A 57–years–old man with a history of smoke and hypertension was transferred to our unit with chest pain and dyspnoea, lasting few days. Electrocardiography revealed the presence of ST elevation in the infero–lateral leads with Q waves and Transthoracic Echocardiographic Study revealed a normal dimension left ventricle with infero–postero–lateral akinesia, moderately reduced EF (40%) in the absence of significant valve disease and an organized pericardial effusion of about one centimetre. In the meantime, the first signs of hemodynamic instability and cardiogenic shock appeared and the ETT revealed the exacerbation of the pericardial effusion. So we did an emergency coronary angiography that revealed a calcified three–vessel disease with occlusion of the middle segment of Cx. Because of the worsening of the cardiogenic shock we used the aortic balloon pump to improve the hemodynamic instability. The concomitant presence of signs of late infarction, pericardial effusion and cardiogenic shock make us suspect a myocardial rupture so we did a cardiac computed tomography (CT ) scan that was suggestive for a cardiac wall rupture within the infarcted left ventricle. The patient was urgently transported to the cardiac surgery room where the patch of inferior wall was performed and then was transferred to the Intensive Care Unit. After the surgery, a residual of pericardial effusion persisted without hemodynamic significant and the revascularization was planned one month after discharge. Heart rupture represents a mechanical complication of MI that we have to suspect every time we find signs of myocardial infarction and pericardial effusion that degenerate into cardiogenic shock. Although it occurs in a very limited number of cases, the postinfarct cardiac free wall rupture is characterized by a poor prognosis and cardiac Computed Tomography provides primary information for the diagnosis.

Background Traditional cardiac rehabilitation (CR) is effective in improving physical performance and prognosis after myocardial infarction (MI). Anyway, it is not consistently recommended to older adults, and its attendance rate is low. Previous studies suggested that alternative, early and tailored exercise interventions are feasible and effective in improving physical performance in older MI patients. Anyway, the demonstration that they are associated also with a significant reduction of hard endpoints is lacking. Aim To describe rationale and design of the “Physical activity Intervention in Elderly patients with myocardial Infarction” (PIpELINe) trial. Methods The PIpELINe trial is a prospective, randomized, multicentre study with a blinded adjudicated evaluation of the outcomes. Patients aged ≥ 65 years, admitted to hospital for MI and with a low physical performance one month after discharge, as defined as short physical performance battery (SPPB) value between 4 and 9, will be randomized to a multi-domain lifestyle intervention (including dietary counselling, strict management of cardiovascular and metabolic risk factors, and exercise training) or health education. The primary endpoint is the one-year occurrence of the composite of cardiovascular death or re-hospitalization for cardiovascular causes. Results The recruitment started in March 2020. The estimated sample size is 456 patients. The conclusion of the enrolment is planned for mid-2023. The primary endpoint analysis will be available for the end of 2024. Conclusions The PIpELINe trial will show if a multi-domain lifestyle intervention is able to reduce adverse events in older patients with reduced physical performance after hospitalization for MI. Trial registration ClinicalTrials.gov NCT04183465.

Introduction Brugada syndrome is an inherited disease characterized by an increased arrhythmic risk and sudden death. The type 1 ECG pattern is the only standard required to make a diagnosis but the stratification of arrhythmic risk remains a controversial element. Some electrocardiographic signs have been described as associated with an increased arrhythmic risk. We present a case of Brugada Syndrome in which different electrocardiographic elements of incremental risk could have predicted the later evolution of the clinical case. Clinical Case A 68–year–old male patient with family history of sudden cardiac death (brother 51aa) and occasional finding of Brugada type 1 ECG pattern (2009), implanted with Medtronic bicameral ICD device in primary prevention. The electrocardiogram shows type 1 Brugada pattern in the right precordials with characteristic ST–elevation, followed by a concave ST segment, one of the signs of association with an increased arrhythmic risk; first–degree AV block with a long PR (323 msec) associated with the presence of the SCN5A mutation and an increased risk of arrhythmic events and sudden cardiac death; in the end a fragmented QRS in V2 with extended duration (153 ms). At the next follow–up the patient had some episodes of arrhythmic storm, effectively treated by the device; in consideration of the arrhythmic burden, he was subjected to epicardial ablation and was also subjected to genetic analysis that was positive for pathological mutation on the SCN5A gene (SCN5A ex 22: c.3929C>T;p.Pro1310Leu). Conclusions Brugada Syndrome can be diagnosed from the type 1 ECG pattern, but the current risk stratification score remains a controversial element. Electrocardiographic signs of malignancy can contribute to create a multiparametric evaluation of the patient in order to predict future arrhythmic events. Fig 1. ECG: RS 74 bpm, first–degree AV block (PR 323 msec), BFA, Brugada type 1 pattern (QRS 153 ms), fragmented QRS in V2. Fig. 2 Family tree.

Introduction Sudden cardiac arrest (SCA) is a high mortality event. Up to 70% of SCAs are caused by an acute coronary syndrome; nevertheless, it is essential to consider also non–ischemic causes while evaluating a post–SCA patient. Clinical Case A 68–year–old male patient with history of hypertension and dyslipidemia, presenting to the emergency room (ER) for syncope. While waiting in the ER, another sincopal episode happened and ventricular fibrillation was detected, therefore he was treated with a DC shock. At the ECG record after SCA, any acute alteration was seen. At the blood tests, an early rise of myocardial injury markers was found. At bedside echocardiography, a slight apical hypokinesia with hypertrabeculation was reported. Hence, coronarography was performed and a multivasal ateromasic coronaropathy was treated with angioplasty and drug–eluting stenting of left main artery, left anterior descending artery and left circumflex artery. In the following days, other ventricular tachyarrhythmias episodes happened and were treated with DC shocks. Due to ventricular arrhythmias relapses and echocardiographic findings, a cardiac MRI was performed, showing subepicardial fatty infiltration in the mid–apical lateral wall with parietal bulging suggesting left ventricle arrhythmogenic cardiomyopathy. So, a cardiac defibrillator was implanted in secondary prevention. Genetic analysis was run and reported a VUS mutation on RYR2 gene, still under evaluation as a possible cause for the clinical events. Conclusions The present clinical case shows that many causes may lead to SCA. Our patient experienced syncopal episodes related to ventricular arrhythmias and an arrhythmic storm which were most likely caused by an ischemic event on the base of an undiagnosed left ventricle arrhythmogenic cardiomyopathy.