Background: The impact of COVID-19 on heart transplant (HTx) recipients remains unclear, particularly in the early post-transplant period. Methods: We share novel insights from our experience in five HTx patients with COVID-19 (three within 2 months post-transplant) from our institution at the epicenter of the pandemic. Results: All five exhibited moderate (requiring hospitalization, n = 3) or severe (requiring ICU and/or mechanical ventilation, n = 2) illness. Both cases with severe illness were transplanted approximately 6 weeks before presentation and acquired COVID-19 through community spread. All five patients were on immunosuppressive therapy with mycophenolate mofetil (MMF) and tacrolimus, and three that were transplanted within the prior 2 months were additionally on prednisone. The two cases with severe illness had profound lymphopenia with markedly elevated C-reactive protein, procalcitonin, and ferritin. All had bilateral ground-glass opacities on chest imaging. MMF was discontinued in all five, and both severe cases received convalescent plasma. All three recent transplants underwent routine endomyocardial biopsies, revealing mild (n = 1) or no acute cellular rejection (n = 2), and no visible viral particles on electron microscopy. Within 30 days of admission, the two cases with severe illness remain hospitalized but have clinically improved, while the other three have been discharged.

We evaluated the association between two-dimensional (2D) echocardiography (echo) determined myocardial contraction fraction (MCF) and adverse cardiovascular outcomes including incident heart failure (HF), atherosclerotic cardiovascular disease (ASCVD) and mortality. The MCF, the ratio of left ventricular (LV) stroke volume (SV) to myocardial volume (MV), is a volumetric measure of myocardial shortening that can distinguish pathologic from physiologic hypertrophy. Using 2D-echo-guided M-mode data from the Cardiovascular Health Study, we calculated MCF among individuals with LV ejection fraction (EF)≥55%, and used Cox models to evaluate its association with incident HF, ASCVD, and all-cause mortality after adjusting for clinical and echo parameters. We assessed whether log2(SV) and log2(MV) were consistent with the expected 1:−1 ratio used in the definition of MCF. Among 2147 participants (age 72±5), average MCF was 59±13%. After controlling for clinical and echo variables, each 10% absolute increment in MCF was associated with lower risk of HF (HR=0.88; 95% CI=0.82, 0.94), ASCVD (HR=0.90; 95% CI=0.85, 0.95) and death (HR=0.93; 95% CI=0.89, 0.97). Moreover, the MCF was still significantly associated with ASCVD and mortality, but not HF, after adjustment for percent predicted LV mass. Significant departure from the 1:−1 ratio was not observed for ASCVD or death, but did occur for HF, driven by a stronger association for MV than SV. In conclusion, among older adults without CVD or low LVEF, 2D-echo-guided M-mode-derived MCF was independently associated with lower risk of adverse cardiovascular outcomes, but this ratiometric index may not capture the full relationship that is apparent when its components are modeled separately in the case of HF.

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BackgroundPatients with hypertrophic cardiomyopathy (HCM) and an identified sarcomere mutation have worse outcomes than those without though the underlying mechanism is incompletely understood. The presence of replacement fibrosis measured by late gadolinium enhancement (LGE) and diffuse fibrosis measured by extracellular volume (ECV) using cardiac magnetic resonance imaging (CMR) are associated with ventricular arrhythmias and cardiac mortality. We aimed to associate these two forms of fibrosis with identified sarcomere mutations. Methods and ResultsThree hundred and thirty-six (336) patients with HCM underwent CMR at a single quaternary referral centre between January 2012 and February 2017. Genetic testing was performed in 73 of these patients, yielding an identified sarcomeric mutation in 29 (G1), no mutation in 39 (G-), and a variant of unknown significance (VUS) in five. LGE was more prevalent in G1 compared to G-patients (86 vs. 56%, OR 4.3, p=0.01) and was more extensive (7.565.5% of [left ventricular] LV mass vs. 3.063.0%, p,0.001). Global ECV from myocardial segments excluding LGE was similar among both groups (26.962.9 vs. 25.662.8%, p=0.46). However, in G1 patients ECV was greater in the hypertrophied regions of the basal anteroseptum (30.267.0 vs. 26.863.6%, p=0.004) and basal inferoseptum (28.164.3 vs. 26.262.9%, p=0.005). ConclusionsGenotyped HCM patients with an identified sarcomere mutation have greater LGE and greater regional, but not global, ECV than HCM patients without an identified mutation. This difference in fibrosis may contribute to worse outcomes in patients with an identified HCM mutation.