- Email: [email protected]
Transmural differences in myocardial perfusion related to preload
ABSTRACTS
LIMITATIONSOF POST-EXTRASYSTOLICPOTENTIATION(PEP) IN PREDICTINGMYOCARDIAL VIABILITY DURINGACUTEISCHEMIA Henry G. Hanley, MD, Thomas Patrick, James S. Cole, VD, FACC, and William O’Connor, MD, VA Hospital, Wenner-Gren Lab, and Univ. of Ky., Col. of Med., Lexington, Kentucky PEP has been suggested to be of value in identifying ischemic but viable myocardium whose function may be improved by coronary artery bypass surgery. To evaluate this, 10 dogs were instrumented with left circumflex coronary artery (LCCA) flow probes and occluders, pacing wires, left ventricular pressure (LVP) gauges and ultrasonic segment length gauges placed near the LCCA. The dogs were studied in the conscious, chronically instru1 hour mented state following recovery from surgery. LCCA occlusions followed by reperfusion (4 days) were During LCCA occlusion timed premature ventristudied. cular contractions (PVC's) (n=411) were induced and PEP LCCA occlusion decreased LVP (133/6 to 117/7 measured. mmHg) (pc.001) (Student t test) and LV dp/dt (3240 to 2698 mm/set) (pc.001). Both diastolic (10.00 to 10.2Omm) (p<.OOl) and systolic (9.07 to 9.77 mm) (pc.001) segment lengths increased and segment shortening decreased markedly (0.96 to 0.44 mm) (p<.OOl) (all 15 segments). In the hypokinetic segments (n=9), PEP increased ischemic shortening (0.74 to 0.89) (pc.05). However shortening did not occur in segments (n=6) that were akinetic or dyskinetic (-.29 to -.33 mm) (pc.4). On reperfusion all segments showed improvement in shortening and at histological examination after sacrifice al1 segments were found to be in areas of viable myocardium. These results demonstrate that when acute ischemia is severe enough to produce akinesis or dyskinesis PEP is not useful in predicting myocardial viability. When these conditions are present in the clinical setting caution should be utilized in the interpretation of PEP data.
TUESDAY, MARCH 7, 1978 AM BASIC SCIENCE INVESTIOATION-I 8:30 to 12:OO
DETECTIONOF FUNCTIONALVENTRICULARRESERVEBY EXERCISE HFHODYNAMICSIN PATIENTSWITH SEVERECONGESTIVEHEART FAILURE. Harris Gelberg MD; Stanley Rubin MD; Bruce Brundage MD, FACC; WilliamParmleyMD, FACC; Ranu Chatterjee MO, FACC; Universityof California,San Francisco,CA. Eighteenpatientson digoxinand diureticain Claw 3 or 4 congestiveheart failurewere exercisedin recumbency, using a bicycleergometerwith a Swan-Ganzrhermodilution catheterin the pulmonaryartery position.Tuo groupswere Identifiedby their responseto rymptom limitedmaxlmum exercise.Group I showedmodest increasesin pulmonary capillarywedge pressuretieh an increasein strokework index while Group II showed substantialincreasein pulwnary capillarywedge pressurewith little &an e In
TRANSMUPAL DIFFERENCES IN MYOCARDIAL PERFUSION RELATED TO PBELOAD. Avery K. Ellis, MD; Francis J. Klocke, MD, FACC, State Univ. of N. Y. at Buffalo, Buffalo, N. Y.
~~
Mean maximumworkloadwas 191 kilopond/minute in Group I and 167 kilopond/minute In Group II. Conclusion: Despitesimilar history,congestiveheart fallure class and restinghemodyna- 40. mics. there is a differencein ventricularreserve in response to exercisein these groups. Exercisehemodynamlcsmay be anI importanttest in evaluating the status of patientsin congestiveheart failure. I.
* gm.m/m2 ** mm Hg
* 0
0
pew**
rb
EPICARDIAL VASODILATOR RESERVE IN THE PRESENCE OF Klm P. Gallagher, MS, John D. “CRITICAL STENOSIS”. BS, George G. Rowe, M.R Folts, Ph.D. , Ronald Shebuskl, FACC, Dept. Med.,Univ. Wlsc., Madison, WI. 53706. Coronary “crltlcal stenosis” 1s the term used to describe partlal obstruction which ellmlnates reactive hyperemla (presumably because downstream arterioles have dllated maximally to compensate for a proxlmal stenosis). Evldence of dlstal vasomotor capacity exlsts, however, desplte the presence of severe constrlctlon. Coronary blood flow (CBF) In the circumflex (LCC) artery and blood pressure ln the aorta and dlstal LCC was studled In 6, open chest, anesthetlzed dogs. The LCC artery was obstructed sufflclently to ellmlnate 95-98% of reactive hyperemla but malntaln restlng blood flow. The reglonal dlstrlbutlon of myocardlal blood flow (MBF) was studied wlth tracer mlcrospheres (15 Fdlameter) before and after lntracoronary (In dlstal LCC catheter) admlnlstratlon of adenoslne (ADEN, The lnner (I) to outer (0) ratlo of flow In the ob5 PM). structed bed was not changed by the stenosls (I/O = 1. 27 f .04 to I/O = 1. 29 * . 04, NS). ADEN decreased I flow from 1.00 f .04 ml/mln/g to 0.75 f .04 ml/mln/g (pc. 001) and Increased 0 flow from 0.77 f .02 ml/mln/g to 1. 28 * .06 ml/mln/g (p <. 001). The I/O ratlo decreased from 1.29 f .04 to 0.65 f .04 (p <. 001). Simultaneously measured LCC CBF (by electomagnetlc flowprobe) increased from 29 f 2 ml/mln to 36 * 2 ml/mln (p < . 01). Thus, arterlolar vasodllator reserve perslsts In the presence of severe proxlmal stenosls but the vasomotor capacity Is llmlted to 0 layers of myocardlum and shuntlng of flow from I to 0 layers can occur.
The effect of preload on the transmural distribution of myocardial blood flow is controversial. The left circumflex artery [LCA] was cannulated and perfused from the left subclavian artery in 7 open-chest dogs. An in-line solenoid, triggered by the R-wave of the ECG, was adjusted so that perfusion, monitored by an in-line flowmeter, occurred only during diastole. Autoregulation was abolished by maximal vasodilation with Chromonar (5 mg/kg). Under these conditions, any differences in local myocardial blood flow measured by radioactive microspheres are presumably due to local differences in diastolic resistance. Measurements were made at normal preload (mean left atria1 pressure [MAPI = 5 ? 1.0 [SEMI mm Hg) and at increased preload (MAP = 20 t 2.0 mm Hg). Despite diastolic perfusion and a significant pressure drop across the perfusion circuit at high flow velocities, overall microsphere flow in the LCA distribution was 1.55 t 0.16 cc/min/g at normal preload and 1.45 + 0.14 cc/min/g at increased preload. The ratio of endocardial flow to epicardial flow decreased from 0.76 f 0.05 at normal preload to 0.54 ?:0.02 at increased preload (p c 0.01). The LCA pressure at which inflow ceased [PC], determined by stepwise constriction of the perfusion circuit, was 14 f 1.7 mm Hg at normal preload and increased to 22 + 1.2 mm Hg at elevated preload (p < 0.01). Local diastolic resistance was calculated as the quotient of driving pressure and local flow, with driving pressure taken as the difference between downstream LCA pressure and PC. With increasing preload, subepicardial resistance remained constant while subendooardial resistance increased significantly. We conclude that small differences in transmural resistance, present at normal preload, are accentuated with increasing preload.
February 1979
The American Journal ol CARDIOLOGY
Volume 41
393
LIMITATIONSOF POST-EXTRASYSTOLICPOTENTIATION(PEP) IN PREDICTINGMYOCARDIAL VIABILITY DURINGACUTEISCHEMIA Henry G. Hanley, MD, Thomas Patrick, James S. Cole, VD, FACC, and William O’Connor, MD, VA Hospital, Wenner-Gren Lab, and Univ. of Ky., Col. of Med., Lexington, Kentucky PEP has been suggested to be of value in identifying ischemic but viable myocardium whose function may be improved by coronary artery bypass surgery. To evaluate this, 10 dogs were instrumented with left circumflex coronary artery (LCCA) flow probes and occluders, pacing wires, left ventricular pressure (LVP) gauges and ultrasonic segment length gauges placed near the LCCA. The dogs were studied in the conscious, chronically instru1 hour mented state following recovery from surgery. LCCA occlusions followed by reperfusion (4 days) were During LCCA occlusion timed premature ventristudied. cular contractions (PVC's) (n=411) were induced and PEP LCCA occlusion decreased LVP (133/6 to 117/7 measured. mmHg) (pc.001) (Student t test) and LV dp/dt (3240 to 2698 mm/set) (pc.001). Both diastolic (10.00 to 10.2Omm) (p<.OOl) and systolic (9.07 to 9.77 mm) (pc.001) segment lengths increased and segment shortening decreased markedly (0.96 to 0.44 mm) (p<.OOl) (all 15 segments). In the hypokinetic segments (n=9), PEP increased ischemic shortening (0.74 to 0.89) (pc.05). However shortening did not occur in segments (n=6) that were akinetic or dyskinetic (-.29 to -.33 mm) (pc.4). On reperfusion all segments showed improvement in shortening and at histological examination after sacrifice al1 segments were found to be in areas of viable myocardium. These results demonstrate that when acute ischemia is severe enough to produce akinesis or dyskinesis PEP is not useful in predicting myocardial viability. When these conditions are present in the clinical setting caution should be utilized in the interpretation of PEP data.
TUESDAY, MARCH 7, 1978 AM BASIC SCIENCE INVESTIOATION-I 8:30 to 12:OO
DETECTIONOF FUNCTIONALVENTRICULARRESERVEBY EXERCISE HFHODYNAMICSIN PATIENTSWITH SEVERECONGESTIVEHEART FAILURE. Harris Gelberg MD; Stanley Rubin MD; Bruce Brundage MD, FACC; WilliamParmleyMD, FACC; Ranu Chatterjee MO, FACC; Universityof California,San Francisco,CA. Eighteenpatientson digoxinand diureticain Claw 3 or 4 congestiveheart failurewere exercisedin recumbency, using a bicycleergometerwith a Swan-Ganzrhermodilution catheterin the pulmonaryartery position.Tuo groupswere Identifiedby their responseto rymptom limitedmaxlmum exercise.Group I showedmodest increasesin pulmonary capillarywedge pressuretieh an increasein strokework index while Group II showed substantialincreasein pulwnary capillarywedge pressurewith little &an e In
TRANSMUPAL DIFFERENCES IN MYOCARDIAL PERFUSION RELATED TO PBELOAD. Avery K. Ellis, MD; Francis J. Klocke, MD, FACC, State Univ. of N. Y. at Buffalo, Buffalo, N. Y.
~~
Mean maximumworkloadwas 191 kilopond/minute in Group I and 167 kilopond/minute In Group II. Conclusion: Despitesimilar history,congestiveheart fallure class and restinghemodyna- 40. mics. there is a differencein ventricularreserve in response to exercisein these groups. Exercisehemodynamlcsmay be anI importanttest in evaluating the status of patientsin congestiveheart failure. I.
* gm.m/m2 ** mm Hg
* 0
0
pew**
rb
EPICARDIAL VASODILATOR RESERVE IN THE PRESENCE OF Klm P. Gallagher, MS, John D. “CRITICAL STENOSIS”. BS, George G. Rowe, M.R Folts, Ph.D. , Ronald Shebuskl, FACC, Dept. Med.,Univ. Wlsc., Madison, WI. 53706. Coronary “crltlcal stenosis” 1s the term used to describe partlal obstruction which ellmlnates reactive hyperemla (presumably because downstream arterioles have dllated maximally to compensate for a proxlmal stenosis). Evldence of dlstal vasomotor capacity exlsts, however, desplte the presence of severe constrlctlon. Coronary blood flow (CBF) In the circumflex (LCC) artery and blood pressure ln the aorta and dlstal LCC was studled In 6, open chest, anesthetlzed dogs. The LCC artery was obstructed sufflclently to ellmlnate 95-98% of reactive hyperemla but malntaln restlng blood flow. The reglonal dlstrlbutlon of myocardlal blood flow (MBF) was studied wlth tracer mlcrospheres (15 Fdlameter) before and after lntracoronary (In dlstal LCC catheter) admlnlstratlon of adenoslne (ADEN, The lnner (I) to outer (0) ratlo of flow In the ob5 PM). structed bed was not changed by the stenosls (I/O = 1. 27 f .04 to I/O = 1. 29 * . 04, NS). ADEN decreased I flow from 1.00 f .04 ml/mln/g to 0.75 f .04 ml/mln/g (pc. 001) and Increased 0 flow from 0.77 f .02 ml/mln/g to 1. 28 * .06 ml/mln/g (p <. 001). The I/O ratlo decreased from 1.29 f .04 to 0.65 f .04 (p <. 001). Simultaneously measured LCC CBF (by electomagnetlc flowprobe) increased from 29 f 2 ml/mln to 36 * 2 ml/mln (p < . 01). Thus, arterlolar vasodllator reserve perslsts In the presence of severe proxlmal stenosls but the vasomotor capacity Is llmlted to 0 layers of myocardlum and shuntlng of flow from I to 0 layers can occur.
The effect of preload on the transmural distribution of myocardial blood flow is controversial. The left circumflex artery [LCA] was cannulated and perfused from the left subclavian artery in 7 open-chest dogs. An in-line solenoid, triggered by the R-wave of the ECG, was adjusted so that perfusion, monitored by an in-line flowmeter, occurred only during diastole. Autoregulation was abolished by maximal vasodilation with Chromonar (5 mg/kg). Under these conditions, any differences in local myocardial blood flow measured by radioactive microspheres are presumably due to local differences in diastolic resistance. Measurements were made at normal preload (mean left atria1 pressure [MAPI = 5 ? 1.0 [SEMI mm Hg) and at increased preload (MAP = 20 t 2.0 mm Hg). Despite diastolic perfusion and a significant pressure drop across the perfusion circuit at high flow velocities, overall microsphere flow in the LCA distribution was 1.55 t 0.16 cc/min/g at normal preload and 1.45 + 0.14 cc/min/g at increased preload. The ratio of endocardial flow to epicardial flow decreased from 0.76 f 0.05 at normal preload to 0.54 ?:0.02 at increased preload (p c 0.01). The LCA pressure at which inflow ceased [PC], determined by stepwise constriction of the perfusion circuit, was 14 f 1.7 mm Hg at normal preload and increased to 22 + 1.2 mm Hg at elevated preload (p < 0.01). Local diastolic resistance was calculated as the quotient of driving pressure and local flow, with driving pressure taken as the difference between downstream LCA pressure and PC. With increasing preload, subepicardial resistance remained constant while subendooardial resistance increased significantly. We conclude that small differences in transmural resistance, present at normal preload, are accentuated with increasing preload.
February 1979
The American Journal ol CARDIOLOGY
Volume 41
393