Acta cardiologica最新文献

Uric acid to HDL ratio (UHR) is a new measure of inflammation that has been widely used to study cardiovascular disease relationships. The aim of this study was to investigate the relationship between uric acid to HDL ratio and hypertension. We found that UHR was positively associated with hypertension prevalence in a nationally representative sample of U.S. participants. In model 3 corrected for multiple confounders, the HR (95% CI) was 1.49 (1.30, 1.70), 2.11 (1.74, 2.54), and 2.97 (2.40, 3.68) for Q2, Q3, and Q4, respectively, compared with the reference value (Q1). There was a nonlinear relationship between the ratio of uric acid to HDL and blood pressure, with an inflection point value of approximately 17. The correlation between the ratio of uric acid to HDL and hypertension was more pronounced before the inflection point value, a finding that was consistent across subgroups except for coronary artery disease. Uric acid, HDL and UHR were predictive of the prevalence of hypertension to varying degrees, with Area Under the Curve (AUC) of 0.62, 0.53, and 0.59, respectively. Therefore, rational monitoring of the ratio of uric acid to HDL can help us in the early prevention of hypertension.

Background: TIMI (Thrombolysis In Myocardial Infarction) frame count is a quantitative method that objectively assesses slow coronary blood flow. In our study, corrected TIMI frame count and non-invasive parameters such as Tp-e interval and Tp-e/QT ratio were investigated after revascularization in patients with ST Elevation Myocardial Infarction (STEMI).

Methods: Patients who were admitted to our hospital with a preliminary diagnosis of STEMI between January 2020 and July 2020 were included in our study. From coronary angiography views, post-procedure corrected TIMI frame counts were measured. Pre and post-procedure Tp-e interval and Tp-e/QT ratios from ECGs were recorded. The patients were divided into 2 groups based on the corrected TIMI frame count of 27. TP-e interval and Tp-e/QT ratios between these two groups were examined.

Results: When the changes in corrected TIMI frame counts and Tp-e interval time were compared, an inverse correlation was found between the changes in Tp-e interval time and corrected TIMI frame count (r= -0.349; p = 0.001). Similarly, an inverse correlation was observed in the change in the Tp-e/QT ratio (r= -0.343; p = 0.002). Patients were divided into 2 groups based on the corrected TIMI frame count (upper limit value of 27). There was a significant difference between the two groups in terms of Tp-e interval (p = 0.003; p < 0.01) and Tp-e/QT ratios (p = 0.023; p < 0.05) measured in the 90th minute ECGs after revascularization.

Conclusions: Coronary antegrade blood flow can be demonstrated invasively by the non-invasive parameters TP-e interval and Tpe/QT ratio instead of corrected TIMI frame count.

Background: Cardioprotective response of ischaemic postconditioning (iPoCo) is blunted in conditions of vascular endothelial dysfunction (ED) associated with hypercholesterolaemia, diabetes, hypertension, etc.

Objective: The current study investigates the effect of metformin on the blunted cardioprotective response of iPoCo in rats subjected to high fat diet (HFD).

Methodology: Wistar rats were subjected to HFD for 56 days. Myocardial ischaemia-reperfusion (I/R) injury was induced by subjecting the heart to global ischaemia of 30 min followed by reperfusion of 120 min after mounting on Langendorff Power Lab apparatus. iPoCo consisting of 6 alternative cycles of ischaemia and reperfusion of 10 sec each, was given after the global ischaemia at the onset of reperfusion. Metformin (25 µM and 50 µM) treatment was given after the global ischaemia just before reperfusion. Myocardial injury was assessed by estimation of infarct size, specific biomarkers of myocardial injury, oxidative stress, inflammation and hemodynamic index.

Results: HFD animal showed significant rise in serum total cholesterol and nitrate levels reflecting hypercholesterolaemia and ED. I/R produced significant myocardial damage indicated by an increase in infarct size, specific biomarkers (LDH, CK-MB, cTn I), oxidative stress- inflammatory parameters (heart Nrf-2, TBARS, TNF-α and decreased GSH and catalase levels) and altered hemodynamic index. iPoCo significantly alleviated I/R induced myocardial injury with respect to above parameters in normal rats but failed to produce such an effect in HFD rats. Treatment of metformin (25 µM and 50 µM) not only mimicked the cardioprotective effect of iPoCo in normal rats but also restored the lost effect of iPoCo in HFD rats.

Myocardial inflammation is a hallmark of inflammatory cardiomyopathy, a heart condition that impairs heart function. This condition encompasses a variety of aetiologies including viral infections, autoimmune disorder, toxin exposures, etc which collectively contribute to its heterogeneity. The classification of ICM varies including Hypertrophic, inflammatory, dilated, left ventricular non-compaction, diabetic, restrictive, etc which are its notable subtypes central to the progression of ICM are inflammatory mechanisms such as cytokine release, immune cell activates, activation of Signalling pathways like NF-κB, NLRP3 inflammasome, etc. These pathways exacerbate inflammatory response & cause cardiac damage. Biomarkers like cardiac troponin- c reactive protein, etc are used for diagnosis &prognosis however, they possess some limitations including specificity & predictive value complicating their chemical utility. Emerging therapies after promising avenues for improved treatment outcomes clinical implications understand the necessity of timely diagnosis & personalised treatment approaches, emphasis the balance between immunosuppression & antiviral therapy. Future perspectives emphasise integrating omics technologies & advanced imaging for more precise diagnostics, alongside developing innovative treatments aimed at modulating inflammation without compromising cardiac function ongoing CT & research on novel molecular targets will likely expand the therapeutic landscape, offering hope for better management & prognosis of ICM.

Background: Intravascular ultrasound (IVUS) guidance shows benefits in various PCI settings; however, its impact in acute myocardial infarction (AMI) patients is not fully understood. This study aims to systematically review and meta-analyse the outcomes of IVUS-guided versus angiography-guided PCI in AMI.

Methods: A comprehensive search across PubMed, Cochrane Library, Embase, Web of Science, and CNKI identified studies comparing IVUS- and angiography-guided PCI in AMI patients. Primary outcomes were all-cause mortality, major adverse cardiac events (MACE), cardiac death, and target vessel revascularization (TVR). A random-effects model was used to calculate pooled risk ratios (RRs) with 95% confidence intervals (CIs).

Results: Nine studies with 838,902 patients (38,949 IVUS-guided and 796,953 angiography-guided) were included. IVUS-guided PCI significantly reduced all-cause mortality (RR 0.74, 95% CI 0.70-0.78, p < 0.001), MACE (RR 0.88, 95% CI 0.82-0.95, p = 0.001), cardiac death (RR 0.67, 95% CI 0.52-0.87, p = 0.003), and TVR (RR 0.86, 95% CI 0.75-0.98, p = 0.024) compared to angiography-guided PCI. Moderate heterogeneity was observed, but sensitivity analyses confirmed result stability.

Conclusion: This meta-analysis indicates that IVUS-guided PCI in AMI patients improves clinical outcomes, including lower mortality, MACE, cardiac death, and TVR rates, compared to angiography guidance. Further research is needed to address barriers to wider IVUS adoption.