Although major pathogenesis mechanisms of heart failure (HF) are well established, the significance of early (mal)adaptive structural changes of cardiomyocytes preceding symptomatic ischemic HF remains ambiguous. The aim of this study is to present the morphological characterization of changes in cardiomyocytes and their reorganization of intermediate filaments during remodeling preceding symptomatic ischemic HF in an adult human heart. A total of 84 myocardial tissue samples from middle-left heart ventricular segments were analyzed histomorphometrically and immunohistochemically, observing the cardiomyocyte’s size, shape, and desmin expression changes in the remodeling process: Stage A of HF, Stage B of HF, and Stages C/D of HF groups (ACC/AHA classification). Values p < 0.05 were considered significant. The cellular length, diameter, and volume of Stage A of HF increased predominantly by the diameter vs. the control group (p < 0.001) and continued to increase in Stage B of HF in a similar pattern (p < 0.001), increasing even more in the C/D Stages of HF predominantly by length (p < 0.001). Desmin expression was increased in Stage A of HF vs. the control group (p < 0.001), whereas it was similar in Stages A and B of HF (p > 0.05), and most intense in Stages C/D of HF (p < 0.001). Significant morphological changes of cardiomyocytes and their cytoskeletal reorganization were observed during the earliest remodeling events preceding symptomatic ischemic HF.

Background and objective: carotid artery stenosis contributes significantly to ischemic strokes, with management options including carotid endarterectomy (CEA) and carotid artery stenting (CAS) ischemic stroke risk can be reduced. Controversies persist regarding their efficacy and factors influencing complications, and understanding the relationship between atherosclerotic plaque characteristics and stent restenosis after CAS is crucial. Methods: we conducted a retrospective study involving 221 patients who underwent CAS for symptomatic or asymptomatic carotid artery stenosis. Comprehensive assessments of plaque morphology were performed using contrast-enhanced ultrasound (CEUS) before CAS. Patient demographics, including smoking status and diabetes, were also recorded. Stent restenosis was diagnosed using various imaging modalities, including ultrasound, angiography, and digital subtraction angiography (DSA). Results: plaque analysis using CEUS revealed a significant association between plaque grade and restenosis incidence (p < 0.001), particularly with grade 0 (11.1%) and grade 2 plaques (66.7%). Smoking was notably associated with plaque vascularization and restenosis (p < 0.001), while diabetes did not significantly impact plaque characteristics or restenosis risk (p > 0.05). The mean duration of restenosis was 17.67 months. Stenting was the most frequent treatment modality for restenosis (70.6%). However, no significant relationship was found between restenosis type and plaque morphology (p = 0.268). Furthermore, while no clear relationship was observed between plaque morphology and the type of restenosis, our findings underscored the importance of plaque characterization in predicting post-CAS outcomes. Conclusions: this study highlights the utility of CEUS in predicting stent restenosis following CAS. There was a significant association between stent restenosis within 12–24 months after the carotid stenting procedure and an elevated grade of plaque vascularization. Moreover, one of the main factors possibly determining the grade of plaque vascularization was smoking. Further research is warranted to elucidate the underlying mechanisms and refine risk stratification in this patient population.

Matrix metalloproteinase 3 (MMP3), in conjunction with other MMPs, plays a key role in myocardial remodeling by breaking down the extracellular matrix of the heart and the development of heart failure (HF). However, the existing data on MMP3 protein expression in human myocardium remains insufficient. The objective of the present study was to determine the expression of MMP3 protein in left ventricular myocardial cells at varying stages of ischemic HF. To this end, a quantitative and semi-quantitative immunohistochemical analysis was performed on 113 samples of left ventricular myocardium. A non-selective digital myocardial image analysis revealed that the stage A HF group exhibited higher MMP3 protein expression compared to the control group (p < 0.001). Subsequent increases in immunostaining intensity of MMP3 were observed in the stage B HF group (p < 0.001). In the stage C/D HF group, MMP3 expression reached its highest level (p < 0.001). The intensity of immunostaining exhibited comparable tendencies in both cardiomyocytes and non-cardiomyocytes. Increased levels of MMP3 immunostaining in both types of cells were associated with increased left ventricular mass. Subjects who carried the 5A allele and patients with the 5A homozygous genotype exhibited a higher propensity for increased immunostaining levels in both cardiomyocytes and non-cardiomyocytes when compared to those with the 6A/6A and 5A/6A genotype. These changes in MMP3 protein expression were associated with left ventricular myocardial remodeling in the progression of ischemic HF.