Acta cardiologica最新文献

Background: In patients presenting with ST-segment elevation myocardial infarction (STEMI), the prevalence of having concomitant severe non-culprit lesion(s) is ≥40%. While timely primary PCI (pPCI) for the culprit lesion is the standard practice, management of the non-culprit lesions remains unsettled.

Results: This prospective multi-center observational study recruited 492 acute STEMI patients who underwent successful pPCI for the culprit lesion. Culprit-only versus complementary non-culprit lesion(s) PCI (either immediate or staged during the same hospital stay) was according to the operator's discretion. Clinical, echocardiographic, and angiographic data were collected and tabulated. The residual SYNTAX score (rSS) was completed by the time of discharge considering the residual lesions after all in-hospital revascularization procedures. Through a minimum follow-up of 12 months, older age, presentation with heart failure Killip class ≥ II, lower estimated glomerular filtration rate (eGFR) on admission, lower left ventricular ejection fraction (LVEF), and higher rSS by discharge were significantly associated with recurrent MACE. In multivariate regression analysis, Killip class ≥ II, LVEF, and rSS were found to be independent predictors for recurrent MACE. In the Receiver Operating Characteristics curve, an rSS of >8 had a sensitivity of 70.1%, and specificity of 75.3% to predict 1-year MACE.

Conclusions: Residual syntax score proved to be an independent predictor for recurrent MACE through the subsequent year post STEMI. Patients with rSS >8 seem to be at the highest risk for adverse events and are likely to be the most deserving for completing revascularization to reduce the disease burden.

Background: Cardiovascular diseases remain a leading cause of global mortality, particularly among diabetic patients undergoing percutaneous coronary intervention (PCI). Chronic kidney disease (CKD) poses an additional risk in this population. Yet, its specific impact on major adverse cardiovascular events (MACEs), mortality, and triple vessel disease (TVD) post-PCI remains a topic of debate, specifically in patients with type 2 diabetes mellitus (T2DM).

Objective: This study aimed to examine the impact of renal function on MACE, mortality, and TVD among diabetic patients undergoing PCI.

Methods: Diabetic patients undergoing PCI were analysed for renal function and outcomes. Participants were stratified by glomerular filtration rate (GFR). Logistic regression and receiver operating characteristic (ROC) analysis assessed associations and predictive capabilities.

Results: A total of 505 patients enrolled in the study. A significant difference was observed regarding age, creatinine levels, and number of culprit vessels between diabetics with and without CKD. Severe CKD was associated with higher odds of 1-month mortality (OR: 15.694, p value <.001), 1-month MACE (OR: 7.734, p value <.001), and TVD (OR: 3.740, p value <.001). Patients with severe CKD also had significantly higher odds of 6-months mortality (OR: 12.192, p value <.001) and 6-months MACE (OR: 3.848, p value: .001). Moreover, GFR showed significant predictive accuracy for mortality at one- and six-months follow-up (AUC: 0.77 and 0.71, respectively).

Conclusions: Renal dysfunction, particularly severe CKD, significantly elevates risks of MACE, mortality, and TVD. Strategies to optimise renal function and tailor cardiovascular management could mitigate adverse outcomes in this high-risk population.

Background: Inflammation plays a crucial role in the progression of acute coronary syndrome.

Aims: The aim of this study was to investigate the relationship between the SYNTAX score and new inflammatory markers including albumin-globulin ratio (AGR), C-reactive protein-to-albumin ratio (CAR), fibrinogen-to-albumin ratio (FAR), neutrophil-to-albumin ratio (NAR), and neutrophil percentage-to-albumin ratio (NPAR) in STEMI and NSTEMI patients.

Methods: The study involved 53 STEMI and 64 NSTEMI patients, and each patient group was evaluated separately. Multivariate linear regression analysis was utilised to identify independent risk factors associated with SYNTAX scores.

Results: Out of the 64 NSTEMI patients, 42 had low SYNTAX score (65.6%), and 22 had high SYNTAX score (34.4%). Patients with high SYNTAX scores had significantly higher levels of age, glucose, fibrinogen, monocyte, and FAR, and lower levels of albumin and total protein. We found that FAR and monocyte levels were independent predictors of the high SYNTAX score. The study also determined that the cut-off value for FAR as 9.99, with a sensitivity of 81% and a specificity of 73% for predicting high SYNTAX score in NSTEMI patients. Out of the 53 STEMI patients, 42 had low SYNTAX score (79.2%), and 11 had high SYNTAX score (20.8%). Patients with high SYNTAX scores exhibited significantly higher total cholesterol, LDL, and glucose levels, and lower albumin and total protein levels.

Conclusions: The FAR level is significantly linked with the high SYNTAX score and can be a useful marker for predicting the severity of disease in NSTEMI patients.

Background: Coronary artery disease (CAD) remains the leading cause of mortality and morbidity around the world. Despite significant progress in the diagnosis and treatment of cardiovascular diseases, still there is a clinical need to identify novel biomarkers for early diagnosis and treatment of CAD. The aim of the study is to investigate circulating miRNAs in CAD patients to identify potential biomarkers for early detection and therapeutic management of CAD.

Methods: We assessed the expression of different candidate miRNAs (miR-21-5p, miR-133a-3p, miR-221-3p, miR-451a and miR-584-5p) in plasma from 50 CAD patients and 50 controls by qRT-PCR analysis.

Results: The expression levels of miR-133a-3p (fold change (FC): 28.05, p < 0.0001), miR-451a (FC: 27.47, p < 0.0001), miR-584-5p (FC: 7.89, p < 0.0001), miR-21-5p (FC: 5.35, p < 0.0001) and miR-221-3p (FC: 5.03, p < 0.0001) were significantly up-regulated in CAD patients compared to controls. Receiver operating characteristic curve analysis showed that miR-133a-3p and miR-451a were powerful biomarkers for detecting CAD.

Conclusions: Our results suggested that miR-21-5p, miR-133a-3p, miR-221-3p, miR-451a and miR-584-5p may serve as independent biomarkers for CAD. Further, the combination of miR-133a-3p and miR-451a could be used as a specific signature in CAD diagnosis.

Background: Rs1333040 is the single-nucleotide polymorphisms (SNP) related with coronary heart disease (CHD). The aim of the present study is to examine the association between rs1333040 polymorphism genotypes and CHD and to further explore the molecular mechanism in Chinese population.

Methods: A case-control study was used in this study, including 500 CHD patients and 500 control subjects. CHD patients and controls were distinguished by coronary angiography. Genotypes of rs1333040 were determined on the Agena MassARRAY system. Statistical analysis was conducted by SPSS (Ver 16.0) and plink (Ver. 1.07, Shaun Purcell).

Results: Fisher's exact test by plink indicated a significant difference in the allele distribution between cases and controls, the allele T may be associated with a higher risk of CHD (p = 0.012, odds ratio (OR) = 1.258). The serum levels of low-density lipoprotein cholesterol (LDL-C) (p = 0.029) and Gensini score (p = 0.008) distributed differently in patients with various alleles. In the recessive model, the levels of high-density lipoprotein (HDL) and apolipoprotein A (ApoA) were higher in the TC + CC genotype than in the TT genotype. The TC + TT genotype was found to be risk factors against CHD in a dominant model (OR = 1.278, p = 0.014). The TC + TT genotype along with multiple risk factors significantly positively correlated with the risk of CHD.

Conclusions: The present study investigates the association between the rs1333040 polymorphism genotypes and CHD. The T allele of rs1333040 is the susceptibility site of CHD. The interaction between SNP and various risk factors plays an important role in the development of CHD.

Background: Chronic intermittent hypoxia (CIH) is the primary cause of myocardial inflammation in obstructive sleep apnea-hypopnea syndrome (OSAHS). Pyroptosis is a newly discovered form of programmed cell death accompanying inflammatory reactions. Our previous study showed that TRPC5 is upregulated in the myocardial injury of CIH rats. The present study aimed to explore the role of TRPC5 in CIH-induced myocardial cell pyroptosis.

Methods: A model of CIH in OSA rats was established. SD rats were randomly divided into control group(8rats) and OSA group(8rats). Scanning electron microscope(SEM) was performed on left ventricular tissues slides. Western blot were used to detect the expression levels of pyroptosis-related factors and TRPC5 and its downstream proteins in myocardia tissue.

Results: The pyroptosis of myocardial cells by SEM revealed damaged cell membrane integrity of OSA group rats, with fibrous tissue attached to the cell membrane surface, and vesicular protrusions and pyroptotic bodies were observed. Compared to the control group, the expression of pyroptosis-related proteins, such as caspase1, pro-IL-1β, IL-1β, IL-18, GSDMD, and GSDMD-N was upregulated in the OSA group (p < 0.05). Compared to the control group, the expression of TRPC5, NLPR3, p-CaMKIIβ + δ+γ, and HDAC4 was higher in the OSA group (p < 0.05).

Conclusions: These findings indicated that the pyroptosis response increases in CIH-induced myocardial injury, and the mechanism that TRPC5 is upregulated, promoting the expression of NLRP3 and inflammasome formation through CaMKII phosphorylation and HDAC4 cytoplasmic translocation. This might be a potential target for the treatment of OSA-induced myocardial injury.