Transient myocardial ischemia in patients with chronic angina: relation to heart rate changes and variability in exercise threshold. BAY r 1999 in Chronic Angina Study Group.

This study was undertaken to assess the relation of ambulatory myocardial ischemia to heart rate changes and variability in exercise threshold in patients with chronic angina. The study involved 118 patients with chronic angina and proven coronary artery disease who had a 'positive' exercise test result. All patients underwent a first exercise test followed by a 48-h period of ambulatory electrocardiographic monitoring. A second exercise test was performed 4 days later. A total of 101 ischemic episodes were recorded in 35 patients. The heart rate at the appearance of 1-mm ST segment depression during ambulatory electrocardiographic monitoring was > or = 20 beats/min lower than that during exercise testing in 58 ischemic episodes (57%, Group A), 10-19 beats/min lower in 26 (26%, Group B), and < or = 9 beats/min lower or higher in 17 (17%, Group C). Thirty-five percent of the Group A ischemic episodes, 69% of Group B, and 71% of Group C were preceded by an increase in heart rate of > or = 10 beats/min. Thirty patients showed a variable exercise threshold. The prevalence of Group A and B ischemic episodes was not significantly different in patients with fixed or variable exercise threshold, whereas that of Group C episodes was 22% in the former and 0% in the latter (P = 0.036). These results suggest that increased coronary tone may be one of the mechanisms contributing to modulate the occurrence of transient myocardial ischemia in most patients with chronic angina and transient myocardial ischemia at ambulatory electrocardiographic monitoring. This occurs regardless of whether the patients have a variable or fixed exercise threshold.

Percent achieved of predicted peak exercise oxygen uptake and kinetics of recovery of oxygen uptake after exercise for risk stratification in chronic heart failure.

To investigate whether percent achieved of predicted peak exercise oxygen uptake (%VO2max) and recovery of oxygen consumption after exercise may provide prognostic information in chronic heart failure (CHF), we prospectively studied 196 patients with mild to moderate CHF. The following variables were examined: age, etiology of CHF, functional class, ejection fraction (EF), peak exercise oxygen uptake normalized for body weight (VO2max), %VO2max, time to reach 50% of the peak oxygen uptake after exercise (T1/2VO2max), presence of nonsustained ventricular tachycardia (NSVT) and inability to take ACE-inhibitors. VO2max was the most powerful predictor of cardiac death (P<0.0001). Other independent predictors of death were EF, T1/2VO2max, NSVT and inability to take ACE-inhibitors. The discriminatory accuracy of VO2max for cardiac death was not significantly greater than that of %VO2max. In conclusion, the determination of %VO2max does not enhance risk stratification in CHF whereas the kinetics of oxygen consumption after exercise can provide prognostic information.

Propionyl-L-carnitine: a new compound in the metabolic approach to the treatment of effort angina.

The effects of propionyl-L-carnitine on exercise tolerance of 12 patients with stable exertional angina were assessed in a double-blind, placebo-controlled, cross-over protocol using serial exercise tests. Compared to placebo, propionyl-L-carnitine significantly increased total work from 514 +/- 199 to 600 +/- 209 W (P less than 0.05) (17%) and prolonged exercise time and time to ischemic threshold from 515 +/- 115 to 565 +/- 109 sec (P less than 0.05) (10%) and from 375 +/- 102 to 427 +/- 93 sec (P less than 0.01) (14%), respectively. ST segment depression at the highest common work level was significantly reduced from 0.19 +/- 0.08 to 0.15 +/- 0.08 mV (P less than 0.05) (21%). No significant changes in heart rate, systolic blood pressure, and rate-pressure product at rest, at the highest common work level, on appearance of the ischemic threshold, or at peak exercise were observed after propionyl-L-carnitine treatment. No side effects were observed under propionyl-L-carnitine treatment. This study shows that propionyl-L-carnitine can significantly improve exercise tolerance in patients with stable angina. Our data seem to confirm that propionyl-L-carnitine most likely exerts its protective action via the metabolic pathway.

Prediction of cardiac events after uncomplicated myocardial infarction by cross-sectional echocardiography during transesophageal atrial pacing.

Atrial pacing can safely be utilized shortly after myocardial infarction. To evaluate the prognostic value of wall motion abnormalities induced by such pacing 83 consecutive patients with recent uncomplicated myocardial infarction underwent transthoracic cross-sectional echocardiography during transesophageal atrial pacing and upright bicycle exercise stress test. Patients were followed-up for 14 +/- 5 months. During the atrial pacing and the echocardiography, patients were defined at high risk if abnormalities of wall motion were detected in left ventricular regions remote from the infarcted area. Then, during the exercise stress test, high risk patients were those with ST segment depression greater than or equal to 1 mm. On the other hand, patients were considered to be at low risk if they had no abnormalities of wall motion during atrial pacing in remote regions or, in the case of the stress test, if they did not develop ST depression greater than or equal to 1 mm. Of the 83 patients, 21 had major cardiac events during the period of follow-up. Cardiac events occurred in 15/23 (65%) and 5/60 (8%, P less than 0.001) patients assigned to the groups adjudged to be at high and low risk, respectively, on the basis of echocardiographic results. Exercise testing was less reliable in identifying patients at risk of future cardiac events. Major events occurred in only 6 of the 19 patients with a positive stress test (32%, P less than 0.05 vs positive stress echocardiography) and in 14 of the 64 patients with a negative exercise stress test (22%, P = NS vs positive exercise stress test, P less than 0.05 vs negative atrial pacing echocardiography).

Ticlopidine treatment for patients with unstable angina at rest. A further analysis of the study of ticlopidine in unstable angina. Studio della Ticlopidina nell'Angina Instabile Group.

Data collected to investigate the effects of ticlopidine in a subset of 489 patients with angina at rest accompanied by transient ischaemic electrocardiographic changes have been analysed. Of the 489 patients, 255 received conventional treatment including beta-blockers, nitrates, or calcium antagonists (control group); 234 received conventional treatment plus ticlopidine 250 mg b.i.d. (ticlopidine group). The predefined end-points were vascular death and acute myocardial infarction (AMI). The incidence of end-points was assessed according to the intention-to-treat principle. The post-hoc estimated statistical power was 80%. The rate of death or AMI in the 6-month follow-up period was reduced from 14.9 to 6.8% (-54.4%) (odds ratio: 0.42; confidence intervals: 0.22, 0.80). The incidence of fatal or nonfatal AMI was reduced from 12.2 to 4.3% (-65%) (odds ratio: 0.32; confidence intervals: 0.14, 0.70) and of nonfatal AMI from 10.2 to 3.8% (-63%) (odds ratio: 0.35; confidence intervals: 0.15, 0.80). Nineteen patients died; 12 in the control group (4.7%) and seven in the ticlopidine group (83%) (-36%) (odds ratio: 0.62; confidence intervals: 0.21, 1.74); five patients in the control group and only one in the ticlopidine group died of an AMI. The post-hoc estimated statistical power was 80%. However, we cannot draw definitive conclusions about the clinical effect of ticlopidine treatment in the patients with angina at rest accompanied by transient ischaemic electrocardiographic changes because the subgroup analysis was not planned a priori. Nevertheless, this report strongly suggests that such patients can benefit from antiplatelet treatment with ticlopidine; the benefit mainly depends on the protective effect against myocardial infarction.

Prediction of mortality in mild to moderately symptomatic patients with left ventricular dysfunction. The role of the New York Heart Association classification, cardiopulmonary exercise testing, two-dimensional echocardiography and Holter monitoring.

In order to investigate the value of peak oxygen consumption (peak VO2) in predicting mortality in mild to moderately symptomatic patients with left ventricular dysfunction, we studied 103 NYHA II/III class patients with a left ventricular ejection fraction (LVEF) < or = 40%. Heart failure was due to coronary artery disease (CAD) in 39 patients, idiopathic dilated cardiomyopathy in 54, hypertension in eight and surgically corrected valvular disease in two. The following variables were analysed: age, cause of heart failure (CAD vs no CAD), NYHA class, peak VO2, LVEF, left ventricular end-systolic volume index (LVESVI), ventricular tachycardia (VT) on Holter monitoring and the use of antiarrhythmic drugs. Statistical analysis was performed by Cox's proportional-hazards regression model. During a mean follow-up period of 20 months, there were 25 deaths. The estimated cumulative probabilities of survival were 88%, 73% and 58% at 1, 2 and 3 years, respectively. Cox's model identified CAD (P = 0.01), NYHA III class (P = 0.04) and LVEF (P = 0.02) as independent, statistically significant predictors of mortality. Peak VO2 had only a marginal statistical significance (P = 0.07). Age, LVESVI, VT on Holter monitoring and use of antiarrhythmic drugs were not related to mortality. These data can be important in patient clinical management and clinical trial design.

Randomized placebo-controlled comparative study of nifedipine, verapamil and isosorbide dinitrate in the treatment of angina at rest.

Twenty-nine patients with angina at rest took part in a randomized placebo-controlled short-term study to assess the relative effectiveness of different dosages of nifedipine (N), verapamil (V) and isosorbide dinitrate (ISDN) versus placebo and to evaluate the antianginal effects of a sustained-release preparation of ISDN (sr), of N retard form (r) and of V retard form (r). The 29 patients were divided into 3 groups: the first group of patients (10 patients, group A) was treated with N 10 mg six times daily, V 80 mg three times daily and ISDN 10 mg six times daily; the second group of patients (9 patients, group B) was treated with N 20 mg six times daily, V 120 mg four times daily and ISDN 20 mg six times daily; the third group of patients (10 patients, group C) was treated with N r 20 mg four times daily, V r 120 mg three times daily and ISDN sr 40 mg four times daily. The daily frequency of ischaemic episodes (IE) was assessed by Holter monitoring. The effect of each drug on the mean frequency of IE was compared with the placebo using a one-way analysis of variance and the Newman-Keuls test. In group A, the mean daily frequency of IE per patient was 8.1 +/- 5.9 with the placebo, 1.4 +/- 1.9 with N (P less than 0.001; -82%), 4 +/- 3.6 with V (P: NS; -50%) and 4.3 +/- 3.6 with ISDN (P: NS; -46%). In group B it was 6.4 +/- 3.4 with the placebo, 0.5 +/- 1.6 with N (P less than 0.01; -91%), 0.3 +/- 0.5 with V (P less than 0.01; -95%) and 1.2 +/- 1 with ISDN (P less than 0.01; -82%). In group C it was 10.3 +/- 8.7 with the placebo, 0.7 +/- 1.6 with N r (P less than 0.01; -93%), 1 +/- 2.5 with V r (P less than 0.01; -90%) and 5.1 +/- 7.7 with ISDN sr (P: NS; -50%). In group A a reduction of 100% in the number of recorded IEs was achieved in 5/10 patients by using N, in none by V, and in 1/10 by ISDN. In group B, in 8/9 patients by N, in 6/9 by V and in 3/9 by ISDN. In group C, in 8/10 patients by both N r and V r in 4/10 patients by ISDN sr.(ABSTRACT TRUNCATED AT 400 WORDS)

Low-dose dobutamine responsiveness in idiopathic dilated cardiomyopathy: relation to exercise capacity and clinical outcome.

AIMS: To evaluate myocardial contractile reserve using low-dose dobutamine echocardiography in patients with chronic heart failure secondary to idiopathic dilated cardiomyopathy stratified by peak exercise oxygen consumption (VO(2)). METHODS AND RESULTS: Sixty clinically stable patients (56+/-11 years; 45 males) with idiopathic cardiomyopathy and NYHA class I to III symptoms of heart failure were studied and followed-up for 13+/-3 months. All patients underwent cardiopulmonary exercise testing and low-dose dobutamine. The dobutamine infusion protocol consisted of an initial dose of 2.5 micro. kg(-1)per 3 min, increasing by 2.5 micro. kg(-1)per min every 3 min; the maximal dose was 10 micro. kg(-1)per min. The end-systolic volume index, left ventricular ejection fraction and cardiac output were measured at baseline and peak dobutamine dose and their change calculated as ((peak dose value-baseline value)/baseline value]x100. Ten normal subjects with normal left ventricular function and no coronary artery lesions served as a control group to compare low-dose dobutamine results. All analysed echocardiographic variables either at baseline or following dobutamine infusion were significantly lower in patients with chronic heart failure as a whole compared to the control group. When the patients were grouped according to Weber's classification, a statistically significant decrease in percentange changes in end-systolic volume index (rho=-0.77;P<0.0001), left ventricular ejection fraction (rho=-0.72;P<0.0001) and cardiac output (rho=-0. 82;P<0.0001) from class A to class C was observed. The mean percentage decrease in end-systolic volume index following the dobutamine infusion was 28.7+/-9% in class A (peak VO(2)>20 ml. kg(-1). min(-1)), 18.6+/-8% in class B (peak VO(2)between 16 and 20 ml. kg. min(-1)), and only 6.4+/-6% in class C (peak VO(2)between 10 and 16 ml. kg(-1). min(-1)) patient groups. At multivariate analysis, only the percentage change in end-systolic volume index was significantly associated with a peak VO(2)<15 ml. kg(-1). min(-1)(P=0.006). During the follow-up, 17 patients had events (15 readmissions for worsening heart failure and two deaths). At multivariate analysis, only the percentage change in end-systolic volume index was significantly associated with the occurrence of events (P=0.003). The area under the receiver operating characteristic curve for percentage change in end-systolic volume index was not significantly different from that for peak VO(2)(0. 86+/-0.04 vs 0.80+/-0.06;P:ns). CONCLUSION: This study indicates that in patients with chronic heart failure secondary to idiopathic cardiomyopathy, the cardiac response to low-dose dobutamine, as assessed by echocardiography, is correlated with peak VO(2), an objective and accurate measure of the severity of the disease and clinical outcome.

[Value of peak oxygen consumption during exercise for the prognostic stratification of patients with severe systolic dysfunction of the left ventricle]. / Valore del consumo massimo di ossigeno durante esercizio per la stratificazione prognostica di pazienti con severa disfunzione sistolica del ventricolo sinistro.

We sought to assess the prognostic value of peak exercise oxygen consumption (peak VO2) in patients with severe left ventricular systolic dysfunction and mild to moderate symptoms of chronic heart failure. We focused on 1-year mortality. We prospectively studied 77 patients with left ventricular ejection fraction (EF) < or = 25% and NYHA functional class I/II (61%) or III (39%). All patients underwent cardiopulmonary exercise test, two-dimensional echocardiography and 24-hour Holter monitoring. Examined variables were age, etiology, NYHA functional class, EF, peak VO2, and presence of nonsustained ventricular tachycardia. Overall 1-year mortality rate was 23%. At univariate analysis, age > or = 60 years, ischemic etiology, and peak VO2 < 14 ml/kg/min were significantly associated with mortality. At multivariate analysis, peak VO2 was the most powerful predictor of death (p = 0.0001). In the subgroup of patients with a peak VO2 < 14 ml/kg/min, the actuarial 1-year mortality rate was 56%. One additional patient underwent heart transplantation because of severe hemodynamic deterioration. By contrast, in the subgroup of patient with a peak VO2 > 14 ml/kg/min, 1-year mortality rate was 11%. This study provides evidence that patients with severe left ventricular dysfunction and mild to moderate symptoms of chronic heart failure can be accurately stratified into subgroups with strikingly divergent prognosis by an objective criteria such as peak VO2.

Efficacy and duration of the effect of gallopamil sustained release in patients with chronic stable effort angina.

This double-blind, placebo-controlled, cross-over study was designed to evaluate the effects and duration of action of gallopamil sustained release (SR) in patients with stable effort angina. Exercise tests were performed 3, 8, and 12 hours after the last administration of placebo or gallopamil SR. Blood samples for plasma gallopamil concentration were taken just before each exercise test. Statistical analysis was performed using an analysis of variance for multiple comparisons with evaluation of interaction between sequence and period according to a cross-over design. Compared to placebo, gallopamil SR significantly prolonged exercise time from 412 +/- 100 to 481 +/- 71 s (p less than 0.02; 17%), from 416 +/- 88 to 484 +/- 67 s (p less than 0.01; 16%), and from 364 +/- 88 to 440 +/- 85 s (p less than 0.02; 21%) at 3, 8 and 12 hours respectively after administration. Time to -1 mm ST segment depression was also significantly prolonged from 263 +/- 56 to 336 +/- 76 s (p less than 0.001; 28%), from 262 +/- 81 to 356 +/- 70 s (p less than 0.001; 36%), from 231 +/- 65 to 291 +/- 76 s (p less than 0.001; 26%), respectively. No significant relationship between plasma levels and anti-ischemic activity was observed. In conclusion, our data show that gallopamil slow-release is effective in improving exercise tolerance of patients with chronic angina and that its therapeutic effect persists, substantially unchanged, up to 12 hours after administration.

[Efficacy and length of action of a slow-release formulation of isosorbide-5-mononitrate in stable effort angina]. / Efficacia e durata d'azione di una formulazione a lento rilascio di isosorbide-5-mononitrato nell'angina da sforzo stabile.

This double-blind randomized placebo-controlled study was designed to evaluate the acute effects of orally administered slow-release isosorbide-5-mononitrate (SR IS-5-MN) in 12 patients with chronic stable angina. After a prestudy screening to assess the reproducibility of exercise response, the patients entered the study lasting 5 days. On the first and fourth day of the trial, each patient underwent a bicycle exercise test 4, 8 and 24 hours after acute administration of SR IS-5-MN 50 mg or placebo. Statistic analysis of the results was performed using a 2-way analysis of variance for cross-over design. Compared to placebo, 4 hours after administration, SR IS-5-MN prolonged the exercise time from 525 +/- 162 s to 685 +/- 207 s (p less than 0.05; 30%) and - 1mm time from 437 +/- 147 s to 562 +/- 219 (p less than 0.05; 29%). After 8 hours SR IS-5-MN prolonged the exercise time from 510 +/- 145 s to 615 +/- 189 s (p:ns; 21%), and - 1mm time from 415 +/- 128 s to 522 +/- 205 s (p less than 0.05; 26%). No significant changes were observed 24 hours after SR IS-5-MN administration. The maximal rate-pressure product was significantly increased by SR IS-5-MN 4 hours after administration.(ABSTRACT TRUNCATED AT 250 WORDS)

[Comparison of the efficacy of propafenone and hydroquinidine in stabilized extrasystolic ventricular arrhythmia by means of dynamic electrocardiographic Holter monitoring]. / Confronto dell'efficacia del propafenone e dell'idrochinidina nella aritmia extrasistolica ventricolare stabilizzata mediante monitoraggio elettrocardiografico dinamico secondo Holter.

The aim of our study has been to evaluate the efficacy of Propafenon by a reliable experimental method. We have compared the efficacy of Propafenon (300 mg three times daily) with that of Dihydroquinidine Chloride at an elevated dose (300 mg six times daily). Twelve patients, with chronic arrhythmia (at least 1500 premature ventricular beats - PVBs - during a preliminary 24-hour dynamic electrocardiographic Holter monitoring), have been studied. The study has been performed in a double-blind cross-over fashion, and the drugs were administered according to a randomized sequence by the double dummy technique for 4 days. Placebo administration periods of similar duration were established before, after and between the two periods of drug administration. At the end of each Propafenon Dihydroquinidine Chloride and Placebo administration period a 48-hour Holter monitoring was performed. The number of PVBs/hour measured during the 3 periods of Placebo administration (714 +/- 418, 804 +/- 422, 779 +/- 433 respectively) confirmed the chronic nature of the ventricular arrhythmia and the absence of spontaneous variations during the study. Treatment with Propafenon and Dihydroquinidine Chloride significantly reduced the number of PVBs/hour to 87 +/- 130 and to 216 +/- 453 respectively. The reduction observed during Propafenon administration was more than observed during Dihydroquinidine Chloride administration, but it was not statistically significant because of the different behaviour of the individual patients. All patients but one had an over 65% reduction of PVBs/h; only 8/12 patients showed a reduction greater than 65% during Dihydroquinidine Chloride administration.(ABSTRACT TRUNCATED AT 250 WORDS)

Ischaemia related ventricular arrhythmias in patients with variant angina pectoris.

UNLABELLED: Twenty-three patients with variant angina were studied by Holter monitoring both to assess the incidence of serious ventricular arrhythmias (a risk factor of sudden death in variant angina), during ischaemic episodes and to examine the time-relation of the arrhythmias to ST changes. Serious ventricular arrhythmias were observed in 12/23 patients (52%). In the 23 patients, a total of 491 episodes of ST segment elevation were recorded during 954 h of Holter monitoring; serious ventricular arrhythmias were found in only 46 ischaemic episodes (9.4%). Six out of 12 patients showed serious ventricular arrhythmias at the onset of ischaemic episodes or during maximal ST elevation (phase 1), one patient during return or immediately after return of ST to baseline (phase 2) and five patients during both phases. Thirty-three out of 46 ischaemic episodes (76%) showed serious ventricular arrhythmias during phase 1, eight (17%) during phase 2, and five (11%) during both phases. Serious ventricular arrhythmias were neither related to previous myocardial infarction nor to the presence of serious ventricular arrhythmias during inter-crisis periods, whereas a good relationship with severity of ischaemic episodes, as assessed by the magnitude and duration of ST elevation, was found. A modest relationship with anterior ST elevation was also found. IN CONCLUSION: (1) serious ventricular arrhythmias occur in a high percentage of variant angina patients, but in only a small proportion of ischaemic episodes; (2) serious ventricular arrhythmias are related to the severity of ischaemia and occur predominantly at the onset of ischaemic episodes and/or during maximal ST elevation; in only a few cases do they occur during resolution of ischaemic episodes.

Objective evaluation of gallopamil in patients with chronic stable angina. Exercise testing, Holter monitoring, cross-sectional echocardiography and plasma levels.

In this double-blind, randomized placebo-controlled study the effects of two dosages of gallopamil on exercise tolerance were evaluated in 12 patients with stable effort angina. After a pre-study screening aimed at assessing the reproducibility of the exercise response, the patients entered the study which consisted of three 7-day consecutive periods during which placebo or gallopamil 50 mg t.i.d. or gallopamil 75 mg t.i.d. were administered according to a randomized sequence. 24-hour Holter monitoring and cross-sectional echocardiography were performed on the 6th and 7th day of each treatment period, respectively. On the 7th day of each treatment period, patients underwent an exercise test 2 and 8 h after the last administration of gallopamil or placebo. Blood samples for plasma gallopamil concentrations were taken just before each exercise test. The results were analysed using a three-way analysis of variance; intergroup differences were evaluated by the Newman-Keuls test. At 2 h, 11 patients with placebo and three with gallopamil experienced angina; both dosages of gallopamil significantly prolonged exercise time and -1 mm time and also reduced ST segment depression and the rate-pressure product at submaximal workload. No significant change in the rate-pressure product was observed either on the appearance of 1 mm ST depression or at peak exercise. At 8 h, 11 patients with placebo and gallopamil 50 mg t.i.d. and 10 with gallopamil 75 mg t.i.d. experienced angina; although exercise time was significantly prolonged by both dosages of gallopamil, the increase in -1 mm time and reduction of ST segment depression at submaximal workload did not reach statistical significance.(ABSTRACT TRUNCATED AT 250 WORDS)

[Effects of the partial dopamine receptor agonist, terguride, on the field-stimulated vas deferens in the mouse]. / Effetti di un agonista dopaminergico parziale, terguride, sul dotto deferente elettrostimolato di topo.

Transdihydrolisuride (terguride), a 9,10-dihydrogenated analogue of the ergot dopamine agonist lisuride, is characterized as partial dopamine receptor agonist at CNS level. This compound was investigated for its effects on peripheral neurotransmission in the attempt to delineate its pharmacological profile. The contractile responses of field-stimulated mouse vas deferens were slightly inhibited by terguride at very high concentrations (10(-5)-10(-2) M); the selective antagonists for alpha 2-adrenergic and dopamine receptors failed to counteract this effect. Terguride was very effective in blocking the inhibitory effects of LY 171555 (selective DA2 agonist), SK&F 38393 (selective DA1 agonist) and clonidine (selective alpha 2 agonist). In no case the antagonism was competitive: the control dose-response curves were not shifted in a parallel and dose-dependent manner. Therefore terguride displays a mixed DA1, DA2 and alpha 2 antagonistic activity.

[Complicated ventricular arrhythmias in angina at rest]. / Le aritmie ventricolari complicate in corso di angina a riposo.

To assess the incidence of serious ventricular arrhythmias (SVA) during transient ischemic attacks (IA), 27 patients with severe angina at rest were submitted to Holter monitoring for a total period of 1344 hours. The recorded IA's were 565. To evaluate the time/relation between SVA and ST segment changes, the IA's complicated by SVA were divided in 2 parts: one for the upstroke and plateau phase of ST changes; Hse other for the period of resolution of ST changes and the first 3 minutes after ST return to baseline. SVA's were found in 12 of the 27 patients (44.4%), but only in 29 of the 565 IA's (5.1%). The recorded arrhythmias consisted of: frequent ventricular premature beats (VPB) (greater than or equal to 5/min) in 8 patients, multifocal VPB in 6, paired VPB in 10, ventricular tachycardia in 5, R on T phenomenon in 2. No correlations were found between the occurrence of SVA during IA and type of ST changes, location of ST changes, occurrence of the same arrhythmias outside the IA's. SVA's were significantly more frequent during IA associated with pain than during silent IA. When considering only IA associated with ST elevation, a relation was found between the occurrence of SVA and amplitude and duration of ST displacement. The same relation was not observed when IA's associated with ST depression were taken in consideration. Among the 29 IA's complicated by SVA, 22 showed the arrhythmias during the first phase (3.8% of all IA's) and 7 during the second phase (1.3% of all IA's); 6 of these 7 IA's were associated with ST elevation.