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The issue of suboptimal drug regimen adherence in secondary cardiovascular prevention presents a significant barrier to improving patient outcomes. To address this, the utilization of drug combinations, specifically single pill combinations (SPCs) and polypills, was proposed as a strategy to simplify treatment regimens. This approach aims to enhance treatment accessibility, affordability, and adherence, thereby reducing healthcare costs and improving patient health. The document is an Associazione Nazionale Medici Cardiologi Ospedalieri (ANMCO) scientific statement on simplifying drug regimens for secondary cardiovascular prevention. It discusses the underuse of treatments despite available, effective, and accessible options, highlighting a significant gap in secondary prevention across different socio-economic statuses and countries. The statement explores barriers to implementing evidence-based treatments, including patient, healthcare provider, and system-related challenges. The paper also reviews international guidelines, the role of SPCs and polypills in clinical practice, and their economic impact, advocating for their use in secondary prevention to improve patient outcomes and adherence.

Cardio-oncology rehabilitation (CORE) is not only an essential component of cancer rehabilitation but also a pillar of preventive cardio-oncology. Cardio-oncology rehabilitation is a comprehensive model based on a multitargeted approach and its efficacy has been widely documented; when compared with an ‘exercise only’ programme, comprehensive CORE demonstrates a better outcome. It involves nutritional counselling, psychological support, and cardiovascular (CV) risk assessment, and it is directed to a very demanding population with a heavy burden of CV diseases driven by physical inactivity, cancer therapy-induced metabolic derangements, and cancer therapy-related CV toxicities. Despite its usefulness, CORE is still underused in cancer patients and we are still at the dawning of remote models of rehabilitation (tele-rehabilitation). Not all CORE is created equally: a careful screening procedure to identify patients who will benefit the most from CORE and a multidisciplinary customized approach are mandatory to achieve a better outcome for cancer survivors throughout their cancer journey. The aim of this paper is to provide an updated review of CORE not only for cardiologists dealing with this peculiar population of patients but also for oncologists, primary care providers, patients, and caregivers. This multidisciplinary team should help cancer patients to maintain a healthy and active life before, during, and after cancer treatment, in order to improve quality of life and to fight health inequities.

It has been well assessed that women have been widely under-represented in cardiovascular clinical trials. Moreover, a significant discrepancy in pharmacological and interventional strategies has been reported. Therefore, poor outcomes and more significant mortality have been shown in many diseases. Pharmacokinetic and pharmacodynamic differences in drug metabolism have also been described so that effectiveness could be different according to sex. However, awareness about the gender gap remains too scarce. Consequently, gender-specific guidelines are lacking, and the need for a sex-specific approach has become more evident in the last few years. This paper aims to evaluate different therapeutic approaches to managing the most common women’s diseases.

Obesity is a chronic and relapsing disease characterized by the interaction between individual predispositions and an obesogenic environment. Recent advances in understanding the mechanisms of energetic homoeostasis paved the way to more effective therapeutic approaches compared with traditional treatments. Since obesity is a complex disease, it necessitates a multi-disciplinary approach whose implementation remains challenging. Nonetheless, emerging pharmacological interventions appear promising. Currently, therapeutic success is discreet in the short term but often fails to maintain long-term weight loss due to a high likelihood of weight regain. Cardiologists play a key role in managing patients with obesity, yet often lack familiarity with its comprehensive management. The aim of this document is to summarize knowledge to consolidate essential knowledge for clinicians to effectively treat patients living with obesity. The paper emphasizes the pivotal role of a strong patient–clinician relationship in navigating successful treatment. We analyse the criteria commonly used to diagnose obesity and point out the strengths and limitations of different criteria. Furthermore, we discuss the role of obesiologists and the contributions of cardiologists. In addition, we detail key components of effective therapeutic strategies, including educational aspects and pharmacological options.

Late patentials (LPs) detected on the signal-averaged (SA) electrocardiogram (ECG) predict arrhythmic events after acute myocardial infarction (AMI). The effect of thrombolysis on the incidence of LPs after AMI is controversial and its impact on subsequent arrhythmic events is not known. Moreover, the effects of [beta] blockers on the SAECG have not been studied. Six hundred eighteen patients with AMI were studied; thrombolysis was given to 228 (37%). In comparison with patients treated conventionally, those receiving thrombolysis were significantly younger and more frequently male, had higher peak values of creatine kinase, a lower prevalence of non-Q-wave AMI, and a higher incidence of ventricular fibrillation in the acute phase, and more frequently received [beta] blockers. An SAECG obtained 6 to 8 days after AMI showed LPs in 24% of patients receiving and in 25% not receiving thrombolysis (p = NS). On admission, intravenous [beta] blockers were administered to 110 patients (18%); those receiving [beta] blockers were younger, had lower peak values of creatine kinase and more frequently received thrombolysis. LPs were less frequently found in patients treated than in those not treated with [beta] blockers (15 vs 27%; p = 0.007); however, this effect was found only in those with an ejection fraction [greater than or equal to] 40%. independent predictors of LPs by multivariate analysis were an ejection fraction The most frequent mechanism leading to sudden death after acute myocardial infarction (AMI) is considered to be ventricular tachycardia or fibrillation. It was shown that 70 to 90% of patients with episodes of ventricular tachycardia have low-amplitude, high-frequency signals, called late potentials (LPs) on the signal-averaged electrocardiogram (SAECG).[1-3] In patients recovering from AMI, the presence of LPs is a strong predictor of subsequent arrhythmic events.[4-7] Thus, any intervention that reduces the incidence of LPs may be expected to improve the outcome of these patients. Prognosis after AMI can be improved by thrombolytic therapy[8,9] and [beta] blockers.[10,11] The effects of thrombolysis on the SAECG are controversial,[12-18] and those of [beta] blockers are unknown. In addition, there are no studies that have systematically explored the relation between reduction of arrhythmic events by thrombolysis and [beta] blockers, and the effects of these treatments on the incidence of LPs. In 1987, we initiated a prospective, multicenter study to determine the prognostic significance of LPs after AMI. Data from that study were retrospectively analyzed to: (1) assess the effects of thrombolytic therapy and [beta]-blocking agents on the incidence of LPs after AMI, and (2) determine whether the improved survival observed after thrombolysis and therapy with [beta]-blocking agents could be attributed to a reduced incidence of LPs. METHODS Study patients: Between July 1987 and March 1990, 702 patients admitted with the diagnosis of AMI to the coronary care units of the 6 institutions participating in the Late Potentials Italian Study (LAPIS) were recruited. Patients were included in the study if they had: (1) a confirmed diagnosis of AMI on the basis of clinical (typical chest pain lasting >30 minutes), electrocardiographic (ST elevation [greater than or equal to]1 mV in the peripheral leads, and [less than or equal to]2 mV in the precordial leads) and creatine kinase changes; and (2) an SAECG recorded before discharge. Patients were excluded from the study if: (1) they had cardiogenic shock, atrial fibrillation or pacemaker rhythm at the time of the SAECG; (2) they needed antiarrhythmic therapy at the time of the SAECG; or (3) the noise level of the SAECG was [greater than or equal to]0.5 [mu]V All patients gave informed consent. Fifty-four patients (8%) were lost to follow-up and were excluded from analysis. For the objectives of the present study, 30 patients (5%) who presented in Killip class 3 or 4 on admission to the coronary care unit were also excluded, because they had clear contraindications to acute [beta]-blocking treatment. Thus, the study population comprised 618 patients with a mean age of 61 [+ or -] 12 years. The relevant clinical data of the study group included in the analysis are presented in Table I. [TABULAR DATA I OMITTED] Treatment: All patients admitted to the coronary care unit within 6 hours from the onset of symptoms and with no contraindications to thrombolysis were administered intravenous streptokinase (1,500,000 U in 60 minutes) or recombinant tissue-type plasminogen activator (a bolus of 10 mg, followed by 50 mg in 60 minutes, and another 40 mg in 120 minutes). In the absence of specific contraindications, [beta]-blocking agents were also given at the discretion of the attending physician; atenolol or metoprolol (5 mg in 10 minutes) was administered and then repeated after 10 minutes if heart rate was [greater than or equal to]60 beats/min or systolic blood pressure was [greater than or equal to]100 mm Hg, or both. After intravenous administration, 1 oral dose of 100 mg/die of atenolol, or 100 mg twice daily of metoprolol was given. Any other therapy, either acute or chronic, was not standardized and was at the discretion of the attending physician. Therapeutic decisions were not obtained on the basis of the results of the SAECG. Signal-averaged electrocardiogram: All patients had an SAECG obtained 6 to 8 days from AMI. The SAECG was obtained with an Arrhythmia Research Technology-101 or 1200 System, with bidirectional Butterworth filtering (25 to 250 Hz), as previously described.[3] The following quantitative SAECG variables of the filtered QRS were evaluated: (1) total duration, (2) root-mean-square voltage of the last 40 ms (RMS-40), and (3) duration of the low-amplitude signals (114 ms, (2) RMS-40 32 ms. In this study, 44 patients (7%) with bundle branch block patterns on the standard ECG were also included (30 with right and 14 with left bundle branch block). In these patients, the SAECG was analyzed using different filters (40 to 250 Hz) and criteria, according to Buckingham et al.[19] In this group, criteria for the presence of LPs ([greater than or equal to]2) were as follows: (1) total QRS duration [greater than or equal to] ms, (2) RMS [less than or equal to]17 [mu]V, and (3) LAS-40 [greater than or equal to]45 ms. Echocardiography: A 2-dimensional echocardiographic examination was performed at each center by experienced cardiologists before discharge of patients. Ejection fraction was calculated in the apical 4-chamber view by the single-plane ellipse area-length method. The average of 3 measurements was considered as the ejection fraction for each patient. A technically good echocardiographic examination was obtained in 587 patients (95%). Follow-up: Patients were followed up every 3 months at the clinics, by telephone and through their private physician. In the case of death, detailed information was obtained from the patient's relatives, the attending physician or, in the case of death in a hospital not participating in the study, clinical records to determine the cause. Furthermore, clinical records were examined in the case of admission to the hospital for any event. Definitions: Sudden death was defined as instantaneous, unexpected death, or death occurring within 1 hour of the onset of symptoms or during sleep. Sustained ventricular tachycardia was defined as a ventricular rhythm at a rate [greater than or equal to]120 beats/min, lasting [greater than or equal to]30 secon or leading to hemodynamic compromise. Arrhythmic events were considered the occurrence of either sudden death or sustained ventricular tachycardia. Statistics: Analysis of variance was used for comparing continuous variables, whereas discrete data were compared by chi-square test. Bonferroni's correction was used for multiple comparisons. Multivariate analysis was performed using stepwise logistic regression to evaluate independent predictors of LPs; variables were inserted in the model when the p value was For purposes of analysis, patients were dichotomized with regard to ejection fraction ([greater than or equal to] and and [less than or equal to] 1,168 mU/ml) and age (> and [less than or equal to]60 years). To reduce possible bias when patients were assigned to specific treatment, a further analysis was performed by comparing retrospectively matched patients, receiving and not receiving thrombolysis (n = 205 and 203, respectively) and [beta]-blocking therapy (n = 92 and 341, respectively), with similar age, gender, site of AMI, previous AMI, peak creatine kinase and ejection fraction. When not otherwise indicated, values are reported as mean [+ or -] SD. A p value RESULTS Incidence of late potentials: LPs were recorded in 152 of 618 patients (24.5%) (Table II). Age, gender and Killip class were similar in patients with and without LPs. However, patients with LPs had higher mean values of peak creatine kinase, and a higher incidence of ventricular fibrillation in the acute phase ( Characteristics of patients with and without thrombolysis (Table III): There were 228 patients (37%) who received thrombolysis (122 streptokinase and 106 recombinant tissue-type plasminogen activator) and 390 (63%) who did not. Patients who received thrombolysis were significantly younger and more frequently male, had higher mean values of peak creatine kinase, a lower prevalence of non-Q-wave AMI, and a higher incidence of ventricular fibrillation in the acute phase of the infarction, and were more frequently treated with acute [beta]-blocking therapy. There was no difference between the 2 groups with regard to previous AMI, sustained ventricular tachycardia in the acute phase of the infarction, and mean ejection fraction, although patients treated with thrombolysis tended to have a lower incidence of ejection fraction Effects of thrombolysis on late potentials (Table IV): LPs were found in 54 patients (24%) treated with thrombolysis and in 98 (25%) treated conventionally, with a nonsignificant reduction of 6% (95% confidence limits -33%, +22%). Similarly, no difference was found in mean values of the duration of the filtered QRS and LAS-40, and the amplitude of RMS-40. [TABULAR DATA IV OMITTED] Thrombolytic therapy had no effect on the incidence of LPs also in the subgroups of patients with ejection fractions [greater than or equal to] and and [less than or equal to]60 years. Characteristics of patients with and without beta blockers (Table V): Atenolol or metoprolol was administered to 110 of 618 patients (18%). Patients treated with [beta]-blocking agents were younger, had lower mean values of peak creatine kinase and more frequently received thrombolytic agents. The mean ejection fraction was not significantly different between the 2 groups, but the incidence of an ejection fraction Effects of beta blockers on late potentials (Table VI): LPs were recorded in 16 patients (14.5%) treated and in 136 (27%) not treated with [beta]-blocking agents, a significant reduction of 46% (95% confidence limits -13%, -79%; p = 0.007). Beta-blocking agents did not significantly modify the duration of the filtered QRS and LAS-40, but reduced the mean value of RMS-40. Analysis of subgroups, however, showed that [beta]-blocking agents reduced LPs only in the group of patients with an ejection fraction [greater than or equal to]40% (Table VI); in this subgroup, LPs were present in 11% of those treated and in 24% not treated (reduction of 55%; p = 0.006); conversely, in those with an ejection fraction Multivariate analysis: Stepwise logistic regression analysis showed that the most powerful predictor of LPs in patients with AMI was an ejection fraction Results of retrospective matching: Because patients had not been randomized to either thrombolysis or [beta] blockers, we selected 2 groups for each type of treatment (thrombolytic and [beta] blockade) with similar mean age, type of AMI, peak creatine kinase, previous AMI and ejection fraction to reduce bias. Again, the incidence of LPs was similar in the 2 retrospectively matched groups of patients with (52 of 205; 25%) and without (55 of 203; 27%) thrombolysis, whereas it differed significantly between those receiving and not receiving [beta] blockers (13 and 23%, respectively; p = 0.03). Follow-up: During a mean follow up of 12 [+ or -] 7 months, there were 47 deaths (total mortality 8%), with 39 cardiac deaths (6%), of which 13 (2%) were sudden. In addition, 9 patients (1.4%) had [greater than or equal to]1 episode of documented sustained ventricular tachycardia. Thus, in all, 22 arrhythmic events (3.5%) were recorded. Thrombolytic therapy reduced total and cardiac mortality, whereas it did not influence the occurrence of arrhythmic events (3.5 and 3.6% in patients with and without thrombolysis, respectively) (Table VII). The effects of thrombolysis were similar in patients both with and without LPs. [TABULAR DATA VII OMITTED] Furthermore, [beta]-blocking agents reduced both total and cardiac death (Table VIII). Moreover, arrhythmic events were decreased >50% (1.8 vs 3.9%), although this result did not reach statistical significance. However, sudden death did not appear to be influenced by [beta]-blocking agents, whereas no patient on [beta]-blocking therapy had sustained ventricular tachycardia during follow-up. The 2 events (both sudden death) recorded in patients treated with [beta]-blocking agents occurred in those without LPs. Thus, no patient treated with [beta]-blocking agents and with LPs had events during follow-up. [TABULAR DATA VIII OMITTED] DISCUSSION Thrombolysis and signal-averaged electrocardiogram: There are several potential mechanisms by which thrombolysis may decrease LPs and electrical instability after AMI, including: (1) a complete salvage of myocardium; (2) a substantial limitation of necrosis, with reduction of the 'border zone' of the infarct from which LPs occur; and (3) a beneficial impact on scar healing, infarct expansion, ventricular remodeling and dilation.[20,21] Several studies have reported a significant reduction of LPs in patients with AMI treated by thrombolysis.[12-18] However, these results are contradictory and should be interpreted with caution. Gang et al[12] reported incidences of LPs of 5% in patients treated and 23% in those not treated with thrombolysis (p = 0.01) on the SAECG recorded within 48 hours of admission; however, the SAECG obtained at discharge did not show significant differences in LPs between the 2 groups (5 and 18%, respectively). Chew et al[14] found incidences of LPs of 16% in patients treated and 43% in those not treated with streptokinase (p = 0.003), using a 40 Hz filter, but the incidence was not significantly different using a 25 Hz filter. In another study, Zimmermann et al,[15] using high-resolution beat-to-beat analysis, reported incidences of LPs of 10 and 24% in patients receiving and not receiving thrombolysis, respectively; however, there was no difference when LPs were evaluated by the SAECG. Moreover, other studies did not observe any significant difference in the incidence of LPs between patients treated and not treated with thrombolytic agents,[6,17,18] making the effects of thrombolysis on LPs controversial. The results of the present large multicenter study are in agreement with those latter studies, showing no significant effect of thrombolytic therapy per se on LPs. There are several possible explanations for the contradictory results reported on the effects of thrombolysis on the SAECG, including: (1) different techniques, times of recording, and definitions of abnormality; (2) different times of administration and types of thrombolytic agents; (3) different degrees of efficacy of thrombolysis (however, thrombolytic therapy appeared to be effective in the present study, because we observed, as expected, a lower mortality in treated patients); and (4) different clinical characteristics of patients treated with and without thrombolysis (however, this possibility is unlikely in our study, because thrombolysis did not reduce LPs in any comparable subgroup, such as anterior and inferior AMI, low and high ejection fraction, and so forth). Furthermore, it should be considered that thrombolysis could have no apparent effect on the incidence of LPs, because patients with unsuccessful reperfusion are included, whereas a significant effect would be evident only in those with a documented patent infarct artery[12,14,15,17,22-25]; this possibility cannot be ruled out in this study, because coronary angiography was not part of the protocol. However, effective thrombolysis also has the potential of increasing the incidence of LPs after AMI; heterogeneous infarcts have been observed after coronary occlusion and reperfusion in animals[26] and humans,[27] with secondary hemorrhage and patchy fibrosis, which could facilitate the occurrence of LPs. Beta blockers and the signal-averaged electrocardiogram: The effects of [beta]-blocking agents on the SAECG were not investigated previously, although Farrell et al[6] recently reported a lower, although not significant, incidence of LPs in patients with AMI who received in-hospital [beta]-blocking therapy. The present data show that [beta] blockers significantly decrease the incidence of LPs in AMI. Although patients treated with [beta] blockers showed some differences indicating a lower risk than that of those not treated, thus suggesting a selection bias, [beta] blockers maintained their independent effect on LPs when included in the multivariate analysis. This effect was confirmed in the retrospective analysis of 2 well-matched groups of patients treated with and without blockers. In the setting of acute ischemia, [beta] blockers have been shown to induce a favorable redistribution of blood flow to ischemic subendocardial regions, to reduce infarct size and improve regional myocardial function,[28-30] all factors that have potential beneficial effects on the electrophysiologic substrate and thus on the occurrence of LPs. Recently, Grines et al[30] showed a significant improvement in infarct zone wall motion in patients treated with intravenous [beta] blockers after reperfusion therapy. In agreement with that finding, [beta] blockers were more effective in reducing the incidence of LPs when associated with thrombolytic therapy in the present study. Thus, we can speculate that the lower incidence of LPs that we observed in patients treated with [beta] blockers may reflect a reduced extent of the infarcted area or peri-infarctual ischemia, or a decreased infarct area dyssynergy, or a combination. The observation that [beta] blockers decreased the incidence of LPs only in patients with an ejection fraction >40% further confirms that their effect was related to a successful limitation of infarct extension, with a possible reduced risk of border zones constituted by vital and fibrotic areas. Follow-up: Some studies have suggested that the enhanced survival associated with thrombolytic therapy may also depend on a reduced incidence of LPs and, consequently, arrhythmic events.[6,12] In the present study, thrombolysis reduced mortality but had no effect on the incidence of arrhythmic events. Because the occurrence of LPs was not affected by thrombolysis, we suggest that the improvement of prognosis after thrombolytic therapy is not due to a reduction of electrical instability as indicated by the SAECG. Several studies have demonstrated that [beta] blockers prevent sudden death and recurrent AMI,[10,11] but the mechanism of this beneficial effect is not clear. Beta blockers significantly decreased cardiac death and the incidence of arrhythmic events by >50%; it is tempting to speculate that the reduction of mortality by [beta] blockers is, at least in part, secondary to an increased electrical stability, as indicated by a lower incidence of LPs in the present study, and that this effect is potentiated by thrombolytic treatment also. Study limitations: These findings are the results of a retrospective analysis of a prospective study. Because patients were not randomized to separate groups with and without thrombolytic and [beta]-blocking therapy, the results should be interpreted with caution. Possible bias in the selection of patients for specific treatment cannot be excluded, and it is probable that patients with more depressed left ventricular function may have been excluded from [beta]-blocking treatment. However, the results of multivariate analysis and retrospective matching both indicate a beneficial effect of [beta]-blocking therapy on the SAECG and may thus have important implications for future research in this field. Acknowledgment: We are grateful to Attilio Maseri, MD, for helpful suggestions in reviewing the manuscript. APPENDIX Participants of the Late Potentials Italian Study (LAPIS): Istituto di Cardiologia, Universita' Cattolica, Roma, Italy (Pietro Santarelli, MD, Gaetano A. Lanza, MD, Francesco Biscione, MD, and Andrea Natale, MD); Divisione di Cardiologia, Ospedale Civile, Caserta, Italy (Giancarlo Corsini, MD, and Carmine Riccio, MD); Divisione di Cardiologia, Ospedale Maggiore della Carita', Novara, Italy (Eraldo Occhetta, MD, and Paolo Rossi, MD); Divisione di Cardiologia, Ospedale Poveri Infermi, Borgosesia, Italy (Maurizio Gronda, MD, and Johannes Makmur, MD); Divisione di Cardiologia, Ospedale SS. Trinita', Borgomanero, Italy (Marco Zanetta, MD, and Umberto Parravicini, MD); and Divisione di Cardiologia, Ospedale S. Filippo Neri, Roma, Italy (Salvatore Toscano, MD). [1.] Simson MB. Identification of patients with ventricular tachycardia after myocardial infarction from signals in the terminal QRS complex. Circulation 1981; 64:235-242. [2.] Breithardt G, Borggrefe M. Recent advances in the identification of patients at risk of ventricular tachyarrhythmias: role of ventricular late potentials. Circulation 1987;75:1091-1097. [3.] Denes P, Santarelli P, Hauser RG, Uretz EF. Quantitative analysis of the high frequency components of the terminal portion of the body surface QRS in normal subjects and in patients with ventricular tachycardia. Circulation 1983;67:1129-1138. [4.] Kuchar DL, Thorburn CW, Sammel NL. Prediction of serious arrhythmic events after myocardial infarction: signal averaged electrocardiogram, Holter monitoring and radionuclide ventriculography. J Am Coll Cardiol 1987;9:531-538. [5.] Gomes JA, Winters SL, Martinson M, Machac J, Stewart D, Targonski A. The prognostic significance of quantitative signal-averaged variables relative to clinical variables, site of myocardial infarction, ejection fraction and ventricular premature beats: a prospective study. J Am Coll Cardiol 1989;13:377-384. [6.] Farrell TG, Bashir Y, Cripps T, Malik M, Poloniecki J, Bennett ED, Ward DE, Camm AJ. Risk stratification for arrhythmic events in postinfarction patients based on heart rate variability, ambulatory electrocardiographic variables and the signal averaged electrocardiogram. J Am Coll Cardiol 1991;18:687-697. [7.] Steinberg JS, Regan A, Sciacca RR, Bigger JT, Fleiss JL. Predicting arrhythmic events after acute myocardial infarction using the signal averaged electrocardiogram. Am J Cardiol 1992;69:13-21. [8]. Gruppo Italiano per lo Studio della Streptochinasi nell' Infarto miocardico (GISSI). Long term effects of intravenous thrombolysis in acute myocardial infarction: final report of the GISSI study. Lancet 1987;ii:871-874. [9.] ISIS-2 (Second International Study of Infarct Survival) Collaborative Group. Randomised trial of intravenous streptokinase, oral aspirin, both, or neither among 17,187 cases of suspected acute myocardial infarction: ISIS-2. Lancet 1988;2: 349-360. [10.] ISIS-I (First International Study of Infarct Survival) Collaborative Group. Randomized trial of intravenous atenolol among 16027 cases of suspected acute myocardial infarction: ISIS-I. Lancet 1981;2:823-827. [11.] MIAMI Trial Research Group. Metoprolol In Acute Myocardial Infarction (MIAMI): a randomized placebo-controlled international trial. Eur Heart J 1985;6: 199-226. [12.] Gang ES, Lew AS, Hong MM, Wang FZ, Siebert CA, Peter T. Decreased incidence of ventricular late potentials after successful thrombolytic therapy for acute myocardial infarction. N Engl J Med 1989;321:712-716. [13.] Eldar M, Leor J, Hod H, Rotstein Z, Truman S, Kaplinsky E, Abboud S. Effect of thrombolysis on the evolution of late potentials within 10 days of infarction. Br Heart J 1990;63:273-276. [14.] Chew E-W, Morton P, Murtagh JG, Scott ME, O'Keef DB. Intravenous streptokinase for acute myocardial infarction reduces the occurrence of ventricular late potentials. Br Heart J 1990;64:5-8. [15.] Zimmermann MM, Adamec R, Ciaroni S. Reduction in the frequency of ventricular late potentials after acute myocardial infarction by early thrombolytic therapy. Am J Cardiol 1991;67:697-703. [16.] Leor J, Hold H, Rotstein Z, Truman S, Gansky S, Goldbourt U, Abboud S, Kaplinsky E, Eldar M. Effects of thrombolysis on the 12-lead signal-averaged ECG in the early postinfarction period. Am Heart J 1990; 120:495-502. [17.] Turitto G, Risa AL, Zanchi E, Prati PL. The signal averaged electrocardiogram and ventiricular arrhythmias after thrombolysis for acute myocardial infarction. J Am Coll Cardiol 1990;15:1270-1276. [18.] de Chillou C, Sadoul N, Briancon S, Etienne A. Factors determining the occurrence of late potentials on the signal averaged electrocardiogram after a first myocardial infarction: a multivariate analysis. J Am Coll Cardiol 1991;18:1638-1642. [19.] Buckingham TA, Thessen CC, Stevens LL, Redd RM, Kennedy HL. Effect of conduction defects on the signal averaged electrocardiographic determination of late potentials. Am J Cardiol 1988;61:1265-1271. [20.] Morgan CD, Roberts RS, Haq A, Baigrie RS, Daly PA, Gent M, Armstrong PW, for the TPAT Study Group. Coronary patency, infarct size, and left ventricular function after thrombolytic therapy for acute myocardial: results from the Tissue Plasminogen Activator Toronto (TPAT) placebo-controlled trial. J Am Coll Carol 1991;17:1451-1457. [21.] Lavie CJ, O'Keefe JH Jr, Chesebro JH, Clements IP, Gibbons RJ. Prevention of late ventricular dilatation after acute myocardial infarction by successful thrombolytic reperfusion. Am J Cardiol 1990;66:31-36. [22.] Vatterott PJ, Hammill SC, Bailey KR, Wiltgen CM, Gersh BJ. Late potentials on signal averaged electrocardiogram and patency of the infarct-related artery in survivors of acute myocardial infarction. J Am Coll Cardiol 1991;17:330-337. [23.] Lange RA, Cigarroa RG, Wers PJ, Kremers MS, Hills LD. Influence of anterograde flow in the infarct artery on the incidence of late potentials after acute myocardial infarction. Am J Cardiol 1990;65:554-558. [24.] Tranchesi B, Verstraete M, Van de Werf F, de Abuquerque CP, Carameni B, Gebara OC, Pereira WI, Moffa P, Renotti G, Pileggi F. Usefulness of high-frequency analysis of signal-averaged surface electrocardiograms in acute myocardial infarction before and after coronary thrombolysis for assessing coronary reperfusion. Am J Cardiol 1990,66:1196-1198. [25.] Aguirre FV, Kern MJ, Hsia J, Serota H, Janosik D, Greenwalt T, Ross AM, Chaitman BR. Importance of myocardial infarction artery patency on the prevalence of ventricular arrhythmia and late potentials after thrombolysis in acute myocardial infarction. Am J Cardiol 1991;68:1410-1416. [26.] Smith GT, Soeter JR, Haston HH, McNamara JJ. Coronary reperfusion in primates. Serial electrocardiographic and histologic assessment. J Clin Invest 1974;54: 1420-1427. [27.] Fujiwara H, Onodera T, Tanaka M, Fujiwara T, Wu DJ, Kawai C, Hamashima Y. A clinicopathologic study of patients with hemorrhagic myocardial infarction treated with selective coronary thrombolysis with urokinase. Circulation 1986;73: 749-757. [28.] Vatner SF, Baig H, Manders TW, Ochs H, Pagani M. Effects of propranolol on regional myocardial function, electrocardiogram and blood flow in conscious dogs with myocardial infarction. J Clin Invest 1977;60:353-360. [29.] Steingart RM, Matthews R, Gambino A, Kantrowitz N, Katz S. Effects of intravenous metoprolol on global and regional left ventricular function after coronary arterial reperfusion in acute myocardial infarction. Am J Cardiol 1989;63:767-771. [30.] Grines CL, Booth DC, Nissen SE, Gurley JC, Bennet KA, DeMaria EN. Acute effects of parenteral beta-blockade on regional ventricular function of infarct and noninfarct zones after reperfusion therapy in humans. J Am Coll Cardiol 1991;17: 1382-1387. From the Institute of Cardiology, Catholic University, Rome, and the Late Potentials Italian Study (LAPIS) sites (see Appendix), Italy. Manuscript received December 31, 1992; revised manuscript received April 9, 1993, and accepted April 12. Address for reprints: Pietro Santarelli, MD, Istituto di Cardiologia, Universita' Cattolica del S. Cuore, L. go A. Gemelli, 8, 00168 Roma, Italy.