BACKGROUND: Disappearance of left ventricular hypertrabeculation/noncompaction (LVHT) has been reported only in myocarditis. We report disappearance of LVHT after implantation of a biventricular pacemaker in a 68-year-old female. She suffered from symmetrical polyneuropathy and heart failure New York Heart Association Class IV due to dilated cardiomyopathy despite angiotensin-converting enzyme inhibitors, beta-blockers, digitalis, and diuretics. Echocardiographically, she showed an enlarged poorly contracting left ventricle with LVHT involving the lateral and apical wall. METHODS AND RESULTS: In January 2001, a biventricular pacemaker system was implanted. From that time, her condition and left ventricular systolic function improved and the left ventricular size decreased. Surprisingly, LVHT could no longer be detected echocardiographically. CONCLUSIONS: We explain LVHT disappearance as follows: (1) the trabeculations are still existing, but not visible any more because of the better contraction state of the left ventricle; (2) the trabeculations have regressed because they are not needed anymore; and (3) the trabeculations have been falsely diagnosed and were in fact ventricular thrombi, which is quite unlikely because no embolic events occurred. LVHT can disappear if dilatation of the cardiac cavities and severely reduced systolic function regress. The dynamics of LVHT may represent an adaption mechanism of the cardiac function to compensate for a temporary failing myocardium.
BACKGROUND: Disappearance of left ventricular hypertrabeculation/noncompaction (LVHT) has been reported only in myocarditis. We report disappearance of LVHT after implantation of a biventricular pacemaker in a 68-year-old female. She suffered from symmetrical polyneuropathy and heart failure New York Heart Association Class IV due to dilated cardiomyopathy despite angiotensin-converting enzyme inhibitors, beta-blockers, digitalis, and diuretics. Echocardiographically, she showed an enlarged poorly contracting left ventricle with LVHT involving the lateral and apical wall. METHODS AND RESULTS: In January 2001, a biventricular pacemaker system was implanted. From that time, her condition and left ventricular systolic function improved and the left ventricular size decreased. Surprisingly, LVHT could no longer be detected echocardiographically. CONCLUSIONS: We explain LVHT disappearance as follows: (1) the trabeculations are still existing, but not visible any more because of the better contraction state of the left ventricle; (2) the trabeculations have regressed because they are not needed anymore; and (3) the trabeculations have been falsely diagnosed and were in fact ventricular thrombi, which is quite unlikely because no embolic events occurred. LVHT can disappear if dilatation of the cardiac cavities and severely reduced systolic function regress. The dynamics of LVHT may represent an adaption mechanism of the cardiac function to compensate for a temporary failing myocardium.