Abstract 23: N -Terminal Fragment of the Prohormone Brain-Type Natriuretic Peptide (NT-proBNP) vs. BNP for Predicting Heart Failure in Patients with Stable Coronary Artery Disease: the Heart and Soul Study.

Author(s):  
Rakesh K Mishra ◽  
Mathilda Regan ◽  
Alan H Wu ◽  
Mary A Whooley

Background The B-type natriuretic peptide (brain natriuretic peptide [BNP] and its amino terminal pro-BNP [NT-proBNP]) are powerful predictors of adverse cardiovascular outcomes, including heart failure (HF), in patients with coronary artery disease (CAD). However, their relative prognostic utility remains uncertain. We compared the ability of NT-proBNP and BNP to predict HF hospitalizations in patients with stable CAD. Methods We studied the relative prognostic utility of NT-proBNP and BNP in 983 participants with stable CAD from the Heart and Soul Study. The primary outcome was time to HF hospitalization. Results During an average of 6.7 ± 3.0 years follow-up, there were 173 hospitalizations for HF. NT-proBNP and BNP levels were strongly correlated with one another (r=0.87; p<0.001). In demographically-adjusted models, HF hospitalization was predicted similarly by NT-proBNP (HR per 1-SD increase in log-transformed level: 3.1; 95% C.I. 2.7 - 3.7; p<0.001) and BNP (HR per 1-SD increase in log-transformed level: 3.0; 95% C.I. 2.5 - 3.6; p<0.001). This finding persisted after adjustment for traditional coronary risk factors, history of HF, left ventricular (LV) systolic and diastolic function and LV mass index, with NT-proBNP (HR per 1-SD increase in log-transformed level: 3.4; 95% C.I. 2.5 - 4.5; p<0.001) and BNP (HR per 1-SD increase in log-transformed level: 3.0; 95% C.I. 2.3 - 3.8; p<0.001) continuing to predict the primary outcome similarly. Moreover, in fully adjusted ROC analyses, NT-proBNP (AUC 0.87) and BNP (AUC 0.86; p=0.19 for comparison) performed similarly for predicting HF hospitalization. Conclusions NT-proBNP and BNP are secreted in equimolar amounts and perform similarly for predicting HF hospitalization in patients with stable CAD. This suggests that their relative prognostic utility is not affected by differences in their biological half-lives, in vitro stability and mechanisms of clearance.

Cardiology ◽  
2017 ◽  
Vol 137 (4) ◽  
pp. 201-206 ◽  
Author(s):  
Rakesh K. Mishra ◽  
Gregory Judson ◽  
Robert H. Christenson ◽  
Christopher DeFilippi ◽  
Alan H.B. Wu ◽  
...  

Background: The N-terminal fragment of the prohormone brain-type natriuretic peptide (NT-proBNP) is a powerful predictor of adverse outcomes in patients with coronary artery disease (CAD). However, little is known regarding the prognostic significance of longitudinal changes in NT-proBNP levels. Methods: We evaluated the ability of 5-year changes in NT-proBNP levels to predict subsequent heart failure (HF) hospitalization or cardiovascular (CV) death in 635 participants with stable CAD enrolled in the Heart and Soul Study. Results: The median (IQR) 5-year change in NT-proBNP was 50 pg/mL (-5 to +222). During an average of 4.0 ± 1.4 years follow-up (i.e., 9 years from the baseline measurement), there were 67 events. Participants with 5-year changes in the highest quartile (≥ 223 pg/mL increase in NT-proBNP) had an almost 4-fold greater risk of subsequent HF or CV death than those in the lowest quartile of ≤-5 pg/mL (HR 3.8; 95% CI 2.0-7.3; p < 0.001). This association remained strong after adjustment for demographic variables, comorbidities, left ventricular mass index, systolic and diastolic function, and baseline and follow-up NT-proBNP levels (HR 3.9; 95% CI 1.1-13.4; p = 0.01). Conclusion: Changes in NT-proBNP levels at 5 years predict subsequent HF or CV death in patients with stable CAD, independent of other prognostic markers, including baseline and follow-up NT-proBNP levels. A stable NT-proBNP level predicts a low risk of subsequent events.


2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Olga Mironova ◽  
Olga Perekosova ◽  
Alina Ushanova ◽  
Georgy Isaev ◽  
Alexander Ermolaev ◽  
...  

Abstract Background and Aims Contrast-induced acute kidney injury (CI-AKI) remains one of the major obstacles to perform percutaneous coronary interventions (PCI), especially in older patients and in patients with comorbidities. The number of cases of stable coronary artery disease (CAD) requiring such kind of interventions, in spite of optimal medical treatment received, remains high. Diabetes, hyperuricemia and other components of metabolic syndrome, as well as heart failure, are well known risk factors predisposing to the development of CI-AKI after contrast exposure. Anaemia is diagnosed in a number of patients without underlying chronic kidney disease (CKD), when they seek for medical help due to CAD. The aim of our study was to assess the prevalence of CI-AKI (primary outcome) and the prognostic significance of anaemia as a its possible risk factor (secondary outcome) in different groups of patients with stable CAD requiring PCI using the contrast media. Method We conducted a single-centre prospective observational cohort study. 561 patients aged 18-89 with stable CAD undergoing PCI were enrolled from June 2012 until October 2013. The CI-AKI was defined as a rise in serum creatinine of ≥0,5 mg/dl (≥44μmol/l) or a 25% increase from baseline value, assessed at 48-72 hours after PCI. Anaemia was defined according to the WHO definition – haemoglobin level &lt;12,0 g/dl in women and &lt;13,0 g/dl in men. The contrast media used was either iodixanol (iso-osmolar contrast) or iopromide (low-osmolar contrast), which are both known to cause less adverse events than high-osmolar types of contrast. Nephrotoxic drugs were stopped 48 hours before PCI. The 5-year prognosis including all-cause and cardiovascular mortality, myocardial infarction, stroke, gastrointestinal bleeding, decompensation of chronic heart failure, repeat revascularizations (PCI and coronary artery bypass grafting), end-stage renal disease (ESRD) development, was assessed via phone calls and appointments according to the clinical situation and severity of the condition. Results The prevalence of CI-AKI in this group of patients was 104 cases (18,5%) (primary outcome). The number of patients with anaemia was higher in the group of patients who developed CI-AKI after PCI (6% [7/104] vs 4,4% [20/457]). The female patients with anaemia were more likely to develop CI-AKI (71% [5/7] vs 35% [7/20]). The number of patients who suffered from MI having anaemia at the inclusion date was 2 (28,6%) vs 6 (30%) in patients with and without CI-AKI respectively. Acute heart failure decompensation in patients with anaemia was significantly higher in patients with CI-AKI (43% [3/7] vs 10% [2/20]). This fact needs further evaluation in larger studies but anaemia may be one of the prognostic factors, worsening the kidney damage and leading to worse cardiorenal outcomes. Conclusion Patients with stable CAD suffering from anaemia are more likely to develop CI-AKI even without underlying CKD or ESRD. Female patients with anaemia and stable CAD have higher risk of development of CI-AKI. The combination of CI-AKI and anaemia may lead to a higher 5-year risk of acute heart failure decompensation.


Author(s):  
Mariusz Piechota ◽  
Maciej Banach ◽  
Anna Jacoń ◽  
Jacek Rysz

AbstractThe natriuretic peptide family comprises atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), C-type natriuretic peptide (CNP), dendroaspis natriuretic peptide (DNP), and urodilatin. The activities of natriuretic peptides and endothelins are strictly associated with each other. ANP and BNP inhibit endothelin-1 (ET-1) production. ET-1 stimulates natriuretic peptide synthesis. All natriuretic peptides are synthesized from polypeptide precursors. Changes in natriuretic peptides and endothelin release were observed in many cardiovascular diseases: e.g. chronic heart failure, left ventricular dysfunction and coronary artery disease.


2020 ◽  
Vol 16 (5) ◽  
pp. 678-685
Author(s):  
O. A. Yepanchintseva ◽  
K. A. Mikhaliev ◽  
I. V. Shklianka ◽  
O. J. Zharinov ◽  
B. M. Todurov

Aim. To determine the role of adherence to the basic drug treatment of heart failure (HF) in prevention of late major adverse events (MAEs) after isolated coronary artery bypass grafting (CABG) in patients with stable coronary artery disease (CAD) and left ventricular (LV) dysfunction at three-year follow-up.Material and methods. A prospective non-controlled single-center study included 125 consecutive patients with stable CAD and LV EF<50% (62±8 years; 114 [91.2%] males), after isolated CABG. At three-year follow-up MAЕs occurred in 40 (32.0%) patients. The data on pharmacotherapy at followup were obtained in 124 patients: 85 (68.6%) patients without MAEs and 39 (31.4%) patients with MAEs.Results. The enrolled sample of patients was characterized by high discharge prescription rate of renin-angiotensin system (RAS; 86.3%) blockers (angiotensin-converting enzyme inhibitors or angiotensin-II receptors blockers), beta-blockers (BBs; 97.6%) and mineralocorticoid receptors antagonists (MRAs; 79.0%), being comparable in MAEs and non-MAEs groups. The total coverage of basic HF pharmacotherapy (the combination of RAS blockers, BBs and MRAs) at discharge was 66.1%. At follow-up, about one third of patients in both groups withheld previously prescribed triple HF therapy. The MAEs were associated with more frequent withhold of previously prescribed RAS blockers, as opposed to patients without MAEs (20.5% and 7.1%, respectively; р=0.009). The majority of patients in both groups continued BBs therapy at follow-up (95.0% and 92.9%, respectively; p=0.187). Additionally, we observed the decline of MRAs intake frequency at follow-up (to 43.6% and 49.4%, respectively; p=0.547).Conclusion. During 3-year follow-up after isolated CABG, about one third of patients with stable CAD and baseline LVEF<50% interrupted triple basic HF therapy (including RAS blockers, BBs and MRAs), mainly due to decrease of RAS blockers and MRAs usage. MAEs in patients with stable CAD and baseline LVEF<50% after CABG were associated with suboptimal use and more frequent interruption of RAS blockers.


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.


2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
S Z Zamani ◽  
T J Samuel ◽  
J Wei ◽  
L E J Thomson ◽  
B Tamarappoo ◽  
...  

Abstract Background Women with signs and symptoms of ischemia but no obstructive coronary artery disease (INOCA) are at increased risk of developing heart failure with preserved ejection fraction (HFpEF); however, the exact mechanism for HFpEF progression remains to be elucidated. Prior studies have focused specifically on impaired left ventricular diastolic function in INOCA. We hypothesized that extending our evaluation to include the left atrium (LA)– a key constituent of the transmitral pressure gradient and left ventricular filling– would provide additional, novel, pathophysiological insight. Purpose To evaluate LA function in women with INOCA using cardiac MRI (CMR). Methods We performed retrospective feature tracking analysis of cine images from CMR (Figure 1A), to evaluate LA strain, in 58 INOCA women with normal sinus rhythm (three were excluded due to suboptimal image quality). All strain measurements were performed in duplicate by an experienced investigator blinded to clinical status. We subdivided the cohort by an established threshold of resting left ventricular end diastolic pressure (LVEDP) <12 mmHg vs >12 mmHg, performed invasively within a median of 27 days of the CMR. As illustrated in Figure 1B, LA function was divided into three established phases: (1) reservoir strain, passive expansion of the left atrium from the pulmonary circulation while the mitral valve is closed; (2) conduit strain, passive emptying of the atrium into the ventricle; and (3) booster strain, active emptying of the left atrium following atrial depolarization. Results Reservoir strain was higher in the elevated LVEDP group (n=20, 26.1 + 1.3%) vs. not elevated group (n=35, 22.8 + 0.9%, p=0.03; Figure 1C). In contrast, we observed no group difference in conduit strain (16.5 + 1.0 and 16.5 + 0.7, p=0.78, respectively; Figure 1D), resulting in significantly higher atrial booster strain in the elevated LVEDP group (10.0 + 1.1% and 7.0 + 0.6, p<0.01, respectively; Figure 1E). Conclusions To our knowledge, this is the first report of LA function in women with INOCA. That reservoir strain was higher in subjects with elevated LVEDP provides important pathophysiologic insight regarding diastolic hemodynamics of the LA. The similar conduit function between groups– despite different LVEDP's– strongly suggests a ventricular contribution to the impaired transmitral pressure gradient. Together, these initial proof-of-concept data support the evaluation of LA function in our quest to better understand heart failure progression in INOCA.


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