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Assessment of Myofilament Ca2+ Sensitivity Underlying Cardiac Excitation-contraction Coupling
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Published on: August 1, 2016

Reduced myocardial sarcoplasmic reticulum Ca(2+)-ATPase mRNA expression and biphasic force-frequency relations in

F Somura1, H Izawa, M Iwase

  • 1Cardiovascular Division, Department of Clinical Pathophysiology, the First Department of Internal Medicine, Nagoya University, Japan.

Circulation
|August 8, 2001
PubMed

Insights

In hypertrophic cardiomyopathy (HCM), lower SERCA2 gene expression is linked to reduced left ventricular (LV) contractile reserve. This suggests SERCA2 downregulation contributes to impaired heart function in severe HCM.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Genetics

Background:

  • Hypertrophic cardiomyopathy (HCM) is a genetic heart disease.
  • The link between left ventricular (LV) contractile reserve and Ca(2+)-handling protein gene expression in HCM is unclear.

Purpose of the Study:

  • To investigate the relationship between LV contractile functional reserve and gene expression of Ca(2+)-handling proteins in patients with HCM.

Main Methods:

  • Measured LV pressure and its first derivative during pacing in 14 nonobstructive HCM patients and 7 controls.
  • Quantified mRNA levels of key Ca(2+)-handling proteins (SERCA2, ryanodine receptor-2, phospholamban, calsequestrin, Na+/Ca(2+) exchanger) using real-time PCR.
  • Categorized HCM patients into two groups based on their response of LV dP/dt(max) to pacing.

Main Results:

  • Patients with a biphasic heart rate-LV dP/dt(max) relation (Group B) had greater LV hypertrophy than those with a progressive rise (Group A).
  • SERCA2 mRNA levels were significantly lower in Group B (0.34±0.15) compared to Group A (0.72±0.27) and controls (0.85±0.47).
  • Expression of other studied Ca(2+)-handling proteins remained similar across all groups.

Conclusions:

  • Downregulation of SERCA2 mRNA contributes to impaired LV contractile reserve in HCM patients with severe hypertrophy.
  • Altered Ca(2+) handling due to reduced SERCA2 may explain functional deficits even without baseline systolic dysfunction.
Abstract

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