Elevated Plasma Brain Natriuretic Peptide Research Articles

Routine assessment of cardiotoxicity in patients undergoing long-term immune checkpoint inhibitor therapy.

The indications for immune checkpoint inhibitors (ICIs) are expanding in cancer drug therapy, and while cardiac events associated with ICIs are often fatal, there are few reports regarding cardiac complications associated with long-term ICI therapy. We aimed to study cardiac complications in patients undergoing long-term ICI therapy. From the database of our local cardio-oncology unit, we enrolled patients with cancer undergoing ICI therapy for more than 6months and for whom cardiologists continuously performed routine follow-ups. We defined the primary endpoint as discontinuation of ICI due to cardiac events. We also analyzed changes in cardiac biomarkers and echocardiographic parameters. We retrospectively analyzed 55 consecutive patients (43 males, mean age: 65 ± 11years) treated with ICI therapy in our hospital between January 2017 and June 2021. None of the patients discontinued ICI therapy due to cardiac events more than 6months after treatment was initiated. Among the participants, we observed four patients with elevated serum troponin I levels, seven patients with decreased global longitudinal strain values, and two patients with elevated plasma brain natriuretic peptide levels. No patient required drug intervention for these cardiac events; furthermore, there were no cases of clinically diagnosed myocarditis. In the present study, there were no cardiac events causing ICI discontinuation in patients undergo ICI therapy for more than 6months.

Arrhythmogenic right ventricular cardiomyopathy patients with a markedly enlarged RV compressing LV to left side have an atypical distribution of epsilon waves and elevated plasma BNP

Abstract Funding Acknowledgements Type of funding sources: None. Background Epsilon waves on V1-3 leads are specific ECG findings in patients with arrhythmogenic right ventricular (RV) cardiomyopathy (ARVC) suggesting RV conduction delay. Four dimensional (4D) cardiac CT visualizes ARVC characteristics, such as fibro-fatty invasion into RV and left ventricular (LV) myocardium (RVM, LVM), an enlarged RV, reduced RV motion, and bulging. Purpose We hypothesize that Epsilon waves in V4-6 leads suggest LV invasion in ARVC. Alternatively, extreme RV enlargement may compress the LV and cause clockwise rotation; an enlarged RV may itself cause epsilon waves in V4-6 leads. Methods Retrospective analysis of 17 patients (11 males, 57 ± 17 yrs) with suspected ARVC undergoing cardiac CT and ECG, 9 of whom met 2010 ARVC task force criteria. Results All 9 patients had epsilon waves on ECG; 5 had fibro-fatty invasion into the LVM. We divided the 9 into 5 groups by CT: 1) markedly enlarged RV compressing the LV to the left side with fibro-fatty changes exclusively in RVM (N = 1); 2) similar findings in both RVM and LVM (N = 2); 3) moderately enlarged RV without compression of the LV to the left side and fibro-fatty changes exclusively in RVM (N = 3); 4) the same in both RVM and LVM (N = 2); 5) severe mitral valve regurgitation, a markedly enlarged LV, and a fibro-fatty change in both RVM and LVM (N = 1). The patient in group (gp) 1 showed epsilon waves in V1-6 leads, patients in gp 2 had epsilon waves in V1-6 (N = 1), and V3-5 (N = 1) leads; patients in gp 3 had epsilon waves in V1-4 (N = 2), and V1-3 (N = 1) leads, patients in gp 4 had epsilon waves in V1-3 (N = 1), and V1, 2 (N = 1) leads; finally, the patient in gp 5 had epsilon waves in V4-6 leads. Plasma brain natriuretic peptide (BNP) levels were significantly greater in patients in gp 1 & 2 than gp 3 & 4 (1255 ± 838 vs 80 ± 52 pg/ml, P = 0.016). Conclusions ARVC patients with a markedly enlarged RV compressing the LV to the left side (gp 1,2) had a broad (V1-6) or different range (V3-5) distribution of epsilon waves and significantly elevated plasma BNP independent of fibro-fatty invasion of the LV, different from typical ARVC (gp 3,4). Additionally, structural change due to complicated heart disease, such as valvular disease (gp5), may also influence the distribution of epsilon waves in ARVC. Abstract Figure. CT and ECG in ARVC group 1

Technology Applications of Capnography Waveform Analytics for Evaluation of Heart Failure Severity

This study aimed to elucidate the influential parameter, acquired from the analyses of nasal capnography waveforms, for the elevated plasma brain natriuretic peptide (BNP) levels in patients (n = 34) with heart failure (HF). The capnography waveforms were analyzed to evaluate changes in end-tidal CO2 (ETCO2) values and expiratory and inspiratory durations. The relationship between these parameters, estimated from capnography analyses and plasma BNP, was then evaluated. Mean ETCO2 values and BNP levels showed a strong negative correlation (R2 = 0.6355, p < 0.0001) in HF patients with chronic kidney disease (CKD) (R2 = 0.6355, p < 0.0001). The ETCO2 value was the most influential parameter that indicated elevated BNP levels in HF patients with CKD (β = - 0.577; p = 0.031). The mean ETCO2 level could be a potentially influential parameter reflecting elevated BNP levels in HF patients, especially in HF patients with CKD. Respiratory parameters, acquired from detailed nasal capnography analyses, might be reasonable for evaluating the severity of HF. Graphical abstract.

Heart Failure With Midrange Ejection Fraction in Patients Admitted for Acute Decompensation: A Report from the Japanese Multicenter Registry

Patients having heart failure with midrange ejection fraction (HFmrEF: 40% ≤ EF < 50%) are increasingly being considered a new subset of the population with heart failure. Despite recent advances in heart-failure treatment strategies, the prognosis of these patients has not improved substantially over time. In addition, the significance of this new phenotype in hospitalized patients with acute decompensated heart failure (ADHF), another population whose prognosis has not improved, also remains poorly understood. This study aimed to describe the clinical characteristics, prognosis and treatment responses of patients with HFmrEF hospitalized for ADHF. On the basis of consecutive inpatient data from a multicenter ADHF registry, 651 of 3572 patients (17.1%) were classified as having HFmrEF. Prognostic factors predicting composite outcomes, defined as all-cause death and heart failure readmission, as well as all-cause death alone, were analyzed. In the median follow-up duration of 724 days, both composite endpoints and all-cause death alone were comparable in those with heart failure with preserved ejection fraction, HFmrEF and heart failure with reduced ejection fraction. Age, anemia, hyponatremia, elevated blood urea nitrogen, chronic kidney disease, and elevated plasma brain natriuretic peptide levels were significant predictors of composite outcomes in HFmrEF. Roughly one-sixth of the patients with ADHF had HFmrEF. The long-term prognosis of patients with HFmrEF was not significantly different from that of patients with heart failure with preserved ejection fraction and heart failure with reduced ejection fraction in the population with ADHF. Risk factors for adverse outcomes in HFmrEF were also similar to those for heart failure with preserved ejection fraction and HFmrEF in the hospitalized population with ADHF.

Factors associated with elevated brain natriuretic peptide level in acute ischemic stroke patients with non-valvular atrial fibrillation

Background: Elevated plasma brain natriuretic peptide (BNP) levels are associated with cardioembolic stroke mainly because of atrial fibrillation (AF). In the present study, we evaluated an array of variables, including BNP level, to determine significant predictors of functional outcome in patients who had non-valvular atrial fibrillation (NVAF) after an acute ischemic stroke (AIS). However, the mechanisms of increased serum BNP levels are hitherto unclear.

Abstract WP209: Plasma Brain Natriuretic Peptide Should be a Predictor for 3-Month Mortality in Non-Cardioembolic Stroke

Background: Plasma brain natriuretic peptide (BNP) is primarily released from the ventricular myocardium and is a biomarker of cardioembolic stroke. Previous studies have shown that elevated plasma BNP level predicts short and long term mortality in cardioembolic stroke. However, the relationship between BNP and mortality in non-cardioembolic stroke has not been fully examined. The present study tested the hypothesis that admission plasma BNP level can serve as a marker of 3-month mortality in non-cardioembolic stroke. Methods: From a prospective stroke registry, we examined acute non-cardioembolic stroke patients within 7 days after symptom onset who measured plasma BNP on admission from September 2014 to March 2016. We divided all patients into the non-survivors and the survivors within 3 month of non-cardioembolic stroke, and compared clinical characteristics between the two groups. The factors associated with 3-month mortality were investigated by multivariate logistic regression analysis. Results: Three hundred and one patients (198 males, 71 [61-80] years old) were enrolled in the study. Thirteen patients (3.8%) died within 3 month of non-cardioembolic stroke. There were no significant differences in male (61.5% vs. 66.0%, P=0.769), age (71 years old vs. 68 years old, P=0.450), hypertension (61.5% vs. 65.6%, P=0.771), diabetes (15.4% vs. 28.7%, P=0.525), dyslipidemia (30.8% vs. 43.4%, P=0.409), and smoking (61.5% vs. 50.0%, P=0.573) between the non-survivors and the survivors. The NIHSS score was significantly higher in the non-survivors than in the survivors (15 vs. 2, P&lt;0.001). The plasma BNP was significantly higher in the group of non-survivors than in the group of survivors (85 pg/ml vs. 31 pg/ml, p =0.005). A cut off plasma BNP level of 65.0 pg/ml could predict death within 3 month of non-cardioembolic stroke. Multivariate logistic regression analysis showed that a plasma BNP level of &gt;65.0 pg/ml (odds ratio [OR] 6.49; 95% confidence interval [CI], 1.79-23.56, P=0.04) was independently associated with 3-month mortality in non-cardioembolic stroke. Conclusions: A high plasma BNP level on admission should be a predictor for 3-month mortality in non-cadioembolic stroke.

Noninvasive Predictors of Malignant Arrhythmias

Background: Prediction and potential prevention of sudden cardiac death (SCD) due to malignant ventricular arrhythmia (MVA) represent an obvious unmet medical need. We estimated the prognostic relevance of numerous biomarkers associated with future MVA development in patients with coronary artery disease (CAD) over 2 years of follow-up. Methods: Patients with stable documented CAD (n = 97) with a mean age of 61 ± 10 years were prospectively enrolled in a single-center observational cohort study. Heart failure was diagnosed in 68% of the patients (NYHA class II-III). The mean left ventricular ejection fraction (LVEF) was 50 ± 13%, while 20% of patients had LVEF ≤35%. Sixty-two patients underwent myocardial revascularization during the follow-up (mean 25 ± 11 months). Clinical characteristics (age, gender, diabetes, history of coronary disease and arrhythmias, prior interventions and antecedent medications), noninvasive electrophysiological markers [microvolt T-wave alterations, signal-averaged electrocardiography, QT interval duration and alteration, and heart rate turbulence (HRT) and HR variability], laboratory indices [serum creatinine and creatinine clearance, brain natriuretic peptide (BNP), NT-proBNP, and C-reactive protein and troponin T levels] were assessed with regard to the MVA prognosis. Results: MVA was diagnosed in 11 patients during the prospective follow-up. Prior percutaneous coronary intervention (p < 0.05), MVA or syncope (p < 0.05), on-pump coronary artery bypass grafting during follow-up (p < 0.01), LVEF ≤47% (p < 0.01), a left atrium size ≥4.7 cm (p < 0.05), left atrium index (p = 0.01), filtered QRS duration (p < 0.05), abnormal HRT (χ² = 6.2, p = 0.01) or turbulence slope (χ² = 9.5, p < 0.01), BNP ≥158 pg/ml (p < 0.01) and NT-proBNP ≥787 pg/ml (χ² = 4.4, p < 0.05) were significantly associated with MVA risk by univariate analysis. However, only prior MVA or syncope [odds ratio (OR) 11.1; 95% confidence interval (CI) 2.8-44.4; p < 0.01], abnormal HRT (ОR 13.6; 95% CI 2.8-66.1; p < 0.01) and plasma BNP (ОR 14.3; 95% CI 3.2-65.0; p < 0.01) remained independent predictors of MVA occurrence by multivariate Cox regression analysis. Conclusion: Prior syncope or MVA, HRT and elevated plasma BNP were independent MVA predictors, advocating for the prospective screening of high-risk CAD patients for potential SCD awareness.

Levels of brain natriuretic peptide as a marker for the diagnosis and prognosis of acute ischemic stroke.

IntroductionThe relationships between plasma levels of brain natriuretic peptide (BNP) and severity and location of stroke, prognosis, and infarct volume were investigated in acute ischemic stroke patients who presented within the first 24 hours (h) of stroke.Material and methodsBrain natriuretic peptide levels were tested in 40 patients and 30 healthy controls. Infarct volume was automatically calculated by multi-slice computed tomography. Disease severity was assessed using the National Institutes of Health Stroke Scale (NIHSS) at presentation, 24 h, 72 h and the 28th day. Progression was defined as an increase of more than two points in the NIHSS scores.ResultsThe mean BNP levels were 284.16 ±382.79 at presentation and 273.78 ±451.91 at 72 h in the patient group, whereas the mean BNP level was 25.29 ±13.47 in controls. There was a statistically significant difference between the two groups (p < 0.001). Differences in BNP levels among patient subgroups according to the TOAST and OCSP classifications were not statistically significant (p = 0.534, p = 0.943, respectively). There was no significant correlation between plasma BNP level and infarct volume or NIHSS scores (p = 0.5, p = 0.07). A positive correlation was found between BNP levels and the length of the hospitalization period (p = 0.03 and r = 0.33). There was no statistically significant relationship between elevated plasma BNP levels and progression of disease (p = 0.08).ConclusionsPlasma BNP levels were increased in the acute phase of stroke; therefore, BNP could be used as a biomarker for morbidity and mortality, even in patients without cardiac failure.

Elevated plasma brain natriuretic peptide levels predict left atrial appendage dysfunction in patients with acute ischemic stroke

It is well known that left atrial appendage (LAA) dysfunction plays an important role in the occurrence of cardioembolic stroke. The atrium is the main source of brain natriuretic peptide (BNP) in patients with atrial fibrillation (AF). We hypothesized that the plasma BNP level would be a sensitive predictor of LAA dysfunction in patients with acute ischemic stroke. Transesophageal echocardiography was performed and plasma BNP levels were measured in 223 patients (145 males, age 69 ± 14 years), within 7 days after the onset of acute ischemic stroke. None of the patients had a history of congestive heart failure. LAA thrombus was detected in 23 of 77 (30%) patients with AF. Plasma BNP levels were markedly higher in patients with cardioembolic stroke compared to those without (144 pg/ml vs. 35 pg/ml, p<0.05). Plasma BNP levels were significantly correlated with LAA emptying flow velocity regardless of sinus rhythm (R=-0.352) or AF (R=-0.436). Furthermore, among patients with cardioembolic stroke, plasma BNP levels were markedly higher in patients with cardiogenic stroke, as diagnosed by transesophageal echocardiography, than in those with cryptogenic stroke (193 pg/ml vs. 14 pg/ml, p<0.05). Multivariate logistic regression analysis showed that a BNP concentration >90 pg/ml was an independent predictor of cardiogenic stroke (odds ratio 41.39, 95% confidence interval 1.28-138; p=0.0358). Elevated plasma BNP concentrations may be a reliable surrogate marker for the prediction of LAA dysfunction and cardiogenic stroke in patients with acute ischemic stroke.

Brain Natriuretic Peptide Production and Secretion in Inflammation

Gene expression and secretion of the cardiac polypeptide hormones atrial natriuretic factor (ANF) and brain natriuretic peptide (BNP) are simultaneously upregulated in various cardiac disorders such as congestive heart failure, ischemic heart disease, and hypertensive heart disease, in which hemodynamic or neuroendocrine changes are key components in the progression of disease. However, during acute cardiac allograft rejection, plasma BNP levels are increased but not those of ANF. Successful treatment of the rejection episode decreases the elevated plasma BNP to prerejection values suggesting that substances related to inflammation may selectively influence BNP gene expression. Indeed, cytokines such as TNFα and IL-1β selectively stimulate cardiac BNP at the transcriptional and translational levels in cardiomyocyte cultures without affecting ANF. This selective BNP increase is seen in vivo, in addition to acute cardiac allograft rejection, in several circumstances where inflammation significantly contributes to the pathogenesis of disease such as in sepsis and in acute myocarditis.

Abstract 9569: Circulating Plasma Brain Natriuretic Peptide Predicts Longitudinal Change in Blood Pressure: The Jackson Heart Study

INTRODUCTION: Elevation in circulating brain natriuretic peptide (BNP) concentrations has been associated with hypertension in studies of non-Hispanic whites. However, the relation of plasma BNP concentration to progression in blood pressure (BP) category and to incident hypertension in African Americans is unknown. HYPOTHESIS: We assessed the hypothesis that higher circulating BNP concentrations in non-hypertensive African Americans will be associated with change in BP category and incident hypertension. METHODS: Our study population consisted of non-hypertensive participants of the Jackson Heart Study with BP, anthropometry and phlebotomy measures in both exam 1 (2000-04) and exam 2 (2005-08), and plasma measures of BNP in exam 1 only. We examined the relation of circulating BNP concentrations (categorical measures by quartile) to BP progression and to incident hypertension using multivariable logistic regression. The model adjusted for age, sex, BP categories (optimal; normal and high normal), systolic and diastolic BP, smoking, diabetes, body mass index, echo LV mass (all measured at baseline) and change in age between the two exam cycles. RESULTS: The study population consisted of 1,158 participants (mean age 49±12 years, 59% women). The median follow-up period was 5.0± 0.8 years. We observed 38.1% of the participants progressed to a higher BP stage and 20.1% of the participants developed incident hypertension. In the multivariable regression model, elevated plasma BNP concentrations (based on highest quartile) were significantly and positively associated with BP progression [p=0.006; OR, 1.8; 95% CI (1.2, 2.6)] and marginally and positively associated with incident hypertension [p=0.06; OR, 1.3; 95% CI (0.8, 2.1)]. Categorical BNP was significantly and positively associated with both BP progression (p=0.006) and incident hypertension (p = 0.04). CONCLUSION: In our community-based sample of middle-aged and elderly African Americans, higher plasma BNP concentrations were associated with increased risk of BP progression and incident hypertension in all participants.

Eponym

Barth syndrome (OMIM #302060) (BTHS) is an X-linked disorder of lipid metabolism characterized by skeletal myopathy, neutropenia, growth delay, and cardiomyopathy. It is caused by mutations in the tafazzin gene (TAZ), which lead to decreased production of an enzyme required to produce cardiolipin, a component of the inner mitochondrial membrane necessary for proper functioning of the electron transport chain. The most common initial presentation of BTHS is significant heart failure due to cardiomyopathy, which is the main cause of death in infancy or childhood. On the other hand, some patients have limited clinical features of BTHS. These patients may be overlooked or misdiagnosed with unclassified congenital myopathy, especially when heart failure is not clinically significant. However, these patients could also develop significant heart failure or life-threatening arrhythmias during or even after childhood. Heart failure in BTHS is often responsive to standard medical therapy, indicating early diagnosis is critical. Diagnostic clues of BTHS in the subclinical stage of heart failure include family histories, findings of lipid storage myopathy in the skeletal muscle biopsy, and elevated plasma brain natriuretic peptide levels. The genetic analysis of TAZ is the only confirmatory method for the diagnosis of BTHS. physicians should be aware of the possibility of this disease and carry out genetic studies when it is considered.

Barth syndrome diagnosed in the subclinical stage of heart failure based on the presence of lipid storage myopathy and isolated noncompaction of the ventricular myocardium

Barth syndrome (BTHS) is an X-linked disorder characterized by skeletal myopathy, neutropenia, growth delay, and cardiomyopathy. It is caused by mutations in the tafazzin gene (TAZ). Although early diagnosis is critical to prevent the progression of heart failure, this disease remains unrecognized when heart failure is not clinically significant. Here we report on a 13-year-old boy with no family history of BTHS who was diagnosed with the syndrome in the subclinical stage of heart failure. The clues to the diagnosis of BTHS in this patient were the findings of lipid storage myopathy in the skeletal muscle biopsy, elevated plasma brain natriuretic peptide, and the diagnosis of isolated noncompaction of the ventricular myocardium in echocardiography. Genetic studies of TAZ revealed a disease-causing mutation (p.Gly216Arg) in this patient. Physicians should be aware of the possibility of this disease and carry out genetic studies when it is considered.

Successful bosentan therapy in a case of pulmonary arterial hypertention developed during immunosuppressive therapy for lupus nephritis.

We report a 43-year-old female who developed pulmonary arterial hypertension (PAH) during intensive immunosuppressive therapy for systematic lupus erythematosus (SLE). She was diagnosed as SLE at the age of 32 years based on serological and hematological abnormalities, oral ulcers, and facial erythema. She experienced frequent flare-ups of disseminated discoid lupus between the ages of 33 and 36 years and developed immune thrombocytopenia at the age of 39 years. In 2007 when she was 43 years old, she developed lupus nephritis (LN) with elevated serum anti-double stranded DNA antibodies and urine protein of less than 1 g/day. Combination therapy for the LN with 35 mg/day prednisolone and intravenous cyclophosphamide (IVCY) led to renal remission. After the seventh monthly session of IVCY, she developed dyspnea on exertion. PAH was diagnosed based on enlarged main pulmonary arteries on the chest x-ray, right ventricular outflow and a peak tricuspid regurgitant pressure gradient exceeding 45 mmHg on echocardiography, an elevated plasma brain natriuretic peptide (BNP) level of 260 pg/ml, the exclusion of pulmonary thromboembolism, and no lung fibrosis. The PAH was treated successfully with bosentan. At present the tricuspid regurgitation has disappeared, and the plasma BNP level has normalized.

Abstract 4852: High Resting Velocity in Intramyocardial Coronary Artery is Related to Elevated Plasma Brain Natriuretic Peptide Levels in Patients With Hypertension

Narrowings in intramyocardial coronary arteries (IMCA) and elevated plasma brain natriuretic peptide (BNP) levels have been demonstrated in hypertensive heart disease. To clarify the relation between abnormalities in IMCA and plasma BNP levels, 228 consecutive patients with hypertension were studied using high-frequency transthoracic Doppler echocardiography. We defined IMCA flow as abnormal one if acceleration flow in IMCA, indicating the presence of vessel narrowing, was detected by color flow mapping and the pulsed Doppler study demonstrated higher peak diastolic flow velocity than 32cm/sec (i.e. normal value + 2SD) in the site. Such abnormal flow in IMCA was demonstrated in 59 (56%) of 102 hypertensive patients with left ventricular hypertrophy (LVH) and in 36 (24%) of the other 126 hypertensive patients without LVH. Independent of LVH, the 95 hypertensive patients with abnormal IMCA flow had higher peak diastolic velocities in the IMCA (47.9±16.5 cm/s vs. 24.3±5.4 cm/s, p&lt;0.01) and more elevated plasma BNP levels (131.0±24.4 pg/ml vs. 45.8±5.7 pg/ml, p&lt;0.01) than those without abnormal IMCA flow. Furthermore, peak diastolic velocities had a significant correlation with log BNP values (p&lt;0.01). The index of % area stenosis (IAS) estimated by the continuity equation was 46±14% at the site of acceleration flow, indicating the presence of mild to moderate lumen narrowing in the IMCA. The patients with the IAS of 50% and over had significantly higher log BNP values as compared to those with the IAS of less than 50% (p&lt;0.05), indicating plasma BNP levels may be elevated by factors associated with lumen narrowing in the IMCA. Conclusions: High resting velocity in IMCA is at least partly related to elevated BNP levels in patients with hypertension independent of LVH.

Delayed gadolinium enhancement and elevated plasma brain natriuretic peptide are useful in differentiating hypertrophic cardiomyopathy from athlete's heart

Delayed gadolinium enhancement and elevated plasma brain natriuretic peptide are useful in differentiating hypertrophic cardiomyopathy from athlete's heart

Preoperative plasma brain natriuretic peptide level is an independent predictor of postoperative atrial fibrillation following off-pump coronary artery bypass surgery

Atrial fibrillation (AF) is a frequent complication after coronary artery bypass surgery. Postoperative AF can lead to thromboembolic events, prolonged hospital stay, and increased costs. Recent reports have shown that an elevated plasma brain natriuretic peptide (BNP) level is associated with AF. The purpose of this prospective study was to test the hypothesis that preoperative BNP level is a predictor of postoperative AF following off-pump coronary artery bypass surgery (OPCAB). One hundred and fifty patients without a history of AF undergoing elective isolated OPCAB were enrolled. Plasma BNP level was measured preoperatively. Heart rate and rhythm were continuously monitored during the first 72 h after surgery. Twenty-six patients (17.3%) exhibited postoperative AF. This proportion is similar to those reported in earlier studies. Univariate analysis demonstrated that age (odds ratio [OR], 1.060; 95% confidence interval [CI], 1.008 to 1.114; P = 0.023), previous myocardial infarction (MI; OR, 2.628; 95% CI, 1.031 to 6.697; P = 0.043), and BNP level (OR, 7.336; 95% CI, 2.401 to 22.409 / log BNP level; P < 0.001) were accurate predictors of postoperative AF. Stepwise multivariate regression analysis indicated age (OR, 1.059; 95% CI, 1.002 to 1.120; P = 0.043) and BNP level (OR, 6.272; 95% CI, 1.980 to 19.861/log BNP level; P = 0.002) as the only independent predictors of postoperative AF. Preoperative BNP level is an independent predictor of postoperative AF following OPCAB. Our findings permit us to stratify the risk of AF and to plan prophylactic strategies in high-risk patients.

Elevated Serum Cobalamin in Patients With Decompensated Biventricular Failure

Serum cobalamin (vitamin B12), bound to transcobalamin II, is taken up by the endothelium of the hepatic vasculature via a receptor-mediated membrane transport process. We hypothesized hepatic congestion is associated with elevated serum B12 without hepatocyte necrosis. Serum B12, aspartate and alanine transaminases, alkaline phosphatase, bilirubin (Bili), and brain natriuretic peptide (BNP) were monitored at the time of admission in 91 hospitalized patients: (a) 38 with decompensated biventricular failure having systemic venous distention, tricuspid regurgitation (TR), and echocardiographic evidence of inferior vena cava dilation and moderate to marked TR; (b) 18 with acute left heart failure having a myocardial infarction, an ischemic cardiomyopathy, or hypertensive heart disease; and (c) 35 without clinical evidence of failure despite myocardial infarction, pericarditis, or atrial arrhythmia. Serum cobalamin (normal 180-600 pg/mL) was elevated with biventricular failure (861.4 +/- 53.0 pg/mL) compared with (P < 0.0001) left heart or no failure, where B12 remained normal. Serum aspartate, alanine, and alkaline phosphatase were normal in each group whereas Bili was increased (1.8 +/- 0.2 mg/dL; P < 0.05) with biventricular failure. Plasma BNP was elevated in each group. Elevated cobalamin and Bili are respective biomarkers of hepatocellular dysfunction and cholestasis in patients having decompensated biventricular failure with systemic venous distention and TR without hepatocyte necrosis vis-à-vis left heart failure or in the absence of clinical failure. Elevated plasma BNP did not distinguish between the presence or absence of systemic venous congestion.

Symptomatic ventricular tachyarrhythmia is associated with delayed gadolinium enhancement in cardiac magnetic resonance imaging and with elevated plasma brain natriuretic peptide level in hypertrophic cardiomyopathy

Delayed gadolinium enhancement (DGE) in cardiac magnetic resonance (CMR) imaging indicates the areas with myocardial fibrosis, which are suggested to be arrhythmogenic substrate in hypertrophic cardiomyopathy (HCM). Elevated brain natriuretic peptide (BNP) is associated with cardiovascular events in HCM. We investigated the grade of DGE in CMR and plasma BNP levels in HCM patients with or without symptomatic ventricular tachycardia (VT) or ventricular fibrillation (VF). We recruited 26 consecutive untreated HCM patients without any symptoms of heart failure. They were divided into 2 groups: (1) patients with symptomatic VT/VF [VT/VF(+) group, n=6]; (2) patients without symptomatic VT/VF [VT/VF(-) group, n=20]. CMR was performed to evaluate left ventricular geometry and the grade of DGE. Plasma BNP levels, left ventricular mass index, and the number of segments with positive DGE were greater in the VT/VF(+) group than in the VT/VF(-) group (698.1+/-387.6 vs. 226.9+/-256.8 pg/ml, p=0.006; 152.3+/-49.5 vs. 89.5+/-24.1 g/m(2), p=0.003; 9.7+/-5.7 vs. 3.5+/-3.3, p=0.013). On logistic regression, adjusted odds ratio for symptomatic VT/VF was 214 for logBNP (95% confidence interval [CI] 1.2-37,043, p=0.04) and 1.54 for DGE score (95% CI 1.01-2.34, p=0.04). High plasma BNP levels and the enlarged area of DGE in CMR were associated with symptomatic ventricular tachyarrhythmia. These factors may be useful markers for detecting high-risk patients of sudden cardiac death in HCM.

Diminished mesenteric vaso- and venoconstriction and elevated plasma ANP and BNP with simulated microgravity

Diminished constriction of arteries and veins following exposure to microgravity or bed rest is associated with a reduced ability to augment peripheral vascular resistance (PVR) and stroke volume during orthostasis. We tested the hypothesis that small mesenteric arteries and veins, which are not exposed to large pressure shifts during simulated microgravity via head-down tail suspension (HDT), will exhibit decrements in adrenergic constriction after HDT in rats. Small mesenteric arteries and veins from control (Con; n = 41) and HDT (n = 35) male Sprague-Dawley rats were studied in vitro. Vasoactive responsiveness to norepinephrine (NE) in arteries (10(-9) to 10(-4) M) and veins (pressure-diameter responses from 2 to 12 cmH(2)O after incubation in 10(-6) or 10(-4) M NE) were evaluated. Plasma concentrations of atrial (ANP) and NH(2)-terminal prohormone brain (NT-proBNP) natriuretic peptides were also measured. In mesenteric arteries, sensitivity and maximal responsiveness to NE were reduced with HDT. In mesenteric veins there was a diminished venoconstriction to NE at any given pressure in HDT. Plasma concentrations of both ANP and NT-proBNP were increased with HDT, and maximal arterial and venous constrictor responses to NE after incubation with 10(-7) M ANP or brain natriuretic peptide (BNP) were diminished. These data demonstrate that, in a vascular bed not subjected to large hydrodynamic differences with HDT, both small arteries and veins have a reduced responsiveness to adrenergic stimulation. Elevated levels of circulating ANP or NT-proBNP could adversely affect the ability of these vascular beds to constrict in vivo and conceivably could alter the intrinsic constrictor properties of these vessels with long-term exposure.