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BACKGROUND The right ventriculoarterial coupling (R-V/A), a measure of right ventricular systolic dysfunction (RVSD) adaptation/maladaptation to chronic overload, and consequent pulmonary hypertension, has been little investigated in nonischemic dilated cardiomyopathy (NIDCM). We examined the correlates of R-V/A and traditional echocardiographic indices of RVSD, over the spectrum of pulmonary hypertension and tertiles of mean pulmonary artery pressures (PAPm). METHODS In 2016-2017, we studied 81 consecutive patients for heart transplant/advanced heart failure. Inclusion criteria were NIDCM, reduced ejection fraction (≤40%) and sinus rhythm. R-V/A was computed as the RV/pulmonary elastances ratio (R-Elv/P-Ea), derived from a combined right heart catheterization/transthoracic- echocardiographic assessment [right heart catheterization/transthoracic-echocardiographic (RHC/TTE)]. RESULTS A total of 68 patients (mean age 64 ± 7 years, 82% men) were eligible. After adjustments, R-Elv and P-Ea were higher in isolated postcapillary-pulmonary hypertension (Ipc-PH) than combined-pulmonary hypertension (Cpc-PH) (P = 0.004 and P = 0.002, respectively), whereas R-V/A progressively decreased over Ipc-PH and Cpc-PH (P = 0.006). According to PAPm increment, P-Ea congruently increased (P-Trend = 0.028), R-Elv progressively decreased (P-Trend

Necrotizing eosinophilic myocarditis (NEM) is a life-threatening condition that needs rapid diagnosis by endomyocardial biopsy and hemodynamic support usually by mechanical circulatory systems. We present the case of a 25-year-old Caucasian man who developed a refractory cardiogenic shock due to a NEM that was supported with a peripheral veno-arterial extracorporeal membrane oxygenation associated with intravenous steroids and recovered after 2 weeks. Further instrumental investigations lead to the final diagnosis of NEM as first presentation of eosinophilic granulomatosis with polyangiitis (formerly Churg-Strauss syndrome), remarking the importance of identifying the systemic disorder that usually triggers the eosinophilic damage of the myocardium.

A 31-year-old man presenting with cardiogenic shock and left ventricular ejection fraction of 10% received the diagnosis of giant cell myocarditis by endomyocardial biopsy. The patient was successfully treated with high-dose inotropes, intra-aortic balloon pump and venoarterial extracorporeal membrane oxygenation for 21 days associated with combined immunosuppression (thymoglobulin, steroids, cyclosporine). Immunosuppression including thymoglobulin is the regimen associated with the highest probability of recovery in case of giant cell myocarditis. Immunosuppression needs time to be effective; thus, hemodynamic support must be guaranteed. In the present case, we observed that full recovery can be obtained up to 21 days of support with extracorporeal membrane oxygenation and adequate immunosuppression.

Fulminant myocarditis is a distinct entity within the acute forms of myocarditis characterized by a rapidly progressive clinical course. Lymphocytic forms have been historically reported to generally resolve spontaneously with early appropriate aggressive supportive care alone. We describe the case of a 28-year-old man with lymphocytic fulminant myocarditis presenting with out-of-hospital cardiac arrest, treated with veno-arterial extracorporeal membrane oxygenation, progressed to end stage cardiac failure requiring heart transplantation. In line with recent evidence, we highlight the need for prolonged supportive treatment and the eventual persistent long-term ventricular dysfunction in patients with fulminant myocarditis