Left-Ventricular Plication Reduces Wall Stress and Cardiomyocyte Hypertrophy in a Rat Model of Ischemic Cardiomyopathy.

Background: The indications of left-ventricular plication (LVP) are controversial, although several studies have reported favorable outcomes in heart failure patients. The aim of this study was to assess left-ventricular (LV) wall stress and myocardial remodeling after LVP in a rat model of myocardial infarction (MI).

Methods: Sixteen rats underwent LVP by excluding the LV anterior wall scar 4 weeks after ligation of the left anterior descending artery. After 4 weeks, LV wall stress was assessed using transthoracic echocardiography and an LV catheter. Gene expression of the wall stress markers, atrial natriuretic factor (ANF) and brain natriuretic peptide (BNP), were evaluated via reverse transcription polymerase chain reaction. Cardiomyocyte area and myocardial fibrosis were also examined through histological examinations. These parameters were compared to those in 16 rats that underwent coronary artery ligation but not LVP.

Results: We noted that the LV end-diastolic dimension was smaller (9.9 ± 0.3 vs. 11.2 ± 0.2 mm, p < 0.05) and fractional shortening was greater (25 ± 2 vs. 15 ± 1%, p < 0.05) in LVP rats than in sham rats. Moreover, systolic wall stress was lower in LVP rats (71 ± 7 vs. 111 ± 9 × 103 dyn/cm2, p < 0.05). Myocardial ANF and BNP expression levels were lower in LVP rats (2.6 ± 0.3 vs. 4.4 ± 0.5 and 1.0 ± 0.1 vs. 1.5 ± 0.2 arbitrary units, respectively; p < 0.05). Cardiomyocyte area was significantly decreased in LVP rats (556 ± 15 vs. 670 ± 28 μm2, p = 0.003) and was correlated with LV wall stress (r = 0.669, p = 0.002). The reduction in myocardial fibrosis after LVP was not significant.

Conclusion: LVP reduced LV wall stress and cardiomyocyte hypertrophy in a rat model of MI.