scholarly journals Role of N Terminal-Pro Brain Natriuretic Peptide in predicting the Severity of Coronary Artery Disease in Patients with Chronic Stable Angina

Author(s):  
Sankalan Saha ◽  
Indrajit Mandal
2019 ◽  
Vol 06Sp, 07 & 07h (1 & 1) ◽  
Author(s):  
Seyed Mohammad Hassan Adel ◽  
◽  
Seyed Mohammadreza Afshani ◽  
Nehzat Akiash ◽  
Seyed Amir Ali Adel ◽  
...  

Medicina ◽  
2021 ◽  
Vol 57 (7) ◽  
pp. 706
Author(s):  
Kamila Marika Cygulska ◽  
Łukasz Figiel ◽  
Dariusz Sławek ◽  
Małgorzata Wraga ◽  
Marek Dąbrowa ◽  
...  

Background and Objectives: Resistance to ASA (ASAres) is a multifactorial phenomenon defined as insufficient reduction of platelet reactivity through incomplete inhibition of thromboxane A2 synthesis. The aim is to reassess the prevalence and predictors of ASAres in a contemporary cohort of coronary artery disease (CAD) patients (pts) on stable therapy with ASA, 75 mg o.d. Materials and Methods: We studied 205 patients with stable CAD treated with daily dose of 75 mg ASA for a minimum of one month. ASAres was defined as ARU (aspirin reaction units) ≥550 using the point-of-care VerifyNow Aspirin test. Results: ASAres was detected in 11.7% of patients. Modest but significant correlations were detected between ARU and concentration of N-terminal pro-brain natriuretic peptide (NT-proBNP) (r = 0.144; p = 0.04), body weight, body mass index, red blood cell distribution width, left ventricular mass, and septal end-systolic thickness, with trends for left ventricular mass index and prothrombin time. In multivariate regression analysis, log(NT-proBNP) was identified as the only independent predictor of ARU—partial r = 0.15, p = 0.03. Median concentrations of NT-proBNP were significantly higher in ASAres patients (median value 311.4 vs. 646.3 pg/mL; p = 0.046) and right ventricular diameter was larger, whereas mean corpuscular hemoglobin concentration was lower as compared to patients with adequate response to ASA. Conclusions: ASAres has significant prevalence in this contemporary CAD cohort and NT-proBNP has been identified as the independent correlate of on-treatment ARU, representing a predictor for ASAres, along with right ventricular enlargement and lower hemoglobin concentration in erythrocytes.


2020 ◽  
Author(s):  
José Tuñón ◽  
Álvaro Aceña ◽  
Ana Pello ◽  
Sergio Ramos-Cillán ◽  
Juan Martínez-Milla ◽  
...  

Abstract Background N-terminal pro-brain natriuretic peptide (NT-proBNP) plasma levels are increased in patients with cancer. In this paper we test whether NT-proBNP may identify patients who are going to receive a future cancer diagnosis (CD) in the short term. Methods We studied 962 patients with stable coronary artery disease and free of cancer and heart failure at baseline. NT-proBNP, galectin-3, monocyte chemoattractant protein-1, high-sensitivity C-reactive protein, high-sensitivity cardiac troponin I (hsTnI), and calcidiol (vitamin D) plasma levels were assessed. The primary outcome was new CD. Results After 5.40 (2.81-6.94) years of follow-up, 59 patients received a CD. NT-proBNP [HR 1.036 CI (1.015-1.056) per increase in 100 pg/ml; p=0.001], previous atrial fibrillation [HR 3.140 CI (1.196-8.243); p=0.020], and absence of previous heart failure [HR 0.067 CI (0.006-0.802); p=0.033] were independent predictors of a receiving a CD in first three years of follow-up. None of the variables analyzed predicted a CD beyond this time. A previous history of heart failure was present in 3.3% of patients receiving a CD in the first three years of follow-up, in 0.0% of those receiving this diagnosis beyond three years, and in 12.3% of patients not developing cancer (p=0.036). Conclusions In patients with coronary artery disease, NT-proBNP is an independent predictor of CD in the first three years of follow-up but not later, suggesting that it could be detecting subclinical undiagnosed cancers. The existence of previous heart failure does not account for these differences. New studies in large populations are needed to confirm these findings.


2017 ◽  
Author(s):  
Benjamin J Scirica ◽  
J. Antonio T. Gutierrez

By definition, chronic stable angina is angina that has been stable with regard to frequency and severity for at least 2 months. Chronic stable angina is the initial manifestation of coronary heart disease in approximately 50% of patients. Typically, this type of angina occurs in the setting of atherosclerotic coronary arterial narrowing, although other causes are possible. This review covers the epidemiology, pathophysiology, initial evaluation, differential diagnosis, management, and treatment of patients with chronic stable angina. Figures show noninvasive testing and the probability of coronary artery disease; diagnosis of patients with suspected ischemic heart disease; probability of severe coronary artery disease; coronary outcomes for high- versus low-intensity statin therapy; optimal medical therapy (OMT) versus OMT and percutaneous coronary intervention for chronic angina; OMT versus percutaneous coronary intervention for stable coronary heart disease; and coronary artery bypass grafting versus percutaneous coronary intervention for diabetes and coronary artery disease. Tables list the grading of angina pectoris by the Canadian Cardiovascular Society classification system, the differential diagnosis of chest pain, conditions promoting myocardial oxygen supply and demand mismatch, the features of typical angina, the classification of chest pain, a comparison of the pretest likelihood of coronary heart disease (CHD) in low-risk and high-risk symptomatic patients, the posttest probability of significant CHD based on pretest probabilities of CHD and normal or abnormal results of noninvasive studies, survival according to risk groups based on Duke treadmill scores, high- and moderate-intensity statin therapy, revascularization to improve survival compared with medical therapy, revascularization to improve symptoms with significant anatomic (≥ 50% left main or ≥ 70% nonleft main coronary artery disease) or physiologic (fractional flow reserve ≤ 0.80) coronary artery stenoses, and questions recommended by an expert panel for patients with chronic stable angina at follow-up visits. This review contains 7 highly rendered figures, 13 tables, and 109 references.


2018 ◽  
Vol 10 (2) ◽  
pp. 164-170 ◽  
Author(s):  
Ratan Kumar Datta ◽  
Md Mamunur Rashid ◽  
MG Azam ◽  
Md Salahuddin Ulubbi ◽  
Mohammad Khalilur Rahman Siddiqui ◽  
...  

Background: Neutrophil to lymphocyte ratio (NLR) has been proposed as a new prognostic marker in patients with chronic stable angina (CSA). NLR is a cheap, easily available, non-invasive and routinely done procedure to predict the severity of coronary artery disease.Methods: 110 patients with stable coronary artery disease were evaluated to calculate the NLR from January, 2016 to September, 2016. The patients were divided into two groups: Group I NLR>2.38 and group II NLRd”2.38. Coronary angiogram was done during index hospitalization. The severity of the coronary artery disease was assessed by vessel score and Gensini score and was compared between the groups.Results: NLR was significantly higher in the group of high vessel score and high Gensini score. We found significant weak association between NLR and vessel score (r=0.30, p=0.004) and a moderate positive correlation between NLR and Gensini score (r =0.65, P=0.001). With the increase of NLR, vessel score and Gensini score increases demonstrating more severe coronary artery disease. Univariate logistic regression analysis of variables of interest revealed that age, hypertension, dyslipidemia, serum creatinine, total WBC count and NLR were independent predictor of severe coronary artery disease with odds ratio (OR) being 1.88, 3.93, 5.01, 5.54, 4.05 and 5.70 respectively. In multivariate logistic regression analysis, after adjustment of factors NLR remain independent predictors of severe CSA (OR = 5.73; p = 0.002).Conclusion: Increased neutrophil to lymphocyte ratio is associated with angiographically severe coronary artery disease in chronic stable angina and this association is independent of conventional cardiovascular risk factors.Cardiovasc. j. 2018; 10(2): 164-170


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