CRAX: A simple cardiovascular risk assessment tool to predict risk of acute myocardial infarction or death.

BACKGROUND: Determining the risk of cardiovascular events is essential to optimize patient management. METHODS AND RESULTS: 5842 individuals underwent SPECT myocardial perfusion imaging (MPI) with 4.4 ± 1.2 years of follow-up. Models (the CRAX tool) were derived to predict the cumulative risk of death and acute myocardial infarction (AMI) at 1, 3, and 5 years using clinical and MPI variables. Predictors of AMI and death included age, number of hospitalizations in the 3 years preceding MPI, and left ventricular ejection fraction (LVEF). Additional predictors of death were the use of pharmacological stress, and global stress total perfusion deficit (sTPD), while transient ischemic dilation (TID), and ischemic total perfusion deficit (iTPD) change were predictive of AMI. CRAX predictions were significantly (P < .001) more accurate than clinical variables or MPI results alone, resulting in a significant net reclassification improvement (NRI, 7.5% for AMI, 14.5% death) compared to clinical variables alone. Accuracy for predicting major adverse cardiac events (MACE, comprising all-cause death, AMI, unstable angina, late revascularization) was comparable to that of AMI or death. CONCLUSIONS: CRAX is a risk assessment tool that predicts the risk of AMI, death, or MACE, and improves prediction compared to clinical variables or MPI results alone.

Extracellular ubiquitin levels are increased in coronary heart disease and associated with the severity of the disease.

Aim: This study aimed to evaluate concentration of plasma extracellular ubiquitin (UB) in coronary heart disease (CHD) patients and its correlation with the disease severity.Methods: Levels of UB and stromal cell-derived factor-1a (SDF-1a) were measured in 60 healthy controls and 67 CHD cases. Coronary atherosclerosis was assessed with Gensini scoring system. Spearman correlation was used to evaluate the correlation between UB and low-density lipoprotein cholesterol (LDL-C), C-reactive protein (CRP), creatine kinase-MB (CK-MB), cardiac troponin I (cTnI) or SDF-1a. The receiver-operating characteristic (ROC) curve was established to assess the predictive value of UB.Results: Plasma UB levels were significantly higher in CHD patients than in controls (p < .0001), and the levels in those with acute myocardial infarction (AMI) were higher than stable angina pectoris (SAP) and unstable angina pectoris (UAP) groups (both p < .01). UB was also positively correlated with Gensini score, CRP, CK-MB and cTnI in CHD. ROC analysis of UB showed that the area under the curve (AUC) were 0.711 (95%CI, 0.623-0.799) and 0.778 (95%CI, 0.666-0.890) for CHD and acute coronary syndrome (ACS), respectively. Plasma SDF-1a levels were elevated in CHD patients but showed no significant correlation with UB concentration or the severity of the disease.Conclusion: Plasma UB concentration was increased in CHD and the change of UB levels may reflect the progression of CHD.

Association of plasma apolipoprotein CIII, high sensitivity C-reactive protein and tumor necrosis factor-α contributes to the clinical features of coronary heart disease in Li and Han ethnic groups in China.

BACKGROUND: Apolipoprotein CIII (apoCIII) is an independent risk for coronary heart disease (CHD). In this study, we investigated the associations among plasma apoCIII, hs-CRP and TNF-α levels and their roles in the clinical features of CHD in the Li and Han ethnic groups in China. METHODS: A cohort of 474 participants was recruited (238 atherosclerotic patients and 236 healthy controls) from the Li and Han ethnic groups. Blood samples were obtained to evaluate apoCIII, TNF-α, hs-CRP and lipid profiles. Chi-squared, t-tests, and Kruskal-Wallis or Wilcoxon-Mann-Whitney tests, Pearson or Spearman correlation tests and multiple unconditional logistic regression were employed to analyze lipid profiles and variations in plasma apoCIII, TNF-α, hs-CRP in subgroups of CHD and their contributions to CHD using SPSS version 20.0 software. RESULTS: Compared to healthy participants, unfavorable lipid profiles were identified in CHD patients with enhanced systolic pressure, diastolic pressure, fasting blood sugar (FBS), TG, TC, LDL-C, apoB, Lp(a) (P < 0.05, TC and Lp(a); P < 0.01, FBS, TG, LDL-C, apoB); and lower HDL-C and apoAI (P < 0.05). Plasma apoCIII, TNF-α and hs-CRP levels were higher in CHD individuals (16.77 ± 5.98 mg/dL vs. 10.91 ± 4.97 mg/dL; 17.23 ± 6.34 pg/mL vs. 9.49 ± 3.88 pg/mL; 9.55 ± 7.32 mg/L vs. 2.14 ± 1.56 mg/L; P < 0.01 vs. healthy participants). Identical patterns were obtained in the Li and Han groups (16.46 ± 6.08 mg/dL vs. 11.72 ± 5.16 mg/dL; 15.71 ± 5.52 pg/mL vs. 9.74 ± 4.31 pg/mL; 8.21 ± 7.09 mg/L vs. 2.15 ± 1.51 mg/L in Li people; 17.05 ± 5.90 mg/dL vs. 10.07 ± 4.63 mg/dL; 18.59 ± 6.73 pg/mL vs. 9.23 ± 3.38 pg/mL; 10.75 ± 7.44 mg/L vs. 2.12 ± 1.63 mg/L in Han people; P < 0.01). Paired comparisons of subgroups with stable angina, unstable angina, and acute myocardial infarction (AMI) revealed significant variation in plasma levels of apoCIII, TNF-α and hs-CRP (P < 0.01), but not among subgroups with mild, moderate and severe stenosis (P > 0.05). Plasma apoCIII, TNF-α and hs-CRP contributed to the development of CHD (OR = 2.554, 7.252, 6.035, P < 0.01) with paired correlations in CHD patients (apoCIII vs. TNF-α, r = 0.425; apoCIII vs. hs-CRP, r = 0.319; TNF-α vs. hs-CRP, r = 0.400, P < 0.01). CONCLUSIONS: Association among plasma apoCIII, hs-CRP and TNF-α interacts with unfavorable lipid profiles to contribute to the clinical features of CHD with stable angina, unstable angina, and AMI in the Li and Han ethnic groups in China.

MMP1 and MMP3 gene polymorphisms in patients with acute coronary syndromes.

Matrix metalloproteinases (MMPs) are the group of proteolytic enzymes that break down the components of the connective tissue matrix leading to unstable atherosclerotic plaques. The aim of this study was to examine the association between MMP1-1607dupG (rs1799750) and MMP3-1171dupA (rs3025058) gene polymorphisms and acute coronary syndromes (ACS) in the form of unstable angina. This study included 197 patients with ACS in the form of unstable angina confirmed by coronary angiography (defined by >70% stenosis in at least one major coronary artery) and 144 healthy controls. There was no statistically significant difference in the distribution of the MMP1-1607dupG (rs1799750) polymorphism between patients with unstable angina and the control group. With regard to the MMP3-1171dupA (rs3025058) polymorphism, a significant increase in the frequency of the 6A/6A genotype among patients with unstable angina was detected. This association was confirmed in multivariate logistic regression analysis, where male sex and rs3025058 6A/6A genotype were significantly associated with an increased risk of ACS. © 2017 IUBMB Life, 69(11):850-855, 2017.

Intermediate and nonclassical monocytes show heterogeneity in patients with different types of acute coronary syndrome.

This study was performed to gain further insight in the heterogeneity of monocytes in the different categories of acute coronary syndrome (ACS), especially between patients with unstable angina pectoris, ST-elevation myocardial infarction (STEMI), and non-ST-elevation myocardial infarction (NSTEMI). For this purpose, blood samples were collected in the acute phase from patients presenting with an ACS. These samples were examined with multiparameter flow cytometry to identify the different monocyte subsets and to analyze the expression of monocyte-associated molecules. Leukocytes, as well as an absolute number of monocytes, showed a clear and significant increase in patients with STEMI. This increase was seen in all subtypes of monocytes. The classical monocytes (CD14++CD16-) of patients with an NSTEMI had a significantly increased CD11b expression when compared to the control group, while these cells showed a decreased expression pattern in STEMI patients. This increased CD11b-expression was also seen in the intermediate monocytes of NSTEMI, while it was almost completely downregulated on the intermediate monocytes of STEMI. Finally, CX3CR1, which is almost exclusively expressed on intermediate and nonclassical monocytes, showed a significant decrease in expression in patients with STEMI. In conclusion, intermediate and nonclassical monocytes have a different immunophenotypic pattern in patients with STEMI versus NSTEMI. These differences reflect the pro-inflammatory state of the monocytes in NSTEMI and can be used as target molecules for novel therapeutic strategies to diminish the migration of proinflammatory monocytes into the myocardial tissue. © 2017 International Society for Advancement of Cytometry.

Serum miRNA-499 and miRNA-210: A potential role in early diagnosis of acute coronary syndrome.

In clinical practice, there is still a need for novel biomarkers, which can reliably rule in or rule out acute coronary syndrome (ACS) immediately on admission. This is of particular interest in patients with unstable angina (UA) and non-ST-segment elevation myocardial infarction (NSTEMI) in whom diagnostic uncertainty is high. The aim of the present study is to evaluate the potential role of miRNA-499 and miRNA-210 as novel molecular biomarkers for early diagnosis of UA and NSTEMI suspected patients presented at the emergency unit. A total of 110 patients presenting to the intensive care unit (ICU) within 24 h of onset of chest pain suggestive of ACS were enrolled in the study. They included 37 UA, 48 NSTEMI and 25 noncardiac chest pain (NCCP) patients. Immediately at enrollment, blood samples were taken for estimation of serum miRNA-499 and miRNA-210 expression levels by real time PCR. miRNA-499 and miRNA-210 expression levels were significantly increased in UA and NSTEMI patients compared with NCCP patients (P < 0.001). Receiver operating characteristic (ROC) curve analysis revealed that the area under curve (AUC) of miR-499 for the diagnosis of UA and NSTEMI was 0.98 and 0.97, respectively; while the AUC of miRNA-210 was 0.84 and 0.90, respectively. The important finding of our study was that the AUC of miRNA-499 for the diagnosis of ACS patients with symptoms onset <3 h was 0.89, while the AUC of miRNA-210 was 0.86. Interestingly, combining miRNA-499 and miRNA-210 significantly improved the diagnostic value by increasing the AUC to 0.96, P < 0.001. In conclusion, serum miRNA-499 and miRNA-210 are associated with UA and NSTEMI and with those presenting within 3 h of symptom onset. Both miRNAs might be potentially novel biomarkers for accelerating the diagnosis of ACS patients in emergency unit. © 2016 IUBMB Life, 68(8):673-682, 2016.

Platelet-bound cyclophilin A in patients with stable coronary artery disease and acute myocardial infarction.

OBJECTIVE: Recently, we reported that extracellular cyclophilin A (CyPA) is an important agonist for platelets. Whereas soluble CyPA-levels have been associated with cardiovascular risk factors, cell-bound CyPA has not been investigated yet. In this study, we analyzed for the first time platelet-bound CyPA in patients with symptomatic coronary artery disease (CAD). METHODS AND RESULTS: blood was obtained from 388 consecutive patients: 204 with stable CAD and 184 with acute coronary syndrome (76 with unstable angina, 78 with non ST-elevation myocardial infarction (NSTEMI), and 30 with STEMI). In vitro stimulation of platelets with classical agonists revealed an enhanced expression of CyPA on the platelet surface. In patients with stable CAD, platelet-bound CyPA correlated excellently with platelet activity measured by P-selectin exposure in flow cytometry. The analysis of classical risk factors for atherosclerosis revealed that patients with hypertension and hypercholesterolemia had significantly enhanced platelet-bound CyPA, whereas diabetes and smoking were not associated with enhanced CyPA-binding to the platelet surface. In multivariate analysis, hypercholesterolemia was the only significant predictor of enhanced platelet-bound CyPA. Interestingly, in patients with acute myocardial infarction (AMI) platelet-bound CyPA was significantly decreased compared with patients with stable CAD. CONCLUSIONS: Enhanced platelet-bound CyPA is associated with hypertension and hypercholesterolemia in stable CAD patients. In patients with AMI platelet-bound CyPA is significantly decreased.

Circulating Endothelial Progenitor Cells were Increased in Patients with Thin-Cap Fibroatheroma.

BACKGROUND: We used virtual histology-intravascular ultrasound (VH-IVUS) to evaluate the relationship between circulating endothelial progenitor cells (EPC) and thin-cap fibroatheroma (TCFA). METHODS: This study included 52 patients with unstable angina who underwent coronary angiography and IVUS examination. Patients were divided into a TCFA group (n = 21) or a non-TCFA group (n = 31) based on VH-IVUS performance. Before angiography, peripheral blood levels of EPC were measured by flow cytometry. TCFA was defined as a necrotic core (NC) ≥ 10% of the plaque area without overlying fibrous tissue in the presence of ≥ 40% plaque burden. RESULTS: Levels of circulating EPCs were 72.45 ± 31.73 (count/105) in the TCFA group and 23.93 ± 11.87 (count/ 105) (p < 0.01). Mean levels of CRP were 0.38 ± 0.21 mg/L in the TCFA group and 0.23 ± 0.17 mg/L (p < 0.01). Levels of EPCs correlated positively with necrotic core volume(r = 0.421, p = 0.005), CRP (r = 0.405, p = 0.011) and negatively with fibrous tissue volume(r = -0.411, p = 0.009). In multivariate logistic regression analysis, level of EPC (OR: 1.815, 95% CI: 1.12 - 2.798, p = 0.016), plaque burden (OR: 1.26, 95% CI: 1.07 - 1.86, p = 0.027), and CRP (OR; 1.14, 95% CI: 0.74 - 1.56, p = 0.029) were independent predictors of TCFA. CONCLUSIONS: Circulating EPCs were increased in patients with TCFA, level of EPCs could predict the presence of TCFA.

Resting angina due to papillary fibroelastoma of the right coronary cusp.

A 63-year-old man with chest pain at rest was referred to our hospital. Transthoracic echocardiography showed a mobile ball-like mass at the top of the right coronary cusp. Subsequently, transesophageal echocardiography also showed a mobile mass at the right coronary cusp. Aortic valve replacement with a mechanical valve was performed under general anesthesia. We diagnosed this condition as papillary fibroelastoma based upon the pathological findings with hematoxylin and eosin staining, and Elastica van Gieson staining. Coronary angiography revealed no organic lesions. The operation was successful, and the patient remains asymptomatic. We speculate that the resting chest pain was induced by transient occlusion of the right coronary orifice by the tumor. We describe this rare case in detail including a review of the literature.

Anatomical criteria of malignancy by computed tomography angiography in patients with anomalous coronary arteries with an interarterial course.

PURPOSE: We sought to determine the relation between major adverse cardiac events (MACE) and anatomical criteria assessed by coronary computed tomography angiography (CCTA) in patients with an anomalous coronary artery with an interarterial course (ACAIAC). MATERIAL AND METHODS: We selected CCTA studies of patients with an ACAIAC from a database of 4,160 examinations and studied anatomical criteria according to the presence of prior MACE, defined as syncope, unstable angina, myocardial infarction and resuscitated sudden cardiac death. RESULTS: There were 19 patients (18 males) with an ACAIAC during the study period (incidence 0.46 %). Seven patients with prior MACE were younger (26 years vs 59 years, p < 0.001), had a smaller minimal lumen area (3.6 mm(2) vs 9.0 mm(2), p = 0.001), a higher degree of area stenosis (57 % vs 24 %, p = 0.001), a longer interarterial course (14.7 vs 8.6 mm, p = 0.003) and a smaller proximal segment width (1.6 mm vs 2.5 mm, p = 0.02) compared with the 12 patients without prior MACE. All patients with MACE had the following concomitant anatomical characteristics: minimum lumen area ≤4 mm(2), an area stenosis ≥50 % and intra-arterial length >10 mm CONCLUSIONS: Prior MACE is associated with specific anatomical CCTA characteristics among patients with ACAIAC. CCTA may therefore contribute to distinguish patients at risk of adverse events.

Metabolic syndrome and long-term cardiovascular outcomes in NSTEMI with unstable angina.

BACKGROUND AND AIM: Metabolic syndrome (MS) is associated with cardiovascular mortality and morbidity in patients with acute coronary syndrome. The purpose of this study was to evaluate the impact of MS on long-term clinical outcomes in patients with pure non-ST segment myocardial infarction (NSTEMI) or unstable angina pectoris (USAP). METHODS AND RESULTS: We prospectively enrolled 310 consecutive NSTEMI/USAP patients (74 females; mean age, 59.3 ± 11.9 years). The study population was divided into two groups: MS(+) and MS(-). The clinical outcomes of the patients were followed for up to 3 years. Increased 3-year cardiovascular mortality and reinfarction were observed in the MS(+) group, as compared to the MS(-) group (15 vs. 3.4%, p = 0.001, and 22.2 vs. 8.3%, p = 0.001, respectively). Hospitalization rates for heart failure and stroke were not significantly different between the two groups on follow-up. By a Cox multivariate analysis, a significant association was noted between MS and the adjusted risk of 3-year cardiovascular mortality (odds ratio 3.4, 95% confidence interval, 1.24-9.1, p = 0.02). CONCLUSION: These results suggest that MS is associated with an increased risk of 3-year cardiovascular mortality and reinfarction in patients with NSTEMI/USAP.

Circulating CD36 and fractalkine levels are associated with vulnerable plaque progression in patients with unstable angina pectoris.

The chemokine, fractalkine, independently enhances the vulnerability of coronary atherosclerotic plaques. The present study investigated the combined effects of CD36 and fractalkine on coronary plaque progression in patients with unstable angina pectoris. In the present study, 120 unstable angina pectoris patients undergoing coronary angiography and intravascular ultrasound were divided into two groups: an intermediate lesion group (lumen diameter stenosis 50-70%, 80 patients) and a severe lesion group (at least one lesion with lumen diameter stenosis > 70%, 40 patients). The control group consisted of 40 healthy age- and sex-matched subjects. Concentrations of CD36 and fractalkine were measured by enzyme-linked immunosorbent assay. Major adverse cardiovascular events were monitored over a 2-year follow up. Intravascular ultrasound showed that patients with severe lesions had more calcified and mixed plaques, and a larger plaque area and plaque burden than patients with intermediate lesions (P < 0.05-0.01). More patients with severe lesions underwent stent deployment (P < 0.05) than those with intermediate lesions. CD36 and fractalkine concentrations were significantly higher in the severe lesion patients (P < 0.05), and both had significant positive correlations (P < 0.05) with the plaque burden of atherosclerotic lesions. Using the matched nested case-control study, we found that CD36 and fractalkine levels were higher in patients with recurrent major adverse cardiovascular events than controls (P < 0.05). In conclusion, CD36 and fractalkine both promote, and might synergistically enhance, the progression of coronary atherosclerotic plaques.

Remote ischemic preconditioning immediately before percutaneous coronary intervention does not impact myocardial necrosis, inflammatory response, and circulating endothelial progenitor cell counts: a single center randomized sham controlled trial.

AIMS: Percutaneous coronary intervention (PCI) is frequently accompanied by myocardial injury. The present study was performed to determine whether remote ischemic preconditioning (IP) induces cardioprotection during PCI. METHODS: We enrolled 95 patients requiring nonemergency PCI for stable disease or unstable angina into this prospective clinical trial. Patients were randomized to either remote IP (induced by three 3-min cycles of blood pressure cuff inflations to 200 mm Hg around the upper arm, followed by 3-min of reperfusion n = 47) or sham control (n = 48) immediately preceding PCI. The primary outcome measure was the frequency of post-PCI myonecrosis, defined as a peak postprocedural cTnT T ≥ 0.03 ng/dL. Secondary outcome measures were the change in plasma high-sensitivity C-reactive protein (hsCRP) levels following PCI and in endothelial progenitor cells (EPC) counts following IP. RESULTS: There was no difference in the primary endpoint of the frequency of PCI related myonecrosis which occurred in 22 (47%) and 19 (40%) patients in the remote IP and control groups, respectively, P = 0.42. There was significant increase in hsCRP post-PCI in both groups (P < 0.001), but there was no difference between the groups (median %change in hsCRP 46% vs. 54%, P = 0.73). There was no significant change in circulating early (CD34 -/CD133+/KDR+), intermediate (CD34+/CD133+/KDR+), or late (CD34+/CD133-/KDR+) EPC in the two groups immediately following IP. The composite rate of death, myocardial infarction, and target lesion revascularization at 1 year was 14.1% versus 13.7% (P = 0.90). CONCLUSIONS: Our study indicates that remote IP immediately before PCI does not induce cardioprotection in low to moderate risk patients.

A decrease in the percentage of circulating mDC precursors in patients with coronary heart disease: a relation to the severity and extent of coronary artery lesions?

Inflammation plays a pivotal role in coronary heart disease. Dendritic cells (DCs) are principal players in inflammation and atherosclerosis. Although the percentage of circulating DC precursors in coronary heart disease have been investigated, circulating myeloid DC (mDC) and plasmacytoid DC (pDC) precursors have not been extensively studied, particularly in relation to the severity of coronary artery lesions in patients with coronary heart disease. In this study, we recruited controls (n = 29), patients with stable angina pectoris (SAP, n = 30), patients with unstable angina pectoris (UAP, n = 56), and patients with acute myocardial infarction (AMI, n = 50). The severity and extent of coronary artery lesions was evaluated by Gensini score, following coronary angiograms. The percentage of circulating mDC and pDC precursors was determined by fluorescence-activated cell sorting (FACS). Plasma levels of MCP-1 and MMP-9, which correlate with atherosclerosis and DC migration, were also measured. The percentage of circulating mDC precursors was reduced in patients with AMI and UAP compared with control and SAP patients, respectively (p < 0.01 for AMI vs. SAP and Control, p < 0.05 for UAP vs. SAP and Control). The percentage of circulating pDC precursors was not significant changed. The levels of plasma MMP-9 and MCP-1 and Genisi score were all increased in patients with AMI and UAP, compared to control and SAP patients, respectively (p < 0.01 for AMI vs. SAP and control, p < 0.05 for UAP vs. SAP and control). Overall, the percentage of circulating mDC precursors was negatively correlated with MCP-1 (p < 0.001), MMP-9 (p < 0.001) and Genisi scores (p < 0.001). Genisi scores were positively correlated with the levels of MCP-1 (p < 0.001) and MMP-9 (p < 0.001). Our study suggested that the percentage of circulating mDC precursors is negatively correlated with the severity and extent of coronary artery lesions in patients with coronary heart disease.

Relationship between serum neopterin levels and coronary heart disease.

The relationship between serum neopterin levels and coronary heart disease (CHD) was investigated. Eighty-six CHD patients were divided into an acute myocardial infarction (AMI) group (N = 21), an unstable angina pectoris (UAP) group (N = 35), and a stable angina pectoris (SAP) group (N = 30), based on coronary angiography (CAG), 30 subjects without CHD served as the control group. Serum neopterin levels were determined by enzyme linked immunosorbent assay (ELISA), and relationships between neopterin and the severity of stenosis, stenosis number, and the stability of coronary artery were analyzed. Serum neopterin levels were higher in the AMI and UAP groups than in the SAP and control groups (P < 0.01), but no significant differences were observed between the AMI and UAP groups or between the SAP and control groups (P > 0.05). Mean serum neopterin levels were higher in the single, double, and three vessel lesion groups than in the control group (P < 0.05), whereas there were no significant differences among the lesion groups (P > 0.05). Serum levels of neopterin were significantly higher in the type II than in the type I or type III, plaque groups (P < 0.01), the incidence of type II plaque was significantly higher in the AMI and UAP groups compared to the SAP group (P < 0.01). Neopterin likely plays a role in the occurrence and development of athermanous plaque and can serve as a useful biomarker of vulnerable plaques. Immunoreaction may be involved in the pathophysiological process of CHD.

[The lipid acids spectrum of platelet in patients with new-onset and progressive angina].

The coronary thrombosis is the main factor which leads to acute coronary syndrome. The mechanisms of the coronary thrombogenesis are not found out in detail. It was investigated the changes of the lipid acids spectrum of platelet membrane phospholipids in patients with unstable angina.

[Clinic pathogenetic features of gastroduodenal erosions and ulcers in patients with unstable stenocardia].

OBJECTIVE: To reveal the clinical, morphological and pathogenic features of gastroduodenal erosions and ulcers in unstable angina. METHODS: 135 patients with unstable angina were examined and divided into 2 groups, depending on the presence of a pathological process in the gastroduodenal zone. The state of microcirculation in the tissues of the gastroduodenal zone, secretory and motor function of the stomach were estimated by complex of techniques, adapted to the severity of the patients. RESULTS: It is found that the pathological process in the gastroduodenal zone in patients with unstable angina was presented primarily by acute erosions, less - acute ulcers or recurrent peptic ulcer disease. In this case, the leading symptom of acute erosions was dyspepsia, that as a rule prevailed over the indistinct abdominal pain, and often disappeared in the first few days of treatment. Clinical picture of acute ulcers was determined by gastric dyspepsia and was often combined with abdominal pain and symptoms of gastrointestinal bleeding. The recurrence of peptic ulcer disease was characterized by the combination of moderate abdominal pain, often with migration in retrosternal and cardiac area and loss of circadian rhythm inherent in anthro-duodenal ulcer localization, and dyspeptic disorders. The severity of symptoms of ulcerous process was gradually decreased with time, but in most patients, they had remained by the end of the 2nd week of treatment. The basis of development of erosions and ulcers in unstable angina were the focal mainly thrombohaemorrhagic disorders of the terminal blood flow in the gastroduodenal mucosa. Its were combined with changes in the functional state of the stomach, manifested with an increase activity of acid-peptic factor, reduced production of gastromucoproteins, hypomotor dyskinesia and discoordination of anthro-duodenal propulsion on the hypotonic type. CONCLUSION: Erosive and ulcerative lesions of gastroduodenal zone in unstable angina have a number of clinical and pathogenetic features that should be considered in the process of diagnosis and treatment.

Neutrophil-to-lymphocyte ratio predicts coronary artery lesion severity and long-term cardiovascular mortality in patients with unstable angina pectoris.

OBJECTIVES: Neutrophil-to-lymphocyte ratio (NLR), one of the composite biomarker of systemic inflammatory status, was proved promising in predicting clinical outcomes of acute coronary syndrome (ACS). However, there were no evidences that NLR was directly relative to the clinical outcomes of unstable angina pectoris (UAP). Therefore, this study was aimed to detect whether NLR could predict the coronary artery lesion severity (indicated as SYNTAX score) and clinical outcomes (especially long-term cardiovascular mortality) in patients with. METHODS: In the single-centre retrospective study, 4110 patients with UAP were enrolled and divided into two groups according to their primary NLR values and followed up at a median time duration of 36 months. The differences of SYNTAX score and cardiovascular mortality between groups were analysed, and the predictive value of NLR was determined. RESULTS: NLR was positively and linearly correlated with SYNTAX score (r = 0.270). Diabetes (p = 0.049), lymphocyte (p = 0.004), NLR (p = 0.002) and SYNTAX score (p < 0.001) were independent predictors of long-term cardiovascular mortality in patients with UAP. Kaplan-Meier analysis revealed higher occurrence of cardiovascular mortality when NLR > 2.38 (p = 0.015). Receiver operating characteristic (ROC) analysis showed that NLR = 2.76 is an effective cut point for predicting cardiovascular mortality (69.2% sensitivity, 64.8% specificity). CONCLUSIONS: NLR value was positively related to the severity of coronary artery lesion and proved to be an independent predictor of cardiovascular mortality in patients with UAP. This study would contribute to therapy and prognosis optimisation of UAP.