1 gery were congestive failure and progressive cardiac enlargement.

2 at lower, at 89.0%, in the 167 patients with cardiac enlargement.

3 eft ventricular hypertrophy, and symmetrical cardiac enlargement.

4        Magnetic resonance analysis confirmed cardiac enlargement.

5 he inflammasome and limited infarct size and cardiac enlargement after AMI.

6 tration) is the primary factor in triggering cardiac enlargement and arrhythmogenesis.

7  Id cKO mice exhibited fibrotic vasculature, cardiac enlargement and decreased cardiac function.

8         Postnatal demise was associated with cardiac enlargement and defects in the ventricular septu

9 (2) a large reversible defect (n=36), or (3) cardiac enlargement and either increased pulmonary uptak

10                             Pulmonary edema, cardiac enlargement, and left ventricular ejection fract

11 lly silenced in the postnatal heart, induces cardiac enlargement because of cardiomyocyte hyperplasia

12 ing severe hypertriglyceridemia, hepatic and cardiac enlargement, growth retardation, and premature m

13                                Nevertheless, cardiac enlargement in both models can be effectively at

14        We have investigated the mechanism of cardiac enlargement in these hearts.

15                                              Cardiac enlargement in TNF1.6 mice is partly attributabl

16 a proapoptotic Bcl2 family protein, mediates cardiac enlargement, reshaping, and dysfunction in mice

17                        Near-normal scans and cardiac enlargement were independent predictors of time

18  The appropriate management of patients with cardiac enlargement will remain a matter of clinical jud

19                    Echocardiography revealed cardiac enlargement with impaired chamber function in he