Attenuated L-type Ca²⁺ current (I_Ca,L), or current-contraction gain have been proposed to explain impaired cardiac contractility in congestive heart failure (CHF). Six weeks after coronary artery ligation, which induced CHF, left ventricular myocytes from isoflurane-anesthetized rats were current or voltage clamped from 70 mV. In both cases, contraction and contractility were attenuated in CHF cells compared with cells from sham-operated rats when cells were only minimally dialyzed using high-resistance microelectrodes. With patch pipettes, cell dialysis caused attenuation of contractions in sham cells, but not CHF cells. Stepping from 50 mV, the following variables were not different between sham and CHF, respectively: peak I_Ca,L (4.5 ± 0.3 vs. 3.8 ± 0.3 pApF¹ at 23°C and 9.4 ± 0.5 vs. 8.4 ± 0.5 pApF¹ at 37°C), the bell-shaped voltage-contraction relationship in Cs⁺ solutions (fractional shortening, 15.2 ± 1.0% vs. 14.3 ± 0.7%, respectively, at 23°C and 7.5 ± 0.4% vs. 6.7 ± 0.5% at 37°C) and the sigmoidal voltage-contraction relationship in K⁺ solutions. Caffeine-induced Ca²⁺ release and sarcoplasmic reticulum Ca²⁺-ATPase-to-phospholamban ratio were not different. Thus CHF contractions triggered by I_Ca,L were normal, and the contractile deficit was only seen in undialyzed cardiomyocytes stimulated from 70 mV.