Survival outcomes correlate with the level of cell-free circulating DNA in ST-elevation myocardial infarction.

Background: Myocardial infarction (MI) can lead to higher cellular damage, making cell-free DNA (cfDNA) a potential biomarker for assessing disease severity. The aim of this study is to evaluate survival predictions using cfDNA measurements and assess its correlation with MI. Materials and Methods: A direct fluorescence assay was employed to measure cfDNA content in the blood samples of participants. The inclusion criteria included patients who gave informed consent, suffering from ST-elevation myocardial infraction (STEMI) based on established diagnostic criteria (joint ESC/ACC guidelines), between the age of 18 and 80 years old, and had elevated troponin biomarker levels. The study included 150 patients diagnosed with STEMI and 50 healthy volunteers as controls. Serial monitoring of patients was conducted to track their postdisease status. The rate of change of cfDNA was calculated and daily measurements for 7 days were recorded. Results: Mean levels of cfDNA were found to be 5.93 times higher in patients with STEMI compared to healthy controls, providing clear evidence of a clinical correlation between cfDNA and STEMI. Patients were further categorized based on their survival status within a 90-day period. The study observed a strong predictive relationship between the rate of change of cfDNA during daily measurements and survival outcomes. To assess its predictive capability, a receiver operating characteristics (ROC) curve analysis was performed. The ROC analysis identified an optimal cutoff value of 2.50 for cfDNA, with a sensitivity of 81.5% and specificity of 74.0% in predicting disease outcomes. Conclusion: This study demonstrates a robust association between cfDNA and STEMI, indicating that cfDNA levels can be a valuable early prognostic factor for patients. Serial measurements of cfDNA during early disease onset hold promise as an effective approach for predicting survival outcomes in MI patients.

Safety and efficacy of perioperative continuous renal replacement therapy for percutaneous coronary intervention in severe acute myocardial infarction patients.

This retrospective study aimed to evaluate the safety and efficacy of continuous renal replacement therapy (CRRT) during percutaneous coronary intervention (PCI) in patients with severe acute myocardial infarction (AMI). The study analyzed data from 945 AMI patients hospitalized between January 2016 and December 2017, out of which 21 patients underwent perioperative CRRT for PCI. We assessed the baseline characteristics of severe AMI patients before and after CRRT and examined the effect of CRRT on cardiac, renal, and liver function, as well as other indicators. The heart rate of patients undergoing CRRT was significantly lower at 24 h and 48 h after CRRT than before CRRT (p=0.038). There was a moderate but not significant decrease in the mean systolic blood pressure or diastolic blood pressure (p>0.05). Importantly, we found that significantly more patients showed Killip class I-II and significantly improved cardiac function after CRRT (23.8% vs. 57.1%, p=0.001). The levels of urea nitrogen, creatinine, aspartate aminotransferase, glutamic pyruvic transaminase, and total bilirubin were significantly lowered after CRRT treatment (p<0.05). Perioperative management of CRRT was safe and effective for severe AMI patients.

Association of LT-alpha Ala252Gly gene polymorphism and the genetic predisposition of coronary heart disease in Chinese.

About the role of lymphotoxin alpha (LTA) gene in coronary heart disease, controversy reports exists. So the purpose of the present study was to investigate the possible involvement of LTA in the pathogenesis of atherosclerosis and MI in Chinese. In a cross-sectional design, we studied 57 coronary heart disease patients with family history of coronary heart disease and in another control group of 62 healthy subjects (mean age 56 years; range 32-78 years). Body mass index, the levels of blood pressure, the plasma levels of lipoproteins, cholesterol, and triglycerides were measured, smoking data were self-reported, and LTA genotypes were determined. LTA Ala252Gly gene polymorphism had two alleles (LTA1 and LTA2) and three kinds of genotype: homozygote LTA G/G, LTA A/A, and heterozygote LTA A/G. No population significant differences were detected in LTA genotypes and allele frequencies between coronary heart disease patients or healthy controls (chi(2) = 1.479, P = 0.477 > 0.05). LTA Ala252Gly gene polymorphism was not associated with the genetic predisposition of coronary heart disease.

Acute proximal left anterior descending thrombosis manifested by persistent hiccups: A case report.

INTRODUCTION: Hiccup is usually a benign and self-limited phenomenon. Therefore, if hiccups do not resolve by themselves and even last for a long time, it may be the marker of serious medical conditions. PATIENT CONCERNS: We encountered a case presenting with recurrent abdominal discomfort. Diffuse ST-segment elevation in V2-V6 and elevated Troponin I was identified. He had complained about constipation and incomplete intestinal obstruction was ever suspected. Four days later, he exhibited persistent hiccups. DIAGNOSIS: He was diagnosed with acute anterior wall myocardial infarction. And elective coronary angiography showed that proximal left anterior descending (LAD) was occluded by fresh thrombus with TIMI 1 flow. INTERVENTIONS: The lesion in proximal LAD was dilated with low pressure. Interestingly, the hiccups reduced. And after stent implantation the hiccup disappeared in 24 hours. OUTCOMES: The patient was discharged in good general condition, with maintenance therapy and a follow-up protocol. CONCLUSION: Hiccup is only rarely described in the context of acute proximal LAD thrombosis. However, if this special symptom occurs intractably during disease progression, thrombus is revealed to be the probable cause, prompt opening of the criminal vessel should be performed besides strengthening of anticoagulant and antiplatelet.

A case report of spontaneous coronary artery dissection complicated by stent fracture.

RATIONALE: Spontaneous coronary artery dissection (SCAD) is a rare, complex disease, and nowadays poorly understood. The overall incidence of SCAD ranges from 0.28% to 1.1% in angiographic studies. Therefore, the true incidence of SCAD is most likely underestimated due to asymptomatic or sudden cardiac death before diagnosis. Stent fracture (SF) is a multifactorial issue. Longer vessel remodeled by 2 stents can be more prone to have SF due to higher radial force. PATIENT CONCERNS: In this paper we report a 48-year-old man with chest pain for 2 years. DIAGNOSES: Elective coronary angiography revealed a linear dissection in obtuse marginal branch (OM). INTERVENTIONS: He underwent percutaneous coronary intervention (PCI) with the guidance of intravascular ultrasound (IVUS). OUTCOMES: Then SF was revealed 9 months later. LESSONS: This is the first case report of SF after coronary intervention therapy in SCAD patients.

Plasma neutrophil gelatinase-associated lipocalin levels are associated with the presence and severity of coronary heart disease.

OBJECTIVE: This study aimed to compare the levels of plasma neutrophil gelatinase-associated lipocalin (NGAL), matrix metalloproteinase (MMP)-9, high-sensitivity C-reactive protein (hs-CRP), and interleukin (IL)-1ß across different clinical presentations of coronary artery disease and to evaluate the relationship between those biomarkers and the severity of coronary artery lesions in patients without kidney disease. METHODS: We examined 365 eligible patients who underwent coronary angiography. A total of 124 ST-segment elevation myocardial infarction (STEMI) patients, 117 stable angina pectoris (SAP) patients and 124 patients without atherosclerotic plaques were enrolled in the study. Plasma NGAL, MMP-9, hs-CRP, and IL-1ß were measured in all patients using the enzyme-linked immunosorbent assay (ELISA) method. According to the SYNTAX score, the STEMI patients and SAP patients were divided into another set of 2 groups: a high score group (≥ 33, n = 29) and a low score group (<33, n = 212). The relationship between those biomarkers and the severity of coronary stenosis was examined by Spearman correlation analysis; the ability for NGAL to discriminate severe coronary stenosis was examined by receiver operating characteristic (ROC) curve; the influencing factors for the SYNTAX score were determined by logistic regression analysis. RESULTS: Plasma NGAL, MMP-9, and hs-CRP levels in STEMI patients were higher than in the SAP patients and control subjects (P<0.05, respectively), and plasma NGAL and hs-CRP levels were significantly higher in the SAP patients than in control subjects (P<0.05, respectively), while plasma IL-1ß was similar among the 3 groups (P>0.05, respectively). The SYNTAX score was positively related to NGAL (r = 0.363, P<0.001), MMP-9 (r = 0.377, P<0.001), and hs-CRP (r = 0.163, P<0.011); the SYNTAX score was not related to IL-1ß (r = -0.043, P = 0.510). Plasma NGAL was positively related to MMP-9 (r = 0.601, P<0.001) and IL-1ß (r = 0.159, P = 0.014). The area under the ROC curve for NGAL discriminating severe coronary stenosis was 0.838 (95% CI: 0.752-0.923, P<0.001), which was greater than that for MMP-9 [0.818, (95% CI: 0.724-0.912, P<0.001)], IL-1ß [0.485, (95% CI: 0.369-0.601, P = 0.791)], and hs-CRP [0.607, (95% CI: 0.492-0.722, P = 0.061)]. Multivariate regression analysis showed that plasma NGAL levels were independently related to high SYNTAX scores [OR = 1.109, (95% CI: 1.104-1.114), P<0.001]. CONCLUSION: Plasma NGAL, MMP-9, and hs-CRP levels in STEMI patients were higher than those in the SAP patients and control subjects. NGAL had a better ability to discriminate severe coronary stenosis than MMP-9, IL-1ß, and hs-CRP. NGAL may be a novel biomarker to aid in risk stratification in coronary heart disease patients.

Genome-Wide Linkage Analysis of Large Multiple Multigenerational Families Identifies Novel Genetic Loci for Coronary Artery Disease.

Coronary artery disease (CAD) is the leading cause of death, and genetic factors contribute significantly to risk of CAD. This study aims to identify new CAD genetic loci through a large-scale linkage analysis of 24 large and multigenerational families with 433 family members (GeneQuest II). All family members were genotyped with markers spaced by every 10 cM and a model-free nonparametric linkage (NPL-all) analysis was carried out. Two highly significant CAD loci were identified on chromosome 17q21.2 (NPL score of 6.20) and 7p22.2 (NPL score of 5.19). We also identified four loci with significant NPL scores between 4.09 and 4.99 on 2q33.3, 3q29, 5q13.2 and 9q22.33. Similar analyses in individual families confirmed the six significant CAD loci and identified seven new highly significant linkages on 9p24.2, 9q34.2, 12q13.13, 15q26.1, 17q22, 20p12.3, and 22q12.1, and two significant loci on 2q11.2 and 11q14.1. Two loci on 3q29 and 9q22.33 were also successfully replicated in our previous linkage analysis of 428 nuclear families. Moreover, two published risk variants, SNP rs46522 in UBE2Z and SNP rs6725887 in WDR12 by GWAS, were found within the 17q21.2 and 2q33.3 loci. These studies lay a foundation for future identification of causative variants and genes for CAD.

Genome-wide linkage scan identifies two novel genetic loci for coronary artery disease: in GeneQuest families.

Coronary artery disease (CAD) is the leading cause of death worldwide. Recent genome-wide association studies (GWAS) identified >50 common variants associated with CAD or its complication myocardial infarction (MI), but collectively they account for <20% of heritability, generating a phenomena of "missing heritability". Rare variants with large effects may account for a large portion of missing heritability. Genome-wide linkage studies of large families and follow-up fine mapping and deep sequencing are particularly effective in identifying rare variants with large effects. Here we show results from a genome-wide linkage scan for CAD in multiplex GeneQuest families with early onset CAD and MI. Whole genome genotyping was carried out with 408 markers that span the human genome by every 10 cM and linkage analyses were performed using the affected relative pair analysis implemented in GENEHUNTER. Affected only nonparametric linkage (NPL) analysis identified two novel CAD loci with highly significant evidence of linkage on chromosome 3p25.1 (peak NPL  = 5.49) and 3q29 (NPL  = 6.84). We also identified four loci with suggestive linkage on 9q22.33, 9q34.11, 17p12, and 21q22.3 (NPL  = 3.18-4.07). These results identify novel loci for CAD and provide a framework for fine mapping and deep sequencing to identify new susceptibility genes and novel variants associated with risk of CAD.