SVT-induced cardiomyopathy in pigs reduced LV fractional shortening by 61% and increased cytoskeletal protein mRNA, with no change in contractile protein content or mRNA.
Does SVT-induced cardiomyopathy alter contractile and cytoskeletal protein content, structure, and mRNA levels in a pig model?
SVT-induced cardiomyopathy in a pig model is associated with increased cytoskeletal protein abundance and altered cytoarchitecture, rather than changes in contractile protein content or mRNA.
Chronic supraventricular tachycardia (SVT)-induced cardiomyopathy is associated with left ventricular (LV) dilatation, increased wall stress, neurohormonal activation, and no change in LV mass. To determine mechanisms for changes in LV geometry and function with SVT cardiomyopathy, LV and myocyte function, contractile protein content and mRNA levels, and cytoskeletal protein structure and mRNA levels were examined in 12 pigs with SVT cardiomyopathy (paced at 240 beats/min for 3 wk) and in 12 controls. With SVT cardiomyopathy, LV fractional shortening fell by 61%, and end-diastolic dimension increased by 42%, with no change in LV mass-to-body weight ratio (3.36 +/- 0.15 vs. 3.14 +/- 0.13 g/kg). Myocyte contractile function was reduced by 33%, myocyte length was increased by 28%, and cross-sectional area was decreased by 19% with SVT cardiomyopathy. Total protein, myosin heavy chain (MHC), and actin appeared unchanged with SVT cardiomyopathy at the LV or myocyte level. Moreover, there was no change in mRNA levels for MHC (0.57 +/- 0.05 vs. 0.59 +/- 0.09 mRNAOD/rRNAOD) or cardiac alpha-actin (0.58 +/- 0.08 vs. 0.58 +/- 0.04 mRNAOD/rRNAOD) with SVT cardiomyopathy. In contrast, mRNA levels for specific cytoskeletal proteins were significantly increased with SVT cardiomyopathy, and immunofluorescent localization of contractile and cytoskeletal proteins in isolated myocytes revealed alterations in cytoskeletal architecture. Thus changes in LV and myocyte geometry with SVT cardiomyopathy were associated with no change in contractile protein content or mRNA at the chamber or myocyte level. Furthermore, increased cytoskeletal protein abundance and mRNA and reorientation of cardiocyte cytoarchitecture may have contributed to the LV and myocyte remodeling with SVT cardiomyopathy.
Eble et al. (Thu,) conducted a other in SVT-induced cardiomyopathy (n=24). Supraventricular tachycardia (SVT) pacing vs. Controls was evaluated on LV and myocyte function, contractile and cytoskeletal protein content and mRNA levels. SVT-induced cardiomyopathy in pigs reduced LV fractional shortening by 61% and increased cytoskeletal protein mRNA, with no change in contractile protein content or mRNA.