gms | German Medical Science

Question: Previously we have reported decreased values of QRS amplitude and of the QRS to LVM ratio in the stage of developing left ventricular hypertrophy (LVH) of different experimental models and formulated the hypothesis on the relative voltage deficit. We hypothesize that this relative voltage deficit is conditioned by changes in electrogenetic properties of myocardium. Connexin43 (Cx43) is the predominant gap-junction protein in the working ventricular myocardium and its reduction has been implicated in the genesis of conduction abnormalities and re-entry arrhythmia. In this study we assessed the Cx43 expression in the early stage of LVH in spontaneously hypertensive rats (SHR).

Method Used: We investigated 20 week old male SHR and age- and sex-matched normotensive Wistar rats. Systolic blood pressure was measured using the tail-cuff method. Orthogonal electrocardiogram was recorded and the maximum spatial QRS vector magnitude (QRSmax) was calculated from the maximum QRS deflections of X, Y, Z electrocardiograms. LVM was weighed after rats were sacrificed. The specific potential of myocardium (SP) was calculated as the QRSmax to LVM ratio. Left ventricular protein level of Cx43 was analysed using SDS-PAGE and Western blotting (n = 5, per group).

Results: SHR showed significantly higher values of sBP (206±13 mmHg and 126±8 mmHg, respectively; p<0.05) and LVM (848±54 mg and 620±101 mg, respectively; p<0.05) as compared to the normotensive controls. Values of QRSmax in SHR were significantly lower as compared to Wistar rats (0.50±0.15 mV and 0.79±0.50 mV, respectively, p<0.05), as well as the SP values (0.54±0.14 mV/g and 1.08±0.20 mV/g, respectively, p<0.05). A 40% decrease in Cx43 level was observed in SHR as compared to the control animals.

Conclusion: We showed in this study that the lower values of QRSmax and SP in SHR in the early stage of LVH were associated with lower values of Cx43. Cx43 reduction is associated with slowing of impulse propagation, what could lead to the decrease in extracellulary recorded voltage in terms of the spatial angle theory. We assume that the relative voltage deficit, manifested as the decreased in QRS amplitude and/or SP values, is caused by altered electrical properties of the myocardium in LVH and can be considered as an early sign of the hypertrophic remodeling of myocardium in LVH.

Supported by grants: VEGA 1/3406/06 from The Science Grant Agency, Slovak Republic and FaF UK/005/2005 from the Pharmaceutical Faculty of Comenius University, Slovak Republic.