Flavia Casolaro

Acute extracardiac conditions can occasionally produce electrocardiographic abnormalities that closely mimic acute coronary occlusion, posing a diagnostic challenge and increasing the risk of unnecessary activation of invasive cardiac pathways. Severe gastrointestinal distension, although uncommon, is a recognized cause of transient ST-segment elevation due to mechanical displacement of the heart, autonomic imbalance, and abrupt changes in ventricular loading conditions. These alterations may be particularly misleading in patients with chronic regional wall motion abnormalities, in whom new ECG changes risk being misinterpreted as recurrent ischemia. We report the case of a 68-year-old man with a history of inferior myocardial infarction who presented with marked abdominal distension secondary to a closed-loop small bowel obstruction. Despite the absence of chest pain, his ECG showed significant anterolateral ST-segment elevation. High-sensitivity troponin I remained negative, and transthoracic echocardiography demonstrated preserved anterior and apical motion, chronic inferior akinesia, and unchanged global longitudinal strain. Following nasogastric decompression, the ST-segment normalized completely within fifteen minutes. Subsequent imaging confirmed a closed-loop volvulus requiring urgent surgical intervention, with full bowel viability preserved. This case underscores the importance of integrating clinical context, biomarkers, and rapid echocardiographic assessment when evaluating ST-segment elevation, helping avoid unnecessary coronary angiography in the presence of extracardiac causes.

Obesity, sleep-disordered breathing (SDB), and epicardial adipose tissue (EAT) are increasingly recognized as interconnected contributors to cardiometabolic and cardiovascular disease, although they are often addressed as distinct clinical conditions. This narrative review aims to integrate current evidence on the reciprocal pathophysiological interactions linking these entities and their contribution to cardiovascular remodeling. A comprehensive literature search up to May 2025 was performed, focusing on clinical, imaging, and mechanistic studies examining obesity, SDB, EAT, and cardiovascular outcomes. Available data indicate that obesity promotes visceral and epicardial fat expansion, systemic inflammation, and altered cardiopulmonary mechanics, thereby facilitating the development of SDB. In turn, intermittent hypoxia and sympathetic activation associated with SDB further aggravate adipose tissue dysfunction and inflammatory activation of EAT. As a metabolically active fat depot in direct anatomical continuity with the myocardium and coronary arteries, EAT contributes to myocardial fibrosis, atrial remodeling, diastolic dysfunction, and coronary atherosclerosis through paracrine inflammatory and neurohumoral pathways. The convergence of these mechanisms delineates a high-risk cardiometabolic phenotype associated with atrial fibrillation, coronary artery disease, and heart failure with preserved ejection fraction. Recognizing obesity, SDB, and EAT as components of an integrated cardiometabolic system may support improved phenotypic stratification and inform more comprehensive approaches to residual cardiovascular risk.

Acute extracardiac conditions can occasionally produce electrocardiographic abnormalities that closely mimic acute coronary occlusion, posing a diagnostic challenge and increasing the risk of unnecessary activation of invasive cardiac pathways. Severe gastrointestinal distension, although uncommon, is a recognized cause of transient ST-segment elevation due to mechanical displacement of the heart, autonomic imbalance, and abrupt changes in ventricular loading conditions. These alterations may be particularly misleading in pa-tients with chronic regional wall motion abnormalities, in whom new ECG changes risk being misinterpreted as recurrent ischemia. We report the case of a 68-year-old man with a history of inferior myocardial infarction who presented with marked abdominal dis-tension secondary to a closed-loop small bowel obstruction. Despite the absence of chest pain, his ECG showed significant anterolateral ST-segment elevation. High-sensitivity troponin I remained negative, and transthoracic echocardiography demonstrated pre-served anterior and apical motion, chronic inferior akinesia, and unchanged global longitudinal strain. Following nasogastric decompression, the ST-segment normalized completely within fifteen minutes. Subsequent imaging confirmed a closed-loop volvulus requiring urgent surgical intervention, with full bowel viability preserved. This case underscores the importance of integrating clinical context, biomarkers, and rapid echo-cardiographic assessment when evaluating ST-segment elevation, helping avoid un-necessary coronary angiography in the presence of extracardiac causes.

Background and Clinical Significance: Early lead failure after dual-chamber pacemaker implantation is rare but clinically significant, particularly when associated with thromboembolic complications. Technical pitfalls at the time of implantation, such as suture fixation without protective sleeves, may be predisposed to premature lead damage and abrupt device malfunction. This case highlights the role of device interrogation in diagnosing arrhythmia-related stroke, the challenges of reimplantation in the setting of venous occlusion and anticoagulation, and the value of leadless pacing as a safe rescue strategy. Case Presentation: A 78-year-old man with a history of complete atrioventricular block underwent dual-chamber pacemaker implantation one year earlier. He presented to the emergency department with acute aphasia, right-sided hemiparesis, and facial asymmetry. Stroke was diagnosed, and new-onset atrial fibrillation was documented. Device interrogation revealed an abrupt fall in lead impedance followed by a sharp rise consistent with lead insulation failure and premature battery depletion. Fluoroscopy demonstrated multiple focal narrowings of the leads and complete left subclavian vein occlusion, making conventional transvenous reimplantation unfeasible, while extraction was judged high risk. Right-sided reimplantation was avoided due to hemorrhagic risk under anticoagulation. A leadless pacemaker was implanted successfully in the apico-septal region of the right ventricle via ultrasound-guided femoral access. Hemostasis was secured with a figure-of-8 suture fixed inside a 3-way tap, providing constant compression and preventing hematoma. At two-months follow-up, device function was stable and neurological recovery was favorable (mRS = 2). Conclusions: This case underscores how multiple adverse factors—stroke, arrhythmia detection, early device failure, venous occlusion, and anticoagulation—may converge in a single patient, and demonstrates leadless pacing as a safe and effective rescue strategy in such complex scenarios.

Background and Clinical Significance: Early lead failure after dual-chamber pacemaker implantation is rare but clinically significant, particularly when associated with throm-boembolic complications. Technical pitfalls at the time of implantation, such as suture fixation without protective sleeves, may predispose to premature lead damage and abrupt device malfunction. This case highlights the role of device interrogation in diagnosing arrhythmia-related stroke, the challenges of reimplantation in the setting of venous oc-clusion and anticoagulation, and the value of leadless pacing as a safe rescue strategy. Case Presentation: A 78-year-old man with a history of complete atrioventricular block underwent dual-chamber pacemaker implantation one year earlier. He presented to the emergency department with acute aphasia, right-sided hemiparesis, and facial asym-metry. Stroke was diagnosed, and new-onset atrial fibrillation was documented. Device interrogation revealed an abrupt fall in lead impedance followed by a sharp rise con-sistent with lead insulation failure and premature battery depletion. Fluoroscopy demonstrated multiple focal narrowings of the leads and complete left subclavian vein occlusion, making conventional transvenous reimplantation unfeasible, while extraction was judged high risk. Right-sided reimplantation was avoided due to hemorrhagic risk under anticoagulation. A leadless pacemaker was implanted successfully in the api-co-septal region of the right ventricle via ultrasound-guided femoral access. Hemostasis was secured with a figure-of-8 suture fixed inside a 3-way tap, providing constant com-pression and preventing hematoma. At one-month follow-up, device function was stable and neurological recovery was favorable (mRS = 2). Conclusions: This case underscores how multiple adverse factors—stroke, arrhythmia detection, early device failure, venous occlusion, and anticoagulation—may converge in a single patient, and demonstrates leadless pacing as a lifesaving bailout strategy in such complex scenarios.