Background—The clinical profile and arrhythmic outcome of competitive athletes with isolated nonischemic left ventricular (LV) scar as evidenced by contrast-enhanced cardiac magnetic resonance remain to be elucidated.Methods and Results—We compared 35 athletes (80% men, age: 14–48 years) with ventricular arrhythmias and isolated LV subepicardial/midmyocardial late gadolinium enhancement (LGE) on contrast-enhanced cardiac magnetic resonance (group A) with 38 athletes with ventricular arrhythmias and no LGE (group B) and 40 healthy control athletes (group C). A stria LGE pattern with subepicardial/midmyocardial distribution, mostly involving the lateral LV wall, was found in 27 (77%) of group A versus 0 controls (group C; P<0.001), whereas a spotty pattern of LGE localized at the junction of the right ventricle to the septum was respectively observed in 11 (31%) versus 10 (25%; P=0.52). All athletes with stria pattern showed ventricular arrhythmias with a predominant right bundle branch block morphology, 13 of 27 (48%) showed ECG repolarization abnormalities, and 5 of 27 (19%) showed echocardiographic hypokinesis of the lateral LV wall. The majority of athletes with no or spotty LGE pattern had ventricular arrhythmias with a predominant left bundle branch block morphology and no ECG or echocardiographic abnormalities. During a follow-up of 38±25 months, 6 of 27 (22%) athletes with stria pattern experienced malignant arrhythmic events such as appropriate implantable cardiac defibrillator shock (n=4), sustained ventricular tachycardia (n=1), or sudden death (n=1), compared with none of athletes with no or LGE spotty pattern and controls.Conclusions—Isolated nonischemic LV LGE with a stria pattern may be associated with life-threatening arrhythmias and sudden death in the athlete. Because of its subepicardial/midmyocardial location, LV scar is often not detected by echocardiography.

Remodelling of the extracellular matrix (ECM) and cell surface by matrix metalloproteinases (MMPs) is an important function of monocytes and macrophages. Recent work has emphasised the diverse roles of classically and alternatively activated macrophages but the consequent regulation of MMPs and their inhibitors has not been studied comprehensively. Classical activation of macrophages derived in vitro from un-fractionated CD16+/− or negatively-selected CD16− macrophages up-regulated MMP-1, -3, -7, -10, -12, -14 and -25 and decreased TIMP-3 steady-state mRNA levels. Bacterial lipopolysaccharide, IL-1 and TNFα were more effective than interferonγ except for the effects on MMP-25, and TIMP-3. By contrast, alternative activation decreased MMP-2, -8 and -19 but increased MMP -11, -12, -25 and TIMP-3 steady-state mRNA levels. Up-regulation of MMPs during classical activation depended on mitogen activated protein kinases, phosphoinositide-3-kinase and inhibitor of κB kinase-2. Effects of interferonγ depended on janus kinase-2. Where investigated, similar effects were seen on protein concentrations and collagenase activity. Moreover, activity of MMP-1 and -10 co-localised with markers of classical activation in human atherosclerotic plaques in vivo. In conclusion, classical macrophage activation selectively up-regulates several MMPs in vitro and in vivo and down-regulates TIMP-3, whereas alternative activation up-regulates a distinct group of MMPs and TIMP-3. The signalling pathways defined here suggest targets for selective modulation of MMP activity.

Background The new designation of arrhythmogenic cardiomyopathy defines a broader spectrum of disease phenotypes, which include right dominant, biventricular, and left dominant variants. We evaluated the relationship between electrocardiographic findings and contrast‐enhanced cardiac magnetic resonance phenotypes in arrhythmogenic cardiomyopathy. Methods and Results We studied a consecutive cohort of patients with a definite diagnosis of arrhythmogenic cardiomyopathy, according to 2010 International Task Force criteria, who underwent electrocardiography and contrast‐enhanced cardiac magnetic resonance. Both depolarization and repolarization electrocardiographic abnormalities were correlated with the severity of dilatation/dysfunction, either global or regional, of both ventricles and the presence and regional distribution of late gadolinium enhancement. The study population included 79 patients (60% men). There was a statistically significant relationship between the presence and extent of T‐wave inversion across a 12‐lead ECG and increasing values of median right ventricular ( RV ) end‐diastolic volume ( P <0.001) and decreasing values of RV ejection fraction ( P <0.001). The extent of T‐wave inversion to lateral leads predicted a more severe RV dilatation rather than a left ventricular involvement because of the leftward displacement of the dilated RV , as evidenced by contrast‐enhanced cardiac magnetic resonance. A terminal activation delay of >55 ms in the right precordial leads (V1‐V3) was associated with higher RV volume ( P =0.014) and lower RV ejection fraction ( P =0.053). Low QRS voltages in limb leads predicted the presence ( P =0.004) and amount ( P <0.001) of left ventricular late gadolinium enhancement. Conclusions The study results indicated that electrocardiographic abnormalities predict the arrhythmogenic cardiomyopathy phenotype in terms of severity of RV disease and left ventricular involvement, which are among the most important determinants of the disease outcome.

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In survivors of OHCA, early CMR with a comprehensive tissue characterization protocol provided additional diagnostic and prognostic value. The identification of myocardial edema was associated with a favorable long-term outcome.

A 52‐year‐old male with no history of familiar sudden death arrived at our Emergency Department after syncope with loss of consciousness occurred during high fever. The thoracic high‐resolution computed tomography demonstrated bilateral multiple ground‐glass opacities. The nose‐pharyngeal swab resulted positive for SARS‐CoV‐2. The 12‐lead ECG presented a “coved‐type” aspect in leads V1 and V2 at the fourth intercostal space and a first degree atrio‐ventricular block. As soon as the temperature went down, the 12‐lead ECG resumed a normal aspect, maintaining a long PR interval.

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Aims Pocket hematoma is a common complication of cardiac implantable electronic device (CIED) procedures. the aim of the study was to research the clinical factors associated with pocket hematoma formation after CIED implantation or replacement and to identify the best perioperative antithrombotic management. Methods We retrospectively analyzed 500 consecutive patients who underwent to CIED implantation or replacement at our center from November 2014. Results Among our population, 206 patients (41.2%) were on anticoagulant therapy at the time of the intervention: 68 (13.6%) on ongoing Warfarin; 111 (22.2%) on low-molecular-weight heparin (LMWH); and 27 (5.4%) on ongoing direct oral anticoagulants. Antiplatelet therapy was present in 262 (52.4%) patients: in particular, 50 (10%) were on dual antiplatelet therapy, 64 (12.8%) were on single antiplatelet therapy and anticoagulant therapy, whereas 12 (2.4%) were on anticoagulant with dual antiplatelet therapy. Incidence of pocket hematoma after CIEDs implantation was of 4.6%. Considering the different perioperative anticoagulant strategies, patients on LMWH presented the higher hematoma rate [11/100 patients (11.0%), P < 0.001]. At the multivariate analysis, anticoagulant with dual antiplatelet therapy (P = 0.021, OR 6.3, IC 1.3–30.8), left ventricular ejection fraction (LVEF) less than 30% (P < 0.001, OR 7.4, IC 2.7–20.4), and use of LMWH (P = 0.008, OR 3.8, IC 1.4–10.6) resulted the strongest predictors of pocket hematoma (Hosmer test = 0.899). Considering replacement procedures, incidence of pocket hematoma was of 4.4%. The incidence was higher after ICD/CRT-D replacement. The majority of pocket hematoma occurred in patients with mechanical valve prosthesis (3/4 cases, 75%, P < 0.001). Conclusion The use of LMWH and a low LVEF expose patients to a higher risk of pocket hematoma after CIED procedures. Anticoagulant with dual antiplatelet therapy and LMWH should be avoided.