Aim: 

Disarrayed structure and kinetics of heart molecular motors are primary anomalies associated with dilated cardiomyopathy (DCM). We investigated whether a coformulation of PLC, CoQ₁₀ and omega-3 positively affects ultrastructure and functions of failed myocardial molecular machinery in BIO TO-2 cardiomyopatic Syrian Hamsters.

Methods: 

Mechanical features of electrically-driven control and treated papillary muscles were in vitro recorded in isometric and isotonic conditions. Using Huxley's formalism (Huxley 1957) the effects of the coformulation on number and kinetics of isolated muscle crossbridges (CB) were determined. Electron microscopy was also performed in order to compare muscle sarcomeral structures to mechanical findings.

Results: 

There was a 87% increase in the total number of active CB per mm² in treated hamsters as compared to control (p < 0.05). The single CB force did not differ between control an treated muscles. The rate constant for CB attachment (f₁) and detachment (g₂) were 98% and 124% higher, respectively (p < 0.05). Electron microscopy revealed that unlike in controls, distinct actin and myosin filaments were uniform and in register, and I, A, H and M bands were clearly observed in treated hamsters. Measured sarcomere length was found 45% increased in treated papillary muscles when compared to control preparations.

Conclusions: 

Treatment with PLC, CoQ₁₀ and omega-3 was effective in reversing structural and functional anomalies in cardiomyopathic hamsters. Results will be discussed at the light of the possibility that altered cardiac metabolism may play a role in the mechanisms that lead to cardiac maladaptative remodelling (Giordano 2005).