title: Comparison of mortality rates and progression of left ventricular dysfunction in patients with idiopathic dilated cardiomyopathy and dilated versus nondilated right ventricular cavities.
abstract: This study assesses the influence of right ventricular (RV) dilation on the progression of left ventricular (LV) dysfunction and survival in patients with idiopathic dilated cardiomyopathy (IDC). Using transthoracic echocardiography, we studied 100 patients with IDC aged 20 to 80 years (mean 55 +/- 14); 67% were men. In the apical 4-chamber view, diastolic LV and RV chamber area measurements classified patients into 2 groups: group RV enlargement+ (RV area/LV area > 0.5) included 54 patients; group RV enlargement- (no RV enlargement) had RV area/LV area < or = 0.5. Echocardiographic studies were repeated in all patients after a mean of 33 +/- 16 months. At the time of the initial study, the 2 groups did not differ in age, gender, incidence of atrial fibrillation and diabetes, left ventricular mass, and LV ejection fraction, but the RV enlargement+ group had more severe tricuspid regurgitation and less LV enlargement. After 47 +/- 22 months (range 12 to 96), patients in group RV enlargement+ had lower LV ejection fraction (29% vs 34%, p = 0.006) than patients with initial RV enlargement-. At clinical follow-up, mortality was higher (43%) in patients with initial RV enlargement+ than the RV enlargement- patients (15%), p = 0.002. For survivors, the mitral deceleration time averaged 157 +/- 36 ms; for nonsurvivors or patients who required transplant, the mitral deceleration time averaged 97 +/- 12 ms (p < 0.0001). With use of a multivariate Cox model adjusting for LV ejection fraction, LV size, and age, the relative risk ratio of mortality from initial RV enlargement+ was 4.4 (95% confidence limits 1.7 to 11.1) (p = 0.002). Thus, patients with significant RV dilation had nearly triple the mortality over 4 years and more rapidly deteriorating LV function than patients with less initial RV dilation. In IDC, RV enlargement is a strong marker for adverse prognosis that may represent a different morphologic subset.
authors.affiliation: Cardiovascular Imaging Center, Department of Cardiology, The Cleveland Clinic Foundation, Ohio 44195, USA.
authors.forename: J P
authors.initials: JP
authors.lastname: Sun
authors.forename: K B
authors.initials: KB
authors.lastname: James
authors.forename: X S
authors.initials: XS
authors.lastname: Yang
authors.forename: N
authors.initials: N
authors.lastname: Solankhi
authors.forename: M S
authors.initials: MS
authors.lastname: Shah
authors.forename: K L
authors.initials: KL
authors.lastname: Arheart
authors.forename: J D
authors.initials: JD
authors.lastname: Thomas
authors.forename: W J
authors.initials: WJ
authors.lastname: Stewart
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D002311:Cardiomyopathy, Dilated / Q000150:complications / Q000000981:diagnostic imaging / Q000401:mortality* / Q000473:pathology; D004108:Dilatation, Pathologic; D018450:Disease Progression; D004452:Echocardiography; D005260:Female; D006352:Heart Ventricles / Q000000981:diagnostic imaging / Q000473:pathology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D012307:Risk Factors; D015996:Survival Rate; D018487:Ventricular Dysfunction, Left / Q000150:complications* / Q000000981:diagnostic imaging / Q000473:pathology