Abnormal intra-atrial conduction induced by premature stimulation in patients with atrial flutter or fibrillation. A basis for reentry?

Abnormal intra-atrial conduction induced by premature stimulation in patients with atrial flutter or fibrillation. A basis for reentry?

ABSTRACTS AN IMPROVEDCARDIOPLEGIC TECHNIQUE MDNDAY, APRIL 26, 1982 PM ATRIAL ARRHYlHMlAS I AND II 2:00-3:30 A CELLULAR ELECTROPHYSIOLOGIC STUDY OF H...

157KB Sizes 0 Downloads 60 Views

ABSTRACTS

AN IMPROVEDCARDIOPLEGIC TECHNIQUE

MDNDAY, APRIL 26, 1982 PM ATRIAL ARRHYlHMlAS I AND II 2:00-3:30 A CELLULAR ELECTROPHYSIOLOGIC STUDY OF HUMAN ATRIAL FIBRILLATION. Michael R. Rosen MD FACC, Allan .I. Hordof MD, James R. Malm MD, Luc Mary-Rabine MD, Columbia Univ., New York, NY

Richard D. Weisel, MD, FACC; Lynda L. Mickleborough, MD; Ronald J. Baird, MD; Joan Ivanov, RN; Hugh E. Scully, MD; Bernard S. Goldman, MD, FACC,Toronto General Hospital, Toronto, Ontario.

Construction of proximal (PA) as well as distal (DA) anastomoses during a single cross-clamp (XC) period permits more uniform cardioplegic cooling and allows immediate reperfusion. This technique was evaluated in a prospective concurrent trial of 42 patients (pts) undergoing elective triple bypass. Group A (25 pts) had 500 ml of a crystaloid cardioplegic solution (CPS) infused initially and 200 ml infu,sedafter each DA. Group B (17 pts) received a similar amount of CPS, but a PA was constructed after each DA to permit cardioplegic delivery to ischemic areas. Group B pts had a longer XC time (A: 43.7 f 14.5, B: 56.6 + 19.5 min, p< .Ol), a lower mean nlyocardial temperature (A: lg.2 + 3.7, B: 12 + 3.3"C, p<.Ol) and a lower temperature in the most ischemic region (A: 16.2 + 4.5, B: 9.5 + 3.4' C, p<.Ol). Group A patients had higher postoperative (PO) CK-MB levels (A: 47.3 + 36, B: 20.8 I g III/L,pc.01). Cardiac lactate production reverted to lactate extraction (LEx) at 4 hrs PO in Group A and at 1 hr PO in Group B (p<.Ol). A volume challenge 2 hrs PO resulted in a similar increase in LA pressure and stroke work index in the two groups, but an opposite lactate response. Group A pts produced lactate and Group B extracted lactate in response to the volume challenge (change in LEx, A: -1.7 * 2.3, B: 2.5 + 5.1 mg/dl, ~4.05). The construction of PA as well as DA during a prolonged XC period permits more uniform cardiac hypothermia and innnediate reperfusion. This technique resulted in less CK-MB release, an earlier restoration of LEx and a normal lactate response to volume loading.

The relationship of atria1 dilatation and hypertrophy to depolarization of cardiac fibers and chronic atria1 fibrillation (AF) is uncertain. Therefore, we used microelectrode techniques to study the electrophysiology of AF in isolated right and left atria1 tissues from patients (pts) undergoing open heart surgery. We studied 9 pts aged 55.9 9.3 (&SD) years with chronic AF (Grp I). All had markedly dilated atria. For comparison we selected pts of = age who had atria of normal size and no AF (Grp II) or comparably dilated atria and no AF (Grp III). Maximum_diastolic potential (MDP), phase 0 upstroke velocity (Vmax) and atria1 pressure were: Grp I Grp II Grp III n 18 9 5 74.9*4.9* MDP (-mV) 66.s3.9 73.6*1.7* 130r49 179*51* 1a5+34* 'max (Vlsec) At. pres. 8.721.6 6.2+1.8* Okl.1" *p<.o5 cf Grp I (mmHg) In Grp I, 8 pts had rheumatic heart disease (RHD) and 1 atherosclerotic heart disease (ASHD). In Grp II, 10 pts had ASHD, and 8 had RHD. Grp III included 3 pts with RHD and 2, ASHD. Our results suggest (1) AF can occur in human atria having depressed fast response action potentials (AP), (2) marked atria1 dilatation occurs in all atria showing AF; but the presence of dilatation alone does not ensure the occurrence of depolarization and AF (compare Grps I and III), (3) the addition of 4 atria1 pressure to dilatation appears prerequisite for membrane depolarization and AF. In conclusion, a combination of atria1 dilatation, 4 atria1 pressure and depressed fast response AP are see" in depolarized atria during chronic AF.

GRAFT PATENCY IN PATIENTS WITH CORONARY ARTERY BYPASS OPERATION COMPLICATED BY PERIOPERATIVE MYOCARDIAL INFARCTION Ralph G. Brindis, MD, MPH; Martin J. Lipton, MD, FACC; .___ Charles R. McKay, MD; Bruce A. Brundage, MD, FACC, University of California, San Francisco, Ca.

ABNORMAL INTRA-ATRIAL CONDUCTION INDUCED BY PREMATURE STIMULATION IN PATIENTS WITH ATRIAL FLUTTER OR FIBRILLATION. A BASIS FOR REENTRY? Francisco G. Casio, MD, FACC; Jose Palacios, MD; Ciudad Sanitaria 1 de Ootubre. Madrid, Spain

Perioperative myocardial infarction (POMI) occurs in approximately 5-10% of coronary artery bypass grafting (CABG) procedures. We examined the graft patency in 17 patients (PTS) with POMI after CABG to assess the role of graft occlusion in the pathogenesis of POMI. Graft patency was evaluated by contrast enhanced computed tomography. Preoperative coronary angiograms were reviewed to assess native coronary disease and visible collaterals in the distribution of POMI. Documentation of POMI was by elevation of CPK-MB bands, ECG changes, and in the majority of cases a positive pyrophosphate scan. Twelve PTS (70%) had open grafts and a POMI in distribution of grafted vessel. Five PTS had a closed graft and a POMI in distribution of grafted vessel. Of the 12 PTS with open grafts, 10 PTS had a 90-99% diameter narrowing without visible collaterals to vessels in the distribution of POMI, one PT had a 75% diameter narrowing without visible collaterals, and one PT had a 100% occlusion associated with 90% narrowing of the major collateral vessel to the distribution of POMI. We conclude that a majority of POMI in CABG operations are unassociated with graft occlusions. The severity of coronary obstruction and lack of collaterals to the region of POMI in PTS with open grafts suggests a" island of jeoparized myocardium may exist vulnerable to inadequate intraoperative preservation.

909

March 1992

The American Journal ol CARDlOLOGY

Because animal experiments have shown that conduction through incompletely recovered myocardium is important for the precipitation and maintenance of atria1 flutter and fibrillation (AFF), we have studied intra-atria1 conduction during premature stimulation of the high right atrium in a group of 15 patients with paroxysmal AFF. The interval from the stimulus to the atria1 electrogram was measured on the His Bundle (HBE) and the coronary sinus (CS) electrograms. The results were compared with those of a control (C) group of 24 patients with and without heart disease but without a history of AFF. Premature stimuli produced little or no atria1 conduction delay (ACD) during sinus rhythm, but during atria1 pa@ing a conduction delay zone (CDZ) was defined in the proximity of the At paced cycle atria1 effective refractory period (AERP). lengths of 500-650 ms the AERP was shorter in AFF (209 f 22.6 ms) than C (240 f 27, p < 0.01). The CDZ was wider in AFF (77 f 19.9 ms) than C (49 f 18.8, p < 0.01) and ACD was longer in AFF than C; both to the HBE (65 f 24.1 vs 37 2 21.5 ms, p < 0.01) and to the CS (71 f 20 vs 35 ? 16.1 ms, p < 0.001). The correlation of ACD with P wave duration was weak (r = 0.3). Repetitive atrial responses occurred in 54% of AFF and 44% of C patients. In summary: Our patients with atria1 flutter or fibrillation had an increased tendency to develop slow intra-atria1 Co"duction during premature stimulation and this abnormality may help to explain their propensity to sustain atria1 reentrant A short atria1 effective refractory period may arrhythmias. further facilitate reentry in this group. Repetitive atria1 rasponses to single extrastimuli were not a pod index of a spontaneous tendency to develop atria1 flutter or fibrillation.

Volume 49