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Right ventricular remolding, dysfunction, and pulmonary arterial hypertension following left ventricular myocardial infarction (648.7)
Author(s) -
Huber Jason,
Platt Mathew,
Romanova Nadya,
Wright David,
Simpson Jeremy
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.648.7
Subject(s) - cardiology , medicine , ventricle , myocardial infarction , ventricular remodeling , contractility , heart failure , hemodynamics , diastole , pulmonary artery , blood pressure
Assessment of cardiac function in patients with heart failure (HF) is generally limited to the evaluation of systolic and diastolic function of the left ventricle (LV). Right ventricle (RV) dysfunction is considered a sequelae of LV HF. However, the pathogenesis of RV remodeling has received little attention. Our objective was to investigate the progression of RV function following LV myocardial infarction (MI). Methods : Left and right ventricle remodeling was assessed using invasive hemodynamics, molecular and histomorphometric approaches at 2, 4 9 and 18 weeks post‐MI induced by permanent ligation of the left anterior descending artery. Results: Invasive hemodynamics revealed a decrease in LV contractility and systolic blood pressure and an increase in end diastolic pressures (EDP), which remained stable until 18 weeks post‐MI. In contrast, RV systolic pressure and contractility initially increased at 2 weeks prior to a drop off from 4 to 18 weeks post‐MI. In addition RV EDP was elevated at all time points. Re‐expression of fetal genes occurred in both ventricles with greater change of several genes in the RV as compared to the LV. Histological analysis revealed significant increases in cardiomyocyte cross sectional area and fibrosis in both LV and RV. Conclusion: Significant RV remodeling and dysfunction is evident immediately following a LV MI and may play an important and underappreciated role in the development of LV HF. Grant Funding Source : Supported by Canadian Institute of Health Research