ObjectiveAn unclear issue is whether gender may influence at cardiac remodeling after myocardial infarction (MI). We evaluated left ventricle remodeling in female and male rats post-MI.MethodsRats were submitted to anterior descending coronary occlusion. Echocardiographic evaluations were performed on the first and sixth week post-occlusion to determine myocardial infarction size and left ventricle systolic function (FAC, fractional area change). Pulsed Doppler was applied to analyze left ventricle diastolic function using the following parameters: E wave, A wave, E/A ratio. Two-way ANOVA was applied for comparisons, complemented by the Bonferroni test. A P≤=0.05 was considered significant.ResultsThere were no significant differences between genders for morphometric parameters on first (MI [Female (FE): 44.0±5.0 vs. Male (MA): 42.0±3.0%]; diastolic [FE: 0.04±0.003 vs. MA: 0.037±0.005, mm/g] and systolic [FE: 0.03±0.0004 vs. MA: 0.028±0.005, mm/g] diameters of left ventricle) and sixth (MI [FE: 44.0±5.0 vs. MA: 42.0±3.0, %]; diastolic [FE: 0.043±0.01 vs. MA: 0.034±0.005, mm/g] and systolic [FE: 0.035±0.01 vs. MA: 0.027±0.005, mm/g] of LV) week. Similar findings were reported for left ventricle functional parameters on first (FAC [FE: 34.0±6.0 vs. MA: 32.0±4.0, %]; wave E [FE: 70.0±18.0 vs. MA: 73.0±14.0, cm/s]; wave A [FE: 20.0±12.0 vs. MA: 28.0±13.0, cm/s]; E/A [FE: 4.9±3.4 vs. MA: 3.3±1.8]) and sixth (FAC [FE: 29.0±7.0 vs. MA: 31.0±7.0, %]; wave E [FE: 85.0±18.0 vs. MA: 87.0±20.0, cm/s]; wave A [FE: 20.0±11.0 vs. MA: 28.0±17.0, cm/s]; E/A [FE: 6.2±4.0 vs. MA: 4.6±3.4]) week.ConclusionGender does not influence left ventricle remodeling post-MI in rats.
BackgroundGender can influence post-infarction cardiac remodeling.ObjectiveTo evaluate whether gender influences left ventricular (LV) remodeling and integrin-linked kinase (ILK) after myocardial infarction (MI).MethodsFemale and male Wistar rats were assigned to one of three groups: sham, moderate MI (size: 20-39% of LV area), and large MI (size: ≥40% of LV area). MI was induced by coronary occlusion, and echocardiographic analysis was performed after six weeks to evaluate MI size as well as LV morphology and function. Real-time RT-PCR and Western blot were used to quantify ILK in the myocardium.ResultsMI size was similar between genders. MI resulted in systolic dysfunction and enlargement of end-diastolic as well as end-systolic dimension of LV as a function of necrotic area size in both genders. Female rats with large MI showed a lower diastolic and systolic dilatation than the respective male rats; however, LV dysfunction was similar between genders. Gene and protein levels of ILK were increased in female rats with moderate and large infarctions, but only male rats with large infarctions showed an altered ILK mRNA level. A negative linear correlation was evident between LV dimensions and ILK expression in female rats with large MI.ConclusionsPost-MI ILK expression is altered in a gender-specific manner, and higher ILK levels found in females may be sufficient to improve LV geometry but not LV function.
There is conflicting data about gender differences with regard to left ventricular (LV) remodeling after myocardial infarction (MI). Moreover, the molecular basis for gender-based differences in LV remodeling remains unknown. This study evaluated whether gender differences exist in LV remodeling after MI. Given that integrin-linked kinase (ILK) influences LV remodeling, we also examined whether gender affects the modulation of ILK post-MI. Female and male Wistar rats were assigned to one of three groups: a sham group, a moderate MI group (size: 20-39% of LV area) and a large MI group (size: ≥40% of LV area). The MI was produced by coronary occlusion and echocardiographic analysis as well as ILK expression was performed six weeks post-MI. The MI resulted in systolic dysfunction and enlargement of end-diastolic as well as end-systolic dimension of the left ventricle as a function of necrotic area size for both genders. However, female rats with large MI showed a lower diastolic (5.4±1 mm 2 ) and systolic dilatation (3.9±0.9 mm 2 ) than respective male rats (8.2±0.7 mm 2 and 5.7±1.1 mm 2 , respectively). Both gene (moderate MI: 1.85±0.15; large MI: 2.35±0.16, p<0.001) and protein (moderate MI: 3.21±0.09; large MI: 4.75±0.24, p<0.001) levels of ILK were increased as a function of MI size in female rats. However, only male rats in the large MI group showed an altered ILK mRNA level (moderate MI: 1.51±0.10; large MI: 1.69±0.08, p<0.001). A negative linear correlation was evident between LV dimensions and ILK protein expression in female rats with large MI (left ventricle diastolic area:ILK protein content: r 2 =0.52, p=0.003; left ventricle systolic area:ILK protein content: r 2 =0.68, p<0.001). In conclusion, post-MI ILK expression is altered in a gender-specific manner and higher ILK levels found in females may be sufficient to improve geometry of LV; however, may not be sufficient to improve LV function.
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