Immunosuppressive drugs and hypertrophic cardiomyopathy

Brand, PaulL P.; Brus, F; Natazuka, Toshiki; Ogawa, Ryoichi; Kizaki, Tomohiko; Ueno, Hiroshi; Shiotani, Hideyuki; Koizumi, Tamio; Nishimura, Ryuichiro; Nakagawa, Toshio; Dhawan, Anil; Mack, DavidR; Langnas, Alan Norman; Shaw, ByersW; Vanderhoof, J. A.

doi:10.1016/s0140-6736(95)90153-1

Cited by 23 publications

(4 citation statements)

References 7 publications

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“…Nakata et al (19) report that elevated blood level of TAC, particularly levels above 15 ng/mL, have a direct effect on the ventricular wall thickness. While cardiac hypertrophy has been partially attributed to concomitant steroid therapy, prednisone tapering did not prevent or cure the problem (19–21). Additionally, myocardial changes have also been linked to the deficiency of trace element selenium (22).…”

Section: Discussionmentioning

confidence: 99%

Reversal of tacrolimus‐related hypertrophic obstructive cardiomyopathy 5 years after kidney transplant in a 6‐year‐old recipient

Jarzembowski

John

Panaro³

et al. 2005

Pediatric Transplantation

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Hypertrophic obstructive cardiomyopathy (HOCM) is an unusual but serious side-effect of tacrolimus (TAC) based immunosuppression primarily affecting pediatric patients after solid organ transplant. TAC-induced HOCM has already been described in patients after liver, bowel and heart transplant shortly after the procedure. Herein, we present the first case report of TAC-induced HOCM in a young renal transplant recipient 5 yr after renal transplant. The condition was diagnosed by ECHO and EKG and successfully treated by discontinuation of TAC followed by conversion to cyclosporine (CsA).

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Section: Discussionmentioning

confidence: 99%

Reversal of tacrolimus‐related hypertrophic obstructive cardiomyopathy 5 years after kidney transplant in a 6‐year‐old recipient

Jarzembowski

John

Panaro³

et al. 2005

Pediatric Transplantation

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“…Hypertrophic cardiomyopathy has also been reported to arise from the administration of steroids. Brand and Brus ( 14) report on three premature infants who developed hypertrophic cardiomyopathy while being treated with dexamethasone for bronchopulmonary dysplasia. Because both dexamethasone and tacrolimus have similar global effects on the immune system in terms of inhibiting cytokine synthesis, it has been proposed that immunomodulating mechanisms may play a role in the development of cardiomyopathy.…”

Section: Discussionmentioning

confidence: 99%

“…Alternatively, tacrolimus and dexamethasone share a number of side‐effects, including fluid retention and hypertension, both of which can be contributing factors to the pathogenesis of hypertrophic cardiomyopathy ( 14). In this scenario, concurrent use of steroids and tacrolimus may accelerate development of hypertrophic cardiomyopathy.…”

Section: Discussionmentioning

confidence: 99%

Sirolimus in pediatric gastrointestinal transplantation: The use of sirolimus for pediatric transplant patients with tacrolimus‐related cardiomyopathy

Pappas¹,

Weppler²,

Pinna³

et al. 2000

Pediatric Transplantation

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Hypertrophic obstructive cardiomyopathy (HOCM) associated with the use of tacrolimus is a rare complication of liver and intestinal transplantation seen almost exclusively among pediatric patients. Reduction of tacrolimus dosage or conversion to cyclosporin A (CsA) has been used as an effective treatment in reviewed cases. We present three pediatric transplant recipients who developed hypertrophic obstructive cardiomyopathy while under tacrolimus immunosuppression and were treated with conversion to sirolimus (Rapamycin). The patients (ages 6 yr, 12 yr and 11 months) were transplant recipients (liver, n = 2; liver and intestine, n = 1) who developed significant cardiomyopathy 15 and 96 months post-transplant. One patient died of post-transplant lymphoproliferative disorder 21 days after starting sirolimus. One patient had received two liver transplants and had been on CsA for 12 yr before conversion to tacrolimus at 60 months post-transplant for acute and chronic rejection. The surviving patients were receiving mycophenolate mofetil, tacrolimus and steroids at the time of diagnosis. Dose reduction of tacrolimus and treatment with beta blockers failed to alleviate the hemodynamic changes. The patients were converted to sirolimus 1.6, 37 and 148 months post-transplant and maintained a whole-blood trough level of 15-20 ng/mL 21 days after starting sirolimus. Repeat echocardiograms in the surviving patients showed improvement in cardiomyopathy. One patient had one rejection episode (intestinal biopsy, mild acute cellular rejection) after starting sirolimus that responded to a transient increase in steroids. The early demise of the third patient after sirolimus conversion prevented an adequate assessment of cardiomyopathy. Conversion to sirolimus was associated with a reduction in the cardiomyopathy of the two surviving patients while still providing effective immunosuppression. To our knowledge this observation has not been previously reported.

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“…Over the next decade, additional reports of obstructive HCM in pediatric solid organ transplant recipients were published, including in kidney, 11 liver, [12][13][14][15] and small bowel. 16 The etiology of LVH was thought to be because of tacrolimus, since the recognition of this clinical entity was coincident with the rise in its use after its approval by the US Food and Drug Administration. Around the same time, caselevel associations between regression of LV hypertrophy after decreasing or discontinuing the tacrolimus dose started to be reported.…”

Section: Introductionmentioning

confidence: 99%

Left Ventricular Hypertrophy and Hypertrophic Cardiomyopathy in Adult Solid Organ Transplant Recipients

Reza

Feria

Wang

et al. 2021

Transplantation Direct

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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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Immunosuppressive drugs and hypertrophic cardiomyopathy

Cited by 23 publications

References 7 publications

Reversal of tacrolimus‐related hypertrophic obstructive cardiomyopathy 5 years after kidney transplant in a 6‐year‐old recipient

Reversal of tacrolimus‐related hypertrophic obstructive cardiomyopathy 5 years after kidney transplant in a 6‐year‐old recipient

Sirolimus in pediatric gastrointestinal transplantation: The use of sirolimus for pediatric transplant patients with tacrolimus‐related cardiomyopathy

Left Ventricular Hypertrophy and Hypertrophic Cardiomyopathy in Adult Solid Organ Transplant Recipients

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