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Objectives: We studied the influence of rate control or rhythm control in patients with persistent atrial fibrillation (AF) on quality of life (QoL).Background: Atrial fibrillation may cause symptoms like fatigue and dyspnea. This can impair QoL. Treatment of AF with either rate or rhythm control may influence QoL.Method: Quality of life was assessed in patients included in the Rate Control Versus Electrical Cardioversion for Persistent Atrial Fibrillation (RACE) study (rate vs. rhythm control in persistent AF). Rate control patients (n = 175) were given negative chronotropic drugs and oral anticoagulation. Rhythm control patients (n = 177) received serial electrocardioversion, antiarrhythmic drugs, and oral anticoagulation, as needed. Quality of life was studied using the Short Form (SF)-36 health survey questionnaire at baseline, one year, and the end of the study (after 2 to 3 years of follow-up). At baseline, QoL was compared with that of healthy control subjects. Patient characteristics related to QoL changes were determined.Results: Mean follow-up was 2.3 years. At baseline, QoL was lower in patients than in age-matched healthy controls. At study end, under rate control, three subscales of the SF-36 improved. Under rhythm control, no significant changes occurred compared with baseline. At study end, QoL was comparable between both groups. The presence of complaints of AF at baseline, a short duration of AF, and the presence of sinus rhythm (SR) at the end of follow-up, rather than the assigned strategy, were associated with QoL improvement.Conclusions: Quality of life is impaired in patients with AF compared with healthy controls. Treatment strategy does not affect QoL. Patients with complaints related to AF, however, may benefit from rhythm control if SR can be maintained. [ABSTRACT FROM AUTHOR]

Background and Purpose: It has been suggested that a higher procedure volume is associated with less complications after hip arthroplasty. In order to investigate the incidence of serious negative outcomes and a possible association with procedure volume, we performed a retrospective nationwide cohort study on total hip replacements in all Dutch hospitals., Methods: All total hip replacements (n = 50,080) that were identified as primary intervention in all general and university medical centers between January 1, 2002 and October 1, 2004 were included. Primary endpoints of follow-up were mortality and complications during admission, and re-admission within 3 months due to complications. Variables that were assessed as potential risk factor were age, sex, duration of (preoperative) admission, specific diagnosis, acute/non-planned admission, co-morbidity, and hospital procedure volume., Results: Age, sex, and comorbidity were associated with complications and mortality. Additionally, acute admission was a risk factor for mortality but not for complications. There was no linear trend indicating that decreasing volume led to an increasing number of complications, and no statistically sginificant effect for mortality was found., Interpretation: After adjustment for several risk factors, we found that the hospitals performing most hip procedures every year had fewer complications during index admission, but that they did not have a lower mortality than groups performing fewer procedures. The lack of a linear trend may be explained by the fact that almost all Dutch hospitals perform a high number of hip arthroplasties each year.

Objectives: This study sought to investigate whether prolongation of the heart rate-corrected QT (QTc) interval is a risk factor for sudden cardiac death in the general population., Background: In developed countries, sudden cardiac death is a major cause of cardiovascular mortality. Prolongation of the QTc interval has been associated with ventricular arrhythmias, but in most population-based studies no consistent association was found between QTc prolongation and total or cardiovascular mortality. Only very few of these studies specifically addressed sudden cardiac death., Methods: This study was conducted as part of the Rotterdam Study, a prospective population-based cohort study that comprises 3,105 men and 4,878 women aged 55 years and older. The QTc interval on the electrocardiogram was determined during the baseline visit (1990 to 1993) and the first follow-up examination (1993 to 1995). The association between a prolonged QTc interval and sudden cardiac death was estimated using Cox proportional hazards analysis., Results: During an average follow-up period of 6.7 years (standard deviation, 2.3 years) 125 patients died of sudden cardiac death. An abnormally prolonged QTc interval (>450 ms in men, >470 ms in women) was associated with a three-fold increased risk of sudden cardiac death (hazard ratio, 2.5; 95% confidence interval, 1.3 to 4.7), after adjustment for age, gender, body mass index, hypertension, cholesterol/high-density lipoprotein ratio, diabetes mellitus, myocardial infarction, heart failure, and heart rate. In patients with an age below the median of 68 years, the corresponding relative risk was 8.0 (95% confidence interval 2.1 to 31.3)., Conclusions: Abnormal QTc prolongation on the electrocardiogram should be viewed as an independent risk factor for sudden cardiac death.

Aims: To assess the association between the use of non-cardiac QTc-prolonging drugs and the risk of sudden cardiac death., Methods and Results: A population-based case-control study was performed in the Integrated Primary Care Information (IPCI) project, a longitudinal observational database with complete medical records from more than 500,000 persons. All deaths between 1 January 1995 and 1 September 2003 were reviewed. Sudden cardiac death was classified based on the time between onset of cardiovascular symptoms and death. For each case, up to 10 random controls were matched for age, gender, date of sudden death, and general practice. The exposure of interest was the use of non-cardiac QTc-prolonging drugs. Exposure at the index date was categorized into three mutually exclusive groups of current use, past use, and non-use. The study population comprised 775 cases of sudden cardiac death and 6297 matched controls. Current use of any non-cardiac QTc-prolonging drug was associated with a significantly increased risk of sudden cardiac death (adjusted OR: 2.7; 95% CI: 1.6-4.7). The risk of death was highest in women and in recent starters., Conclusion: The use of non-cardiac QTc-prolonging drugs in a general population is associated with an increased risk of sudden cardiac death.

Atrial fibrillation (AF) is the most common sustained rhythm disorder observed in clinical practice and predominantly associated with cardiovascular disorders such as coronary heart disease and hypertension. However, several classes of drugs may induce AF in patients without apparent heart disease or may precipitate the onset of AF in patients with preexisting heart disease. We reviewed the literature on drug-induced AF, using the PubMed/Medline and Micromedex databases and lateral references. Successively, we discuss the potential role in the onset of AF of cardiovascular drugs, respiratory system drugs, cytostatics, central nervous system drugs, genitourinary system drugs, and some miscellaneous agents. Drug-induced AF may play a role in only a minority of the patients presenting with AF. Nevertheless, it is important to recognize drugs or other agents as a potential cause, especially in the elderly, because increasing age is associated with multiple drug use and a high incidence of AF. This may contribute to timely diagnosis and management of drug-induced AF.

Aims To evaluate costs between a rate and rhythm control strategy in persistent atrial fibrillation. Methods and results In a prospective substudy of RACE (Rate control versus electrical cardioversion for persistent atrial fibrillation) in 428 of the total 522 patients (206 rate control and 222 rhythm control), a cost-minimisation and cost-effectiveness analysis was performed to assess cost-effectiveness of the treatment strategies. After a mean follow-up of 2.3+/-0.6 years, the primary endpoint (cardiovascular morbidity and mortality) occurred in 17.5% (36/202) of the rate control patients and in 21.2% (47/222) of the rhythm control patients. Mean costs per patient under rate control were euro 7386 and euro 8284 under rhythm control. Cost-effectiveness analysis showed that per avoided endpoint under rate control, the cost savings were euro 24944. Under rhythm control, more costs were generated due to electrical cardioversions, hospital admissions and anti-arrhythmic medication. Costs were higher in older patients, patients with underlying heart disease, those who reached a primary endpoint and women. Heart rhythm at the end of study, did not influence costs. Conclusions Rate control is more cost-effective than rhythm control for treatment of persistent atrial fibrillation. Underlying heart disease but not heart rhythm largely accounts for costs., (Copyright 2004 Elsevier Ltd)

Background: Persistent atrial fibrillation (AF) does not terminate spontaneously and may cause left ventricular dysfunction and thromboembolic complications. For restoration of sinus rhythm electrical cardioversion (ECV) is most effective. However, AF frequently relapses, necessitating re-ECV and institution of potentially harmful antiarrhythmic drugs. If AF is accepted, rate control and prevention of thromboembolic complications using negative chronotropic drugs and warfarin is pursued. It is our hypothesis that rate control therapy is not inferior to ECV therapy in preventing morbidity and mortality., Methods: RACE (RAte Control versus Electrical cardioversion for atrial fibrillation) is a randomised comparison of serial ECV therapy (repeat ECV as soon as possible after a relapse and institution of an antiarrhythmic drug: sotalol, class IC drug and amiodarone) and rate control therapy (resting heart rate <100 bpm using digitalis, calcium channel blockers and/or β-blockers) in patients with persistent AF. Morbidity (heart failure, side effects of drugs, thromboembolic complications, bleeding and pacemaker implantation), mortality, quality of life and cost-effectiveness are primary and secondary endpoints. Included are patients with a recurrence of persistent AF, present episode <1 year and a maximum of two previous successful ECVs during the last two years. This study is a multicentre study in 31 centres throughout the Netherlands. All 520 patients have now been included. Follow-up is two years. The results are expected this year.

Objectives: To describe morbidity and mortality in patients waiting for coronary artery bypass graft (CABG) surgery and to assess determinants for the occurrence of these complications., Methods: A prospective cohort study was carried out in a tertiary referral general teaching hospital. Three hundred and sixty consecutive patients with a priority of routine or urgent who were accepted for CABG or CABG with additional valve surgery were evaluated. Follow-up began from the moment of acceptance until the procedure took place for cardiac death, myocardial infarction and unstable angina requiring hospital admission., Results: The median (25-75th percentile) waiting time in the two priority groups was 100 (79-119) days for the routine group and 69 (38-91) days for the urgent group. Overall, eight patients died, seven suffered a myocardial infarction, and 33 episodes of unstable angina requiring immediate hospitalization occurred. The majority of events took place during the first 30 days on the waiting list. Unstable angina less than 3 months before acceptance was identified as an independent predictor (hazard ratio 2.5, 95% confidence interval 1.2-5.1) for complications during the wait. The prognostic value of smoking and familial cardiovascular disease was found to vary depending on the priority assigned to the patient., Conclusions: Complications occur relatively early during the time on the waiting list. If complications in coronary heart disease cannot be predicted more accurately, the only way to diminish the complication rate is drastic reduction of waiting times.

Objectives: We sought to investigate the effect of angiotensin-converting enzyme (ACE) inhibition <9 h after myocardial infarction (MI) on left ventricular (LV) dilation in patients receiving thrombolysis., Background: The ACE inhibitors reduce mortality after MI. Attenuation of LV dilation has been suggested as an important mechanism., Methods: The data of 845 patients with three-month echocardiographic follow-up after MI were combined from three randomized, double-blind, placebo-controlled studies. The criteria for these studies included: 1) thrombolytic therapy; 2) ACE inhibition within 6 to 9 h; and 3) evaluation of LV dilation as the primary objective., Results: The ACE inhibitor was started 3.2+/-1.7 h after the patients' first (mainly, 85%) anterior MI. After three months, LV dilation was not significantly attenuated by very early treatment with an ACE inhibitor. The diastolic volume index was attenuated by 0.5 ml/m2 (95% confidence interval [CI] -1.5 to 2.5, p = 0.61), and the systolic volume index by 0.5 ml/m2 (95% CI -1.0 to 1.9, p = 0.50). Subgroup analysis demonstrated that LV dilation was significantly attenuated by ACE inhibitor treatment for patients in whom reperfusion failed. In contrast, LV dilation was almost unaffected by ACE inhibitor treatment in successfully reperfused patients., Conclusions: We could not demonstrate attenuation of LV dilation in patients receiving thrombolysis by ACE inhibitor treatment within 6 to 9 h after MI. We speculate that very early treatment with an ACE inhibitor has a beneficial effect on LV remodeling only in patients in whom reperfusion failed. Other mechanisms may be responsible for the beneficial effects of ACE inhibitors in successfully reperfused patients after MI.

Objective: To describe the causes and circumstances of death regarding patients who died in 1994 and 1995 while on a waiting list for cardiac surgery in the Netherlands., Design: Retrospective multicentre case study., Setting: 11 Dutch cardiac surgery centres., Patients: All patients reported as dying while on the waiting list for cardiac surgery in 1994 and 1995., Main Outcome Measures: Classification of death by an independent adjudication committee into "erroneously reported", "waiting list related" or "not waiting list related". Death was judged as "waiting list related" if the clinical course would have been substantially different if there had been unrestricted surgical capacity., Results: 138 and 129 deaths were reported in 1994 and 1995, respectively. 43 deaths (16%) were considered as erroneously reported. 181 of the remaining 224 cases were adjudicated as waiting list related. Median time from acceptance for surgery to death was 35 days (interquartile range 14-75 days). 97 of 181 deaths occurred within six weeks following addition to the waiting list. The estimated incidence of death ranged from 1.33 per 1000 patient-weeks during weeks 2-4 to 0.68 per 1000 patient-weeks after 12 weeks., Conclusions: The causes and circumstances of death are waiting list related for approximately 100 patients per year in the Netherlands. At least half of the deaths may occur within the first six weeks. Waiting lists for cardiac surgery engender high risks for the patients involved.

Aims: To study the absorption kinetics of sotalol following administration of different formulations. A formulation which results in fast absorption might be useful in the episodic treatment of paroxysmal supraventricular tachycardia (SVT), atrial fibrillation (Afib) or atrial flutter (Afl)., Methods: In an open randomized crossover study seven healthy male volunteers were given an intravenous infusion of 20 mg sotalol, for assessing the absolute bioavailability, an oral solution containing 80 mg sotalol, an oral solution containing both 80 mg sotalol and 20 mg cisapride and an 80 mg sotalol tablet, which was taken sublingually., Results: The addition of cisapride decreased the time at which maximum serum concentrations were reached (tmax) from 2.79 (1.85-4.34) h to 1.16 (0.68-2.30) h (P=0.009) [95% CI: -2.59, -0.55] and increased the absorption rate constant (ka) from 0.49 (0.31-0.69) h(-1) to 1.26 (0.52-5.61) h(-1) (P=0.017). The absolute bioavailability of sotalol was reduced by cisapride from 1.00+/-0.15 to 0.70+/-0.26 (P=0.006), while maximum serum concentrations of both oral solutions were not significantly different. Compared with the sublingually administered tablet with a median tmax of 2.12 (0.89-3.28) h, the sotalol/cisapride oral solution gave a smaller tmax (p=0.009) [95% CI: -1.64, -0.36]. The ka of the sotalol/cisapride solution was significantly (P=0.010) larger than the ka of 0.56 (0.33-0.75) h(-1) found after sublingual administration of the tablet., Conclusions: The sotalol/cisapride oral solution might be suitable for the episodic treatment of SVT, Afib or Afl.

Objectives: This study was conducted to test the hypothesis that angiotensin-converting enzyme (ACE) inhibition reduces myocardial ischemia and related events after myocardial infarction (MI)., Background: The oxygen demand/supply ratio of the myocardium is influenced by angiotensin II as a result of its arterial vasoconstrictive and inotropic effects and through its interaction with the sympathetic nervous system., Methods: We studied 244 patients who had been included in a double-blind, randomized, placebo-controlled, post-MI, ACE inhibition intervention study (Captopril and Thrombolysis Study [CATS]). All patients underwent exercise testing before and 3 and 12 months after hospital discharge. After 1-year double-blind treatment, all patients continued receiving single-blind placebo for 1 month., Results: Total exercise time increased in both groups after 3 months (placebo: +86 +/- 13 s; captopril: +69 +/- 12 s, p = 0.8 between groups) and increased further after 1 year (placebo: +13 +/- 11 s; captopril: +33 +/- 13 s, p = 0.7 between groups). There were also no differences in mean ST segment depression. During the 12 months, significantly fewer ischemia-related events occurred in the captopril group (82 vs. 52, p = 0.015). This difference was found between 3 and 12 months but not during the first 3 months. After withdrawal from double-blind medication, nine ischemic events were reported in teh captopril group compared with one in the placebo group (p = 0.006 between groups)., Conclusions: The present data show that captopril may reduce the incidence of ischemia-related events after MI, which becomes apparent after 3 months. However, no anti-ischemic effect was observed during exercise testing. After withdrawal from ACE inhibition, a high incidence of clinical events occurred, suggesting a rebound phenomenon.

Aims: Angiographic studies on the natural course of both focal and diffuse coronary atherosclerosis have not been performed before, but can both be assessed by quantitative coronary angiography. The objective of this study was to describe the natural course of focal and diffuse coronary atherosclerosis over time., Methods and Results: In 129 patients with mild coronary artery disease, but not on lipid-lowering medication, three coronary angiograms were made each 2 years apart. Nine hundred and sixty five angiographically diseased and non-diseased segments were analysed by quantitative coronary angiography. Mean lumen diameter and minimal lumen diameter were used as measures of diffuse and focal coronary atherosclerosis. Mean lumen diameter and minimum lumen diameter decreased by 0.02 and 0.03 mm per year. The rate of progression was similar in the angiographically non-diseased, as in the mildly and moderately diseased segments. Progression of diffuse coronary atherosclerosis was largest in severely stenosed lesions (percentage diameter stenosis > or = 50%) and in the right coronary artery with a loss of 0.19 mm and 0.16 mm in mean lumen diameter. Progression of focal disease was most prominent in new and mild lesions and the right coronary artery, with a decrease in minimum lumen diameter of 0.34 mm and 0.22 mm. In most subgroups, progression occurred gradually over time. On a per segment level, progression and the occurrence of new lesions occurred in 4.4% and 4.2%. Regression and disappearance of a lesions was found in 2.3% and 1.9%. On a per patient level, 36% were progressors, 12% had a mixed response, 36% were stable, and 16% were regressors., Conclusion: Diffuse and focal coronary atherosclerosis progressed at the same rate in the first and second 2 years in stenosed and non-stenosed segments. The rate of coronary atherosclerosis progression was small, but was higher for focal than for diffuse disease. A minority of lesions progressed and spontaneous regression was rare.

Background: Left ventricular dilation after acute myocardial infarction (MI) is mainly determined by infarct size. In addition, this detrimental structural adaptation seems to be augmented in patients with the ACE DD genotype. The ACE DD genotype is associated with increased ACE activity. The aim of the present study was to evaluate whether ACE activity per se may carry prognostic significance for subsequent left ventricular dilation as assessed by echocardiography during 1-year follow-up after acute MI., Methods and Results: Left ventricular end-systolic and end-diastolic volume indexes were assessed by two-dimensional echocardiography. In 102 consecutive patients, plasma ACE activity was determined 3.7 +/- 0.1 hours after the onset of MI. In 64 of these patients, left ventricular volume indexes obtained at baseline and 1 year after MI were used for the present analysis. Patients were divided ino a group having low ACE activity (< or = IU/L, n = 15) and a group having high ACE activity (> 12 IU/L, n = 49). Infarct size was a significant predictor of the increase in left ventricular volume indexes (P = .0001) in these patients. Multivariate regression analysis, after correction for infarct size, demonstrated that elevated plasma ACE activity is a significant predictor of the increase in left ventricular end-diastolic and end-systolic volume indexes (P = .0006 and P = .02, respectively) 1 year after MI., Conclusions: Elevated plasma ACE activity determined soon after the onset of MI may be a significant predictor of the development of left ventricular dilation and may identify patients at risk.

Objective: To evaluate exercise capacity of patients with chronic atrial fibrillation in whom His bundle ablation followed by ventricular rate response pacing (VVIR) was carried out because of drug refractoriness., Design: Prospective study., Patients: 25 consecutive patients, all with chronic symptomatic drug refractory atrial fibrillation, underwent His bundle ablation. Before this intervention all patients were on antiarrhythmic drugs to attain acceptable heart rate control and to relief symptoms., Main Outcome Measures: Exercise capacity, including measurements of VO2, was examined before and after a mean interval of seven months following His bundle ablation., Results: Exercise capacity after His bundle ablation increased from a mean of 109 (SD 49) W to 118 (46) W (P < 0.002), but VO2 at peak exercise did not change significantly. Maximum exercise capacity was achieved with a significantly lower maximum driven heart rate than the spontaneous heart rate before ablation., Conclusions: Exercise capacity of patients who underwent His bundle ablation followed by VVIR pacing remained unchanged or improved during a mean follow up of seven months. Larger patient populations with longer follow up are necessary to examine determinants of improved exercise capacity.

Objectives: In this study we sought to investigate the effect of intervention with captopril within 6 h of the onset of myocardial infarction on left ventricular volume and clinical symptoms of heart failure in relation to infarct size during a 1-year follow-up period., Background: Remodeling of the heart starts in the early phase of myocardial infarction and is associated with an adverse prognosis. Angiotensin-converting enzyme inhibition started in the subacute or late phase after myocardial infarction has been shown to improve prognosis., Methods: In the Captopril and Thrombolysis Study, 298 patients with a first anterior myocardial infarction treated with intravenous streptokinase were randomized to receive either oral captopril (25 mg three times a day) or placebo. The left ventricular volume index was assessed by two-dimensional echocardiography within 24 h, on days 3, 10 and 90 and after 1 year., Results: A small but significant increase in left ventricular volume indexes was observed after 12 months. Using a random coefficient model, no significant treatment effect on left ventricular volumes could be detected. In contrast, when survival models were used, the occurrence of left ventricular dilation was significatnly lower in captopril-treated patients (p = 0.018). In addition, the incidence of heart failure was lower in the captopril group (p < 0.03). This effect appeared early and was most obvious in patients with a medium-sized infarct (p = 0.04) and was not present in large infarcts., Conclusions: Very early treatment with captopril after myocardial infarction significantly reduces the occurrence of early dilation and the progression to heart failure. These data underscore the importance of early treatment. Furthermore, patients with intermediate infarct size benefit the most from this treatment strategy.

Objective: To estimate the costs and effects of preventive treatment with captopril compared with the current treatment policy in patients with asymptomatic left ventricular dysfunction after a myocardial infarction., Methods: Estimates of effects are based on the results of the SAVE trial. Costs are estimated on the basis of current treatment patterns in four Dutch hospitals. All knowledge is incorporated in a mathematical model extrapolating the SAVE results to 20 years., Results and Conclusions: Captopril treatment is expected to increase survival at certain costs. The average additional costs per patient are estimated at DF1 2,491 in 4 years and at DF1 8,723 in 20 years of treatment. Costs per additional survivor after 4 years are estimated at DF1 69,126. After extrapolation of the results of the SAVE trial to 20 years, costs per life-year gained can be estimated at DF1 15,799. From univariate sensitivity analysis it appears that the results are highly sensitive for the costs of treatment with captopril and the occurrence and prevention of clinical heart failure. Varying all estimates randomly between upper and lower limits-in 5,000 simulations-an estimate of costs per life-year gained of DF1 15,729 is made for 20 years of treatment, with 95% of all estimates between DF10 and DF1 50, 000. On a national level, undiscounted costs are expected to increase up to approximately DF1 42 million annually during the first 40 years after introduction of the preventative strategy.

Background: In patients with postinfarction sustained ventricular tachycardia showing one or more antiarrhythmic drug failures, the question is how long to proceed with new drug trials before deciding to perform map-guided arrhythmia surgery. Although the techniques of this surgery developed rapidly in the early 1980s, this therapy may be offset by damage to residual left ventricular function. However, surgery has been shown to be very effective in selected groups of patients., Methods: A randomized study was carried out in patients with postinfarction ventricular tachycardia and eligible for arrhythmia surgery based on residual left ventricular function. Therapy failure was defined by the occurrence of the following events: spontaneous recurrence of ventricular tachycardia or ventricular fibrillation, sudden cardiac death, inducibility of sustained ventricular tachycardia or ventricular fibrillation with programmed stimulation of the heart, symptomatic non-sustained ventricular tachycardia requiring therapy or side-effects of antiarrhythmic drugs requiring withdrawal. In the drug limb, failure of the first antiarrhythmic drug was accepted but failure of a second and different drug was regarded as true therapy failure., Results: After randomization, antiarrhythmic drug therapy was administered in 33 patients, and 30 patients underwent surgery. Neither group differed in baseline characteristics, and the mean number of drug failures before randomization was 2.7. The Kaplan-Meier therapeutic failure of antiarrhythmic drugs was 39 +/- 11%, 42 +/- 11% and 51 +/- 18% at 0.5-, 1- and 4-year follow-up, respectively, whereas the therapeutic failure of cardiac surgery was 37 +/- 11%, 37 +/- 11% and 50 +/- 20% at 0.5, 1 and 4 years, respectively, showing no statistical difference. The 1- and 4-year Kaplan-Meier survival of the antiarrhythmic drug-treated group was 91 +/- 6% and 78 +/- 15%, respectively, and of the surgical group 92 +/- 6% and 59 +/- 20%, respectively, and did not differ between either group. However, the relative risk for total cardiac death was higher in the surgical limb than in the drug limb (relative risk 2.2, CI 0.68-7.48)., Conclusion: This study demonstrated no difference between the therapeutic result of continuation of two different antiarrhythmic drugs and that of arrhythmia surgery. Despite the small number of patients studied, it is recommended that drug therapy should continue as long as this regimen is tolerated by the patient. When true drug refractoriness or side-effects of drugs arise, arrhythmia surgery offers a valuable alternative. However, when additional reasons for cardiac surgery exist, arrhythmia surgery should be undertaken earlier and may become the first choice of treatment of postinfarction ventricular tachycardia.

Background: Progressive left ventricular dilatation after myocardial infarction is associated with a high mortality rate, the majority of which is arrhythmogenic in origin. The underlying mechanism of this relation remains unknown. It has been suggested, however, that left ventricular dilatation is accompanied by changes in repolarization characteristics that may facilitate the occurrence of life-threatening ventricular arrhythmias., Methods and Results: We examined 62-lead body surface QRST integral maps during sinus rhythm in 78 patients at 349 +/- 141 days after thrombolysis for a first anterior myocardial infarction. Visual map analysis was directed at discriminating dipolar (uniform repolarization) from nondipolar (nonuniform repolarization) patterns. In addition, the nondipolar content of each map was assessed quantitatively with the use of eigenvector analysis. Nondipolar map patterns were present in almost one third of the patients (32%). Left ventricular end-systolic and end-diastolic volumes were assessed echocardiographically before discharge and after 3 and 12 months with the use of the modified biplane Simpson rule. The increase in left ventricular end-systolic volume 1 year after myocardial infarction was more pronounced in patients with nondipolar QRST integral map patterns (14.47 +/- 14.10 versus 4.22 +/- 8.44 mL/m2, P = .017). In patients with an increase in end-systolic volume of more than 16 mL/m2 (upper quartile), the prevalence of nondipolar maps was 89% compared with 29% in patients with dilatation of less than 16 mL/m2. In addition, the nondipolar content of maps in patients in the upper quartile was significantly increased compared with the lower quartiles (49 +/- 14% versus 37 +/- 12%, P = .013). Logistic regression analysis revealed that an end-systolic volume of more than 42 mL/m2 after 1 year contributed independently to the appearance of nondipolar maps. Patients with high-grade ventricular arrhythmias showed a higher nondipolar content (49 +/- 17% versus 39 +/- 10%, P = .013). QTc dispersion did not discriminate between patients with and those without high-grade ventricular arrhythmias. Also, the association between left ventricular remodeling and nondipolar map patterns was confirmed prospectively in an additional group of 15 patients., Conclusions: Nondipolar map patterns are present in 32% of patients after thrombolysis for a first anterior myocardial infarction and are associated with increased left ventricular dilatation. These data support the hypothesis that left ventricular dilatation after myocardial infarction leads to changes in repolarization characteristics that may facilitate the occurrence of life-threatening ventricular arrhythmias.

Objectives: This study sought to determine whether patients who are homozygous for the deletion (D)-type allele of the angiotensin-converting enzyme gene display augmented ventricular dilation after myocardial infarction., Background: Recent evidence suggests that the deletion-type allele of the angiotensin-converting enzyme gene (DD genotype) is associated with an increased prevalence of myocardial infarction and myocardial hypertrophy. However, it is unknown whether the DD genotype is associated with adverse cardiac remodeling. To address this question we determined the genotype in patients enrolled in the Captopril and Thrombolysis Study (CATS), a prospective trial in which patients received either captopril or placebo during and after thrombolysis for a first anterior myocardial infarction., Methods: Cardiac volume was determined by echocardiography immediately after thrombolysis and at 1-year follow-up. The genotype for the angiotensin-converting enzyme was determined in 96 patients. Norepinephrine levels were assessed during and immediately after thrombolysis., Results: Immediately after thrombolysis, cardiac volume did not differ between genotype groups. However, at 1-year follow-up, both end-systolic and end-diastolic left ventricular volumes were significantly greater in the DD-genotype group. Norepinephrine increased to higher levels in the DD-genotype group that received placebo therapy. Captopril treatment effectively blunted both the norepinephrine increase and cardiac dilation in the DD-genotype group., Conclusions: This exploratory study suggests that homozygosity for the angiotensin-converting enzyme deletion-type allele is associated with augmented neurohumoral activation as well as augmented cardiac dilation after an acute anterior myocardial infarction, an effect that may be susceptible to angiotensin-converting enzyme inhibition.

Background: Reduced heart rate variability has been identified as an important prognostic factor after myocardial infarction. This factor is thought to reflect an imbalance between sympathetic and parasympathetic activity, which may lead to unfavourable loading conditions and thus promote left ventricular dilatation., Patients and Methods: 298 patients in a multicentre clinical trial were randomised to captopril or placebo after a first anterior myocardial infarction. All patients were treated with streptokinase before randomisation. In the present substudy full data including heart rate variability and echocardiographic measurements were available from 80 patients. Patients were divided into two groups: those with a reduced (< or = 25) heart rate variability index and those with normal heart rate variability index (> 25). Heart rate variability was evaluated by 24 h Holter monitoring before discharge. Left ventricular volumes were assessed by echocardiography before discharge and three and 12 months after myocardial infarction. Extent of myocardial injury, severity of coronary artery disease, functional class, haemodynamic variables, and medication were also considered as possible determinants of left ventricular dilatation., Results: Before discharge end systolic and end diastolic volumes were not different in the two groups. After 12 months in patients with a reduced heart rate variability, end systolic volume (mean (SD)) had increased by 6 (14) ml/m2 (P = 0.043) and end diastolic volume had increased by 8 (17) ml/m2 (P = 0.024). Left ventricular volumes were unchanged in patients with a normal heart rate variability. Also, patients with left ventricular dilatation had a larger enzymatic infarct size and higher heart rates and rate-pressure products. A reduced heart rate variability index before discharge was an independent risk factor for left ventricular dilatation during follow up. Measurement of heart rate variability after three months had no predictive value for this event., Conclusion: Assessment of the heart rate variability index before discharge, but not at three months, gave important additional information for identifying patients at risk of left ventricular dilatation.

Objectives: This study examined the performance of the 62-lead body surface electrocardiogram (ECG) in identifying the site of origin of ventricular tachycardia in patients with a previous myocardial infarction., Background: Because the accuracy of ECG localization of ventricular tachycardia using standard 12-lead recordings is restricted to the identification of rather large ventricular areas, application of multiple torso lead recordings may augment the resolving power of the surface ECG and result in more discrete localization of arrhythmogenic foci., Methods: Thirty-two patients were selected for electrophysiologically guided ablative therapy for drug-resistant postinfarction ventricular tachycardia. In these patients, QRS integral maps of distinct monomorphic ventricular tachycardia configurations were correlated with a previously generated infarct-specific reference data base of paced QRS integral maps. Each paced pattern in the data base corresponded with ectopic endocardial impulse formation at 1 of 18 or 22 discrete segments of the left ventricle with a previous anterior or inferior myocardial infarction, respectively. Electrocardiographic localization was compared with the results obtained during intraoperative or catheter endocardial activation sequence mapping., Results: Body surface mapping was performed during 101 distinct ventricular tachycardia configurations. Compared with the activation mapping data that were acquired in 64 of 101 ventricular tachycardias, body surface mapping identified the correct segment of origin in 40 (62%) of 64 tachycardias, a segment adjacent to the segment where the arrhythmia actually originated in 19 (30%) of 64 tachycardias and a segment disparate from the actual segment of origin in 5 (8%) of 64 tachycardias. With respect to infarct location, the segment of origin was correctly identified in 28 (60%) of 47 ventricular tachycardias in patients with anterior, 7 (70%) of 10 tachycardias in patients with inferior and 5 (71%) of 7 tachycardias in patients with combined anterior and inferior myocardial infarction., Conclusions: This study shows that body surface mapping enables precise localization of the origin of postinfarction ventricular tachycardia in 62% and regional approximation in 30% of tachycardias. The multiple-lead ECG may be used to guide and shorten catheter-based mapping procedures during ventricular tachycardia and to provide relevant information on the origin of tachycardias that cannot be mapped with conventional single-site mapping techniques because of unfavorable characteristics.

Objective: To investigate the long-term results of the corridor operation in the treatment of symptomatic atrial fibrillation refractory to drug treatment., Background: The corridor operation is designed to isolate from the left and right atrium a conduit of atrial tissue connecting the sinus node area with the atrioventricular node region in order to preserve physiological ventricular drive. The excluded atria can fibrillate without affecting the ventricular rhythm. This surgical method offers an alternative treatment when atrial fibrillation becomes refractory to drug treatment., Patients: From 1987 to 1993, 36 patients with drug refractory symptomatic paroxysmal atrial fibrillation underwent surgery. The in hospital rhythm was followed thereafter by continuous rhythm monitoring and with epicardial electrograms. After discharge Holter recording and stress testing were regularly carried out to evaluate the sinus node function and to detect arrhythmias; whereas Doppler echocardiography was used to measure atrial contraction and size., Main Outcome Measures: Maintained absence of atrial fibrillation without drug treatment after operation; preservation of normal chronotropic response in the sinus node., Results: The corridor procedure was successful in 31 (86%) of the 36 patients. After a mean (SD) follow up of 41 (16) months 25 (69%) of the 36 patients were free of arrhythmias without taking drugs (mean (SE) actuarial freedom at four years 72 (9)%)). Paroxysmal atrial fibrillation recurred in three patients; paroxysmal atrial flutter (two patients) and atrial tachycardia (one patient) developed in the corridor in three others. Among the 31 patients in whom the operation was successful sinus node function at rest and during exercise remained undisturbed in 26 and 25 patients respectively (mean (SE) actuarial freedom of sinus node dysfunction at four years (81(7)%)). Pacemakers were needed in five (16%) of the 31 patients for insufficient sinus node rhythm at rest only. Doppler echocardiography showed maintenance of right atrial contribution to right ventricle filling in 26 of the 31 patients after operation in contrast to the left atrium, which never showed such contribution. His bundle ablation was performed and a pacemaker implanted in the five patients in whom the corridor operation was unsuccessful., Conclusion: These results substantiate the idea of this surgical procedure. Modification of the technique is, however, needed to achieve a reliable isolation between left atrium and corridor, which would make this experimental surgery widely applicable in the treatment of drug refractory atrial fibrillation.

Background: The purpose of this study was to assess the value of body surface mapping and the standard 12-lead ECG in localizing the site of origin of postinfarction ventricular tachycardia (VT) during endocardial pace mapping of the left ventricle., Methods and Results: Simultaneous recordings of 62-lead body surface QRS integral maps and scalar 12-lead ECG tracings were obtained in 16 patients with prior myocardial infarction during a total of 26 distinct VT configurations and during subsequent left ventricular catheter pace mapping at 9 to 24 different endocardial sites. Anatomic pacing site locations were computed by means of a biplane cineradiographic method and plotted on a polar projection of the left ventricle. The QRS integral map and the QRS complexes of the 12 standard leads of each VT morphology obtained in a particular patient were compared independently with the different paced QRS integral maps and paced QRS complexes of the 12-lead ECG generated in that same patient. The stimulus site locations of the best matching paced QRS integral map and paced QRS complexes of the 12-lead ECG were indicated on the polar projection and subsequently compared with the endocardial location of the corresponding site of VT origin identified during intraoperative (surgical ablation) or catheter activation sequence mapping (catheter ablation). The localization resolution of pace mapping was established separately for each electrocardiographic technique by computing the size of endocardial areas with similar morphological features of the QRS complex. Pace mapping advocated with body surface mapping or the 12-lead ECG enabled adequate reproduction of the VT QRS morphology in 24 of 26 VTs (92%) and 25 of 26 VTs (96%), respectively. Activation sequence mapping identified the site of origin in 12 of 26 previously observed VT configurations (46%). Ten and 11 VTs were localized by activation sequence mapping and pace mapping combined with body surface mapping or the 12-lead ECG, respectively. Pace mapping applied with body surface mapping identified the site of origin correctly (distance < or = 2 cm) in 8 of 10 compared VTs (80%); an adjacent site (distance between 2 and 4 cm) or a disparate site (distance > or = 4 cm) was identified in the remaining 2 of 10 VTs (20%). Pace mapping used with the 12-lead ECG localized the site of origin correctly in 2 of 11 VTs (18%); the site of origin was identified correctly next to an additional adjacent site in 5 of 11 VTs (55%); and an adjacent site or a disparate site was found in 1 of 11 VTs (9%) and 2 of 11 VTs (18%), respectively. The difference in localization accuracy of both electrocardiographic techniques was statistically significant (P = .02). The mean size of endocardial areas where a comparable QRS morphology was obtained during pace mapping was 6.0 +/- 4.5 cm2 with the application of body surface mapping and 15.1 +/- 12.0 cm2 with the use of the 12-lead ECG., Conclusions: These results demonstrate that application of the 62-lead instead of the 12-lead ECG during endocardial pace mapping enhances the localization resolution of this mapping technique and enables more precise identification of the site of arrhythmogenesis in the majority of compared postinfarction VT episodes.

Self-terminating ventricular fibrillation was recorded in a 47 year old woman without coronary artery or other structural heart disease. Reperfusion was thought to be responsible for the ventricular fibrillation because the arrhythmia started while the ST segment was returning to the baseline during an episode of silent ischaemia that was probably caused by coronary spasm. This case shows that potentially lethal arrhythmias can arise during reperfusion and that ventricular fibrillation during reperfusion may be self-terminating.

To improve electrocardiographic localization of the site of origin of ectopic left ventricular (LV) impulse formation in the heart with prior myocardial infarction, 62-lead body surface QRS integral maps were studied during LV pacing at a total of 221 endocardial sites in 14 patients with previous anterior (AMI), inferior (IMI), lateral (LMI), or anterior and inferior (AMI/IMI) myocardial infarction. The anatomic location of each pacing site was computed using digitized biplane fluoroscopic images and plotted on standardized LV endocardial polar projections. A data base of characteristic AMI and IMI mean QRS integral maps was developed after visually selecting subgroups with nearly identical QRS integral morphology from the ectopic activation sequences produced at 110 sites in eight patients with AMI and at 66 sites in four patients with IMI. Intrasubgroup pattern uniformity and intersubgroup pattern variability were statistically verified. The endocardial pacing site locations belonging to each AMI and IMI subgroup were depicted as segments on the respective LV polar projections. In patients with AMI, a total of 18 typical mean QRS integral patterns were obtained, whereas 22 different mean total QRS integral patterns showing more substantial intersubgroup variation were acquired in patients with IMI. Posterolateral regions exhibited a relatively low electrocardiographic sensitivity (six AMI and five IMI patterns) as compared with anteroseptal regions (12 AMI and 17 IMI patterns). Total QRS integral patterns obtained at 24 sites in one patient with LMI were largely compatible with the IMI mean total QRS integral patterns, whereas the majority of total QRS integral patterns acquired at 21 sites in one patient with AMI/IMI corresponded with the AMI mean total QRS integral patterns. The results show that total body surface QRS integral maps generated during LV pacing in patients with prior myocardial infarction cluster by pattern and that each QRS integral pattern is related to a circumscribed endocardial segment of ectopic impulse formation. The relation between a given QRS integral pattern and the position and size of the corresponding paced segment is dependent on infarct location. The present infarct-specific data base of characteristic total body surface QRS integral patterns provides a clinical tool to obtain detailed electrocardiographic localization of ventricular arrhythmias in patients with previous myocardial infarction.

Patients with paroxysmal atrial fibrillation may be extremely disabled despite medical therapy. Based on recent concepts of atrial fibrillation, a surgical open heart procedure was designed to isolate a "corridor" from the right and the left atrium. The corridor consists of the sinus node area, the atrioventricular nodal junction, and the connecting right atrial mass, small enough to prevent atrial fibrillation. Between 1987 and 1990, 20 patients with severely disabling symptoms due to frequent paroxysmal atrial fibrillation underwent the corridor operation, with permanent success in 16 patients. In 8 patients, left atrium to corridor conduction reappeared shortly after the procedure. Reoperation was performed in these patients without extracorporeal circulation. The site of persistent conduction between the left atrium and the corridor could consistently be localized adjacent to the coronary sinus. Nevertheless, reoperation failed to isolate permanently the corridor in 4 patients. During a mean follow-up of 20 months, atrial fibrillation dominating the ventricles was never observed nor inducible in the corridor in the 16 patients with a successful operation. In all cured patients, sinus node function remained undisturbed. Paroxysmal atrial flutter inside the corridor arose in 1 patient and a paroxysmal focal tachycardia in another. All 16 cured patients experienced a clear improvement in quality of life. Refinement of the surgical technique to obtain persistent isolation between the left atrium and the corridor is needed. These results demonstrate that the concept of the corridor operation is sound and justify its use in the treatment of drug-refractory paroxysmal atrial fibrillation.

In animal studies reperfusion of coronary arteries is commonly accompanied by ventricular arrhythmias. It is not certain, however, whether ventricular arrhythmias can be used as a reliable non-invasive marker of reperfusion in humans. Two-channel Holter recordings were obtained from the start of an intravenous infusion of streptokinase until coronary angiography (2.8 (2.7) hours (mean SD)) afterwards) in 57 patients with acute myocardial infarction of less than four hours who were generally not treated with antiarrhythmic drugs. Ventricular arrhythmias occurred in 21 (37%) of the 57 patients: accelerated idioventricular rhythm in 13 patients and non-sustained ventricular tachycardia in 15 patients. Seven patients had both accelerated idioventricular rhythm and non-sustained ventricular tachycardia. Coronary angiography showed a patent infarct-related vessel in 12 (92%) of the 13 patients with accelerated idioventricular rhythm (95% confidence interval 66 to 99%), in 22 (50%) of the 44 patients without accelerated idioventricular rhythm (95% CI 34 to 66%), in 11 (73%) of the 15 patients with non-sustained ventricular tachycardia (95% CI 45 to 92%), and in 23 (55%) (95% CI 39 to 71%) of the 42 patients who did not have non-sustained ventricular tachycardia. Seventeen (81%) of the 21 patients with accelerated idioventricular rhythm, or non-sustained ventricular tachycardia, or both, had a patent infarct-related vessel (95% CI 58 to 94%) as did 17 (47%) of the 36 patients with no ventricular arrhythmia (95% CI 29 to 65%). In patients with accelerated idioventricular rhythm after thrombolysis the infarct-related vessel is almost certain to be patent; but the infarct-related coronary artery can still be patent when no arrhythmia is seen.

In a single-blind randomized study, the efficacy and safety of intravenous propafenone (2 mg/kg body weight per 10 min) versus flecainide (2 mg/kg per 10 min) were assessed in 50 patients with atrial fibrillation or flutter. Treatment was considered successful if sinus rhythm occurred within 1 h. Conversion to sinus was achieved in 11 (55%) of 20 patients with atrial fibrillation treated with propafenone and in 18 (90%) of 20 with atrial fibrillation treated with flecainide (p less than 0.02). If atrial fibrillation was present less than or equal to 24 h, conversion to sinus rhythm was achieved in 8 (57%) of 14 patients in the propafenone group and 13 (93%) of 14 in the flecainide group (p less than 0.05). Atrial flutter was converted in two (40%) of five patients treated with propafenone and in one (20%) of five with flecainide (p = NS). Mean time to conversion was 16 +/- 10 min in the propafenone group versus 18 +/- 13 min in the flecainide group (p = NS). QRS lengthening (83 +/- 15 to 99 +/- 20 ms) was observed only in the patients treated with flecainide (p less than 0.001). Patients successfully treated with propafenone showed significantly higher plasma levels than those whose arrhythmia did not convert to sinus rhythm. Transient adverse effects were more frequent in the flecainide group (40%) than in the propafenone group (8%) (p less than 0.01). In conclusion, at a dose of 2 mg/kg in 10 min, flecainide is more effective than propafenone for conversion of paroxysmal atrial fibrillation to sinus rhythm. However, considering the propafenone plasma levels and very few adverse effects, the dose or infusion rate, or both, used in the propafenone group may not have been sufficient to achieve an optimal effect. Neither drug seems very effective in patients with atrial flutter.

Supraventricular tachyarrhythmias are reported in up to 40% of patients early after coronary artery bypass graft operations. In a randomized study, we compared the efficacy and safety of the class III antiarrhythmic beta-blocking drug sotalol versus propranolol at low and high doses in the prevention of supraventricular tachyarrhythmias in 429 consecutive patients after coronary artery bypass graft operations. Patients with severely depressed left ventricular function and other contraindications for beta-blockers were excluded. From the fourth hour up to the sixth day after coronary artery bypass, 74 patients received low-dose sotalol (40 mg every 8 hours), 66 patients low-dose propranolol (10 mg every 6 hours), 133 patients high-dose sotalol (80 mg every 8 hours), and 156 patients high-dose propranolol (20 mg every 6 hours). Baseline characteristics were comparable in all groups. Supraventricular tachyarrhythmia was observed in 10 of 72 (13.9%) who received low-dose sotalol, 12 of 64 (18.8%) who received low-dose propranolol, 13 of 119 (10.9%) who received high-dose sotalol, and 19 of 139 (13.7%) who received high-dose propranolol (not significant). Drug-related adverse effects necessitating discontinuation of the drug occurred in four receiving low doses (2.9%) and in 31 receiving high doses (10.7%) (p less than 0.02). In conclusion, no medication was found to be superior, although supraventricular tachyarrhythmias tended to be less prevalent in patients treated with sotalol than in those treated with propranolol. Moreover, significantly fewer adverse effects were noted in both low-dose groups. Therefore, low-dose beta-blocking treatment, especially low-dose sotalol, seems preferable.

In a multicenter study, 390 patients with sustained symptomatic ventricular tachycardia or ventricular fibrillation late after acute myocardial infarction were prospectively followed up to assess determinants of mortality and recurrence of arrhythmic events. Patients were given standard antiarrhythmic treatment, which consisted primarily of drug therapy. During a mean follow-up period of 1.9 years, 133 patients (34%) died; arrhythmic events and heart failure were the most common cause of death (41 patients [11%] died suddenly, 31 [8%] died because of recurrent ventricular tachycardia or ventricular fibrillation and 23 [6%] died of heart failure). One hundred ninety-two patients (49%) had at least one recurrent arrhythmic event; 85% of first recurrent arrhythmic events were nonfatal. Multivariate analysis of data from patients who developed the arrhythmia less than 6 weeks after infarction identified five variables as independent determinants of total mortality: 1) age greater than 70 years (risk ratio 4.5); 2) Killip class III or IV in the subacute phase of infarction (risk ratio 3.5); 3) cardiac arrest during the index arrhythmia (risk ratio 1.7); 4) anterior infarction (risk ratio 2.2); and 5) multiple previous infarctions (risk ratio 1.6). Multivariate analysis of data from patients developing the arrhythmia greater than 6 weeks after infarction identified four variables as independently predictive of total mortality: 1) Q wave infarction (risk ratio 2.1); 2) cardiac arrest during the index arrhythmia (risk ratio 1.7); 3) Killip class III or IV in the subacute phase of infarction (risk ratio 1.7); and 4) multiple previous infarctions (risk ratio 1.4). The results of the two multivariate analyses were used in a model for prediction of mortality at 1 year. The average predicted mortality rate varied considerably according to the model: for 243 patients (62%) with the lowest risk, it was 13%, corresponding to an observed mortality rate of 12%; for 92 patients (24%) with intermediate risk, it was 27%, corresponding to an observed rate of 28%; for 55 patients (14%) with the highest risk, it was 64%, corresponding to an observed rate of 54%. This study shows that patients with symptomatic ventricular tachycardia or ventricular fibrillation late after myocardial infarction who are given standard antiarrhythmic treatment have a high mortality rate. The predictive model presented identifies patients at low, intermediate and high risk of death and can be of help in designing the appropriate diagnostic and therapeutic strategy for the individual patient.

The value of simultaneous 62-lead electrocardiographic recordings in localizing the site of origin of ectopic ventricular activation in a structurally normal heart was assessed by examining body surface QRS integral maps in 12 patients during left and right ventricular (LV and RV) pacing at 182 distinct endocardial sites. A data base of 38 characteristic mean integral maps was composed after visually selecting subgroups with nearly identical total QRS integral morphology and numerically evaluating intrasubgroup pattern uniformity and intersubgroup pattern variability. Corresponding endocardial pacing site locations were computed by a biplane cineradiographic method and outlined as segments on a standardized LV and RV polar projection. LV pacing resulted in 25 markedly different mean total QRS integral patterns, showing higher electrocardiographic sensitivity for anteroseptal (18 patterns) compared with posterolateral regions (seven patterns). RV pacing demonstrated 13 mean total QRS integral patterns, exhibiting less intersubgroup variation and comparatively low electrocardiographic sensitivity for the basal anterior and outflow regions. Comparison of LV with RV pacing revealed that QRS configurations produced at LV apical and LV midseptal sites closely resembled QRS configurations generated at RV apical, RV septal, and RV anterior sites, respectively. Total QRS time integral amplitudes showed considerable intrasubgroup variation but permitted global differentiation of spatially similar QRS patterns obtained during pacing at LV and RV sites. This study demonstrates that the QRS pattern of the total body surface electrocardiogram allows discrimination among 38 different LV and RV segments of ectopic endocardial impulse formation in patients with normal cardiac anatomy.

Combined treatment of beta-adrenoceptor-blocking agents and class I antiarrhythmic drugs can potentially have profound and deleterious effects on cardiac impulse formation and conduction. We studied the effect of 5 mg of oral bisoprolol daily and 10 mg/kg of procainamide intravenously with programmed electrical stimulation of the heart in 10 patients with postinfarction ventricular tachyarrhythmias. Oral bisoprolol slowed sinus rhythm and atrioventricular nodal conduction; ventricular effective refractory periods were increased significantly after several days of oral bisoprolol treatment. Combined treatment of oral bisoprolol and intravenous procainamide did not produce clinically relevant changes in parameters of cardiac impulse formation and conduction. This study shows that combined use of bisoprolol and a class I antiarrhythmic drug appears to be safe in patients with ventricular tachyarrhythrhythmias late after myocardial infarction.

To assess the value of lead V4R during exercise testing for predicting proximal stenosis of the right coronary artery, 107 patients were studied. In all patients, a Bruce exercise test with the simultaneous recording of leads I, II, V4R, V1, V4 and V6 was followed by coronary angiography. Apart from registering ST segment changes in the conventional leads, all patients were classified according to absence or presence of an ST segment deviation of 1 mm or greater in lead V4R. Seventy-nine of the 107 patients were studied because of inadequate control of angina pectoris. Seven patients had had myocardial infarction before 40 years of age. Twenty-one patients were analyzed because of severe cardiac arrhythmias. In the 46 patients who had a previous myocardial infarction, the infarct location was inferior in 28 and anterior in 18. Seven of the 14 patients without myocardial infarction and significant proximal stenosis in the right coronary artery showed an ST segment deviation of 1 mm or greater in lead V4R during exercise. This was also observed in 11 of 18 patients with an old inferior wall infarction and proximal occlusion of the right coronary artery. None of the 53 patients without significant proximal stenosis in the right coronary artery showed exercise-related ST segment changes in lead V4R. Exercise-related ST segment deviation in lead V4R had a sensitivity of 56%, a specificity of 96% and a predictive accuracy of 84% in recognizing proximal stenosis in the right coronary artery. These observations indicate that the recording of lead V4R is of value for predicting or excluding proximal stenosis in the right coronary artery.