Acute myocarditis (AM) is an inflammatory injury of the myocardium secondary to infections, systemic autoimmune disorders, medications, or toxic agents. The patient’s genetic underground is a likely concurrent aetiology/contributory mechanism recently implicated in a proportion of AM. This review focuses on some critical new concepts of AM, updated indications for endomyocardial biopsy when cardiac magnetic resonance imaging is not sufficient or feasible, and estimation of long-term events after discharge. Furthermore, studies exploring AM as the cause of sudden cardiac death will be examined to assess the characteristics of patients who die due to AM before hospital admission. Managing the most severe clinical presentation, termed fulminant myocarditis (FM) characterized by haemodynamic instability due to ventricular arrhythmias or severe acute pump failure, will be summarized. Specific issues aimed to reduce the high mortality rate of FM, like early recognition, referring these patients from spoke centres to a hub centre, timely temporary mechanical circulatory support when indicated, early endomyocardial biopsy, and eventually immunosuppression, will be briefly discussed. Immune checkpoint inhibitors and desmosomal gene variant-associated AM will be highlighted as paradigmatic new forms of myocarditis.

Background: Abnormalities of the mitral valve (MV) apparatus are typical features of hypertrophic cardiomyopathy (HCM). These abnormalities include leaflet elongation, thick leaflets, displacement of papillary muscle, and systolic anterior motion (SAM) of the MV anterior leaflet. Mitral valve chordal rupture associated with HCM is a rare but serious issue capable of change the clinical apparence and the prognosis of the patient.Case summary: A 57-year-old lady with a history of diabetes, dyslipidemia, and a previous single episode of atrial fibrillation (treated with pharmacological cardioversion), presented to the Emergency Department for worsening dyspnea (New York Heart Association Classification class IV). A trans-thoracic echocardiogram (TTE) showed a significant, septal, and asymmetric left ventricular hypertrophy (basal anteroseptal wall diastolic thickness of 19 mm) with normal left ventricle systolic function. A SAM of AML was evident together with a left ventricular outflow tract gradient of 56 mmHg at rest, rising to 136 mmHg during the Valsalva maneuver. In addition, there was evidence of moderate to severe mitral regurgitation (MR) with an anteriorly directed jet, not very typical of MR related to SAM. A 2D-3D trans-esophageal echocardiogram (2D-3D TEE) revealed a combined MR mechanism based on PML degenerative prolapse with P2-flail from ruptured chordae with related eccentric anteriorly directed regurgitant jet, together with a second regurgitant posteriorly directed jet, related to SAM of AML. The patient underwent MV repair together with septal myectomy, with a good final outcome.Conclusion: Pre-operative echocardiography (both TTE and 2D-3D TEE) is an essential tool in order to detect different MV abnormalities in patients with HCM. These types of patients should never be treated by septal reduction alone. Surgical MV repair or replacement, together with septal myectomy, may be the preferred approach.

Although mitral valve prolapse (MVP) is the most prevalent valvular abnormality in Western countries and generally carries a good prognosis, a small subset of patients is exposed to a significant risk of malignant ventricular arrhythmias (VAs) and sudden cardiac death (SCD), the so-called arrhythmic MVP (AMVP) syndrome. Recent work has emphasized phenotypical risk features of severe AMVP and clarified its pathophysiology. However, the appropriate assessment and risk stratification of patients with suspected AMVP remains a clinical conundrum, with the possibility of both overestimating and underestimating the risk of malignant VAs, with the inappropriate use of advanced imaging and invasive electrophysiology study on one hand, and the catastrophic occurrence of SCD on the other. Furthermore, the sports eligibility assessment of athletes with AMVP remains ill defined, especially in the grey zone of intermediate arrhythmic risk. The definition, epidemiology, pathophysiology, risk stratification, and treatment of AMVP are covered in the present review. Considering recent guidelines and expert consensus statements, we propose a comprehensive pathway to facilitate appropriate counseling concerning the practice of competitive/leisure-time sports, envisioning shared decision making and the multidisciplinary “sports heart team” evaluation of borderline cases. Our final aim is to encourage an active lifestyle without compromising patients’ safety.

Objectives: Patients with acute ST-segment elevation myocardial infarction (STEMI) are at high risk for recurrent coronary events (RCE). Non-culprit plaque progression and stent failure are the main causes of RCEs. We sought to identify the incidence and predictors of RCEs. Methods: Eight hundred thirty patients with STEMI were enrolled and followed up for 5 years. All patients underwent blood test analysis at hospital admission, at 1-month and at 12-month follow-up times. Patients were divided into RCE group and control group. RCE group was further categorized into non-culprit plaque progression and stent failure subgroups. Results: Among 830 patients with STEMI, 63 patients had a RCE (7.6%). At hospital admission, HDL was numerically lower in RCE group, while LDL at both 1-month and 12-month follow-up times were significantly higher in RCE group. Both HDL at hospital admission and LDL at 12-month follow-up were independently associated with RCEs (OR 0.90, 95% CI 0.81–0.99 and OR 1.041, 95% CI 1.01–1.07, respectively). RCEs were due to non-culprit plaque progression in 47.6% of cases, while in 36.5% due to stent failure. The mean time frame between pPCI and RCE was significantly greater for non-culprit plaque progression subgroup as compared to stent failure subgroup (27 ± 18 months and 16 ± 14 months, P = 0.032). Conclusion: RCEs still affect patients after pPCI. Low levels of HDL at admission and high levels of LDL at 12 months after pPCI significantly predicted RCEs. A RCE results in non-culprit plaque progression presents much later than an event due to stent failure.