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ABSTRACTS
LONG-TERM RESULTS OF SURGICAL THERAPY FOR REFRACTORY VENTRICULAR ARRHYTHMI :AS William B. Ricks, MD; Roger A. Winkle, MD; Norman E. Shumway, MD; Donald C. Harrison, MD, FACC, Divisions of Cardiology and Cardiovascular Surgery, Stanford University Medical Center, Stanford, Ca.
It has been shown that patients (pts) with ventricular aneurysms and life-threatening ventricular arrhythmias benefit from surgical resection. In order to improve pt selection for operation and to evaluate long-term results, 21 pts with refractory ventricular arrhythmias due to coronary artery disease who underwent surgery from Decem- ber 1970 to January 1975 were reviewed. Eleven pts had aneurysm resection (AR) and ~~onary artery bypass graft- ing (CABG), 4 AR alone, 2 aneurysm plication and CABG, and 4 CABG alone. Follow-up was obtained for 20 pts. Twelve pts were alive an average of 2.7 years after operation (range 9 months to 5 years). Three pts have required five cardioversions for recurrence of ventricular arrhythmias 6 months to 3-l/2 years postoperatively (PO). Twelve-hour ambulatory ECGs in the other nine survivors showed fre- quent multiform premature ventricular contractions in all and asymptomatic ventricular tachycardia in one. There were 8 deaths, 7 during the initial hospitalization and one 4 months PO. Only 20% (l/5) of the pts operated with- in one month of acute myocardial infarction survived to leave the hospital, whereas 81% (13/16) of those operated more than one month after acute infarction survived to leave the hospital. These results suggest that cardiac surgery for refractory ventricular arrhythmias in the relatively unstable post-myocardial infarction period is associated with a high early mortality. Cardiac surgery for refractory ventricular arrhythmias late after infarc- tion is effective and has only a modest mortality. HOW- ever, late failures may occur and all survivors demon- strate persistent ventricular ectopic activity.
SERIAL NON-INVASIVE ASSESSMENT OF LEFT VENTRICULAR
PERFORMANCE AFTER CORONARY BYPASS SURGERY
Albert0 Righetti, MD; Michael Crawford, MD; Robert O’Rourke,
MD, FACC; Pat Daily, MD; William Ashburn, MD; and John
Ross, Jr., MD, FACC, University of California, San Diego.
Twenty-eight potients (pts) undergoing coronary artery bypass graft
surgery (CABG) had echo measurements of left ventricular (LV)
end-diastolic volume (EDV), LV mean normalized septol velocity
(VS) and posterior wall velocity (Vpw) before ond after CABG.
All had pre- and postop x-ray determinations of the left heart
dimension (LHD) and 22 pts had late echo and LHD studies (2 to
9.5 months postop). Thirt?v pts also had pre- and postop LV
ejection fractions (EF) by Tc ongiography. EDV and EF retrained
unchanged early (within I week) after CABG ll30+12 (SE) ml and
6623% vs l44tl2 ml and 6li2%, both p>.21; also, I2 of 25 pts
(48%) with normal septol motion developed paradoxical septol
motion (IO) or okinesis (2). The mean VS decreased from .29?.04
to -.02’.06 (p<.OOl) while Vpw increased from .76?.05 to .93*
.05 (p <.03) early after CABG. Lote postop, the EDV and EF were
unchanged and Vpw had returned to its control value. In contrast,
the mean VS improved to .10+.04 (pc.05) but was still reduced
os compared to control (p<.Ol); abnormal septol motion persisted
in only 4 of 20 (20%) pts with previous y
creased from 45 t.8 to 5O.l+l.2 mm/m 1
normal motion. LHD in-
BSA (pc.002) immediately
postop and then decreased to 47i.8 (pc.03) during outpatient
followup; however, early pericardial effusion (PEf) by echo was
noted in 19 of these pts, which disappeared at late followup. We
conclude: I) Increased heart size after CABG usually indicates
PEf and is transient and 2) LV performance is usually unchanged
early and late after CABG even though obnormol septaf motion
is common and persists in some potients.
REST AND EXERCISE MYOCARDIAL IMAGING WITH THALLIUM-201 - CORRELATION WITH EKG, CORONARY ANATOMY, AND LEFT VENTRI- CULAR FUNCTION James L. Ritchie, MD; Gene B. Trobaugh, MD; Glen W. Hamilton, MD; W. Douglas Weaver, MD; David L. Williams, Ph.D.; K. Lance Gould. MD; University of Washington, Seattle, Washington.
Fifty patients (pts) with suspected coronary heart disease had myocardial imaging at rest after the intra- venous injection of 2 mCi of Thallium-201 c201T1); 18 pts also had images with 2QlT1 during maximal treadmill exer- cise. All pts had coronary angiography and ventriculo-
graehy. At rest, 15 pts had image defects, 25 were nor- mal and 10 were borderline normal. Ten of the 11 pts (91%) with EKG Q waves had image defects in that area. All 12 pts with hypo- or akinesis > 25% of the left ven- tricle had image defects in that area and no pts with normal or borderline normal images had > 25% hypo- or a- kinesis. Ejection fraction was decreased in pts with image defects 49 + 4.9% compared to the remainder 63 + 2% (p < .03). All pts (4) with normal coronary arteries had normal images. Coronary stenosis did not correlate with image defects except when infarction was associated. Exercise images revealed new image defects in I3 of 18 pts (45%). Ih each, there was an associated coronary steno- sis of > 60%.
Myocardial target to background ratios plateaued at 20
minutes post injection and averaged 1.97 + .35:1, which is greater than that reported for other intravenous agents such as Potassium-43. We conclude that 2OlTl is a promising noninvasive agent and that image abnormalities at rest represent infarction while exercise defects cor- relate with ischemia.
DOES VARIANCE IN CPK DISAPPEARANCE RATE IMPAIR
ENZYMATIC ESTIMATION OF INFARCT SIZE?
Robert Roberts, MD; Ronald Karlsberg, MD; Burton E. Sobel, MD,
FACC, Washington University, St. Louis, Missouri.
lt hos been claimed that variance in the fractional rate of CPK dis-
appearance (kd) may impoir enzymatic estimation of infarct size
although kd is not influenced by profound hemodynamic deronge-
ments and individualized estimates, described by Norris, have been
employed to compensate for differences between patients. In the
present study we utilized 40 conscious dogs to examine: I) repro-
ducibility of kd in the some dog with 3 doily i.v. injections of
purified, 14C-lobeled myocardial CPK; 2) kd variance during inter-
cedent myocardial infarction; and 3) changes in kd ofter therapeutic
doses of lidocaine (1 mg/kg), morphine (0.2/kg), Valium (O.l/kg)
and methylprednisolone (3O/kg) and 10 fold greater doses of the
first three agents. Calculations of kd were independent of endog-
enous CPK release because changes in specific radioactivity and
pool size ore inversely proportional. kd wars determined for at
least 3 hr before and 3 hr after each intervention from CPK activity
and radioactivity in plasma samples obtained q 30 min with the
following results: 1) repetitively determined values of kd in the
same dog varied by ~10% (n=5) although values differed subston-
tiolly between animals (3.8 to 6.2~10~~ min-‘, range); 2) kd
remained constant during intercedent myocardial infarction (n=5),
varying by ~8%; and 3) kd varied by <5% after therapeutic doses
of morphine, Valium, lidocaine or high doses of methylpredniso-
lone (n=22), but decreased by 48% and 46% with high doses of
morphine and Valium (n=8). These results suggest that valid esti-
mates of infarct size con be obtained in the clinical setting
without the need for modification due to variance of kd.
166 January 1976 The American Journal of CARDIOLOGY Volume 37