Effects of Cardiac Resynchronisation Therapy on Dilated Cardiomyopathy With Isolated Ventricular Non-Compaction
What are the effects of cardiac resynchronization therapy (CRT) on left ventricular (LV) reverse remodeling among patients with dilated cardiomyopathy (DCM) associated with isolated ventricular noncompaction (IVNC)?
A total of 52 patients with heart failure meeting criteria for CRT were recruited, including 20 patients with DCM associated with IVNC (IVNC-DCM), and 32 patients with DCM without IVNC. Patients were matched for age, sex, body surface area, and LV systolic function. Echocardiography (with contrast enhancement to optimize endocardial border visualization) was used to assess LV volumes and function, and at baseline and at 6-month follow-up. Using a 16-segment model, the number of segments with noncompaction (criteria including a noncompacted/compacted myocardium thickness ratio >2) was determined. Patients with heart failure were subsequently classified as CRT negative responders (LV systolic volume increase at 6 months compared to baseline), nonresponders (LV systolic volume reduction 0-14%), responders (systolic volume reduction 15-29%), or super-responders (systolic volume reduction ≥30%).
Different types of CRT response were observed in IVNC-DCM and non-IVNC DCM patients. In particular, in IVNC-DCM patients, the percentage of super-responders was significantly higher than for other patients (60% vs. 28%, respectively, p = 0.02). In addition, there was a trend toward reduction at 6 months in the number of IVNC segments (3; range, 1-5) compared to baseline (4; range 3-6; p = 0.07). Finally, in patients with IVNC-DCM, patients with a higher number of IVNC segments at baseline (>4) were more likely to be responders or super-responders than were patients with ≤4 IVNC segments (p = 0.003).
Patients with DCM associated with isolated LV noncompaction had greater LV reverse remodeling after CRT than did patients with DCM unassociated with noncompaction. A larger area of noncompaction (higher number of noncompacted myocardial segments) was associated with a greater likelihood of achieving CRT response, and with a greater degree of LV reverse remodeling.
Considered an unclassified cardiomyopathy, it is not clear whether noncompaction is a distinct etiology of DCM or a manifestation of it––possibly caused by incomplete LV hypertrophy. This is an important study in several respects. First, it revealed that, despite similar measures of baseline dyssynchrony, patients with DCM and noncompaction respond more favorably to CRT than do patients with DCM without noncompaction. Second, it suggests (although the trend did not reach statistical significance in this relatively small study) that regions of LV noncompaction can regress with CRT. This could support the theory that hyper-trabeculation might be a compensatory mechanism of a failing ventricle rather than the underlying mechanism of cardiomyopathy.
Keywords: Follow-Up Studies, Ventricular Function, Left, Myocardium, Systole, Cardiac Resynchronization Therapy, Body Surface Area, Cardiomyopathies, Ventricular Remodeling, Heart Failure, Hypertrophy, Cardiomyopathy, Dilated, Echocardiography
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