Background: Aortic valve replacement (AVR) for chronic aortic regurgitation (AR) with a severe dilated left ventricle and dysfunction leads to left ventricle remodeling. But there are rarely reports on the left ventricle reverse remodeling (LVRR) after AVR. This study aimed to investigate the LVRR and outcomes in chronic AR patients with severe dilated left ventricle and dysfunction after AVR. Methods: We retrospectively analyzed the clinical datum of chronic aortic regurgitation patients who underwent isolated AVR. The LVRR was defined as an increase in left ventricular ejection fraction (LVEF) at least 10 points or a follow-up LVEF ≥ 50%, and a decrease in the indexed left ventricular end-diastolic diameter of at least 10%, or an indexed left ventricular end-diastolic diameter ≤ 33 mm/m². The changes in echocardiographic parameters after AVR, survival analysis, the predictors of major adverse cardiac events (MACE), the association between LVRR and MACE were analyzed. Results: Sixty-nine patients with severe dilated left ventricle and dysfunction underwent isolated AVR. LV remodeling in 54 patients and no LV remodeling in 15 patients at 6–12 months follow-up. The preoperative left ventricular dimensions and volumes were larger, and the EF was lower in the LV no remodeling group than those in the LV remodeling group (all p < 0.05). The adverse LVRR was the predictor for MACE at follow-up. The mean follow-up period was 47.29 months (range 6 to 173 months). The rate of freedom from MACE was 94.44% at 5 years and 92.59% at 10 years in the remodeling group, 60% at 5 years, and 46.67% at 10 years in the no remodeling group. Conclusions: The left ventricle remodeling after AVR was the important predictor for MACE. LV no remodeling may not be associated with benefits from AVR for chronic aortic regurgitation patients with severe dilated LV and dysfunction.

Hypertrophic obstructive cardiomyopathy (HOCM) can bring a high risk of sudden cardiac death in young people. It is particularly urgent to understand the development and mechanism of HOCM to prevent unsafe incidents. Here, the comparison between pediatric and adult patients with HOCM has been performed to uncover the signaling mechanism regulating pathological process through histopathological analysis and immunohistochemical analysis. We found SMAD proteins played an important role during myocardial fibrosis for HOCM patients. In patients with HOCM, Masson and HE staining showed that myocardial cells were diffusely hypertrophied with obvious disorganized myocardial fiber alignment, and myocardial tissue was more damaged and collagen fibers increased significantly, which come early in childhood. Increased expressions of SMAD2 and SMAD3 contributed to myocardial fibrosis in patients with HOCM, which happened early in childhood and continued through adulthood. In addition, decreased expression of SMAD7 was closely related to collagen deposition, which negatively expedited fibrotic responses in patients with HOCM. Our study indicated that the abnormal regulation of SMAD signaling pathway can lead to severe myocardial fibrosis in childhood and its fibrogenic effects persist into adulthood, which is a crucial factor in causing sudden cardiac death and heart failure in HOCM patients.

The surgical strategy among patients with malignancy and coronary artery disease (CAD) remains controversial. In this study, we present the experiences of coronary artery bypass grafting (CABG) in patients with malignancy and analyzed the treatment outcomes. From January 2011 to October 2021, eight patients combined with coronary artery disease and malignancy, six of them with three-vessel disease and two with anterior descending branch lesions on coronary angiography. The age ranged from 54 to 73 years (61.8 ± 7.7years). Four patients underwent CABG and staging for surgical oncology, and 2 patients underwent CABG and surgical oncology simultaneously. Four patients underwent CABG procedure with cardiopulmonary bypass (on-pump CABG), and the other patients underwent the procedure without cardiopulmonary bypass (off-pump CABG). All patients were followed up for 3 to 96 months (40.4 ± 31.5 months) postoperatively. The mean number of grafts was 2.6 ± 1.1, there was no in-hospital death, postoperative myocardial infarction, and stroke. Among the eight patients, one patient received chemotherapy and radiation before bypass surgery, which occurred postoperatively pulmonary infection, and the rest of 7 patients had no major adverse cardiovascular events during follow-up periods. Based on the results of the present study, simultaneous or staged CABG and oncologic surgery according to the TNM stage of the tumor and cardiac assessment is an effective treatment for patients with severe CAD combined with malignancy.

Myocardial bridges are congenital coronary artery anomalies. There are still many controversies surrounding surgical treatment strategies for myocardial bridges combined with other heart disorders. The purpose of this study was to evaluate the surgical treatment strategies and outcomes in patients with these conditions. Between March 2004 and October 2021, our institution witnessed 77 patients diagnosed with myocardial bridging who underwent surgical intervention. According to the myocardial bridge and combined heart disorder, four groups were identified: 1. isolated LAD supra-arterial myotomy group, 2. LAD CABG and(or not) myotomy group, 3. LAD supra-arterial myotomy and grafting of other branches group, and 4. LAD supra-arterial myotomy and other cardiac surgery group. The perioperative outcomes, symptoms, life quality, mortality, and major adverse cardiac events (MACEs) were analyzed. There were no deaths during hospitalization and no rethoractomy for postoperative bleeding or major adverse cardiac events (MACEs). The follow-up period ranged from 2 months to 199.2 months (55.61 ± 10.21) months, the 10-year cumulative survival rates for the four groups of patients were 95.0%, 100%, 100% and 74.1%, and the 10-year freedom rates from the MACEs were 83.9%, 92.0%, 87.5% and 76.2%, respectively. Supra-arterial myotomy is preferred in patients with isolated myocardial bridge, and acceptable results can be achieved by choosing supra-arterial myotomy in combination with CABG or other cardiac surgery simultaneously for patients with myocardial bridges and other heart disorders.

Background: Hypertrophic obstructive cardiomyopathy (HOCM) is a genetic cardiomyopathy characterized by microvascular ischemia and myocardial fibrosis. Microvessels play an important role in myocardial fibrosis in HOCM. However, the changes of myocardial microvessels and myocardial fibrosis in pediatric and adult patients with HOCM remain unclear. This study was to investigate the changes in myocardial microvessel density (MVD) and myocardial fibrosis in pediatric and adult patients with HOCM. Methods: We analyzed the changes in MVD and myocardial fibrosis in myectomy left ventricular (LV) septal wall specimens in 12 adult patients and five pediatric patients with HOCM. Control myocardium from the LV septal wall was collected at autopsy of 5 adults and 4 pediatric individuals, who died of non-cardiac causes. Results: There was no significant difference in MVD between pediatric HOCM patients and control subjects (706.4±187.5 vs. 940.2±491.1, P > 0.05), but the myocardial fibrosis area ratio was significantly increased in HOCM than in control subjects (10.6±3.5 vs. 4.9±1.2, P < 0.01). MVD was significantly reduced, and myocardial fibrosis area ratio was significantly higher in adult HOCM patients than in control subjects (i.e. 523.3± 209.4 vs. 845.7±260.7, P < 0.05; 12.8±5.1 vs. 4.4±1.3, P < 0.05). There was no significant difference in MVD and myocardial fibrosis between pediatric and adult HOCM patients (706.4±187.5 vs. 523.3±209.4, P > 0.05; 10.6±3.5 vs. 12.8±5.1, P > 0.05). Conclusions: Pediatric and adult patients with HOCM have high myocardial fibrosis. The present findings suggest that myocardial microvascular density lesions contribute to myocardial fibrosis during childhood.