Key result
In about 20% of patients after myocardial infarction, the left atrium undergoes significant remodeling (volume increase ≥8 ml/m2 over 12 months) driven by left ventricular diastolic dysfunction.
Discusses the pathophysiological relationship between left ventricular diastolic dysfunction and left atrial remodeling following acute myocardial infarction.
Left ventricular diastolic dysfunction (LVDD) usually precedes systolic dysfunction in the early phase after acute myocardial infarction (MI).1,2 Previous studies have shown that in MI patients, LVDD may promote progression of heart failure (HF) from stage B to stage C, even in HF with preserved left ventricular (LV) ejection fraction (HFpEF).3,4 In about one fifth of patients after MI, the left atrium undergoes significant remodeling, defined as increase in left atrial (LA) volume of ≥8 ml/m 2 over a 12-month period (although it may be evident after one month).3,5 It has been reported that after MI, increased LV enddiastolic pressure (LVEDP) induces higher LA afterload and hence mechanical stress on the atrium that leads to higher LA volumes, mechanical dysfunction and increased stiffness, which in turn, by a tandem effect, reduce LA emptying, LV filling and cardiac output during exertion.The backward effects of LA enlargement and dysfunction are pulmonary venous congestion and vascular pulmonary vasoconstriction that may eventually trigger right ventricular overload and dysfunction.Accordingly, the evolving stages of HFpEF are associated with right ventricle-to-pulmonary circulation
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Regina Ribeiras (2018) conducted an editorial in Left ventricular diastolic dysfunction and left atrial remodeling after acute myocardial infarction. In about 20% of patients after myocardial infarction, the left atrium undergoes significant remodeling (volume increase ≥8 ml/m2 over 12 months) driven by left ventricular diastolic dysfunction.
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