Insulin Resistance in Patients With Familial Combined Hyperlipidemia and Coronary Artery Disease

scar (and thus viability of the remaining myocardium) may be important in preventing left ventricular remodeling and long-term prognosis.18 In conclusion, these data further substantiate the hypothesis that low-dose dobutamine echocardiography has a relatively low specificity in segments with mild dyssynergy. This phenomenon can, at least in part, be attributed to the presence of subendocardial scar. 1. Rahimtoola SH. The hibernating myocardium. Am Heart J 1989;117:211–221. 2. Vanoverschelde JLJ, Wijns W, Depre´ C, Essamri B, Heyndrickx GR, Borgers

M, Bol A, Melin JA. Mechanisms of chronic regional postischemic dysfunction in humans. New insights from the study of noninfarcted collateral-dependent myocardium. Circulation 1993;87:1513–1523. 3. Cornel JH, Bax JJ, Fioretti PM. Assessment of myocardial viability by dobutamine stress echocardiography. Curr Opin Cardiol 1996;11:621– 626. 4. Baer FM, Voth E, Deutsch HJ, Schneider CA, Schicha H, Sechtem U. Assessment of viable myocardium by dobutamine transesophageal echocardiography and comparison with fluorine-18 fluorodeoxyglucose PET. J Am Coll Cardiol 1994;24:343–353. 5. Arnese M, Cornel JH, Salustri A, Maat APWM, Elhendy A, Reijs AEM, Ten Cate FJ, Keane D, Balk AHMM, Roelandt JRTC, Fioretti PM. Prediction of improvement of regional left ventricular function after surgical revascularization: a comparison of low-dose dobutamine echocardiography with 201-TL SPECT. Circulation 1995;91:2748 –2752. 6. La Canna G, Alfieri O, Giubbini R, Gargano M, Ferrari R, Visioli O. Echocardiography during infusion of dobutamine for identification of reversible dysfunction in patients with chronic coronary artery disease. J Am Coll Cardiol 1994;23:617– 626. 7. Baer FM, Voth E, Deutsch HJ, Schneider CA, Horst M, de Vivie ER, Schicha H, Erdmann E, Sechtem U. Predictive value of low dose dobutamine transesophageal echocardiography and fluorine-18 fluorodeoxyglucose positron emission tomography for recovery of regional left ventricular function after successful revascularization. J Am Coll Cardiol 1996;28:60 – 69.

8. Perrone-Filardi P, Pace L, Prastaro M, Piscione F, Betocchi S, Squame F,

Vezzuto P, Soricelli A, Indolfi C, Salvatore M, Chiariello M. Dobutamine echocardiography predicts improvement of hypoperfused dysfunctional myocardium after revascularization in patients with coronary artery disease. Circulation 1995;91:2556 –2565. 9. DeFilippi CR, Willett DWL, Irani WN, Eichhorn EJ, Velasco CE, Grayburn PA. Comparison of myocardial contrast echocardiography and low-dose dobutamine stress echocardiography in predicting recovery of left ventricular function after coronary revascularization in chronic ischemic heart disease. Circulation 1995;92:2863–2868. 10. Vanoverschelde J-LJ, D’Hondt A-M, Marwick T, Gerber BL, De Kock M, Dion R, Wijns W, Melin JA. Head-to-head comparison of exercise-redistributionreinjection thallium single-photon emission computed tomography and low dose dobutamine echocardiography for prediction of reversibility of chronic left ventricular ischemic dysfunction. J Am Coll Cardiol 1996;28:432– 442. 11. Qureshi U, Nagueh SF, Afridi I, Vaduganathan P, Blaustein A, Verani MS, Winters WL, Zoghbi WA. Dobutamine echocardiography and quantitative restredistribution 201T1 tomography in myocardial hibernation. Relation of contractile reserve to 201T1 uptake and comparative prediction of recovery of function. Circulation 1997;95:626 – 635. 12. Pigott JD, Kouchoukos NT, Oberman A, Cutter GR. Late results of surgical and medical therapy for patients with coronary artery disease and depressed left ventricular function. J Am Coll Cardiol 1985;5:1036 –1045. 13. Lieberman AN, Weiss JL, Jugdutt JL, Becker LC, Bulkley BH, Garrison JG, Hutchins GM, Kallman CA, Weisfeldt ML. Two-dimensional echocardiography and infarct size: Relationship of regional wall motion and thinning to the extent of myocardial infarction in the dog. Circulation 1981;63:739 –746. 14. Armstrong WF. ‘‘Hibernating’’ myocardium: asleep or part dead? J Am Coll Cardiol 1996;28:530 –535. 15. Kaul S. There may be more to myocardial viability than meets the eye! [editorial]. Circulation 1995;92:2790 –2793. 16. Afridi I, Kleiman NS, Raizner AE, Zoghbi WA. Dobutamine echocardiography in myocardial hibernation. Optimal dose and accuracy in predicting recovery of ventricular function after coronary angioplasty. Circulation 1995;91:663– 670. 17. Kaul S. Response of dysfunctional myocardium to dobutamine. ‘‘The eyes see what the mind knows!’’ [editorial]. J Am Coll Cardiol 1996;27:1608 –1611. 18. Gaudron P, Eilles C, Kugler I, Ertl G. Progressive left ventricular dysfunction and remodeling after myocardial infarction: potential mechanisms and early predictors. Circulation 1993;21:683– 691. AQ1—Give location (city and state or city and country if in Europe) of all manufacturers.

Insulin Resistance in Patients With Familial Combined Hyperlipidemia and Coronary Artery Disease Juan F. Ascaso,

MD, PhD,

Rosario Lorente, MD, Angel Merchante, MD, Jose´ T. Real, Antonia Priego, MD, and Rafael Carmena MD, PhD

amilial combined hyperlipidemia (FCH) is an alteration in the metabolism of lipoproteins initially F described in a study of family members of young survivors of myocardial infarction.1 The etiology of FCH is unknown because the phenotype is variable and the expression of the disease is affected by genetic, metabolic, and environmental factors.2 FCH has a prevalence in the general population of 0.5% to 2% and between 15% and 20% in subjects with premature cardiovascular disease.3 The common factor in subjects with FCH is the increase in low-density lipoprotein (LDL) or very low density lipoprotein (VLDL), or both, with elevations in the apolipoprotein B levels and, frequently, low levels of high-density lipoprotein (HDL), abnormal composition of lipoproteins, central From the Service of Endocrinology and Nutrition, Hospital Clinico, University of Valencia, Valencia, Spain. Dr. Ascaso’s address is: Departament de Medicina, Universitat de Valencia, Avenida Blasco Iban˜ez 15, 46010 Valencia, Spain. Manuscript received June 12, 1997; revised manuscript received and accepted September 8, 1997.

1484

©1997 by Excerpta Medica, Inc. All rights reserved.

MD,

trunk obesity, hyperinsulinemia, and abnormal glucose tolerance.4,5 These associations highlight the considerable metabolic heterogeneity of the FCH condition and arteriosclerosis.6 In the present study we have investigated insulin resistance (quantified using the minimal model of glucose metabolism modified by the administration of insulin) and other known cardiovascular disease risk factors in patients with FCH subgrouped according to the presence or absence of ischemic heart disease (IHD). •••

Patients (33 men) were diagnosed as having FCH after clinical and biochemical assessments of the probands and first-degree relatives. All patients selected were nonsmokers or ex-smokers for at least 1 year. Diagnosis was based on: the presence of hyperlipidemia of variable phenotypes IIa, IIb, or IV in firstdegree relatives of $2 generations, family history of premature arteriosclerosis, elevated concentrations of apoprotein B in plasma (.1.20 g/L), and absence of xanthomas in the proband and in first-degree relatives. The lipoprotein phenotypes were as described by 0002-9149/97/$17.00 PII S0002-9149(97)00737-6

TABLE I Anthropometric and Lipid Values in FCH Patients With and Without Ischemic Heart Disease, and in Control Subjects

Age (yr) Body mass index (kg/m2) Waist-to-hip ratio Systolic blood pressure (mm Hg) Diastolic blood pressure (mm Hg) Total cholesterol (mmol/L) Plasma triglycerides (mmol/L) HDL (mmol/L) LDL (mmol/L) Apo B (g/L) Apo A1 (g/L) LDL pattern B log Lp(a) FFA basal (g/L)

FCH-IHD1 (n 5 14)

FCH-IHD0 (n 5 19)

49 6 9 29 6 3 1.01 6 0.07*‡ 139 6 12*† 87 6 9*† 7.17 6 1.51* 3.88 6 0.48* 0.95 6 0.16* 4.79 6 1.65* 1.59 6 0.40* 1.12 6 0.24 5 (35%)*† 1.06 6 0.12*‡ 5.31 6 1.81*

46 6 10 29 6 2 0.97 6 0.04 131 6 13 78 6 8 7.34 6 1.48* 3.24 6 1.50* 0.95 6 0.20* 5.02 6 1.17* 1.59 6 0.35* 1.08 6 0.19 3 (15%) 0.79 6 0.32 4.94 6 1.64*

Control (n 5 20) 6 6 6 6 6 6 6 6 6 6 6 0 0.71 6 3.53 6 45 27 0.96 128 77 5.26 1.48 1.06 3.42 1.04 1.03

7 3 0.04 9 6 0.64 0.39 0.11 0.57 0.15 0.15 0.51 1.16

*p ,0.02 versus controls; †p ,0.02; ‡p ,0.05 versus FCH-IHD0. Data are expressed as mean 6 SD. Apo A1 5 apolipoprotein A1; Apo B 5 apolipoprotein B; FCH 5 familial combined hyperlipidemia; FFA 5 free fatty acids; HDL 5 high-density lipoprotein; IHD 5 ischemic heart disease; LDL 5 low-density-lipoprotein; log Lp(a) 5 log lipoprotein (a).

North American National Cholesterol Education Program7: phenotype IIa (LDL cholesterol $4.1 mmol/L and plasma triglycerides ,2.3 mmol/L), IIb (LDL cholesterol $4.1 mmol/L and triglycerides $2.3 mmol/L), and phenotype IV (LDL cholesterol ,4.1 mmol/L and triglycerides $2.3 mmol/L). Exclusion criteria were: secondary hyperlipidemia (renal or hepatic insufficiency, hypothyroidism), unstable angina, smoking habit, alcohol consumption .30 g/day, subscription to fitness or dietary programs, weight gain or loss $10% in the previous 3 months, and family history of diabetes or hypertension. Patients were divided into 2 subgroups: those with (FCH-IHD1) and those without IHD (FCH-IHD0). The FCH-IHD1 subgroup had been diagnosed on clinical criteria, electrocardiogram and enzymes indicating infarction at $3 months previously. The FCHIHD0 subgroup had none of these criteria and the resting electrocardiogram was normal. The control group of subjects (n 5 20) were selected among the clinical and laboratory staff. These were ostensibly healthy persons who volunteered to participate and were selected to match the patient group for age and body mass index. Those with plasma levels of triglycerides .2.3 mmol/L, antecedents of diabetes, hyperlipidemia, and premature arteriosclerosis were excluded from the study. All patients and volunteers were fully informed and the procedures in the study were within the guidelines of the ethics committee of Hospital Clinico of Valencia (Spain). All analytic procedures were conducted $1 month after the suspension of any pharmaceutical preparation that could affect lipoprotein and insulin metabolism. After an overnight fast, venous blood was drawn, and the plasma was obtained for analysis of total cholesterol and triglycerides, HDL cholesterol after precipitation with polyanions, VLDL cholesterol after preparative ultracentrifugation was measured by standard methods8 and LDL cholesterol was calculated as the difference from the plasma cholesterol measurement.

Apoprotein B and lipoprotein(a) were measured by immunoassay,8,9 free fatty acids by enzymatic colorimetry,10 and isoforms of LDL by polyacrylamide gel electrophoresis.11 Oral glucose load was done with 75 g of glucose following the recommendations of the World Health Organization, and determination of plasma glucose and insulin were measured by standard techniques.8 After an interval of 1 to 7 days, an intravenous tolerance test of glucose was performed with multiple blood samples taken for the measurement of glucose and insulin. The index of peripheral sensitivity to insulin was calculated by the minimal model of glucose metabolism modified by insulin administration.12 After 12 hours of fast and 15 minutes in the supine position, baseline blood samples were taken (215, 25, and 0 minutes). At time 0, a bolus of 300 mg of glucose per kg body weight was administered as a 50% glucose/saline solution over approximately 60 seconds. This was followed 20 minutes later by a rapid intravenous bolus (0.03 U/kg body weight) of insulin (Actrapid, Novo Nordisk Pharma, S.A., Bagsvaerd, Denmark). After baseline blood extractions, 26 more blood samples were taken (2, 3, 4, 5, 6, 8, 10, 12, 14, 16, 19, 22, 24, 25, 27, 30, 40, 50, 60, 70, 90, 100, 120, 140, 160, and 180 minutes). All analyses were done with the SPSS (version 6.1.3, SPSS Inc., 1995, Chicago, Illinois) statistical package. Results are expressed as mean 6 SD. Because of the sample size and because some of the variables do not fulfill the criteria for normality of distribution, the Mann-Whitney U test was used. For comparison of proportions we used Fisher’s exact test. The impact factor of the variables in IHD was quantified by discriminant analysis and logistic regression analysis. The general characteristics of the FCH-IHD1, FCH-IHD0, and control subject groups are presented in Table I. There were no significant differences with respect to age and body mass index. The waist:hip BRIEF REPORTS

1485

TABLE II Glucose Tolerance, Insulin, and Minimal Model Indexes in FCH Patients With and Without Ischemic Heart Disease and in Control Subjects FCH-IHD1 (n 5 14) Glucose 0 min (mmol/L) Glucose 120 min (mmol/L) AUC glucose (mmol/L/min) Insulin 0 min (pmol/L) Insulin 120 min (pmol/L) AUC insulin (pmol/L/min) Si (3 1024 mU/L/min) Sg (3 1022 min21)

5.7 10.1 1,268 153 1,412 131,251 1.2 0.9

6 6 6 6 6 6 6 6

0.9* 4.2*‡ 325*† 66*† 1050*† 91,938*‡ 0.6*† 1.1*†

FCH-IHD0 (n 5 19) 5.2 7.1 1,007 94 661 82,439 1.9 1.1

6 6 6 6 6 6 6 6

0.6* 2.2* 226* 37 388* 33,437* 1.0* 1.0*

Control (n 5 20) 5.0 5.6 813 86 361 59,255 2.9 2.3

6 6 6 6 6 6 6 6

0.4 1.0 145 24 257 24,294 1.2 0.6

*p ,0.02 versus controls; †p ,0.02; ‡p ,0.05 versus FCH-IHD0. Data are expressed as mean 6 SD. AUC 5 area under the curve; Glucose 0 5 basal (fasting) glucose; Glucose 120 5 plasma glucose at 120 minutes after a 75-g oral glucose load; Insulin 0 5 basal (fasting) insulin; Insulin 120 5 plasma insulin at 120 minutes after a 75-g oral glucose load; Si 5 index of peripheral sensitivity to insulin; Sg 5 index of glucose utilization independent of insulin; other abbreviations as in Table I.

ratio and blood pressure were higher in the FCHIHD1 group than in the FCH-IHD0 and control groups (p ,0.02). The concentrations of plasma lipids, apoprotein B, and LDL cholesterol were significantly higher in the group of FCH patients (p ,0.001) compared with controls, with the exception of the HDL cholesterol which was decreased in patients with FCH (Table I). No differences were observed in these parameters between the FCH-IHD1 and FCH-IHD0 groups. In the FCH-IHD1 group, the concentrations of logtransformed lipoprotein(a) and the percentage of small dense LDL particles were significantly elevated compared with the other 2 groups (p 5 0.05). In response to the oral glucose load, we observed a significant increase in the area under the curve of glucose in FCH patients compared with control subjects. In comparing the FCH-IHD1, FCH-IHD0, and control groups (Table II), the differences were also significant (1,268 6 325, 1,007 6 226, and 813 6 145 mmol/L/min, respectively; p 5 0.02). Concentrations of plasma insulin at baseline and 120 minutes after oral glucose load were significantly increased in patients with IHD compared with the other 2 groups. The differences between the FCH-IHD0 group and controls were significant with respect to insulin at 120 minutes after oral glucose load. The area under the curve for insulin was 131,251 6 91,938, 82,439 6 33,437, and 59,255 6 24,294 pmol/L/min in the FCHIHD1, FCH-IHD0, and control subjects, respectively (p ,0.04). The prevalence of abnormal glucose tolerance was 38.7%. In the FCH-IHD1 group, 7 patients had abnormal glucose tolerance (5 non–insulin-dependent diabetes and 2 glucose intolerance), in the FCHIHD0 group there were 5 (1 non–insulin-dependent diabetes and 4 glucose intolerance), and in the control group of subjects with similar age and body mass index we encountered 1 subject with glucose intolerance—a statistically significant difference of p ,0.01. Insulin resistance, measured as the index of peripheral sensitivity to insulin was 1.2 6 0.6 in the FCHIHD1 group, 1.9 6 1.0 in the FCH-IHD0 group, and 2.9 6 1.2 3 1024 mU/L/min in the controls (p ,0.02) (Table II). 1486 THE AMERICAN JOURNAL OF CARDIOLOGYT

VOL. 80

The discriminant analysis and the logistic regression analysis show a significant relation between the existence/presence of IHD and sensitivity to insulin ,2 3 1024 mU/L/min, diastolic pressure .90 mm Hg and lipoprotein(a) $20 mg/dl. The impact index of the sensitivity to insulin ,2 3 1024 mU/L/min for IHD was 3.37. •••

Several studies have postulated insulin resistance as one of the metabolic alterations implicated in the pathogenesis of FCH and an increase in concentrations of plasma free fatty acids and basal hyperinsulinemia have been described.2 These alterations are confirmed in our group of patients with FCH: elevated free fatty acids, insulinemia (fasting and at 120 minutes after oral glucose load), and increase in the area under the curve of glucose and of insulin. Clinical and experimental studies over the past decades demonstrate a relation between basal insulinemia and atherosclerosis,13 but what is disputable is whether this relation is directly with insulinemia, per se, or because of the accumulation of cardiovascular disease risk factors that appear in subjects with insulin resistance syndromes.14,15 In our study, we observed a significant increase (p ,0.02) in the plasma concentration of insulin at baseline at 120 minutes after oral glucose load, and an increase in the area under the curve of insulin, and a decrease in the sensitivity to insulin (p ,0.01) in the subgroup with FCH-IHD1 compared with the FCH-IHD0 and control subjects. An alteration related to insulin resistance is the presence of pattern B of LDL (small, dense particles) which has been observed with higher frequency in subjects with a higher degree of insulin resistance.16 In our study, there was an increased prevalence of pattern B (35%) in the FCH-IHD1 group of patients, but was slightly lower than that encountered by other investigators (40% to 50%).17 Although we have also observed higher levels of lipoprotein(a) in the FCHIHD1 group, this did not appear to be related to insulin resistance (p 5 0.90). The FCH-IHD1 patients had an increased amount of cardiovascular disease risk factors compared with the other groups. The discriminant and logistic correDECEMBER 1, 1997

lation analysis of all the variables in the FCH-IHD1 and the FCH-IHD0 groups, all nonsmokers, indicated that the IHD discriminant factors were: diastolic pressure $90 mm Hg, concentration of lipoprotein(a) $20 mg/dl, and insulin resistance (sensitivity to insulin ,2 3 1024 mU/L/min). These factors had a sensitivity of 78% and a specificity of 80% which, within the context of the small numbers of subjects studied, have a high prognostic value. In conclusion, FCH subjects with IHD have an index of peripheral sensitivity to insulin significantly lower (p <0.02) than that in patients with FCH without IHD and in control subjects. Insulin resistance appears to be a frequent finding in FCH and could explain, at least in part, its common association with other metabolic abnormalities and elevated IHD risk. 1. Goldstein JL, Hazzard WR, Schrott HG, Bierman EL, Motulsky AG. Hyper-

lipidemia in coronary heart disease. I. Lipid levels in 500 survivors of myocardial infarction. J Clin Invest 1973;52:1533–1543. 2. Castro-Cabezas M, de Bruin TWA, de Valk HW, Shoulders CC, Jansen H, Erkelens EW. Impaired fatty acid metabolism in familial combined hyperlipidemia: a mechanism associating hepatic apolipoprotein B overproduction and insulin resistance. J Clin Invest 1993;92:160 –168. 3. Genest JJ, Martin-Munley SS, McNamara JR, Ordovas JM, Jenner J, Myers RH, Silberman SR, Wilson PWF, Salem DN, Schaeffer J. Familial lipoprotein disorders in patients with premature coronary artery disease. Circulation 1992; 85:2025–2033. 4. Grundy SM, Chait A, Brunzell JD. Familial combined hyperlipidemia workshop. Arteriosclerosis 1987;7:203–207. 5. Hunt SC, Hopkins PN, Stults BM, Kuida H, Ramirez ME, Lalouel JM,

Williams RR. Apolipoprotein, low density lipoprotein subfraction and insulin association in familial combined hyperlipidemia. Arteriosclerosis 1989;9:335– 344. 6. Kwiterovich PO Jr, Coresh J, Bachorick PS. Prevalence of hyperapobetalipoproteinemia and other lipoprotein phenotypes in men (aged #50) and women (#60 years) with coronary artery disease. Am J Cardiol 1993;71:640 – 645. 7. Report of the National Cholesterol Education Program. Expert panel on detection, evaluation and treatment of high blood cholesterol in adults. Arch Intern Med 1988;18:36 –39. 8. Ascaso JF, Sales J, Merchante A, Real J, Lorente R, Martinez-Valls J, Carmena R. Influence of obesity on plasma lipoproteins, glycaemia and insulinaemia in patients with familial combined hyperlipidaemia. Int J Obes Relat Metab Disord 1997;21:360 –366. 9. Labeur C, Michiels G, Burg J, Usher DC, Rosseneau M. Lipoprotein (a) quantified by an enzyme-linked immunosorbent assay with monoclonal antibodies. Clin Chem 1989;35:1380 –1384. 10. Milies J, Glasscock R, Aikens J, Gerich J, Haymond M. A microfluorimetric method for the determination of free fatty acids in plasma. J Lipid Res 1983;24: 96 –99. 11. Nichols AV, Krauss RM, Musliner TA. Nondenaturaring polyacrylamide gradient gel electrophoresis. In: Segrest JP, Albers JJ, eds. Methods in Enzymology. Plasma lipoprotein. Preparation, Structure and Molecular Biology. Orlando: Academic Press, 1986:417– 431. 12. Pacini C, Bergman RN. MINMOD: a computer program to calculate insulin sensitivity and pancreatic responsivity from the frequently sampled intravenous glucose tolerance test. Comput Methods Programs Biomed 1986;23:113–122. 13. Stout RW. Insulin and atherosclerosis. Dev Cardiovasc Med 1992;125:165– 201. 14. Raitakari OT, Porkka KVK, Rom ¨ enaa T, Knip M, Uhari M, Akerblom HK, Viikari JSA. The role of insulin in clustering of serum lipids and blood pressure in children and adolescents. The Cardiovascular Risk in Young Finns Study. Diabetologia 1995;38:1042–1050. 15. Despre´s JP, Lamarche B, Maurie`ge P, Cantin B, Dagenais GR, Moorjani S, Lupien PJ. Hyperinsulinemia as an independent risk factor for ischemic heart disease. N Engl J Med 1996;334:952–957. 16. Haffner SM, Mykka¨nen L, Robbins D, Valdez R, Miettinen H, Howard BV, Stern MS, Bowsher R. A preponderance of small dense LDL is associated with specific insulin, proinsulin and the components of the insulin resistance syndrome in non diabetic subjects. Diabetologia 1995;38:1328 –1336. 17. Krauss RM. Dense low-density lipoprotein and coronary heart disease. Am J Cardiol 1995;75:53B–57B.

Antitachycardia Pacing in Patients With Implantable Cardioverter-Defibrillators: Inverse Circadian Variation of Therapy Success and Acceleration Roland Fries, MD, Armin Heisel, MD, Nikolaus Nikoloudakis, MD, Jens Jung, Hans-Joachim Scha ¨ fers, MD, and Hermann Schieffer, MD n increased morning frequency of spontaneous ventricular tachyarrhythmias has been A demonstrated in patients with an implantable cardioverter-defibrillator (ICD).1,2 Recently, a corresponding morning peak in defibrillation energy requirements and in the failed first shock frequency has been reported.3 Whether there has also been a circadian variation in success and failure of antitachycardia pacing has been unknown until now. We evaluated, in consecutive patients with an ICD, the circadian variation of the antitachycardia pacing termination and acceleration rates during long-term follow-up. From the Innere Medizin III, Kardiologie/Angiologie, and Thorax und Herz-Gefa¨ßchirurgie, Universita¨tskliniken des Saarlandes, Homburg, Germany. Dr. Fries’ address is: Innere Medizin III, Kardiologie/Angiologie, Geb. 40, Universita¨tskliniken des Saarlandes, D-66421 Homburg/Saar, Germany. Manuscript received March 5, 1997; revised manuscript received and accepted August 29, 1997. ©1997 by Excerpta Medica, Inc. All rights reserved.

MD,

•••

We analyzed the results of antitachycardia pacing in a consecutive series of 138 patients with life-threatening ventricular tachyarrhythmias undergoing ICD implantation in our institution. In 57 patients, antitachycardia pacing was programmed; 29 of them experienced spontaneous ventricular tachycardias (VTs) during follow-up, which was treated by antitachycardia pacing. These patients represent our final study population. The mean age of these patients was 61 6 9 years; 27 patients were men; coronary artery disease was present in 26 patients; and idiopathic dilated cardiomyopathy in 3 patients. The mean left ventricular ejection fraction was 33 6 11%. The indications for ICD implantation were sustained monomorphic VTs unresponsive to antiarrhythmic drug therapy in 11 patients. In 18 patients with VTs, an ICD was used as first-line therapy because of documented VT degeneration into ventricular fibrillation. Nine patients (31%) were receiving b blockers, 22 patients (76%) 0002-9149/97/$17.00 PII S0002-9149(97)00731-5

1487