Pathological findings in cardiac apex removed during implantation of left ventricular assist devices (LVAD) are non-specific: 13-year-experience at a German Heart Center

Abstract

Background and aim: Ventricular assist devices (VAD) have become an established therapy for patients with end-stage heart failure. The two main reasons for this development are the shortage of appropriate donor organs and the increasing number of patients waiting for heart transplantation (HTX). Furthermore, the enormous advances in the technical equipment and the rising clinical experience have improved the implantation technique, the durability and the long-term patient outcomes.

Methods: We reviewed all cases of left ventricular assist device (LVAD) implantation at our Erlangen Heart Center during January 2000-July 2013. The main aim of this study was to analyze the underlying pathology from the cardiac apex removed during the implantation. From all patients, we created a follow-up, analyzed the pathological features with the clinical diagnoses and described the overall outcome.

Results: VAD implantation was performed in 266 cases at our center in the last 13 years (2.2% of the total of 12254 cardiac surgical operations in that period). From these patients, 223 underwent LVAD or biventricular (BVAD) implantation; the remaining received a right (RVAD) implantation. The most frequent underlying clinical diagnoses were dilated (n = 84, 37.7%, DCM) or ischemic (n = 61, 27.4%, ICM) cardiomyopathy. The pathological findings in the apex biopsy were generally non-specific and showed variable interstitial myocardial fibrosis with evidence of fibre loss, fatty degeneration and variable irregular atrophy of muscle fibres, consistent with dilated and ischemic cardiomyopathies as the most frequent causes of heart failure in these patients. Only a few cases showed other specific features such as myocarditis and AL-amyloidosis.

Conclusions: Pathological findings in cardiac apex removed during LVAD implantation are rather non-specific and they generally reflect the late stage or consequences of chronic myocardial damage in cases of dilated or ischemic cardiomyopathies. Variable patchy chronic inflammatory changes may be observed in cardiomyopathies as a non-specific reaction caused by myocardial fiber damage and should not lead to misinterpretation as evidence of myocarditis or revision of original diagnosis.

Keywords: Left ventricular assist devices (LVAD); apex pathology; dilatative cardiomyopathy; ischemic cardiomyopathy; myocarditis.

Figure 1

Cardiac Surgery at the University of Erlangen between January 2000 and July 2013. CABG = Coronary Artery Bypass Grafting; VP = Valve Procedures; TAVI = Transcatheter Aortic Valve Implantation; AS = Aortic Surgery; VAD = Ventricular Assist Device; HTX = Heart Transplantation; AOCS = Any Other Cardiac Surgery.

Figure 2

Distribution of the 223 implanted Left Ventricular Assist Devices (LVAD) at he University of Erlangen between January 2000 and July 2013. TAH = Total Artificial Heart.

Figure 3

Distribution of the underlying reasons for the LVAD implantation. AMI = Acute Myocardial infarction; AVD = Aortic Valve Disease; CHD = Congenital Heart Defect; DCM = Dilative Cardiomyopathy; HOCM = Hypertrophic Obstructive Cardiomyopathy; ICM = Ischemic Cardiomyopathy; MCM = Metabolic Cardiomyopathy; MVD = Mitral Valve Disease; PC = Post-Surgery-Cardiomyopathy; PCC = Post-Chemotherapy Cardiomyopathy; RCM = Restrictive Cardiomyopathy.

Figure 4

A: Intraoperative photograph showing the apex of the left ventricle, usually removed for the inflow cannula and then send for further histopathological examination. B: The inflow cannula was inserted into the left ventricle. C: This cannula was connected with the LVAD, then connected with the outflow cannula and inserted into the ascending aorta, finally.

Figure 5

Example of apex pathology in dilated (A) and ischemic (B, C) cardiomyopathy showed variable interstitial fibrosis with occasional reactive mononuclear cell aggregates (C) and myofibre hypertrophy.

Figure 6

A: Case of cardiac failure due to AL-amyloidosis (immunostaining for light chain). B: A case of myocarditis showed increased mononuclear inflammatory cells between muscle fibres. C: severe eosinophilic myocarditis.