Abstract
BackgroundCardiac remodelling after AMI is characterized by molecular and cellular mechanisms involving both the ischemic and non-ischemic myocardium. The extent of right ventricular (RV) dilatation and dysfunction and its relation to pulmonary hypertension (PH) following AMI are unknown. The aim of the current study was to evaluate changes in dimensions and function of the RV following acute myocardial infarction (AMI) involving the left ventricle (LV).MethodsWe assessed changes in RV dimensions and function 1 week following experimental AMI involving the LV free wall in 10 mice and assessed for LV and RV dimensions and function and for the presence and degree of PH.ResultsRV fractional area change and tricuspidal annular plane systolic excursion significantly declined by 33% (P = 0.021) and 28% (P = 0.001) respectively. Right ventricular systolic pressure measured invasively in the mouse was within the normal values and unchanged following AMI.ConclusionAMI involving the LV and sparing the RV induces a significant acute decline in RV systolic function in the absence of pulmonary hypertension in the mouse indicating that RV dysfunction developed independent of changes in RV afterload.
Highlights
Acute myocardial infarction (AMI) is associated with compensatory mechanisms involving both the left and right ventricles
In patients with left ventricle (LV) systolic dysfunction and heart failure the presence of signs and/or symptoms of right ventricular (RV) failure identify a subgroup of patients with a very poor prognosis [6,7,8,9,10]
The mechanisms leading to RV remodelling and dysfunction following acute myocardial infarction (AMI) involving the LV are not completely clear, but it is frequently assumed that LV failure causes pulmonary hypertension (PH) and increased RV afterload leading to RV remodelling and dysfunction
Summary
Acute myocardial infarction (AMI) is associated with compensatory mechanisms involving both the left and right ventricles. Infarction or ischemia of the RV and/or the septum are common in patients with AMI and can contribute to abnormal RV systolic function. In the current study we evaluated the occurrence and extent of RV dilatation and dysfunction in a mouse model of AMI in which the septum and RV are spared eliminating the possibility that RV or septal ischemia/infarction leads to abnormal RV perfusion or mechanics, and in which the RV systolic pressure could be invasively measured. The extent of right ventricular (RV) dilatation and dysfunction and its relation to pulmonary hypertension (PH) following AMI are unknown. The aim of the current study was to evaluate changes in dimensions and function of the RV following acute myocardial infarction (AMI) involving the left ventricle (LV)
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