Right ventricular morphology and systolic function in left ventricular noncompaction cardiomyopathy.
The distinction between normal right ventricular (RV) trabeculations from abnormal has been difficult. We evaluated whether RV volume and function are related to left ventricular (LV) noncompaction (NC) cardiomyopathy and clinical events. Trabeculations or possible LVNC by cardiac magnetic resonance imaging was retrospectively observed among 105 consecutive cases. We measured LV end-systolic (ES) noncompacted-to-compacted ratio, RV ejection fraction (EF), RV apical trabecular thickness, and RV end-diastolic (ED) noncompacted-to-compacted ratio. A control group of 40 subjects was also reviewed to assess the exploratory measures. Comparing those with LVES noncompacted-to-compacted ratio ≥2, those with LVES noncompacted-to-compacted ratio <2, and the normal control group, adjusted means for RV apical trabecular thickness and RVED noncompacted-to-compacted ratio were generated. Logistic regression was used to evaluate the association of composite events traditionally associated with LVNC with RVEF after adjustment for aforementioned covariates, cardiovascular risk factors, delayed enhancement, LVEF, and LVES noncompacted-to-compacted ratio. Analysis of RV morphology found greater apical trabecular thickness among those with LVES noncompacted-to-compacted ratio ≥2 compared with those with LVES noncompacted-to-compacted ratio <2 or normal control group (31 ± 5 vs 27 ± 2.6 vs 22 ± 4 mm; p = 0.03 and p = 0.003, respectively). There was no difference between the groups in relation to the RVED noncompacted-to-compacted ratio. Low RVEF and LVES noncompacted-to-compacted ratio ≥2 had significant association with clinical events in this population even after adjusting for clinical and imaging parameters (p = 0.04 and p <0.001, respectively). In conclusion, RV dysfunction in a morphologic LVNC population is strongly associated with adverse clinical events. LVNC is associated with increased trabeculations of the RV apex.
Department of Internal Medicine Section on Cardiology, Wake Forest University School of Medicine, Winston-Salem, North Carolina. Electronic address: bstacey@wfubmc.edu.
Richard Brandon
RB
Stacey
Department of Internal Medicine Section on Cardiology, Wake Forest University School of Medicine, Winston-Salem, North Carolina.
Mousumi
M
Andersen
Raleigh Cardiology, WakeMed Health and Hospitals, Raleigh, North Carolina.
Jason
J
Haag
Division of Cardiology, Department of Internal Medicine, University of Mississippi Medical Center, Jackson, Mississippi.
Michael E
ME
Hall
Department of Internal Medicine at the University of Texas Southwestern, Dallas, Texas.
George
G
McLeod
Department of Internal Medicine Section on Cardiology, Wake Forest University School of Medicine, Winston-Salem, North Carolina.
Bharathi
B
Upadhya
Department of Internal Medicine Section on Cardiology, Wake Forest University School of Medicine, Winston-Salem, North Carolina; Department of Radiology, Wake Forest University School of Medicine, Winston-Salem, North Carolina.
William Gregory
WG
Hundley
Aurora Cardiovascular Services, Aurora Sinai/Aurora St. Luke's Medical Centers, Milwaukee, Wisconsin.
Vinay
V
Thohan
D005260:Female; D005500:Follow-Up Studies; D006352:Heart Ventricles / Q000473:pathology* / Q000503:physiopathology; D006801:Humans; D056830:Isolated Noncompaction of the Ventricular Myocardium / Q000175:diagnosis* / Q000473:pathology / Q000503:physiopathology; D019028:Magnetic Resonance Imaging, Cine / Q000379:methods*; D008297:Male; D008875:Middle Aged; D009200:Myocardial Contraction / Q000502:physiology*; D009206:Myocardium / Q000473:pathology; D011237:Predictive Value of Tests; D011379:Prognosis; D012189:Retrospective Studies; D013318:Stroke Volume; D013599:Systole; D016277:Ventricular Function, Left; D016278:Ventricular Function, Right / Q000502:physiology*