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Chronic transmural infarction prevents refractory period shortening by sympathetic nerve stimulation in noninfarcted areas apical to infarct
ABSTRACTS
CHRONIC TRANSMUPAL INFARCTION PREVENTS REFRACTORY PERIOD SHORTENING BY SYNPATHETIC NERVE STIMULATION IN NONINFARCTED AREAS APICAL TO INFARCT Michael J. Barber, PhD; Thomas M. Mueller, MD, FACC; Julie D. Phillips; DouylasP. MD, FACC, Krannert Inst. of Cardlol., Indiana Zipes,
Univ. Sch. of Med. and V.A. Med. Ctr., Indianapolis, IN We reported that acute transmural myocardialinfarction (MI) produced by injecting latex into the first diagonal coronary arteryproduced regional sympathetic denervation that prevented effective refractory period(ERP) shortening during stellate stimulation(SS) at noninfarcted epicardial and endocardial sites. In this study, we tested whether chronic MI produced prolonged sympathetic denervation in noninfarcted areas by measuring left ventricular ERP changes duringleft and right(R) SS in lOopen chest dogs 7-21 days after MI. ERP was measuredffixed cycle length) atmultiple endocardial andepicardialsites(N=61) with bipolar electrodes delivering stimulitwice diastolicthreshold. At all 20 sites above(basa1 to) the MI, LSS (138?3 vs 131f3 msec;p<.05) and RSS (13Sf3 vs 13223 msec;p<.05) shortened EP.P. In noninfarcted sites distal(apica1) toMI, LSS did not shorten ERP at 22/41 sites (131+2 vs 130-+2 msec) while RSS was ineffective at 24/41 sites (131+3 vs 131f3 msec). 18/41 sites below MI were unresponsive to both L and R SS (completely denervated) while 12/41 sites showed normal ERP changes (C=148?3 msec;LSS=139?3 msec; RSS=139f2 msec;p<.05) for both. Norepinephrine infusion (0.5Ug/kq/min iv) in 6 dogs shortened ERP in previously nonresponsive sites distal to MI (131+3 to 116f4 msec; pq.051. We conclude that MI after diagonalarteryocclusion resultsin sympathetic denervation to regions below the infarct probably by interrupting sympathetic nerves coursing from base to apex in the epicardium. Sympathetic denervation is heterogeneous and may create nonuniform electrophysiologic responses of viable myocardium SIXrounding the MI conducive to arrhythmogenesis.
MONDAY, APRIL 26, 1982 AM MITRAL REGlJRGITA77ON: FLOPPY MITRAL VALVE PROLAPSE 10:30- 12:oo MECHANISMS “LOCKING”.
SUSTAINING
MITRAL
DIASTOLIC
VALVE AND
MITRAL
VALVE
Daniel David, MD, FACC; Masahito Naito, MD, FACC; Eric L. Michelson, MD, FACC; Chin C. Chen, MD; Mark Schaffenburg; Joel Morganroth, MD, FACC; Leonard S. Dreifus, MD, FACC, The Lankenau Medical Research Center, Philadelphia, PA Atria1 systole induces presystolic closure of the mitral valve (MV). However, during abnormal atrio-ventricular sequencing or irregular cardiac cycles the MV may reopen prior to the next ventricular systole producing mitral regurgitation. To study the mechanisms ensuring diastolic MV “locking”, 15 heart blocked (LVP) and left atria1 pressures (LAP) dogs had left ventricular recorded simultaneously with echocardiography of the MV during programmed pacing and also during atria1 fibrillation. During pacing an atria1 premature prolonged pauses in ventricular contraction (APC) was introduced at varying coupling intervals The time from APC induced MV closure to diastolic 0). reopening (MRT) was plotted versus LV volume (LVV).
At short coupling intervals, atria1 systole caused only transient (left figure). MV closure However as the coupling interval prolonged, LVV increased and the time before reopening of the MV prolonged. At a critical LVV the MV “locked” and did not reopen until the next systole. During atria1 fibrillation the MV
failed to lock independent of the diastolic interval (right figure). Thus, sustained diastolic MV “locking” is dependent upon both effective atria1 systole as well as a critical LV volume.
FUNCTIONAL ANATOMICAL VARIATIONS OF CANINE CARDIAC NERVES Richard B. Schuessler, Ph.D.; John P. Boineau, MD; Linda J. Autry, MS; Anita C. Wylds, BS; Carey B. Miller, PE; Charles W. Brcckus, MS., Veterans Atiinistration Medical Center and Medical College of Georgia, Augusta, GA. Atria1 activation and chronotro ic effect of cardiothoracic nerves were studied in twePve monqrel dogs. Gross anatomy revealed that all dogs had the major cardiothor acic nerves: left and right vagosympathetic trunks (VST), left and right thoracic vaqi (TV), ansa, recurrent cardiac and cardiac stellate. HOwever, these was wide variation in the number and location of caudal and cranial vagal nerves. The right cardiac stellate oriqinated from either the stellate ganqlion, the caudal ansa, or the middle cervical qanglion. Ihe effect of maximum stimulation of each nerve on atria1 activation and heart rate was studied. Vaqal stimulation decreased heart rate and cardiac stellate stimulation increased heart rate in all doqs. Ansa stimulation increased rate in 70% of the dogs and decreased it in 30%. Recurrent cardiac stimulation increased rate in 30% of the doqs and decreased it in 70%. Atria1 activation maps of normal sinus rhythm and each nerve stimulation were made using 360 electrodes fixed on a template attached to the right atrium. I" 77% of the stimulations the site of oriqin of the activation sequence shifted. The VST and TV produced the most consistent shifts, shiftinq the pacemaker caudal from the sinus node. The cardiac stellate shifted the pacemaker cranially 75% of the time, caudally 7% and produced no shift 17% of the time. The recurrent cardiac produced no shift 30% of the time, a caudal shift 55% of the time, and a cranial shift 15% of the time. The ansa, and cauda1 and cranial vagal nerves produced no consistent psttern of shifting. The patterns of activation indicate a tarqetinq of the nerves to different pacemaker sites within the pacemaker complex. Gross anatomy along with the activation maps for each nerve stimulation shows that as the nerves branch away fran the central nervous system, they do not follow consistent anatomic pathways. Previous studies which assume that cardiac nerves, which have a chronotropic effect, are all targeted tD the sinus node, are not supported by these studies.
MYXOMATOUSDEGENERATION AND MITRAL INSUFFICIENCY: A SPECTRUM OF DISEASE Nancy V. Strahan, KD; Nicholas J. Fortuin, MD; Bernadine Healy Bulkley, MD, FACC, The Johns Hopkins Medical Institutions, Baltimore, F?d. Myxomatous degeneration has been described as the typical histologic finding of mitral valve prolapse (MVP). To what extent this change is characteristic of MVP, or is a nonspecific finding, has been a subject of controversy. To study this, we evaluated 116 consecutive patients coming to surgery for pure mitral regurgitation in whom histologic sections of excised valves were present, and in whom clinical findings, angiograms, and echocardiograms were available. Histologic sections of valves were reviewed "blindly" and graded as to extent of myxomatous degeneration on a scale of severe (3-4+), mild (l-2+) or none. Clinical diagnosis included MVP in 53 (46%), coronary artery disease in 20 (17%), rheumatic heart disease in 8 (7%), and miscellaneous in 5 (4%); and was indeterminate in 30 patients. Histologic study of the 116 valves showed 49 (42%) had 3-4+ myxomatous change: 31/49 (63%) had MVP clinically; of the others 22% had mitral regurgitation due to coronary artery disease or endocarditis, and 14% were indeterminate; none had rheumatic heart disease. Of the 67 patients with O-2+, myxomatous change 32% had floppy mitral valve, 34% were indeterminate, 12% had rheumatic heart disease, and 21% coronary artery disiease or infective endocarditis. The findings show that small amounts of myxomatous change may be present in pure mitral regurgitation of a variety of etiologies. Although extensive myxomatous degeneration was more predictive of the floppy mitral valve syndrome, its presence in other diseases also suggests that myxomatous degeneration and floppy mitral valve, together and alone, represent a spectrum of valve disease of diverse cause.
March 1982
The American Journal of CARDIOLOGY
Volume 49
899
CHRONIC TRANSMUPAL INFARCTION PREVENTS REFRACTORY PERIOD SHORTENING BY SYNPATHETIC NERVE STIMULATION IN NONINFARCTED AREAS APICAL TO INFARCT Michael J. Barber, PhD; Thomas M. Mueller, MD, FACC; Julie D. Phillips; DouylasP. MD, FACC, Krannert Inst. of Cardlol., Indiana Zipes,
Univ. Sch. of Med. and V.A. Med. Ctr., Indianapolis, IN We reported that acute transmural myocardialinfarction (MI) produced by injecting latex into the first diagonal coronary arteryproduced regional sympathetic denervation that prevented effective refractory period(ERP) shortening during stellate stimulation(SS) at noninfarcted epicardial and endocardial sites. In this study, we tested whether chronic MI produced prolonged sympathetic denervation in noninfarcted areas by measuring left ventricular ERP changes duringleft and right(R) SS in lOopen chest dogs 7-21 days after MI. ERP was measuredffixed cycle length) atmultiple endocardial andepicardialsites(N=61) with bipolar electrodes delivering stimulitwice diastolicthreshold. At all 20 sites above(basa1 to) the MI, LSS (138?3 vs 131f3 msec;p<.05) and RSS (13Sf3 vs 13223 msec;p<.05) shortened EP.P. In noninfarcted sites distal(apica1) toMI, LSS did not shorten ERP at 22/41 sites (131+2 vs 130-+2 msec) while RSS was ineffective at 24/41 sites (131+3 vs 131f3 msec). 18/41 sites below MI were unresponsive to both L and R SS (completely denervated) while 12/41 sites showed normal ERP changes (C=148?3 msec;LSS=139?3 msec; RSS=139f2 msec;p<.05) for both. Norepinephrine infusion (0.5Ug/kq/min iv) in 6 dogs shortened ERP in previously nonresponsive sites distal to MI (131+3 to 116f4 msec; pq.051. We conclude that MI after diagonalarteryocclusion resultsin sympathetic denervation to regions below the infarct probably by interrupting sympathetic nerves coursing from base to apex in the epicardium. Sympathetic denervation is heterogeneous and may create nonuniform electrophysiologic responses of viable myocardium SIXrounding the MI conducive to arrhythmogenesis.
MONDAY, APRIL 26, 1982 AM MITRAL REGlJRGITA77ON: FLOPPY MITRAL VALVE PROLAPSE 10:30- 12:oo MECHANISMS “LOCKING”.
SUSTAINING
MITRAL
DIASTOLIC
VALVE AND
MITRAL
VALVE
Daniel David, MD, FACC; Masahito Naito, MD, FACC; Eric L. Michelson, MD, FACC; Chin C. Chen, MD; Mark Schaffenburg; Joel Morganroth, MD, FACC; Leonard S. Dreifus, MD, FACC, The Lankenau Medical Research Center, Philadelphia, PA Atria1 systole induces presystolic closure of the mitral valve (MV). However, during abnormal atrio-ventricular sequencing or irregular cardiac cycles the MV may reopen prior to the next ventricular systole producing mitral regurgitation. To study the mechanisms ensuring diastolic MV “locking”, 15 heart blocked (LVP) and left atria1 pressures (LAP) dogs had left ventricular recorded simultaneously with echocardiography of the MV during programmed pacing and also during atria1 fibrillation. During pacing an atria1 premature prolonged pauses in ventricular contraction (APC) was introduced at varying coupling intervals The time from APC induced MV closure to diastolic 0). reopening (MRT) was plotted versus LV volume (LVV).
At short coupling intervals, atria1 systole caused only transient (left figure). MV closure However as the coupling interval prolonged, LVV increased and the time before reopening of the MV prolonged. At a critical LVV the MV “locked” and did not reopen until the next systole. During atria1 fibrillation the MV
failed to lock independent of the diastolic interval (right figure). Thus, sustained diastolic MV “locking” is dependent upon both effective atria1 systole as well as a critical LV volume.
FUNCTIONAL ANATOMICAL VARIATIONS OF CANINE CARDIAC NERVES Richard B. Schuessler, Ph.D.; John P. Boineau, MD; Linda J. Autry, MS; Anita C. Wylds, BS; Carey B. Miller, PE; Charles W. Brcckus, MS., Veterans Atiinistration Medical Center and Medical College of Georgia, Augusta, GA. Atria1 activation and chronotro ic effect of cardiothoracic nerves were studied in twePve monqrel dogs. Gross anatomy revealed that all dogs had the major cardiothor acic nerves: left and right vagosympathetic trunks (VST), left and right thoracic vaqi (TV), ansa, recurrent cardiac and cardiac stellate. HOwever, these was wide variation in the number and location of caudal and cranial vagal nerves. The right cardiac stellate oriqinated from either the stellate ganqlion, the caudal ansa, or the middle cervical qanglion. Ihe effect of maximum stimulation of each nerve on atria1 activation and heart rate was studied. Vaqal stimulation decreased heart rate and cardiac stellate stimulation increased heart rate in all doqs. Ansa stimulation increased rate in 70% of the dogs and decreased it in 30%. Recurrent cardiac stimulation increased rate in 30% of the doqs and decreased it in 70%. Atria1 activation maps of normal sinus rhythm and each nerve stimulation were made using 360 electrodes fixed on a template attached to the right atrium. I" 77% of the stimulations the site of oriqin of the activation sequence shifted. The VST and TV produced the most consistent shifts, shiftinq the pacemaker caudal from the sinus node. The cardiac stellate shifted the pacemaker cranially 75% of the time, caudally 7% and produced no shift 17% of the time. The recurrent cardiac produced no shift 30% of the time, a caudal shift 55% of the time, and a cranial shift 15% of the time. The ansa, and cauda1 and cranial vagal nerves produced no consistent psttern of shifting. The patterns of activation indicate a tarqetinq of the nerves to different pacemaker sites within the pacemaker complex. Gross anatomy along with the activation maps for each nerve stimulation shows that as the nerves branch away fran the central nervous system, they do not follow consistent anatomic pathways. Previous studies which assume that cardiac nerves, which have a chronotropic effect, are all targeted tD the sinus node, are not supported by these studies.
MYXOMATOUSDEGENERATION AND MITRAL INSUFFICIENCY: A SPECTRUM OF DISEASE Nancy V. Strahan, KD; Nicholas J. Fortuin, MD; Bernadine Healy Bulkley, MD, FACC, The Johns Hopkins Medical Institutions, Baltimore, F?d. Myxomatous degeneration has been described as the typical histologic finding of mitral valve prolapse (MVP). To what extent this change is characteristic of MVP, or is a nonspecific finding, has been a subject of controversy. To study this, we evaluated 116 consecutive patients coming to surgery for pure mitral regurgitation in whom histologic sections of excised valves were present, and in whom clinical findings, angiograms, and echocardiograms were available. Histologic sections of valves were reviewed "blindly" and graded as to extent of myxomatous degeneration on a scale of severe (3-4+), mild (l-2+) or none. Clinical diagnosis included MVP in 53 (46%), coronary artery disease in 20 (17%), rheumatic heart disease in 8 (7%), and miscellaneous in 5 (4%); and was indeterminate in 30 patients. Histologic study of the 116 valves showed 49 (42%) had 3-4+ myxomatous change: 31/49 (63%) had MVP clinically; of the others 22% had mitral regurgitation due to coronary artery disease or endocarditis, and 14% were indeterminate; none had rheumatic heart disease. Of the 67 patients with O-2+, myxomatous change 32% had floppy mitral valve, 34% were indeterminate, 12% had rheumatic heart disease, and 21% coronary artery disiease or infective endocarditis. The findings show that small amounts of myxomatous change may be present in pure mitral regurgitation of a variety of etiologies. Although extensive myxomatous degeneration was more predictive of the floppy mitral valve syndrome, its presence in other diseases also suggests that myxomatous degeneration and floppy mitral valve, together and alone, represent a spectrum of valve disease of diverse cause.
March 1982
The American Journal of CARDIOLOGY
Volume 49
899