunnar Grimby, M.D., Ph.D. August Krogh Institute, University of Copenhagen, Denmark. The generally accepted concept that hemodynamic responses to static exercise (Static Ex) are determined by the percent of Maximum Voluntary Contraction (%MVC) but not the ma.ss of muscle activated was reexamined in 10 healthy subjects (S), (7 male, 3 female, 21-24 yrs) on 2 days, 6 weeks apart. Static Handgrip (parallel bar) and knee extension, (Tornvall chair) MVC's were determined (best of 3). S's maintained the contraction (Day 1 20% MVC. Day 2 18% MVC) for 5 minutes with'measures of HR (ECG) and mea" blood pressure (Cuff, l/3 pulse pressure + diastolic) every 30 sec. Order of contraction was varied with 20 min. rest between contractions. Differences between handgrip and knee extension HR and BP responses for the 2 studies were virtually identical. HR beat/min Knee Hand
Rest 82i3 8512
0:30 -__ 97?4 90+3
2:30 108?3 9123
5:oo 109+4 97+4
Bp
89L2 10122 12824 140?4 88+2 Vf?3 10912 12153 (M~~"+s.E.) HR and B were higher with the larger contracting muscle mass throughout both studies (ANOVA p=.OO5). This would suggest that hemodynamic responses to isometric exercise are dependent on the mass of muscle activated. The higher knee extension heart rates suggest a greater cardiac output. This, in the presence of a larger muscle bed with mechanically compromised blood flow could account for the higher m with knee extension. MM Hg
MECHANISMS OF INCREASED R WAVE MAGNITUDE WITH EXERCISE TN PATIENTS WITH CORONARY ARTERY DISEASE. Harisios Boudoulas, MD, FACC; Stephanos Dervenagas, MD; Richard P. Lewis, MD, FACC; The Ohio State University College of Medicine, Columbus, Ohio. An increase of the R wave magnitude with exercise has been used to establish the presence of myocardial ischemia in patients (pts) with coronary artery disease (CAD). The present studies were undertake" in three different groups to define the mechanisms for this phenomenon. I. The effect of Tsoproterenol (Iso) infusion (2 pg/min/lO min) on the R wave magnitude was studied in 10 normals before and after propranolol (Pr) administration 160 mg The R wave magnitude decreased with daily for 2 days. Tso (-10.8 + 1.6X, pcO.001) but remained unchanged when II. A maximal TreadIs0 was given after Pr (-0.9 + 2%). mill exercise test was performed in 25 pts with CAD, not on therapy with stable angina and no resting myocardial perfusion defects or segmental contraction abnormalities. 'The R wave magnitude increased with exercise in 10 pts (+8.2 + 32, ~~0.01) and decreased in 16 (-11.2 + 3%, ).L O.Ol)._ The number of coronary arteries with obstruction 270% was greater in pts in whom the R wave magnitude increased with exercise compared to pts in whom the R wave magnitude decreased (2.1 + .12 vs 1.2 f .l, ~0.01). This suggests that more extensive ischemia was present in pts in whom the R wave magnitude increased with exercise. III. In 10 pts with CAD and stable angina in whom the R wave magnitude decreased with exercise before therapy (-10.8 + 1.6%, p
420
February 1980
The American Journal of CARDIOLOGY
EXERCISE EJECTION FRACTION DIMINISHES AFTER RECOVERY IN POSTOPERATIVE AORTOCORONARY BYPASS PATIENTS. .James L. Cockrell, Jr., BS; Peter N. Zeitler, MS; Lucy S. Goodenday, MD; Richard K. Foster, !Q; Rodney V. Pozderac, MD; V.A.M.C and University of Michigan, Ann Arbor, MI, and Medical College of Ohio, Toledo, OH. Exercise (E) ejection fraction (EF) improves in postoperative coronary artery bypass patients, but serial changes in EEF in the postoperative period have not been We therefore measured EEF in 8 me" using rareported. dionuclide ventriculography approximately 3 weeks following surgery, when they had reached a 3 YET level of exercise tolerance in a" inhospital rehabilitation program After 9 weeks of a home recovery prior to discharge. program the patients were reevaluated, using the identical protocol, and these results compared to the initial studies: At Highest Work Rate: (t S.D.) EEF - Rest EF Pulse EEF Post-Op. .?6 + .lO 129 + 12 .71 + .I0 3 weeks .08 + .08 .61 + .10 12 weeks 136 + 13 .005 .005 P< .02 All 8 patients showed diminished EEF at 12 weeks. Measurements made at matched workloads and heart rates Exercise tolerance imexhibited reduced EEF as well. proved in most cases. We conclude that peak EEF and l?El‘ minus resting EF diminished significantly between the 3rd and 12th weeks This may reflect diminishafter aortocoronary bypass. ed left ventricular performance at 12 weeks following Other possibilities include training-induced surgery. left ventricular enlargement or the existence of a" hyperadrenergic state immediately following surgery which subsides at 12 weeks.
Volume 45
RAPID ONSET EXERCISE STRESS TESTING FOR THE EXPOSURE OF VENTRICULAR ARRHYTHMIA Thomas B. Graboys, MD, FACC; Arno Schoeneberger, MD; ABBREVIATED
Regis A. DeSilva, MD; Virginia Towne; Bernard Lawn, MD, FACC, Cardiovascular Laboratory, Harvard School of Public Health, Boston, Massachusetts Exercise stress testing is a" important method for exposing advanced grades of ventricular premature beats (VPBs). Deletion of the "warn-up" phase produces a physical stress akin to sudden "start-stop" activity and more closely approximates demands of daily life. The provocatjon of VPBs was compared in a standard Bruce protocol (ETT) and a "mini-stress" during which patients (PTs) advanced through each of the eight Bruce protocol stages every 15 seconds. The study involved 52 PTS, 43 males and 9 females average age 49 years. Hemodynamic and ST segment changes were similar during Thirty-eight PTS (73%) both exercise forms of testing. undergoing the Bruce ETT exhibited VPBs while 33 (64%) did so during "mini-stress." In 10 PTS ETT yielded more advanced grades of VPBs than mini-stress while 7 PTS, including 3 with VT, had a greater yield with the mini-stress. Hence, a" abbreviated exercise test may be a valuable adjunct in management of PTS with known or suspect ventricular arrhythmia.
HEMODYNAMIC RESPONSES TO STATIC EXERCISE ARE DEPENDENT ON THE MASS dF MUSCLE ACTIVATED. F. Andrew Gaffney, M.D., Bente Danneskiold-Samsde, M.D., Ula Halskov, M.D., and Gunnar Grimby, M.D., Ph.D. August Krogh Institute, University of Copenhagen, Denmark. The generally accepted concept that hemodynamic responses to static exercise (Static Ex) are determined by the percent of Maximum Voluntary Contraction (%MVC) but not the ma.ss of muscle activated was reexamined in 10 healthy subjects (S), (7 male, 3 female, 21-24 yrs) on 2 days, 6 weeks apart. Static Handgrip (parallel bar) and knee extension, (Tornvall chair) MVC's were determined (best of 3). S's maintained the contraction (Day 1 20% MVC. Day 2 18% MVC) for 5 minutes with'measures of HR (ECG) and mea" blood pressure (Cuff, l/3 pulse pressure + diastolic) every 30 sec. Order of contraction was varied with 20 min. rest between contractions. Differences between handgrip and knee extension HR and BP responses for the 2 studies were virtually identical. HR beat/min Knee Hand
Rest 82i3 8512
0:30 -__ 97?4 90+3
2:30 108?3 9123
5:oo 109+4 97+4
Bp
89L2 10122 12824 140?4 88+2 Vf?3 10912 12153 (M~~"+s.E.) HR and B were higher with the larger contracting muscle mass throughout both studies (ANOVA p=.OO5). This would suggest that hemodynamic responses to isometric exercise are dependent on the mass of muscle activated. The higher knee extension heart rates suggest a greater cardiac output. This, in the presence of a larger muscle bed with mechanically compromised blood flow could account for the higher m with knee extension. MM Hg
MECHANISMS OF INCREASED R WAVE MAGNITUDE WITH EXERCISE TN PATIENTS WITH CORONARY ARTERY DISEASE. Harisios Boudoulas, MD, FACC; Stephanos Dervenagas, MD; Richard P. Lewis, MD, FACC; The Ohio State University College of Medicine, Columbus, Ohio. An increase of the R wave magnitude with exercise has been used to establish the presence of myocardial ischemia in patients (pts) with coronary artery disease (CAD). The present studies were undertake" in three different groups to define the mechanisms for this phenomenon. I. The effect of Tsoproterenol (Iso) infusion (2 pg/min/lO min) on the R wave magnitude was studied in 10 normals before and after propranolol (Pr) administration 160 mg The R wave magnitude decreased with daily for 2 days. Tso (-10.8 + 1.6X, pcO.001) but remained unchanged when II. A maximal TreadIs0 was given after Pr (-0.9 + 2%). mill exercise test was performed in 25 pts with CAD, not on therapy with stable angina and no resting myocardial perfusion defects or segmental contraction abnormalities. 'The R wave magnitude increased with exercise in 10 pts (+8.2 + 32, ~~0.01) and decreased in 16 (-11.2 + 3%, ).L O.Ol)._ The number of coronary arteries with obstruction 270% was greater in pts in whom the R wave magnitude increased with exercise compared to pts in whom the R wave magnitude decreased (2.1 + .12 vs 1.2 f .l, ~0.01). This suggests that more extensive ischemia was present in pts in whom the R wave magnitude increased with exercise. III. In 10 pts with CAD and stable angina in whom the R wave magnitude decreased with exercise before therapy (-10.8 + 1.6%, p
420
February 1980
The American Journal of CARDIOLOGY
EXERCISE EJECTION FRACTION DIMINISHES AFTER RECOVERY IN POSTOPERATIVE AORTOCORONARY BYPASS PATIENTS. .James L. Cockrell, Jr., BS; Peter N. Zeitler, MS; Lucy S. Goodenday, MD; Richard K. Foster, !Q; Rodney V. Pozderac, MD; V.A.M.C and University of Michigan, Ann Arbor, MI, and Medical College of Ohio, Toledo, OH. Exercise (E) ejection fraction (EF) improves in postoperative coronary artery bypass patients, but serial changes in EEF in the postoperative period have not been We therefore measured EEF in 8 me" using rareported. dionuclide ventriculography approximately 3 weeks following surgery, when they had reached a 3 YET level of exercise tolerance in a" inhospital rehabilitation program After 9 weeks of a home recovery prior to discharge. program the patients were reevaluated, using the identical protocol, and these results compared to the initial studies: At Highest Work Rate: (t S.D.) EEF - Rest EF Pulse EEF Post-Op. .?6 + .lO 129 + 12 .71 + .I0 3 weeks .08 + .08 .61 + .10 12 weeks 136 + 13 .005 .005 P< .02 All 8 patients showed diminished EEF at 12 weeks. Measurements made at matched workloads and heart rates Exercise tolerance imexhibited reduced EEF as well. proved in most cases. We conclude that peak EEF and l?El‘ minus resting EF diminished significantly between the 3rd and 12th weeks This may reflect diminishafter aortocoronary bypass. ed left ventricular performance at 12 weeks following Other possibilities include training-induced surgery. left ventricular enlargement or the existence of a" hyperadrenergic state immediately following surgery which subsides at 12 weeks.
Volume 45