Increasing cardiac contractility after myocardial infarction exacerbates cardiac injury and pump dysfunction.

ABSTRACT:

Rationale

Myocardial infarction (MI) leads to heart failure (HF) and premature death. The respective roles of myocyte death and depressed myocyte contractility in the induction of HF after MI have not been clearly defined and are the focus of this study.

Objectives

We developed a mouse model in which we could prevent depressed myocyte contractility after MI and used it to test the idea that preventing depression of myocyte Ca(2+)-handling defects could avert post-MI cardiac pump dysfunction.

Methods and results

MI was produced in mice with inducible, cardiac-specific expression of the β2a subunit of the L-type Ca(2+) channel. Myocyte and cardiac function were compared in control and β2a animals before and after MI. β2a myocytes had increased Ca(2+) current; sarcoplasm

SUBMITTER: Zhang H 

PROVIDER: S-EPMC3021375 | biostudies-literature | 2010 Sep

REPOSITORIES: biostudies-literature