Published online Nov 28, 2017. doi: 10.4254/wjh.v9.i33.1253
Peer-review started: May 10, 2017
First decision: June 30, 2017
Revised: September 1, 2017
Accepted: September 15, 2017
Article in press: September 15, 2017
Published online: November 28, 2017
Patients of acute liver failure and of chronic liver disease, presenting with systolic heart failure within 7 d after the liver transplant surgery in absence of any preoperatively identified and obvious predisposing risk factor.
Systolic heart failure was diagnosed on basis of clinical presentation and echocardiography with greatly reduced left ventricle ejection fraction.
Liver graft dysfunction and severe sepsis may cause hemodynamic instability and were ruled out. Underlying cause for the observed systolic heart failure could not be made.
Creatine kinase-MB was elevated upon diagnosis of systolic heart failure after liver transplant. Troponin T sensitive card test was negative.
Severely reduced left ventricle ejection fraction was diagnosed on echocardiography.
Could not be made conclusively.
Respiration was assisted. Hemodynamics supported using inotropes and inodilators and beta blockers, aimed at preload and after load reduction. Sedation and analgesia were taken care of to reduce sympathetic adrenergic activity.
Cirrhotic cardiomyopathy and alcohol cardiomyopathy have been described as specific clinical entities that describe cardiomyopathy in setting of underlying chronic liver disease and with history of alcohol indulgence respectively. Acute broken heart syndrome describes the cardiomyopathy typically seen under stressful conditions and not necessarily after surgery and is said to resemble acute myocardial infarction.
In absence of established clinical features and limitations of existing prevalent diagnostic modalities, Bio-chemical makers like BNP and Troponin I may be routinely done as part of preoperative workup of patients posted for liver transplant surgery to help identify patients at greater risk of heart failure after the surgery.