Aim: 

We investigated the influence of acidosis on physiological and electrophysiological parameters in dilative cardiomyopathy (DCM).

Methods: 

Dilative cardiomyopathy (DCM) was induced in Sprague Dawley rats (n=6) using 6 weeks doxorubicin treatment (2.5mg/kg). DCM hearts and healthy hearts (n=5) were explanted, perfused with Tyrode solution and attached to the Langendorff system (constant pressure). For epicardial mapping 265 electrodes were placed around the heart surface. Cardiac activation was measured under control conditions (pH7.4, 45min), before acidosis initiation for partial uncoupling of gap junction (pH 6.5, 20min).

Results: 

In spontaneously beating DCM hearts initial QRS was longer than in healthy hearts. During acidosis QRS prolongation was significantly increased, which was more pronounced in DCM compared to healthy hearts (healthy: 32.33±2.9ms vs. DCM: 44.78±3.1ms, p<0.05). Similar changes were observed regarding total activation time (TAT). Under control conditions DCM hearts showed a significant TAT prolongation (DCM: 15.25±2.9ms vs. healthy: 9.95±1.04ms; p=0.05) which was more enlarged during acidosis as compared to healthy hearts (DCM: 44.0±6.6ms vs. healthy: 26.7±5.7ms, p=0.07). These results go along with a significant increase in PQ-interval during acidosis in both groups (p<0.05). Moreover, there were no changes in peak to peak amplitude detectable. However, in DCM and healthy hearts acidosis resulted in a significantly increase in basic cycle length also in a significant decrease of left ventricular pressure and coronary flow.

Conclusion: 

These parameters indicate an increased uncoupling of gap junctions and a retardation of excitation propagation in DCM during acidosis. DCM hearts are more prone to conduction failure during acidosis.