Key result
Solid organ transplant recipients can develop symptomatic obstructive HCM, with ~67% showing asymmetric septal hypertrophy.
Why the study?
Data on the incidence and prevalence of HCM in adult posttransplant patients were limited, despite reports of calcineurin inhibitor-associated HCM in pediatric solid organ transplant recipients.
Observational (n=12)
No
Symptomatic hypertrophic cardiomyopathy with dynamic LVOT obstruction can develop in adult solid organ transplant recipients on calcineurin inhibitors, and can be effectively managed with medical therapy and septal reduction.
Answers are grounded in this paper and cite their sources.
Should not yet change practice in transplant recipients; leaves open calcineurin inhibitor contribution to post-transplant HCM.
Background. Hypertrophic cardiomyopathy (HCM) in pediatric solid organ transplant recipients has been reported in association with use of calcineurin inhibitors. However, data on the incidence and prevalence of HCM in adult posttransplant patients are limited. We sought to describe the clinical characteristics of solid organ transplant recipients who were diagnosed with HCM from 2011 to 2021 at a single center. Methods. Patients who had undergone solid organ transplant and exhibited left ventricular hypertrophy with left ventricular wall thickness ≥13 mm on transthoracic echocardiography were included. Clinical history, pedigree analysis, clinical genetic testing, transthoracic echocardiography, cardiac magnetic resonance imaging, treatment, and follow-up testing results were collected. Categorical variables were described as n (%). Continuous variables were described with medians and interquartile ranges and compared using the Wilcoxon rank-sum and Kruskal-Wallis tests. A 2-sided P < 0.05 was considered statistically significant. Results. Three lung, 5 kidney, and 4 liver transplant recipients from 12 different families were included. Seven patients (58%) did not carry a preexisting diagnosis of hypertension, and none had a history of aortic or subaortic stenosis. A majority of patients exhibited asymmetric septal hypertrophy (67%; medial septal thickness versus left ventricular posterior wall thickness 17 versus 13 mm; P < 0.001) and dynamic left ventricular outflow tract (LVOT) obstruction (58%). All patients were managed long term with calcineurin inhibitors. Clinical genetic testing in 6 patients identified 2 with disease-causing variants in 2 sarcomere genes, myosin binding protein-C and myosin heavy chain 7. Four patients (33%) underwent successful septal reduction therapy for treatment of symptomatic LVOT obstruction. Conclusions. Symptomatic HCM with dynamic LVOT obstruction can develop in solid organ transplant recipients, and genetic testing can identify individuals with sarcomeric HCM. Medical management and septal reduction therapies are treatment options for severe symptomatic disease.
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Reza et al. (2021) conducted an observational in Hypertrophic cardiomyopathy in solid organ transplant recipients (n=12). Solid organ transplant and calcineurin inhibitors was evaluated on Clinical characteristics and echocardiographic findings of HCM. Symptomatic hypertrophic cardiomyopathy with dynamic left ventricular outflow tract obstruction can develop in adult solid organ transplant recipients, with 67% exhibiting asymmetric septal hypertrophy.
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