Updated Strategies in Non-Culprit Stenosis Management of Multivessel Coronary Disease-A Contemporary Review.

The prevalence of multivessel coronary artery disease (CAD) in acute coronary syndrome (ACS) patients underscores the need for optimal revascularization strategies. The ongoing debate surrounding percutaneous coronary intervention (PCI), coronary artery bypass grafting (CABG), hybrid interventions, or medical-only management adds complexity to decision-making, particularly in specific angiographic scenarios. The article critically reviews existing literature, providing evidence-based perspectives on non-culprit lesion revascularization in ACS. Emphasis is placed on nuances such as the selection of revascularization methods, optimal timing for interventions, and the importance of achieving completeness in revascularization. The debate between culprit-only revascularization and complete revascularization is explored in detail, focusing on ST-elevation myocardial infarction (STEMI) and non-ST-elevation myocardial infarction (NSTEMI), including patients with cardiogenic shock. Myocardial revascularization guidelines and recent clinical trials support complete revascularization strategies, either during the index primary PCI or within a short timeframe following the culprit lesion PCI (in both STEMI and NSTEMI). The article also addresses the complexities of decision-making in NSTEMI patients with multivessel CAD, advocating for immediate multivessel PCI unless complex coronary lesions require a staged revascularization approach. Finally, the article provided contemporary data on chronic total occlusion revascularization in ACS patients, highlighting the prognostic impact. In conclusion, the article addresses the evolving challenges of managing multivessel CAD in ACS patients, enhancing thoughtful integration into the clinical practice of recent data. We provided evidence-based, individualized approaches to optimize short- and long-term outcomes. The ongoing refinement of clinical and interventional strategies for non-culprit lesion management remains dynamic, necessitating careful consideration of patient characteristics, coronary stenosis complexity, and clinical context.

Connection between Cardiac Fibrosis Biomarkers and Echocardiography Parameters in Advanced Chronic Kidney Disease Patients.

BACKGROUND: Myocardial fibrosis represents a mainstay pathway in the pathophysiology of uremic cardiomyopathy. This process leads to structural and functional changes in the heart, which can be detected by echocardiography. The purpose of our study was to determine the association between four echocardiographic parameters (ejection fraction (EF), global longitudinal strain (GLS), mean E/e' ratio, and left atrial volume indexed) and biomarkers associated with cardiac fibrosis, such as procollagen type I carboxy-terminal propeptide (PICP), procollagen type III N-terminal peptide (P3NP), and galectin-3 (Gal-3) in patients with end-stage renal disease (ESRD). METHODS: 140 patients with ESRD were enrolled and investigated by echocardiography and the serum levels of the aforementioned biomarkers were determined at baseline. RESULTS: The mean EF was 53.63 ± 8%, the mean GLS was -10.2 ± 5.3%, the mean E/e' ratio was 9.8 ± 4.3, and the mean left atrial volume indexed (LAVI) was 45.8 ± 14.2 mL/m2. The average levels for PICP, P3NP, and Gal-3 were 457.2 ± 240 µg/L, 242 ± 199.9 µg/L, and 10.7 ± 3.7 ng/mL, respectively. In regression analysis, PICP was strongly associated with all four echocardiographic parameters (EF: p = 0.0002, R2 = 0.69; GLS: p = 0.00001, R2 = 0.81; mean E/e': p = 0.00002; R2 = 0.89; LAVI: p = 0.003; R2 = 0.73). P3NP and Gal-3 were only associated with the EF (p = 0.01, R2 = 0.31 and p = 0.02; R2 = 0.35, respectively). CONCLUSION: Our study evidenced that PICP, a collagen-derived biomarker, is associated with important echocardiography parameters, suggesting that it can serve as an indicator of the presence of subclinical systolic and diastolic dysfunction in patients with advanced CKD.

Kidney transplantation: a possible solution to obstructive sleep apnea in patients with end-stage kidney disease.

INTRODUCTION: Obstructive sleep apnea (OSA) is frequently reported among patients with chronic kidney disease resulting in considerable morbidity and mortality. OSA may cause repetitive stimulation of the sympathetic nervous system and elevations in pulmonary artery pressure leading to an elevated risk of cardiac and vascular complications in patients with chronic kidney disease. Furthermore, OSA is associated with progressive worsening of kidney injury and loss of renal function. METHODS: In this systematic review and meta-analysis, we evaluated the effect of renal transplantation on the progression of OSA in patients with end-stage kidney disease. RESULTS: The meta-analysis included eight studies with a total of 401 patients. Findings showed that kidney transplantation does not lead to a statistically significant effect on the apnea-hypopnea index (MD 2.6 events/hr, 95% CI -3.2 to 8.3, p = 0.21), total sleep time (MD 14.7 min/night, 95% CI -8.4 to 37.8, p = 0.76), sleep efficiency (MD 2.5%, 95% CI -1.4 to 6.3, p = 0.57), slow wave sleep (MD 0.4% of total sleep time, 95% CI -7.5 to 8.4, p = 0.05), and rapid eye movement sleep (MD 0.6% of total sleep time, 95% CI -2.2 to 3.3, p = 0.98). There was no statistically significant effect of kidney transplantation on OSA in patients with chronic renal disease.

Kidney transplantation: is it a solution to endothelial dysfunction?

BACKGROUND: Endothelial dysfunction is associated with elevated cardiovascular risk in patients with end-stage renal disease (ESRD). Kidney transplantation has demonstrated significant ability in reducing mortality and improving quality of life in recipients. Recent studies have also reported improvements in endothelial function following kidney transplantation; however, current literature is limited. METHODS: We performed a systematic review of PubMed/Medline, Web of Science, Scopus, Cochrane Library, and CINAHL databases for prospective cohort studies that assessed endothelial function prior to and following kidney transplantation via various clinical markers. Follow-up duration ranged from 1 month to 1 year. A meta-analysis of pooled data was conducted using random-effect models for four key markers: brachial artery flow-mediated dilatation (FMD), high-sensitivity C-reactive protein (hsCRP), nitroglycerin-mediated dilation (NMD), and adiponectin. RESULTS: We included nine studies in our final analysis with a total of 524 patients. Significant improvement of all four biomarkers was observed after transplantation. The mean difference was 2.81% (95% CI 1.92-3.71, p < 0.00001) for FMD, 17.27 mg/L (95% CI 5.82-28.72, p = 0.003) for hsCRP, 1.05%, (95% CI 0.56-1.54, p < 0.0001) for NMD, and 9.27 µg/mL (95% CI 5.96-12.57, p < 0.00001) for adiponectin. CONCLUSION: There is an immediate reversal of endothelial dysfunction in ESRD patients who undergo kidney transplantation, which may explain observed improvements in cardiovascular morbidity in transplant recipients. Future longitudinal studies are needed to understand possible re-emergence of endothelial dysfunction in the long-term postoperative period.