Ventricular defibrillation of heavy weight subjects

Ventricular defibrillation of heavy weight subjects

ABSTRACTS SUDDEN CARDIAC DEATH ON THE LIQUID PROTEIN DIET: CLINICAL AND MORPHOLOGIC FINDINGS IN 16 WOMEN. Jeffrey M. !sner, MDD, Harold E. Sours, MD,...

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ABSTRACTS

SUDDEN CARDIAC DEATH ON THE LIQUID PROTEIN DIET: CLINICAL AND MORPHOLOGIC FINDINGS IN 16 WOMEN. Jeffrey M. !sner, MDD, Harold E. Sours, MD, Allen L. Paris, MD, Victor J. Ferrans, MD, and William C. Roberts, MD, FACC, National Heart, Lung, and Blood Institute, Bethesda, Maryland, and Center for Disease Control, Atlanta, Georgia. Of 58 documented deaths among exclusive users of the liquid protein diet, 16 involved patients (pts) with no prior clinical history of serious medical problems, all of whom died suddenlyand unexpectedly. All 16 pts were women, most were young (aged 23-51 year s [avg=37]), and all had been on the diet for at least 2 months (avg=5 mo). Percent weight loss in all but 2 pts exceeded 25% of initial body weight. Eleven pts were on the diet at the time of death, while 5 were in various stages of refeeding. Ventricular arrhythmias refractory to antiarrhythmic agents caused death in i0 pts, 9 of whom had markedly prolonged Q-T intervals (Q-T interval corrected for rate=0.45 to 0.65 sec). Severely diminished QRS voltage was an additional prominent feature of the electrocardiograms in all but i pt. Gross and light microscopic examination of the hearts in 15 pts disclosed unequivocal myocarditis in only I pt. In the remaining 14 pts studied at necropsy, the myocardial fibers were thin, lipochrome pigment was increased, and nuclear changes were prominent. Similar changes of lesser magnitude were seen at necropsy in 15 control pts, all of whom were cachectic from nondieting causes. Thus, the morphologic findings in pts dying suddenly on the liquid protein diet are probably related to the extent of weight loss and protein or mineral depletion, rather than to the use of the particular liquid-protein products. The clinical expression of such morphologic changes include diminished total electrical activity of the heart and prolongation of repolarization associated with fatal refractory ventricular arrhythmias.

ANTEROSEPTAL ISCHEMIA-PROBABLE MECHANISM OF EXERCISE VENTRICULAR FIBRILLATION AND TACHYCARDIA. Lawrence Griffith, MD. FACC, Charles Angeil, MD, Louise G~nwald, Terry Rehn, MD, Lewis Becker, MD, FACC. Johns Hopkins Un;versity, Baltimore, Maryland. To determine whether a common pattern of regional ischemia is present at the time of exercise induced ventricular fibrillation(VF) or tachycardia(VT), the angiographic, electrocardiographic(ECG) and Thallium'201 myocardial scan(TMS)findings were reviewed in 35 pts(pts) with coronary heart dwsease • (_> 1 arte ry narrowed at least 50%) who developed VF (5 pts) or VT (>,. 3 premature contractions in sequence)(30 pts) dur|ng exercise (Ex) ECG test (31 pts) or ambulatory ECG monitoring (4 pts). On arteriography, main left(MI.CA) or left anterior descending artery(LAD) narrowed ~70% in 34/35(97%) pts. in 31/35 (89%) pts the >70% narrowing proximal to second septal branch(SB); narrowing was 50% in 2 pts. In 24/35 pts, _>70% narrowing proximal to first SB. Nine(26%) pts had >.50% narrowing of MLCA. Five ptshad s|ngle(all LAD), 11 double and 19 triple vessel disease. On left ventriculogram, 32/35 pts had normal or hypokinetic wall motion in anter|or, apical or septal segments. This is likely "vlable" myocard|urn perfused by LAD. Three pts had ak|nes|s of all three segments. During Ex ECG 23/32 pts had angina prior to VF/VT and 29/30 pts had positive ECG test(>. 1 mm ST.b ); one record not available. ST ~, in one or more "anterior" leads (It AVLt V2-V6) was present in 28/30 pts; 13 pts also had ST $ in "inferior" leads (Ilk !11, AVF)° One pt had only inferior ST ~ . Prior data indicates that anterior ECG changes likely reflect LAD myocardium. Twelve pts had rest and stress TMS scans. LAD myocardial segments showed a defect at rest in 2 ptSo Nine other pts had new LAD perfusion defects after exercise. One pt had no LAD defect, Pts with Ex VF/VT have high prevalence of proximal LAD or MLCA narrowings, "vlable" LAD rnyocardium, an d develop angina, anterior ST ¢and new TMS defects in LAD distribution with exercise. Thus, transient ischemia of. "viable" ant,erose,Rtal,~n,l~ocardial segments appears to correlate with exercise |naucea vr-/v~.

TERMINAL CARDIAC ELECTRICAL ACTIVITY IN PEDIATRIC PATIENTS Christine A. Walsh, M.D., Ehud Krongrad, M.D., FACC Columbia University, New York, N.Y. 10032. Ventricular fibrillation (VE) is reported to be the most frequent terminal cardiac electrical activity (TCEA) in adults. No similar data ~re available for pediatric patients (pts). In order to determine the TCEA in children, especially with regard to sudden infant death syndrome (SIDS), the TCEA of i00 pediatric pts was studied. Group (Gr.) A consisted of $4 newborn infants less than 29 days, 18 of whom had congenital cardiac defects (CHD). Gr.B had 46 infants and children from 29 days to 18 years (mean=3.6 years), 29 of whom had CHD. TCEA was correlated with arterial blood gases (ABG), electrolytes (E), and preterminal electrocardiograms (ECG). The TCEA was bradycardic-arrest throughout the death process in 83 pts (S0/$4 from Gr.A and 33/46 from Gr.B). Transient ventricular tachycardia or VF with final bradycardic-arrest was seen in Ii children (I/$4 from Gr.A and 10/46 from Gr.B). Unremitting VF was seen in 6 pts, all with CHD (3/54 from Gr.A and 3/46 from Gr.B). Among 80 pts less than i year, an age group similar to that of SIDS infants, terminal bradycardic-arrest was seen in 76 pts (95%). No correlation Was found between the type of TCEA and ABG, E, or preterminal ECG. The data indicate that bradycardic-arrest is the most common TCEA in pediatric pts, a finding different from that reported for adults. Our clinical observation supports electrophysiologic data suggesting that the development of VF may be related to cardiac mass and is, therefore, less likely to occur in smaller hearts. Thus, the TCEA of pts with no evidence of heart disease, such as SIDS infants, is more likely to be bradycardic-arrest than VF. Our findings are important in attempts to better understand and eventually develop methods of prevention of SIDS.

VENTRICULAR DEFIBRILLATION OF HEAVY WEIGHT SUBJECTS M i c h a e ! L . Chel-wek,_MD, Joseph A. Gascho, MD, James N. Sipes, MD, Frank P. Hunter, BEE, William M. O'Brien, MD and Richard S. Crampton, MD, FACC, University of Virginia, Charlottesville, Virginia 22908 Using conventionaldefibrillators which delivered 360 joules (j) or less, we prospectively assessed defibrillation rate in 12 patients who weighed mean + SE 106 + ii (range 91-225) kg. Of 46 episodes of ventri~ular fibrillation (VF), 45 (98%) defibrillated, 37 (80%) at first shock. Eleven patients received 1.4 + .2 shocks per VF episode to defibrillate; i with cardiomyopathy failed to defibrillate. Delivered energy for all successful shocks was 194 + ii j (1.8 + .i j/kg) and for successful first shocks, 17--4 + i0 j (i~8 ~ .i ~/kg), In 33 VF episodes shocks delivered 200 j or less; 31 (94%) defibrillated, 29 (88%) at first shock. Eight coronary patients defibrillated more easily with i.i + .i shocks per VF episode (pC.01) at less energy, 177 + i0 j (pK.Oi) than noncoronary patients with 3.9 + .i shocks per VF episode and 278 + 25 j. The 225 kg subject had 6 VF episodes ended by 323 j or less (1.4 j/kg) r In 38 of 39 (97%) VF episodes 1.4 - 3.4 j/kg defibrillated. Only 2 of 6 shocks under 1.4 j/kg defibrillated suggesting a threshold about 1.4 j/kg. Defibrillation occurred at half the energy predicted by retrospective studies. Diagnosis, not weight, determined defibrillation. Eight of 12 survived resuscitation; 3 resumed active lives. Shocks from standard devices which stored no more than 400 j defibrillated 98% VF episodes in 12 heavy weight individuals at only one third the energy recommended by proponents of high energy shocks. Thus the costly defibrillators delivering 400 - 800 J, or 6.4 ]/kg or more, now sold by i0 of 14 American manufacturers are superfluous, untested, potentially lethal devices to terminate VF.

February 1979

The American Journal of CARDIOLOGY

Volume 43

421