Reversible Cardiomyopathies—A Review

doi:10.1016/j.transproceed.2010.08.034

Transplantation Proceedings

Volume 42, Issue 9, November 2010, Pages 3673-3678

https://doi.org/10.1016/j.transproceed.2010.08.034 Get rights and content

Abstract

End-stage renal disease, cirrhosis, obesity, tachycardia, and extreme stress have all been shown to result in impaired left ventricular function. It is becoming clear, however, that the cardiomyopathies associated with these states are reversible after resolution of the underlying process. In this article, we present the current data demonstrating that renal transplantation, liver transplantation, and bariatric surgery can lead to reversal of uremic, cirrhotic, and obesity cardiomyopathies, respectively. We also discuss the reversibility of tachycardia-induced cardiomyopathy after radiofrequency ablation or pharmacologic therapy for rate or rhythm control and the reversibility of stress-induced cardiomyopathy with supportive care.

Section snippets

Uremic Cardiomyopathy

Coronary artery disease (CAD) is the most important cause of death among end-stage renal disease (ESRD) patients worldwide, but there are multiple cardiac effects of renal disease, which are often collectively referred to as uremic cardiomyopathy. Concentric left ventricular hypertrophy (LVH) is present in the earliest stages of progressive renal disease.³ Additional characteristics of uremic cardiomyopathy are systolic dysfunction, diastolic dysfunction, and left ventricular (LV) dilatation.

Cirrhotic Cardiomyopathy

Unlike uremic cardiomyopathy, the cardiac dysfunction associated with cirrhosis of the liver can be quite subtle. The prevalence is unknown, because the disease is generally latent, only resulting in overt heart failure after a period of cardiovascular stress, such as exercise, drugs, infection, hemorrhage, or surgery, especially transjugular intraperitoneal shunting (TIPS).¹⁰ Cirrhosis results in hyperdynamic circulation with increased cardiac output and decreased peripheral vascular

Obesity Cardiomyopathy

There is overwhelming evidence that obesity increases the risk of heart disease and, more specifically, heart failure. Longstanding morbid obesity can lead to severe cardiomyopathy called obesity or lipotoxic cardiomyopathy. Obesity leads to an increased blood volume and increased cardiac output as a result of the heightened metabolic activity of the excess adipocytes present in the obese patient. Increased preload and afterload can lead to increased LV wall stress, resulting in LV dilatation

Tachycardia-Induced Cardiomyopathy

As early as 1986, Packer et al described cardiomyopathies resulting from tachyarrhythmias that were present for years but then improved after treatment by radiofrequency ablation.²⁷ Tachycardia-induced cardiomyopathy (TIC) is now a well described widely known reversible cardiomyopathy characterized by LV dilatation and a reduced ejection fraction. Treatment of the tachycardia by either rate or rhythm control is the cornerstone of therapy, which leads to an improvement in cardiac function.28, 29

Stress-Induced Cardiomyopathy

Stress-induced cardiomyopathy, also widely called takotsubo cardiomyopathy, apical ballooning syndrome, or broken heart syndrome, is a reversible cardiomyopathy that is often confused clinically with acute coronary syndromes (ACS), but catheterization fails to reveal evidence of significant obstructive coronary disease. It is associated with hypokinesis or akinesis of the middle and apical segments of the left ventricle, which results in ballooning of the apical wall with sparing of basal

Conclusion

In contrast to many acute heart failure syndromes, only a handful of chronic heart failure problems have been demonstrated to be reversible. We have discussed four such chronic syndromes along with one acute syndrome and the treatments which can reverse these cardiomyopathies: kidney transplantation for uremic, liver transplantation for cirrhotic, gastric bypass surgery for obesity, and heart rate control with either radiofrequency ablation or pharmacotherapy for tachycardia-induced, and

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Cited by (24)

“Obesity paradox” and takotsubo syndrome
2022, International Journal of Cardiology: Cardiovascular Risk and Prevention
An “obesity paradox” has been reported in patients with hypertension and heart failure, in which obese patients fare better than patients with normal-weight. The purpose of this study was to determine whether there is an “obesity paradox” in patients with takotsubo syndrome (TTS).
The prevalence of obesity in databases/registries of patients with TTS was compared to the prevalence of obesity in world general populations. Obese patients with TTS were explored regarding the stress triggers precipitating the illness, hospital outcome, and post-discharge readmission. Finally, the literature on the “obesity paradox” was explored to understand how it could be applied to TTS.
A prevalence of obesity of ∼10–11% has been reported in large cohorts of patients with TTS, which represents 1/3 to ¼ of the prevalence reported in worldwide general populations, suggesting that, normal-weight than obese individuals, are more predisposed to develop TTS, with the latter nevertheless also suffering TTS, when triggered by enormous physical stresses. Obese patients with TTS are likely to have milder hospital outcomes, lower mortality, and lower rate of early readmission. A greater sympathetic nervous system (SNS) response in a number of hyperadrenergic states in normal-weight than obese patients, may explain findings in patients with TTS.
An “obesity paradox” has been identified in patients with TTS. Reporting on body mass index and other markers of obesity in patients with TTS, and implementing some recommendations on monitoring noninvasively the SNS in patients with TTS, may solidify that obesity has a preventive/ameliorating effect for TTS development and its clinical course.
Could Different Thresholds for Tachycardic-Induced Atrial Myopathy Reflect Different Rates Between Atrial Fibrillation and Flutter?
2020, Journal of the American College of Cardiology
A rare case of transient left ventricular apical ballooning syndrome following living donor liver transplantation: A case report and literature review
2019, International Journal of Surgery Case Reports
Citation Excerpt :
Characteristically, hypokinesis or akinesis occurs in the middle and apical segments of left ventricle in the absence of epicardial coronary lesions, which results in ballooning of the apical wall with sparing of basal systolic function. Prognosis of this disease is relatively good and cardiac function of most cases improves to normal levels with a proper conservative management [4,5]. Here, we report the case of transient LV-ABS in liver transplantation recipient several days after LDLT with some literature view.
Transient Left Ventricular Apical Balloon Syndrome (LV-ABS) is an unknown acute dysfunction of the left ventricle, which develops under emotional or physical stress events like the major surgical postoperative period.
A 68-year-old woman diagnosed with hepatitis C cirrhosis was admitted for living donor liver transplantation (LDLT). No evidence for underlying cardiac or pulmonary disease was found. LDLT was performed, and her intra and post-operative course was uneventful. On post-operative day 4, dyspnea and tachycardia were observed. Echocardiography showed a severe wall motion abnormality with ballooning of the apex with normal basilar wall motion and a severely impaired left ventricular function with an ejection fraction (EF) of 40%. Blood tests showed greatly increased level of N-terminal pro-brain natriuretic peptide (NT- pro BNP). Evidence of significant ischemic heart disease was not obtained and a transient LV-ABS was diagnosed. Although she required intensive care, her cardiac function became normal by conservative treatment.
Transient LV-ABS has been reported to occur more frequently in post-menopausal women with reduced estrogens reported to protect myocardium from sympathetic stress after mental or physical stress events. It has been suggested that this disease arises from myocardial stunning with high levels of circulating catecholamines and stress related neuropeptides. However, even in a serious condition, cardiac function has recovered normally in all cases by appropriate care.
Transient LV-ABS is one cause of cardiac dysfunction after LDLT, and it is important to strictly manage cardiac function when diagnosed as transient LV-ABS.
Cardiohepatic Interactions
2017, Encyclopedia of Cardiovascular Research and Medicine
A perspective on obesity cardiomyopathy
2012, Obesity Research and Clinical Practice
Citation Excerpt :
Additionally, pulmonary hypertension as a result of hypoxemia from obstructive sleep apnea syndrome (OSAS) and/or obesity-hypoventilation syndrome (OHS/Pickwickian syndrome) [2,3,5–8] likely plays a role. Structural heart changes related to obesity include increased LV wall thickening (both eccentric and concentric), increased LV mass and LV dilatation [2,9,10]. The evaluation of right ventricular (RV) dysfunction in obese patients is challenging due to the high comorbid rate of OSAS and pulmonary hypertension, however an independent association between obesity and RV dysfunction has been described.
Obesity is a major health concern worldwide as obese individuals have a greater risk of death from any cause than normal-weight individuals. As the number of overweight children and adolescents continues to rise, so too has the scope of the obesity epidemic grown substantially. In this article, the authors discuss the role of obesity in the development of heart failure and the pathophysiology of obesity cardiomyopathy, as well as explore the potential role of bariatric surgery and mechanical circulatory support devices (MCSD) as potential therapeutic targets.
Perioperative management of a patient with morbid obesity and severe cardiomyopathy: a case report and literature review
2023, Journal of International Medical Research

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Thoracic transplantationHeartReversible Cardiomyopathies—A Review

Abstract

Section snippets

Uremic Cardiomyopathy

Cirrhotic Cardiomyopathy

Obesity Cardiomyopathy

Tachycardia-Induced Cardiomyopathy

Stress-Induced Cardiomyopathy

Conclusion

Chest

Kidney Int

Kidney Int

Am J Transplant

Transplant Proc

J Hepatol

Am J Med Sci

J Cardiac Fail

Surg Obes Rel Dis

Am J Cardiol

Am J Med

Heart Rhythm

J Cardiol

Am Heart J

Am Heart J

Cardiovasc Revasc Med

J Obstet Gynaecol Can

J Am Coll Cardiol

Normalization of ejection fraction and resolution of symptoms in chronic severe heart failure is possible with modern medical therapy: clinical observations in 11 patients

Am J Ther

Impact of renal transplantation of uremic cardiomyopathy

Transplantation

Myocardial perfusion and ventricular function assessed by SPECT and gated-SPECT in end-stage renal disease patients before and after renal transplant

Arch Med Res

The effect of kidney transplant on cardiac function: an echocardiographic perspective

Echocardiography

Cirrhotic cardiomyopathy

Orphanet J Rare Dis

Thoracic transplantation
Heart
Reversible Cardiomyopathies—A Review