Mechanical Bridging to Improvement in Severe Acute 'Nonischemic, Nonmyocarditis' Heart Failure

Discussion

The patients described here represent a unique subset with nonischemic cardiomyopathy and acute cardiac decompensation. All four patients were women who needed ventricular assistance for cardiogenic shock. None of them had a history of chronic heart failure or histologic evidence of myocarditis, but they all had histologic characteristics more suggestive of chronic disease. Because the left ventricular apical specimens obtained at VAS implantation measured approximately 2 cm^[3], it is unlikely that myocarditis was missed because of a sampling error. In all cases, improvement occurred during myocardial rest after the ventricle had been unloaded by the VAS.

Improved cardiac function after prolonged VAS support has been well documented. Such support has been shown to result in histologic changes compatible with normalization at the cellular level (Figures 1 and 2), as well as improved physiologic characteristics.^[2] In fact, some patients with chronic heart failure who have required VAS explantation because of pump-related complications or infections have survived long-term with adequate myocardial function.^[3] In our four cases, VAS unloading and medical management resulted in dramatic improvement. Medications known to have positive ventricular remodeling capabilities, such as β blockers, angiotensin-converting enzyme inhibitors, and spironolactone, were continued during the entire VAS support period.

Although there are no clear preoperative predictors of VAS-supported recovery of myocardial function, DSE with concurrent monitoring of hemodynamic values may help identify patients who will recover sufficient myocardial function to tolerate device explantation if indicated.^[8]  Table III shows our protocol for such testing and Table IV lists contraindications for weaning and indications for aborting the test. All four of our patients were able to generate a normal cardiac output while maintaining normal filling and pulmonary artery pressures at maximal dobutamine stress levels. In addition, the left ventricle did not dilate, and LVEF improved as the dobutamine dose was increased. In two patients, significant mitral regurgitation was present during the study and did not improve with dobutamine stress; these two patients required mitral valve replacement. Thus, DSE was particularly useful in determining whether explantation should be done and, if so, the appropriate timing of the procedure and the need for adjunctive valve replacement.

The clinical presentation of acute heart failure without antecedent evidence of cardiac disease is familiar to all physicians involved in cardiac transplantation and the treatment of heart failure. In these four cases, the underlying cause of the cardiomyopathy is unknown. Other causes of acute heart failure such as toxic myocarditis and thyrotoxicosis were ruled out. Given the patients' recent constitutional symptoms and the acuity of onset, the pathophysiology of the illnesses may be similar to that of myocarditis. It is intriguing that all four patients were women, but their condition was not likely postpartum cardiomyopathy because one of them had never been pregnant and the others had been pregnant at a much earlier date. One patient developed heart failure again, but its onset was slow enough to allow successful transplantation. We could not identify any factors that might have predicted this development. The results of this patient's weaning study were similar to those of the other patients.

These patients represent a unique subpopulation with “nonmyocarditis, nonischemic’ acute heart failure. Although this condition may result in a high mortality rate, it also may be successfully treated with prompt mechanical unloading as a bridge to improved ventricular function. Historically, such patients have been at heightened risk for a transplant. Further studies are needed to clarify the pathophysiology of this disease and to determine how to identify similar patients who may benefit from VAS unloading.

CHF. 2004;10(2) © 2004 Le Jacq Communications, Inc.

Cite this: Mechanical Bridging to Improvement in Severe Acute 'Nonischemic, Nonmyocarditis' Heart Failure - Medscape - Mar 01, 2004.