pairment that we observedwas causedby the combined toxic effect of plasmin and plasmin activator, a component of allergic hepatitis and a reaction to hemodynamic A few casereports and a small study documented a derangement,all against a background of a mild basic degreeof hepatic dysfunction after the administration of liver function impairment known to occur in patients with streptokinaseto patients with peripheral arterial obstruc- an AMI. The greater prominence of liver dysfunction tion.*q3q5 Mixed cholestatic and hepatocellular damage with streptokinase than with rt-PA may probably be peaked at 3 days and then declined gradually within 2 ascribed to the more local action of rt-PA on formed months. We measured liver enzymes in patients with thrombi. AM1 and observeda similar trend. Somedegreeof hepatWe conclude that thrombolysis, particularly with ic dysfunction was found in those who did not receive streptokinase,causesan acute, pronounced impairment thrombolytic therapy, a somewhathigher impairment in of hepatic function that does not lead to either acute those treated with rt-PA and a pronounced change in hepatic failure or chronic hepatic diseaseand that heals those treated with streptokinase. No patient went into gradually and completely within 3 months. We suggest hepatic failure, and complete resolution was observed that patients with impaired hepatic function who need thrombolytic therapy should be treated with rt-PA rather within 3 months. The pathophysiologicmechanismof this toxic, hepati- than with streptokinase. tis-like picture has not yet been elucidated. The 3 foremost possibilities are a suddendisturbance of the microcirculation of the liver, hepatotoxicity of the thrombolytic agent or the generatedproteolytic enzymes,or an immu- 1. Ruegsegger P, Nydick I, Freiman A, LaDue J. Serum activity patterns of oxaloacetic transaminase, glutamic pyruvic transaminase and lactic nologic reaction. Some degree of liver function impair- glutamic dehydrogenase following graded myocardial infarction in dogs. Circ Res 1959; ment during AM1 without thrombolytic therapy has pre- 7:4-10. Schmidt E, Poliwoda H, Buhl V, Alexander K, Schmidt F. Observations of viously been described’ and parallels our results. The 2.enzyme elevations in the serum during streptokinase treatment. J Clin Parhol infusion of streptokinase into an isolated hemoglobin- 1972;25:650-652. free and volume-constant perfusedrat liver did not cause 3. Schmidt E, Schmidt p. Streptokinase-induced hepatic dysfunction. Am J 1984;79:328-329. liver enzyme release,whereasthe addition of plasmin or 4.Gastroenterol Siegel S. Nonparametric Statistics for the Behavioral Sciences. New York: plasmin activator led to a marked accelerationof enzyme McGraw Hill, 1956~75-127. release.*Major adverseeffects of streptokinase include 5. Salen M, Efrusy M, Kniaz J, Wolfson P. Streptokinase-induced hepatic dysAm J Gastroenterol 1983;78:523-524. bleeding, transient hypotension and a variety of allergic 6.function. Braunwald E. Heart Disease-A Textbook of Cardiovascular Medicine. Philareactions.6It seemsthat the degreeof liver function im- delphia: W.B. Saunders,1988:1588.

41 patients (27%) in the rt-PA group and I of 31 subjects (3%) in the control group. All these changes normalized at 3 months (Figures 1, 2 and 3).

Influence of Gender on lnducibility of Ventricular Arrhythmias Survivors of Cardiac Arrest with Coronary Artery Disease Paul T. Vaitkus, MD, K. Elizabeth Kindwall, MD, John M. Miller, E. Buxton, MD, and Mark E. Josephson, MD

MD,

Francis E. Marchlinski,

in MD,

Alfred

inducibility may havebeenpartly explained by a differing prevalenceof coronary artery disease.*This observation, however, could not fully explain the difference in outcluded epidemiologic reports on different clinical predic- come of electrophysiologic testing in men and women.* tors of sudden death in men and women’ and disparate We undertook the presentstudy to evaluateif differences results of electrophysiologictesting in survivorsof cardiac in electrophysiologic substrate could explain the differarrest.* Previous studies examining clinical predictors of encein inducibility betweenmen and women with coroarrhythmia inducibility in patients with cardiac arrest nary artery diseaseand cardiac arrest. have documented that male gender is an important preWe studied 52 men and 13 women with coronary dictor of inducibility.* These studies enrolled patients artery disease and cardiac arrest unrelated to recent with a variety of cardiac disorders and the difference in myocardial infarction and not associated with the adhe influence of genderon the clinical manifestations, T results of testing and prognosisof heart diseasehas recently been emphasized.These observations have in-

From the Cardiovascular Division, Department of Medicine, University of Pennsylvania School of Medicine, and the Cardiovascular Division, 9-Founders, Hospital of the University of Pennsylvania, 3400 Spruce Street, Philadelphia, Pennsylvania 19104. This report was supported in part by Grant HL28093 from the National Heart, Lung, and Blood Institute, Bethesda, Maryland. Dr. Josephson is the Robinette Foundation Professor of Medicine in Cardiology. Manuscript received August 15, 1990; revised manuscript received and accepted November 13, 1990.

ministration of antiarrhythmic medications. The following variables were analyzed: age, history of myocardial infarction, ejectionfraction, and number of diseased coronary arteries (defined as 170% obstruction), inducibility of sustained ventricular arrhythmias, endocardial catheter mapping abnormalities, and signal-averaged electrocardiography. Our stimulation protocol,3 endocardial catheter mapping scheme4 and methods of signal-averaged electrocardiography5 have been described THE AMERICAN JOURNAL OF CARDIOLOGY

MARCH 1, 1991

537

TABLE

I Clinical Variables and Results of Endocardial Mapping and Signal-Averaged Electrocardiography in Male and Female Survivors of Cardiac Arrest Men

Number of patients Age W History of MI (%) Number of diseased coronaries Ejection fraction (%) Inducible arrhythmias (%) v-r VF NSVT None Normal sites (%) Abnormal sites (%) Fractionated sites (%) Early sites (%) Late sites (%) Late, abnormal or fractionated sites (%I Duration of longest electrogram (ms) Total endocardial activation time 0-M Offset latest electrogram Filtered QRS duration (ms) Root-mean-square voltage last 40 ms r&V) Abnormal SAECG

Women

p Value

52 60f8 42 (81) 2.3 f 0.8 37f17

13 65i7 10 (77) 1.9f0.9 31i22

0.04 NS NS NS

27 (52) ll(21) 7 (13) 7 (13) 55f27 42f26 3f8 15f 15 7flO 5*9

4(31) l(8) 5 (38) 3 (23) 51f28 43dc25 6f15 16f17 8f12 9f13

NS NS NS NS NS NS

107 f 33 60f32

107 f 22 55f16

NS NS

115f36 122+30 34f30

118zk31 108f24 42f21

NS NS NS

64%

43%

NS

MI = myocardial infarction; NS = difference not significant; NSVT = nonsustained ventricular tachycard!a; SAECG = signal-averaged ekctrocardlogram; VF = ventrlcular fibnllabon; VT = ventricular tachycardia.

in detail previously. Stimulation includes the introduction of 1,2 and 3 extrastimuli at 2 right ventricular sites at 22 drive cycle lengths and rapid ventricular pacing. Nonsustained ventricular tachycardia was not an end point for stopping the electrophysiologic study, and all patients underwent stimulation to refractoriness or induction of hemodynamically compromising sustained ventricular arrhythmia. Patients with bundle branch block (7 men and 4 women) were excludedfrom signalaveragedelectrocardiography. Signal-averaged electrocardiographic data were available for 42 men and 7 women without bundle branch block; catheter mapping data were completefor all patients. Of the patients included for signal-averaged electrocardiography, 71% of the men and 43% of the women were inducible. Endocardial electrograms were classified as normal, abnormal or fractionated according to previously described criteria.4 Total endocardial activation time was defined as time from activation of the earliest to activation of the latest electrogram. Early and late sites were defined as sites exhibiting activity preceding or after the surface QRS, respectively. The signal-averagedelectrocardiograms were comparedfor filtered QRS duration and root-mean-square voltage of the terminal 40 ms. Duration >I 10 ms or voltage of the terminal 40 ms

Influence of gender on inducibility of ventricular arrhythmias in survivors of cardiac arrest with coronary artery disease.

pairment that we observedwas causedby the combined toxic effect of plasmin and plasmin activator, a component of allergic hepatitis and a reaction to...
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