Regional remodeling strain and its association with myocardial apoptosis after myocardial infarction in an ovine model

ObjectiveProgressive left ventricular remodeling after myocardial infarction has been viewed as an important contributor to progressive heart failure. The objective of this study was to investigate the relationship between myocardial apoptosis and strain during progressive cardiac remodeling.MethodsBefore creation of an anterolateral left ventricular infarction by ligation of diagonal arteries, 16 sonomicrometry transducers were placed in the left ventricular free wall of 8 sheep to assess regional deformation in the infarct, adjacent, and normally perfused remote myocardial regions over 8 weeks' duration. Hemodynamic, echocardiographic and sonomicrometric data were collected before infarction and then 30 minutes and 2, 6, and 8 weeks after infarction. At the end of the study, regional myocardial tissues were collected for apoptotic signaling proteins.ResultsAt terminal study, an increase in left ventricular end-diastolic pressure of 8.1 ± 0.1 mm Hg, a decrease in ejection fraction from 54.19% ± 5.68% to 30.55% ± 2.72%, and an end-diastolic volume increase of 46.08 ± 5.02 mL as compared with the preinfarct values were observed. The fractional contraction at terminal study correlated with the relative abundance of apoptotic protein expressions: cytochrome c (r2 = 0.02, P < .05), mitochondrial Bax (r2 = 0.27, P < .05), caspase-3 (r2 = 0.31, P < .05), and poly (adenosine diphosphate–ribose) polymerase (r2 = 0.30, P < .05). These myocardial apoptotic activities also correlated with remodeling strain: cytochrome c (r2 = 0.02, P < .05), mitochondrial Bax (r2 = 0.28, P < .05), caspase-3 (r2 = 0.43, P < .05), and poly (adenosine diphosphate–ribose) polymerase (r2 = 0.37, P < .05).ConclusionIncrease in regional remodeling strain led to an increase in myocardial apoptosis and regional contractile dysfunction in heart failure

Coronary artery bypass grafting outcomes of patients with human immunodeficiency virus: a population-based study of National Inpatient Sample from 2015 to 2020

Abstract Individuals affected by human immunodeficiency virus (HIV) have a growing demand for coronary artery bypass grafting (CABG) due to heightened risk for cardiovascular diseases and extended life expectancy. However, CABG outcomes in HIV patients are not well-established, with insights only from small case series studies. This study conducted a comprehensive, population-based examination of in-hospital CABG outcomes in HIV patients. Patients underwent CABG were identified in National Inpatient Sample from Q4 2015–2020. Patients with age < 18 years and concomitant procedures were excluded. A 1:5 propensity-score matching was used to address preoperative group differences. Among patients who underwent CABG, 613 (0.36%) had HIV and were matched to 3119 out of 167,569 non-HIV patients. For selected HIV patients, CABG is relatively safe, presenting largely similar outcomes. After matching, HIV and non-HIV patients had comparable in-hospital mortality rates (2.13% vs. 1.67%, p = 0.40). Risk factors associated with mortality among HIV patients included previous CABG (aOR = 14.32, p = 0.01), chronic pulmonary disease (aOR = 8.24, p < 0.01), advanced renal failure (aOR = 7.49, p = 0.01), and peripheral vascular disease (aOR = 6.92, p = 0.01), which can be used for preoperative risk stratification. While HIV patients had higher acute kidney injury (AKI; 26.77% vs. 21.77%, p = 0.01) and infection (8.21% vs. 4.18%, p < 0.01), other complications were comparable between the groups

In-hospital outcome of type A aortic dissection repair in patients with chronic obstructive pulmonary disease: A population study of National Inpatient Sample from 2015 to 2020

BACKGROUND: Chronic obstructive pulmonary disease (COPD) is a common comorbidity that has been linked to higher mortality and respiratory complications in cardiac surgery. However, the postoperative outcomes for COPD patients undergoing Type A Aortic Dissection (TAAD) repair remain unexplored. Thus, this study aimed to assess the impact of COPD on in-hospital outcomes of TAAD repair in a national registry. METHODS: Patients undergoing TAAD repair were identified in National Inpatient Sample from the last quarter of 2015-2020. Multivariable logistic regressions were used to compare in-hospital outcomes between patients with and without COPD, where demographics, comorbidities, hospital characteristics, primary payer status, and transfer status were adjusted. RESULTS: There were 701 (16.37 %) COPD patients and 3581 (83.63 %) non-COPD patients who went under TAAD repair, where the prevalence of COPD was higher than in the general population (6 %). COPD and non-COPD patients have comparable rates of in-hospital mortality (14.69 % vs 15.19 %, aOR 1.016, 95 CI 0.797-1.295, p = 0.9) and there was no indication of delayed surgery. However, COPD patients had a higher risk of mechanical ventilation (37.80 % vs 31.42 %, aOR 1.521, 95 CI 1.267-1.825, p \u3c 0.01) and a higher rate of transferring out to other facilities (38.37 % vs 32.23 %, aOR 1.271, 95 CI 1.054-1.533, p = 0.01). In addition, COPD patients had a longer hospital length of stay (14.28 ± 11.32 vs 13.85 ± 12.78 days, F = 5.61, p = 0.01). CONCLUSION: The presence of COPD could be a risk factor for the development of aortic dissection. However, outcomes for COPD patients were largely similar to those without COPD. These findings can be valuable for preoperative assessments and tailoring perioperative care for COPD patients undergoing TAAD repair

Strain-related regional alterations of calcium-handling proteins in myocardial remodeling

BackgroundCardiac remodeling has been shown to have deleterious effects at both the global and local levels. The objective of this study is to investigate the role of strain in the initiation of structural and functional changes of myocardial tissue and its relation to alteration of calcium-handling proteins during cardiac remodeling after myocardial infarction.MethodsSixteen sonomicrometry transducers were placed in the left ventricular free wall of 9 sheep to measure the regional strain in the infarct, adjacent, and remote myocardial regions. Hemodynamic, echocardiographic, and sonomicrometry data were collected before myocardial infarction, after infarction, and 2, 6, and 8 weeks after infarction. Regional myocardial tissues were collected for calcium-handling proteins at the end study.ResultsAt time of termination, end-systolic strains in 3 regionally distinct zones (remote, adjacent, and infarct) of myocardium were measured to be −14.65 ± 1.13, −5.11 ± 0.60 (P ≤ .05), and 0.92 ± 0.56 (P ≤ .05), respectively. The regional end-systolic strain correlated strongly with the abundance of 2 major calcium-handling proteins: sarcoplasmic reticulum Ca2+ adenosine triphosphatase subtype 2a (r2 = 0.68, P ≤ .05) and phospholamban (r2 = 0.50, P ≤ .05). A lesser degree of correlation was observed between the systolic strain and the abundance of sodium/calcium exchanger type 1 protein (r2 = 0.17, P ≤ .05).ConclusionsRegional strain differences can be defined in the different myocardial regions during postinfarction cardiac remodeling. These differences in regional strain drive regionally distinct alterations in calcium-handling protein expression