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Contractile Dysfunction in Heart Failure and Familial Hypertrophic Cardiomyopathy

Cheng, Yi-Hsin

Abstract Details

, Doctor of Philosophy, Case Western Reserve University, Physiology and Biophysics.
Elevations in plasma and myocardial lipids can exacerbate the progression of heart failure (HF). However, our previous studies reported that high saturated fat (SAT) feeding improves in vivo myocardial contractile function after infarction. Since alterations in cardiomyocyte Ca2+ kinetics and myofilament proteins also contribute to contractile dysfunction in HF, in the first study we hypothesize that SAT improves contractile function by ameliorating these alterations in HF. Rats underwent coronary artery ligation or sham surgery (SH) and were fed normal chow (SHNC and HFNC) or SAT (SHSAT and HFSAT) for 8 weeks. SAT reduced in vivo myocyte hypertrophy and improved in vivo (LV dP/dtmax/min) and in vitro contractility (-dL/dt) in HF. MHC isoform switched from fast MHCα to slow MHCβ in HFNC but reversed in HFSAT. Alterations in Ca2+ transients, L-type Ca2+ currents and expression of Ca2+ handling proteins could not account for changes in in vivo contractile properties. Together, the cardioprotective effects associated with SAT in HF occur at the level of cardiomyocyte, specifically involving changes in myofilament function, but not Ca2+ handling properties. Mutations in cardiac myosin binding protein C (MyBP-C) cause familial hypertrophic cardiomyopathy (FHC). Most MyBP-C mutations reduce MyBP-C expression, however, the consequences of MyBP-C deficiency are unclear. In the second study, we employed MyBP-C null (MyBP-C-/-) and heterozygous null (MyBP-C+/-) mice. Complete MyBP-C deficiency altered in vivo and in vitro contractile function, Ca2+ handling, electrical activity, and chamber remodeling of MyBP-C-/- hearts. Partial MyBP-C deficiency and concomitant down-regulated MyBP-C phosphorylation in MyBP-C+/- hearts altered cross-bridge function which contributed to in vitro and in vivo contractile dysfunction and ECG abnormalities in the absence of adaptations in Ca2+ handling or LV chamber remodeling. Contractile dysfunction in MyBP-C+/- myofilaments and intact hearts were normalized by β-agonists, suggesting that their basal contractile dysfunction is partly mediated by impaired MyBP-C phosphorylation. Collectively, our data show that reduced MyBP-C expression and phosphorylation in the sarcomere results in myofilament dysfunction, contributing to contractile dysfunction that precedes adaptations in Ca2+ handling and chamber remodeling. Perturbations in mechanical and electrical activity in these mice could also increase their susceptibility to arrhythmia.
Julian Stelzer (Advisor)

Recommended Citations

Citations

  • Cheng, Y.-H. (n.d.). Contractile Dysfunction in Heart Failure and Familial Hypertrophic Cardiomyopathy [Doctoral dissertation, Case Western Reserve University]. OhioLINK Electronic Theses and Dissertations Center. http://rave.ohiolink.edu/etdc/view?acc_num=case1378894204

    APA Style (7th edition)

  • Cheng, Yi-Hsin. Contractile Dysfunction in Heart Failure and Familial Hypertrophic Cardiomyopathy . Case Western Reserve University, Doctoral dissertation. OhioLINK Electronic Theses and Dissertations Center, http://rave.ohiolink.edu/etdc/view?acc_num=case1378894204.

    MLA Style (8th edition)

  • Cheng, Yi-Hsin. "Contractile Dysfunction in Heart Failure and Familial Hypertrophic Cardiomyopathy ." Doctoral dissertation, Case Western Reserve University. Accessed MAY 21, 2024. http://rave.ohiolink.edu/etdc/view?acc_num=case1378894204

    Chicago Manual of Style (17th edition)