Related Experiment Video
Updated: Oct 9, 2025
Induction of Right Ventricular Failure by Pulmonary Artery Constriction and Evaluation of Right Ventricular Function in Mice
Published on: May 13, 2019
Left Ventricular Hypertrophy and Hypertrophic Cardiomyopathy in Adult Solid Organ Transplant Recipients
Nosheen Reza1, Alejandro De Feria1, Teresa Wang1
1Division of Cardiovascular Medicine, Department of Medicine, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA.
Insights
Hypertrophic cardiomyopathy (HCM) can develop in adult solid organ transplant recipients, often linked to calcineurin inhibitors. Genetic testing helps identify sarcomeric causes, with medical and surgical options available for severe cases.
Area of Science:
- Cardiology
- Transplant Medicine
- Genetics
Background:
- Hypertrophic cardiomyopathy (HCM) is a known complication in pediatric solid organ transplant recipients using calcineurin inhibitors.
- Limited data exists on HCM incidence and prevalence in adult posttransplant patients.
Purpose of the Study:
- To describe the clinical characteristics of adult solid organ transplant recipients diagnosed with HCM.
- To investigate the association between calcineurin inhibitor use and HCM development in this population.
Main Methods:
- Retrospective review of adult solid organ transplant recipients diagnosed with HCM (left ventricular wall thickness ≥13 mm) between 2011-2021.
- Collection of clinical history, genetic testing, echocardiography, cardiac MRI, and treatment data.
- Statistical analysis using Wilcoxon rank-sum and Kruskal-Wallis tests.
Main Results:
- Twelve patients (lung, kidney, liver recipients) were included; 58% had no prior hypertension.
- A majority (67%) presented with asymmetric septal hypertrophy and 58% had dynamic left ventricular outflow tract (LVOT) obstruction.
- Calcineurin inhibitors were used long-term in all patients; genetic testing identified sarcomeric variants in 2/6 patients.
Conclusions:
- Symptomatic HCM with dynamic LVOT obstruction can occur in solid organ transplant recipients.
- Genetic testing is valuable for identifying sarcomeric causes of HCM in transplant patients.
- Medical management and septal reduction therapies are effective for severe symptomatic disease.
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.
Related Concept Videos
01:29Cardiomyopathy III: Hypertrophic Cardiomyopathy
01:29Heart Failure II: Pathophysiology
01:29Cardiomyopathy V: Interprofessional Care
01:30Cardiomyopathy II: Dilated Cardiomyopathy
01:20Mitral Regurgitation I: Introduction
01:25Cardiomyopathy I: Introduction and Classification