End-stage heart failure in humans is associated with reduced contraction of individual cardiomyocytes, smaller Ca transients, and reduced Ca content of the sarcoplasmic reticulum. We investigated whether these alterations were present in mice with congestive heart failure (CHF). Myocardial infarction (MI) was induced by ligation of the left coronary artery, and CHF mice were examined at 10-weeks post-MI. SHAM-operated mice served as controls. Heart weight / body weight ratios were 163 ± 20% higher in CHF than SHAM indicating hypertrophy. Lung weight / body weight ratios were also increased (CHF 221 ± 30% of SHAM values) indicating congestion. Echocardiographic analysis showed marked reductions in cardiac output (SHAM 39 ± 4 ml/min; CHF 25 ± 3 ml/min, P<less-or-equal-to>0.05) and left-ventricular fractional shortening (SHAM 27 ± 4%; CHF 8 ± 1%, P<less-or-equal-to>0.05). However, thickening of the non-infarcted posterior wall was unaltered (SHAM 27 ± 6%, CHF 36 ± 7%). Cardiomyocytes isolated from non-infarcted septum were significantly longer in CHF than SHAM (178 ± 8 mm vs 139 ± 6 mm, P<less-or-equal-to>0.05). During field stimulation (1 Hz, 37C), myocyte contraction magnitude was similar in CHF and SHAM cells (% shortening = 9.1 ± 1.1 vs 9.7 ± 0.4, P=NS). Surprisingly, Ca transients (fluo-4 AM) were larger in CHF than in SHAM at both 1Hz (CHF F/F0 = 3.0 ± 0.2, SHAM F/F0 = 2.3 ± 0.1, P<less-or-equal-to>0.05) and 5 Hz stimulation frequencies, and the rate of Ca decline was unchanged. Caffeine-elicited transients were of similar magnitude in CHF and SHAM (F/F0 = 4.3 ± 0.5 vs 5.0 ± 0.4, P=NS), suggesting that sarcoplasmic reticulum Ca content was unaltered. Therefore, CHF progression in mice does not affect contractions of the viable myocardium to the same extent as in heart failure patients.