natriuretic-peptide--brain and Subarachnoid-Hemorrhage

Cardiac manifestations are recognized complications of subarachnoid hemorrhage. Neurogenic stress cardiomyopathy is one complication that is seen in acute subarachnoid hemorrhage. It can present as transient diffuse left ventricular dysfunction or as transient regional wall motion abnormalities. It occurs more frequently with neurologically severe-grade subarachnoid hemorrhage and is associated with increased morbidity and poor clinical outcomes. Managing this subset of patients is challenging. Early identification followed by a multidisciplinary team approach can potentially improve outcomes.

Topics: Adrenergic beta-Antagonists; Apoptosis; Cardiomyopathies; Cardiotonic Agents; Catecholamines; Electrocardiography; Humans; Intra-Aortic Balloon Pumping; Myocytes, Cardiac; Natriuretic Peptide, Brain; Prognosis; Subarachnoid Hemorrhage; Troponin I; Ventricular Dysfunction, Left

To investigate the association between two cardiac biomarkers, NT-proBNP and TnI, with intracranial pressure (ICP)-/cerebral perfusion pressure (CPP)-insults, cerebral pressure autoregulation, delayed ischemic neurological deficits (DIND), and clinical outcome after aneurysmal subarachnoid hemorrhage (aSAH).. In this retrospective study, 196 aSAH patients treated at the neurointensive care unit, Uppsala University Hospital, Sweden, 2011-2018, with ICP-monitoring and serial NT-proBNP and TnI measurements were included. The first 10 days were divided into early phase (day 1-3) and vasospasm phase (day 4-10).. NT-proBNP and TnI were elevated above the reference interval at least once the first 10 days in 175 (89%) and 116 (59%) patients, respectively. In the vasospasm phase, higher NT-proBNP and TnI were associated with increased percentage of CPP below 60 mmHg. Higher TnI also correlated with more ICP-insults above 20 mmHg. NT-proBNP and TnI did not predict worse pressure autoregulation and DIND. Higher NT-proBNP and TnI were associated with mortality and unfavorable outcome in univariate, but not multivariate, analyses.. Elevated NT-proBNP and TnI correlated with an increased burden of secondary ICP-/CPP-insults, but not with worse pressure autoregulation, DIND, and without independent association with clinical outcome.

Topics: Humans; Natriuretic Peptide, Brain; Retrospective Studies; Subarachnoid Hemorrhage; Troponin I

Cardiac injury and dysfunction following aneurysmal subarachnoid hemorrhage (aSAH) negatively impact the neurological outcomes. This study aimed to determine the association between N-terminal pro-brain-type natriuretic peptide (NT-pro BNP) levels at admission and neurological outcomes at six months in aSAH patients following endovascular treatment. Patients diagnosed with aSAH who underwent NT-pro BNP measurement at admission at our department between January 2018 and April 2021 were retrospectively analyzed. Neurological outcomes were evaluated based on the six-month modified Rankin Scale score. The associations between admission NT-pro BNP levels and neurological outcomes were investigated. In total, 471 patients were included in the analysis. The serum NT-pro BNP levels were significantly lower in patients with a favorable outcome than those with an unfavorable outcome. The area under the receiver operating characteristic curve (AUC) of NT-pro BNP was 0.687. The optimal cutoff value of serum NT-pro BNP level as a predictor of unfavorable outcome was 253.4 pg/mL. Multivariate analysis revealed that admission NT-pro BNP level of >253.4 pg/mL was significantly associated with unfavorable outcomes. After propensity score-matching, admission NT-pro BNP level of >253.4 pg/mL was an independent predictor of unfavorable outcomes. Admission NT-pro BNP level added a slight value to other clinical variables for the prediction of unfavorable outcomes (0.877 vs 0.871 in AUC, respectively; p = 0.084). In conclusion, higher admission NT-pro BNP levels were independently associated with six-month unfavorable outcomes in aSAH patients treated with endovascular treatment. However, it added only minor prognostic value to clinical information alone.

Topics: Biomarkers; Brain; Humans; Natriuretic Peptide, Brain; Peptide Fragments; Prognosis; Retrospective Studies; Subarachnoid Hemorrhage

Brain natriuretic peptide (BNP), often used to evaluate degree of heart failure, has been implicated in fluid dysregulation and inflammation in critically-ill patients. Twenty to 30% of patients with aneurysmal subarachnoid hemorrhage (aSAH) will develop some degree of neurogenic stress cardiomyopathy (NSC) and in turn elevation of BNP levels. We sought to explore the association between BNP levels and development of delayed cerebral ischemia (DCI) in patients with aSAH.. We retrospectively evaluated the records of 149 patients admitted to the Neurological Intensive Care Unit between 2006 and 2015 and enrolled in an existing prospectively maintained aSAH database. Demographic data, treatment and outcomes, and BNP levels at admission and throughout the hospital admission were noted.. Of the 149 patients included in the analysis, 79 developed DCI during their hospital course. We found a statistically significant association between DCI and the highest recorded BNP (OR 1.001, 95% CI-1.001-1.002, p = 0.002). The ROC curve analysis for DCI based on BNP showed that the highest BNP level during hospital admission (AUC 0.78) was the strongest predictor of DCI compared to the change in BNP over time (AUC 0.776) or the admission BNP (AUC 0.632).. Our study shows that DCI is associated not only with higher baseline BNP values (admission BNP), but also with the highest BNP level attained during the hospital course and the rapidity of change or increase in BNP over time. Prospective studies are needed to evaluate whether routine measurement of BNP may help identify SAH patients at high risk of DCI.

Topics: Adult; Aged; Brain Ischemia; Female; Hospitalization; Humans; Male; Middle Aged; Natriuretic Peptide, Brain; Predictive Value of Tests; Retrospective Studies; ROC Curve; Subarachnoid Hemorrhage

Non-traumatic subarachnoid hemorrhage (SAH) is a type of stroke that still has a high mortality rate. Some patients with SAH have electrocardiography (ECG) abnormalities or asymptomatic left ventricular apical ballooning, and requires intervention by cardiologists. However, the impact of cardiac abnormalities after SAH onset remains unclear. We investigated whether ECG abnormalities, myocardial damage, sympathetic nervous activity or echocardiographic left ventricular wall motion abnormalities (WMA) could provide additional risk stratification in patients with SAH.. We studied 118 SAH patients (78 women, age 63 ± 15) without a history of heart disease. Neurological grade (Hunt and Kosnik Grade) and clinical factors were evaluated. A standard 12-lead ECG, echocardiography and blood samples were obtained within 48 h after SAH onset. ECG abnormalities were defined as abnormal Q wave, ST elevation, giant T-wave inversion or QT prolongation.. Twenty of 118 patients (17%) died during the follow-up (35 ± 31 months). Death was significantly associated with higher age (p < 0.0001), neurological grade (p < 0.0001), elevated BNP level (p < 0.0001), increased plasma norepinephrine levels (p < 0.0001) and WMA (p = 0.0070), while ECG abnormalities were not significantly associated. Neurological grade (p < 0.0001), age (p = 0.0047) and BNP (p = 0.0014, hazard ratio 1.0255 for each 1 pg/mL increase in BNP, 95%CI 1.0088 to 1.0499) were independently associated with death. Patients with BNP ≥ 96.6 had a higher risk of death (log- rank p < 0.0001).. Plasma BNP might provide an additional risk stratification in patients with non-traumatic SAH that requires intervention by cardiologists for both its prevention management after onset.

Topics: Adult; Aged; Biomarkers; Female; Heart Diseases; Humans; Male; Middle Aged; Natriuretic Peptide, Brain; Subarachnoid Hemorrhage

We aimed to compare current syncope risk stratification scores and propose a new more feasible and easy-to-use one.. In this prospective cohort study, we enrolled all patients (≥18 years) with chief complaint of syncope if they were not eligible for admission in terms of high-risk features. San Francisco Syncope Rule, Osservatorio Epidemiologico sulla Sincope nel Lazio, and risk stratification of syncope in the emergency department scores were compared in our population.. Overall, 356 patients (mean age: 44.5 years, 46.3% male) were followed for 3 months. Serious adverse events occurred in 26 (7.3%) patients including 4 deaths. Odds ratio for adverse events was 6.8 [95% confidence interval (CI), 2.8-16.1; P < 0.001; area under the curve (AUC): 66.3], 7.7 (95% CI, 3.2-18; P < 0.001; AUC: 72.8), and 18 (95% CI, 7.1-45.4; P < 0.001; AUC: 70.8) when considering San Francisco Syncope Rule, Osservatorio Epidemiologico sulla Sincope nel Lazio, and risk stratification of syncope in the emergency department scores as the predicting tools, respectively. We proposed a relatively more feasible risk score (presenting symptoms, history of cardiovascular diseases, ejection fraction <50%, and predefined electrocardiography abnormalities). According to this syncope score, odds ratio for occurring adverse events was 20.9 (95% CI, 8.4-52; P < 0.001; AUC: 79.8).. The 3 syncope risk scores could somehow predict 3-month adverse events. We found more feasible indicators that could predict serious events better. It suits well for emergency department.

Topics: Adult; Area Under Curve; Cardiac Surgical Procedures; Cardiovascular Diseases; Cohort Studies; Defibrillators, Implantable; Electrocardiography; Emergency Service, Hospital; Feasibility Studies; Female; Follow-Up Studies; Humans; Hypoxia; Incidence; Intracranial Hemorrhages; Male; Middle Aged; Mortality; Myocardial Infarction; Natriuretic Peptide, Brain; Odds Ratio; Oximetry; Pacemaker, Artificial; Peptide Fragments; Prognosis; Prospective Studies; Prosthesis Implantation; Risk Assessment; Stroke; Stroke Volume; Subarachnoid Hemorrhage; Syncope

Neurocardiac injury, a type of myocardial dysfunction associated with neurological insult to the brain, occurs in 31-48% of aneurysmal subarachnoid hemorrhage (aSAH) patients. Cardiac troponin I (cTnI) is commonly used to diagnose neurocardiac injury. Brain natriuretic peptide (BNP), another cardiac marker, is more often used to evaluate degree of heart failure. The purpose of this study was to examine the relationships between BNP and (a) neurocardiac injury severity according to cTnI, (b) noninvasive continuous cardiac output (NCCO), and (c) outcomes in aSAH patients.. This descriptive longitudinal study enrolled 30 adult aSAH patients. Data collected included BNP and cTnI levels and NCCO parameters for 14 days and outcomes (modified Rankin Scale [mRS] and mortality) at discharge and 3 months. Generalized estimating equations were used to evaluate associations between BNP and cTnI, NCCO, and outcomes.. BNP was significantly associated with cTnI. For every 1 unit increase in log BNP, cTnI increased by 0.05 ng/ml ( p = .001). Among NCCO parameters, BNP was significantly associated with thoracic fluid content ( p = .0003). On multivariable analyses, significant associations were found between BNP and poor mRS. For every 1 unit increase in log BNP, patients were 3.16 times more likely to have a poor mRS at discharge ( p = .021) and 5.40 times more likely at 3 months ( p < .0001).. There were significant relationships between BNP and cTnI and poor outcomes after aSAH. BNP may have utility as a marker of neurocardiac injury and outcomes after aSAH.

Topics: Adult; Aged; Aged, 80 and over; Biomarkers; Cardiac Output; Female; Humans; Intracranial Aneurysm; Longitudinal Studies; Male; Middle Aged; Natriuretic Peptide, Brain; Subarachnoid Hemorrhage; Troponin I

Neurogenic stress cardiomyopathy (NCM) has been associated with poor outcomes in the setting of aneurysmal subarachnoid hemorrhage (aSAH). Much less is known regarding recovery of cardiac function. The aim of this prospective cohort study was to study the rate of early cardiac recovery after NCM and the potential effect of NCM on short term functional recovery. A secondary aim sought to determine whether certain biomarkers may be associated with the development of NCM.. Patients with confirmed aSAH between November 2012 and October 2013 were prospectively enrolled and received echocardiograms within 48 h of admission. Ejection fraction (%) and regional wall motion abnormality score index (RWMI) were noted. All patients with confirmed aSAH had a troponin and BNP level drawn on admission. Patients with confirmed NCM received a follow up echocardiogram 7-21 days after the initial echocardiogram. Clinical follow up at 3 months evaluated mortality, mRS and mBI scores.. 63 patients with confirmed aSAH were enrolled. In this cohort 11 (17%) patients were confirmed to have NCM. The NCM group had higher in-hospital mortality [n = 4(36.4%)] compared to the non-NCM group [n = 5(9.6%)] (p = .021). At 3 months the development of NCM was associated with an unfavorable mRS (p = 0.042) and mBI (p = 0.005). Both an elevated BNP (> 100 pg/mL) and elevated troponin (>0.3 mg/dL) were associated with the development of NCM. Follow-up echocardiograms were performed within 21 days of admission on 8 patients with NCM. An abnormal RWMI of 1.5 or higher was present in 5(71%) patients.. NCM is a frequent complication associated with aSAH. The onset of the disease occurs early in the course of aSAH and an elevated BNP and troponin may be associated with the onset of NCM. Cardiac function often remains impaired during the acute recovery phase potentially impeding resuscitation during this period. The routine use of short term follow-up echocardiography may be recommended.

Topics: Adult; Aged; Aged, 80 and over; Electrocardiography; Female; Follow-Up Studies; Humans; Male; Middle Aged; Natriuretic Peptide, Brain; Recovery of Function; Subarachnoid Hemorrhage; Takotsubo Cardiomyopathy; Troponin

Troponin and brain natriuretic peptide (BNP) levels are predictors of mortality following subarachnoid hemorrhage (SAH). Prior studies used strict cutoffs for BNP elevation; however, normal levels of BNP are increased in older persons and women. We explored the association of troponin elevation and BNP elevation adjusted for sex and age with 30-day mortality.. In this retrospective cohort study of patients with SAH, collected data included peak troponin T and BNP levels. Mortality data were obtained from inpatient mortality data and available records. Troponin T elevation was defined as more than 0.10 ng/mL; BNP elevation was defined as greater than the 95th percentile reference limit by age and sex for patients without cardiovascular disease. Associations of elevated troponin T and BNP were estimated from a log-binomial regression model reporting relative risks (RRs), 95 % CIs, and P values; missing data were imputed with the sample median or most frequent category.. This study included 175 SAH patients. In single-variable analysis, peak troponin T level greater than 0.10 ng/mL was associated with increased risk in 30-day mortality (RR 4.38; 95 % CI 2.43-7.89; P < .001); there was no association with elevated peak BNP adjusted for age and sex (RR 1.13; 95 % CI 0.55-2.35; P = .74). There was no evidence suggesting that the combination of elevated peak BNP and elevated peak troponin increased the risk of 30-day mortality.. Elevated troponin was an independent predictor of 30-day mortality following SAH; however, when adjusted for age and sex, elevations in BNP did not have this association.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Female; Humans; Male; Middle Aged; Natriuretic Peptide, Brain; Subarachnoid Hemorrhage; Troponin T; Young Adult

Patients developing stress-induced cardiomyopathy (SIC) after subarachnoid hemorrhage (SAH) have increased risk of vasospasm, delayed cerebral ischemia and death. We evaluated whether high-sensitive troponin T (hsTnT) and N-terminal pro B-type natriuretic peptide (NTproBNP) are useful biomarkers for early detection of SIC after SAH.. Medical records of all patients admitted to our NICU with suspected or verified SAH from January 2010 to August 2014 were reviewed. Patients in whom echocardiography was performed and blood samples for measurements of hsTnT and/or NTproBNP were obtained, within 72 and 48 h, respectively, after onset of symptoms, were included. SIC was defined as reversible left ventricular segmental hypokinesia diagnosed by echocardiography.. A total of 502 SAH patients were admitted during the study period, 112 patients fulfilled inclusion criteria and 25 patients fulfilled SIC criteria. Peak levels of hsTnT and NTproBNP were higher in patients with SIC (p < 0.001). hsTnT had its peak on admission, while NTproBNP peaked at days 2-4 after onset of symptoms. A hsTnT > 89 ng/l or a NTproBNP > 2,615 ng/l obtained within 48 h after onset of symptoms had a sensitivity of 100% and a specificity of 79% in detecting SIC.. The cardiac biomarkers, hsTnT and NTproBNP, are increased early after SAH and levels are considerably higher in patients with SIC. These biomarkers are useful for screening of SIC, which could make earlier diagnosis and treatment of SIC in SAH patients possible.

Topics: Aged; Biomarkers; Early Diagnosis; Female; Humans; Male; Middle Aged; Natriuretic Peptide, Brain; Peptide Fragments; Sensitivity and Specificity; Subarachnoid Hemorrhage; Takotsubo Cardiomyopathy; Troponin T

Myocardial wall motion abnormalities (WMAs) are independent risk factors for a poor outcome in patients with aneurysmal subarachnoid hemorrhage (aSAH).. To study the time course of WMAs during the initial phase after aSAH and to investigate which clinical, electrocardiographic, or myocardial serum markers are predictors of early or late development of WMAs.. In a prospective, multicenter cohort study in patients with aSAH, we performed serial electrocardiography and echocardiography and measured troponin T and N-terminal pro-B-type natriuretic peptide. WMAs present on admission were considered early WMAs; those that developed during the clinical course were considered late WMAs. Using multivariable regression analysis, we calculated odds ratios with corresponding 95% confidence intervals for clinical parameters, electrocardiography, and myocardial serum makers with early or late occurrence of WMAs.. We included 301 patients (mean age ± SD, 57 ± 13) years. Multivariable odds ratios for early WMAs were poor clinical condition, 2.7 (95% confidence interval: 1.1-6.8); sinus tachycardia, 5.0 (1.3-19.9); ST-segment depression, 3.7 (1.02-13.1); ST-segment elevation, 16.6 (1.5-178.9); and increased troponin T, 2.8 (1.1-7.3). Multivariable odds ratios (95% confidence intervals) for late development of WMAs were 6.8 (1.6-30) for a myocardial infarct pattern on admission electrocardiography and 3.4 (1.4-8.5) for increased troponin T on admission.. WMAs may be present on admission or develop during the course of aSAH. Poor neurological condition on admission, sinus tachycardia, ST-segment depression, and ST-segment elevation on admission electrocardiography and increased troponin T are independent predictors of early WMAs; a myocardial infarct pattern on admission ECG and increased troponin T independently predict late WMAs.. NCT00123695.

Topics: Aged; Arrhythmias, Cardiac; Biomarkers; Brugada Syndrome; Cardiac Conduction System Disease; Cohort Studies; Electrocardiography; Female; Heart Conduction System; Hospitalization; Humans; Male; Middle Aged; Natriuretic Peptide, Brain; Odds Ratio; Peptide Fragments; Prospective Studies; Recovery of Function; Regression Analysis; Risk Factors; Subarachnoid Hemorrhage; Troponin T

The rupture of an intracranial aneurysm is followed by increased intracranial pressure and decreased cerebral blood flow. A major systemic stress reaction follows, presumably to restore cerebral blood flow. However, this reaction can also cause adverse effects, including myocardial abnormalities, which are common and can be serious, and increased levels of natriuretic peptides, especially brain natriuretic peptide (BNP). The association of BNP with fluid and salt balance, vasospasm, brain ischemia, and cardiac injury has been studied but almost exclusively regarding events after admission. Brain natriuretic peptide has also been measured at various time points and analyzed in different ways statistically. The authors approached BNP measurement in a new way; they used the calculated area under the curve (AUC) for the first 4 days to quantitatively measure the BNP load during the first critical part of the disease state. Their rationale was a suspicion that early BNP load is a marker of the severity of the ictus and will influence the subsequent course of the disease by disturbing the fluid and salt balance.. The study included 156 patients with acute spontaneous subarachnoid hemorrhage (SAH). Mean patient age was 59.8 ± 11.2 years, and 105 (67%) of the patients were female. An aneurysm was found in 138 patients. A total of 82 aneurysms were treated by endovascular coiling, 50 were treated by surgery, and 6 were untreated. At the time of admission, serum samples were collected for troponin-I analysis and for the N-terminal prohormone of BNP (NT-proBNP); daily thereafter, samples were collected for the NT-proBNP analysis. The cumulative BNP load was calculated as the AUC for NT-proBNP during the first 4 days. The following variables were studied in terms of their influence on the AUC for NT-proBNP: sex, age, World Federation of Neurosurgical Societies grade of SAH, Fisher grade, angiographic result, treatment of aneurysm, clinical neurological deterioration, verified infections, vasospasm treatment, and 6-month outcome.. The AUC for NT-proBNP was larger when variables indicated a more severe SAH. These variables were higher Fisher and World Federation of Neurosurgical Societies grades, high levels of troponin-I at admission, an aneurysm, neurological deficits, and infections. The AUC for NT-proBNP was also larger among women, older patients, and patients with poor outcomes. Linear regression showed that the best predicting model for large AUC for NT-proBNP was the combination of the following: female sex, high levels of troponin-I, an aneurysm, neurological deficits, and advanced age.. The cumulative BNP load during the first days after SAH can be predicted by variables describing the severity of the disease already known at the time of admission. This information can be used to identify patients at risk for an adverse course of the disease.

Topics: Acute Disease; Aged; Biomarkers; Female; Humans; Male; Middle Aged; Natriuretic Peptide, Brain; Peptide Fragments; Predictive Value of Tests; Risk Factors; Rupture, Spontaneous; Subarachnoid Hemorrhage; Time Factors; Troponin I

To assess whether cardiac abnormalities after aneurysmal subarachnoid hemorrhage (aSAH) are associated with delayed cerebral ischemia (DCI) and clinical outcome, independent from known clinical risk factors for these outcomes.. In a prospective, multicenter cohort study, we performed echocardiography and ECG and measured biochemical markers for myocardial damage in patients with aSAH. Outcomes were DCI, death, and poor clinical outcome (death or dependency for activities of daily living) at 3 months. With multivariable Poisson regression analysis, we calculated risk ratios (RRs) with corresponding 95% confidence intervals. We used survival analysis to assess cumulative percentage of death in patients with and without echocardiographic wall motion abnormalities (WMAs).. We included 301 patients with a mean age of 57 years; 70% were women. A wall motion score index ≥1.2 had an adjusted RR of 1.2 (0.9-1.6) for DCI, 1.9 (1.1-3.3) for death, and 1.8 (1.1-3.0) for poor outcome. Midventricular WMAs had adjusted RRs of 1.1 (0.8-1.4) for DCI, 2.3 (1.4-3.8) for death, and 2.2 (1.4-3.5) for poor outcome. For apical WMAs, adjusted RRs were 1.3 (1.1-1.7) for DCI, 1.5 (0.8-2.7) for death, and 1.4 (0.8-2.5) for poor outcome. Elevated troponin T levels, ST-segment changes, and low voltage on the admission ECGs had a univariable association with death but were not independent predictors for outcome.. WMAs are independent risk factors for clinical outcome after aSAH. This relation is partly explained by a higher risk of DCI. Further study should aim at treatment strategies for these aSAH-related cardiac abnormalities to improve clinical outcome.

Topics: Adult; Aged; Cohort Studies; Echocardiography; Female; Heart Diseases; Humans; Kaplan-Meier Estimate; Male; Middle Aged; Natriuretic Peptide, Brain; Netherlands; Odds Ratio; Risk Factors; Subarachnoid Hemorrhage; Tomography, X-Ray Computed; Treatment Outcome

The occurrence of cardiac dysfunction is common after subarachnoid hemorrhage (SAH) and was hypothesized to be related to the release of endogenous catecholamines. The aim of this prospective study was to evaluate the relationship between endogenous catecholamine and cardiac dysfunction at the onset and during the first week after SAH.. Forty consecutive patients admitted for acute SAH without known heart disease were included. Catecholamine plasma concentrations and transthoracic echocardiography (TTE) were documented on admission, on day 1 (D1), and day 7 (D7).. At baseline, 24 patients had a World Federation of Neurosurgical Societies score (WFNS) of one or two; the remaining 16 had a WFNS between three and five. Twenty patients showed signs of cardiac dysfunction on admission, including six with left ventricle (LV) systolodiastolic dysfunction and 14 with pure LV diastolic dysfunction. On admission, norepinephrine, epinephrine, dopamine, B-type Natriuretic Peptide (BNP) and Troponin Ic (cTnI) plasmatic levels were higher in patients with the higher WFNS score and in patients with altered cardiac function (all P <0.05). Among patients with cardiac injury, heart function was restored within one week in 13 patients, while seven showed persistent LV diastolic dysfunction (P = 0.002). Plasma BNP, cTnI, and catecholamine levels exerted a decrease towards normal values between D1 and D7.. Our findings show that cardiac dysfunction seen early after SAH was associated with both a rapid and sustained endogenous catecholamine release and WFNS score. SAH-induced cardiac dysfunction was regressive over the first week and paralleled the normalization of catecholamine concentration.

Topics: Adult; Aged; Biomarkers; Cardiomyopathies; Catecholamines; Echocardiography; Female; Follow-Up Studies; Humans; Male; Middle Aged; Natriuretic Peptide, Brain; Subarachnoid Hemorrhage; Time Factors; Troponin I; Ventricular Dysfunction, Left

The increase of serum brain natriuretic peptide (sBNP) is well known in patients with severe subarachnoid hemorrhage (SAH). However, the pathophysiology between the clinical severity of SAH and the sBNP secretion is still not clear. The aim of this study is thus to clarify the cardiovascular pathophysiological mechanisms of sBNP secretion in severe SAH patients.. From the database of multicenter prospective study (SAH PiCCO study), sBNP level was compared among initial Hunt and Kosnik (H-K) gradings on the first day. Receiver operating characteristics (ROC) analysis was applied to decide the threshold existing between severe (H-K grade 4-5) and non-severe (H-K grade 2-3) patients. Cardiopulmonary parameters were also measured with thermodilution techniques and compared between low and high sBNP groups.. sBNP level was significantly higher in severe patients than in non-severe patients (566.5 ± 204.2 vs. 155.7 ± 32.8 pg/ml, p = 0.034). Based on ROC analysis, the threshold value that divides severe and non-severe was 78.6 pg/ml (AUC = 0.79). In the higher sBNP group (≥78.6 pg/ml), global end-diastolic volume index (GEDI) and intrathoracic blood volume index (ITVI), which indicate the cardiac preload, were significantly higher than in the low sBNP group. The systemic vascular resistance index (SVRI), the indicator for sympathetic activation and cardiac afterload, was also higher in the high BNP group.. In severe SAH patients, sBNP elevation was significantly associated with the increase of both cardiac preload and afterload. sBNP may be a good severity biomarker in SAH patients, reflecting the systemic impact it makes on cardiovascular preload and afterload.

Topics: Aged; Area Under Curve; Biomarkers; Cardiac Output; Databases, Factual; Female; Humans; Immunoradiometric Assay; Japan; Male; Middle Aged; Natriuretic Peptide, Brain; Predictive Value of Tests; Prognosis; Retrospective Studies; ROC Curve; Severity of Illness Index; Subarachnoid Hemorrhage; Thermodilution; Up-Regulation; Vascular Resistance

To investigate aortic functional alterations in the acute phase of aneurysmal subarachnoid hemorrhage and to evaluate the relationship between potential cardiovascular alterations and delayed cerebral infarctions or poor Glasgow Outcome Scale score at discharge from critical care unit.. Prospective observational study.. Critical Care Departments of two tertiary centers.. Thirty-seven patients with aneurysmal subarachnoid hemorrhage.. Patients were evaluated at two time points: on admission (acute aneurysmal subarachnoid hemorrhage phase) and at least 21 days later (stable aneurysmal subarachnoid hemorrhage state). At baseline, the severity of aneurysmal subarachnoid hemorrhage was assessed clinically (Hunt and Hess scale) and radiologically (brain computed tomography Fisher grading). Aortic elasticity was evaluated by Doppler-derived pulse-wave velocity and left ventricular function by echocardiography. Serum B-type natriuretic peptide and troponin I were also assessed at the same time points.. At the acute phase, 23 patients (62%) were found to present supranormal pulse-wave velocity and 14 patients (38%) presented left ventricular systolic dysfunction; there were significant associations between pulse-wave velocity values and left ventricular ejection fraction (p < .001). Left ventricular ejection fraction and pulse-wave velocity were both associated with Hunt and Hess (p ≤ .004) and Fisher grading (p ≤ .03). Left ventricular ejection fraction and pulse-wave velocity were improved between acute aneurysmal subarachnoid hemorrhage and stable state (p ≤ .005); changes (Δ%) were greater in patients who initially had regional wall motion abnormalities compared to patients who had not (28.7% ± 10.2% vs. 2.4% ± 1.8% [p = .002] and -17.9% ± 3.7% vs. -3.5% ± 4.7% [p = .045], respectively). Pulse-wave velocity/left ventricular ejection fraction ratio was the only independent predictor for delayed cerebral infarctions. Left ventricular ejection fraction, B-type natriuretic peptide, pulse-wave velocity, and pulse-wave velocity/left ventricular ejection fraction showed significant diagnostic performance for predicting delayed cerebral infarctions or poor Glasgow Outcome Scale score (1-3).. Our findings suggest that significant cardiovascular alterations in left ventricular function and in aortic stiffness occur during the early phase of aneurysmal subarachnoid hemorrhage. These phenomena were associated with adverse outcomes in this study and their role in the pathogenesis of delayed neurologic complications warrants further investigation.

Topics: Adult; Aorta; Brain; Echocardiography; Female; Heart; Humans; Male; Middle Aged; Natriuretic Peptide, Brain; Neuroimaging; Prospective Studies; Stroke Volume; Subarachnoid Hemorrhage; Tomography, X-Ray Computed; Troponin I; Ventricular Function, Left

Because of the known correlation between the brain natriuretic peptide (BNP) level and the severity of cardiac failure, cardiac function assessment often involves measuring BNP levels. In addition, BNP is produced in the hypothalamus; high BNP levels are reported in patients with subarachnoid hemorrhage (SAH), although the details of this mechanism remain to be clarified. Furthermore, there are unconfirmed reports of high BNP levels during follow up in cases of post-SAH cerebral vasospasm (CVS). In the present study, we retrospectively investigated the correlation between plasma BNP levels and severity of SAH at onset and the utility of the BNP level as a predictor for CVS. Of 149 SAH cases treated as inpatients at our institution between November 2008 and March 2010, our subjects comprised 28 SAH cases in which the plasma BNP level was measured at the time of hospitalization (≦48 hours after SAH onset). There was no significant correlation between BNP levels and SAH severity at the onset, but BNP levels tended to be high in cases accompanied by intracerebral hematoma, particularly in patients with an anterior communicating aneurysm rupture. This is thought to be the result of direct damage to the hypothalamus. The cases with normal BNP levels at the onset of SAH were apt to have favorable outcomes. The incidence of delayed ischemic neurological deficit (DIND) was investigated in 15 cases in which the BNP level was measured multiple times during follow up. The ratio of BNP at SAH onset compared to at days 3 to 7 of the illness was not significant; however, BNP levels tended to be high in cases with DIND complications. BNP levels may constitute a useful early marker for CVS, despite BNP susceptibility to surgical invasion and perioperative management.

Topics: Adult; Aged; Aged, 80 and over; Biomarkers; Cerebral Hemorrhage; Female; Humans; Intracranial Aneurysm; Male; Middle Aged; Natriuretic Peptide, Brain; Retrospective Studies; Subarachnoid Hemorrhage; Vasospasm, Intracranial

Hyponatremia and hypovolemia occur often after aneurysmal subarachnoid hemorrhage (SAH) and are associated with poor outcome. The authors investigated whether brain natriuretic peptide (BNP) is related to hypovolemia and hyponatremia after SAH and whether it can differentiate between hypovolemic and non-hypovolemic hyponatremia.. In 58 SAH patients, the authors daily measured serum BNP and sodium concentrations, and circulating blood volume by means of pulse dye densitometry, during the initial 10 days. For each patient, mean BNP concentrations were calculated until occurrence of the following events: hyponatremia (Na <130 mmol/l), hypovolemia (blood volume <60 ml/kg), and severe hypovolemia (blood volume <50 ml/kg). The median day of onset of each event was calculated. In patients without an event, the authors calculated and used for comparison the mean BNP concentration until the median day of onset of the particular event. Odds Ratio's (OR) for high versus low mean BNP concentrations (dichotomized on median values per event) were calculated for the occurrence of each event and adjusted for relevant baseline characteristics.. Patients with BNP above median more often had severe hypovolemia (adjusted OR 4.2, 95% confidence interval, CI 1.2-15.0) and showed a trend toward hyponatremia (adjusted OR 3.3, 95% CI 0.7-9.2). In the 12 hyponatremic patients, BNP could not differentiate between hypovolemic and non-hypovolemic hyponatremia.. High BNP concentrations are related to the occurrence of severe hypovolemia and possibly hyponatremia. These data do not support a role for BNP measurements to differentiate between hypovolemic and non-hypovolemic hyponatremia in SAH patients.

Topics: Biomarkers; Blood Volume; Diagnosis, Differential; Female; Humans; Hyponatremia; Hypovolemia; Male; Middle Aged; Natriuretic Peptide, Brain; Severity of Illness Index; Sodium; Subarachnoid Hemorrhage

Elevated levels of B-type natriuretic peptide (BNP) have been associated with cardiac dysfunction and adverse neurological outcomes after subarachnoid hemorrhage (SAH). We sought to determine whether elevated levels of BNP are independently associated with radiographic cerebral infarction after SAH.. Plasma BNP levels were measured after admission, a mean of 5.5 ± 3.0 days after SAH onset. Cerebral infarction was determined by retrospective review of computerized tomography (CT) scans. Cerebral vasospasm was confirmed by the presence of vascular narrowing on cerebral angiogram. The association between BNP and cerebral infarction was quantified using multivariable logistic regression and reverse stepwise elimination of clinical covariates. A stratified analysis was performed to quantify the association between BNP levels and infarction in patients with and without angiographic vasospasm.. BNP levels were measured from 119 subjects. The median BNP level was 105 pg/ml (interquartile range 37-275 pg/ml). In our multivariable model, the top quartile of BNP levels (≥ 276 pg/ml) were associated with an increased odds of cerebral infarction (OR 4.2, P = 0.009). The stratified analysis showed that the association between BNP and infarction was strongest in patients without angiographic vasospasm (OR 7.8, P = 0.006).. Elevated levels of BNP are strongly and independently associated with cerebral infarction, and the association is most pronounced in patients without angiographic vasospasm. These results provide further evidence that other mechanisms can contribute to infarction, and BNP may be a useful biomarker in detecting patients at risk for adverse outcomes without large vessel vasospasm.

Topics: Adult; Aged; Biomarkers; Cerebral Infarction; Cohort Studies; Female; Humans; Male; Middle Aged; Natriuretic Peptide, Brain; Subarachnoid Hemorrhage; Tomography, X-Ray Computed; Vasospasm, Intracranial

Serum B-type natriuretic peptide (BNP) is frequently elevated after subarachnoid hemorrhage (SAH), but whether this high BNP level is related to transient elevation of left ventricular filling pressure (LVFP) is unknown. However, in patients with preexistent cardiac pathologies, it is impossible to differentiate between BNP elevation caused by chronic cardiac abnormalities and BNP related to acute neurocardiac injury.. All adult patients with SAH admitted to our intensive care unit were eligible. Patients were excluded for the following reasons: admission >48 hours after aneurysm rupture, pre-existing hypertension, or cardiac disease. Levels of BNP and cardiac troponin Ic were measured daily for 7 days. Echocardiography was performed by a blinded cardiologist on days 1, 2, and 7. Doppler signals from the mitral inflow, tissue Doppler, and the color M-mode-derived flow propagation velocity (FPV) were obtained to assess echo-estimated LVFP.. During a 3-year period, sixty-six consecutive patients with SAH were admitted. Thirty one patients were studied. The BNP level was >100 ng/L in 25 patients (80%) during the first 3 days, with a peak on day 2 (median, 126 ng/L) followed by a gradual decrease (median variation days 1 to 7, 70%). All patients had an ejection fraction >50%. Early transmitral velocity/tissue Doppler mitral annular early diastolic velocity was low: 5.4 (+/- 1.5) on day 1, 5.8 (+/- 1.2) on day 2, and 5.1 (+/- 0.9) on day 7. Early transmitral velocity/FPV was also low: 1.27 (+/- 0.4), 1.25 (+/- 0.3), and 1.1 (+/- 0.2) on days 1, 2, and 7, respectively. Cardiac troponin Ic levels ranged from 0 to 3.67 microg/L and were correlated with BNP (r = 0.63, P < 0.01).. BNP rises gradually over two days and return to normal within a week after SAH. Its release is associated with myocardial necrosis, but is unrelated to elevated LVFP assessed by echocardiography.

Topics: Acute Disease; Adult; Cardiomyopathies; Echocardiography, Doppler; Female; Hemodynamics; Humans; Male; Natriuretic Peptide, Brain; Necrosis; Prospective Studies; Subarachnoid Hemorrhage; Troponin I; Ventricular Dysfunction, Left

Daily changes in serum concentrations of natriuretic peptides and various cardiopulmonary parameters were measured after the onset of subarachnoid hemorrhage (SAH) to investigate the pathogenesis of the cardiac and pulmonary consequences in 15 patients with acute phase SAH, divided into the control group (n = 5) with consciousness continuously preserved from SAH onset to admission, and the consciousness disturbance group (n = 10). Daily changes in serum A-type and B-type natriuretic peptides (ANP and BNP, respectively) were measured for 10 days, and intrathoracic blood volume index and extravascular lung water index (EVLWI) were measured for 5 days by the single transpulmonary thermodilution method. Natriuretic peptides in the consciousness disturbance group showed significantly higher values during the 10-day period, with ANP 119.2 +/- 12.4 pg/ml (mean +/- standard error of the mean, p = 0.005) on day 2 and BNP 354.1 +/- 80.3 pg/ml (p = 0.009) on day 1. EVLWI showed higher values in the consciousness disturbance group compared to the control group throughout the 5-day period. The increases in natriuretic peptide levels and increase in pulmonary extravascular water content found in SAH patients with consciousness disturbance show that load on the left ventricle or atrium as well as pulmonary capillary pressure are increased immediately after onset, supporting the contention that excessive release of catecholamines occurs at this time.

Topics: Adult; Aged; Aged, 80 and over; Atrial Natriuretic Factor; Blood Volume; Catecholamines; Extravascular Lung Water; Female; Humans; Hyponatremia; Male; Middle Aged; Natriuretic Peptide, Brain; Pulmonary Edema; Sodium; Subarachnoid Hemorrhage; Thermodilution; Unconsciousness

Adrenomedullin (AM), a vasorelaxant peptide, is secreted into the cerebrospinal fluid (CSF) from the choroid plexus and can exert natriuretic effects in the kidney. CSF AM concentration is elevated 7-10 days after the onset of aneurysmal subarachnoid hemorrhage (SAH). The aim of the present study was to determine whether CSF AM concentrations correlate with hyponatremia and delayed ischemic neurological deficits (DIND) after SAH.. CSF and plasma concentrations of AM, brain natriuretic peptide, and atrial natriuretic peptide concentrations were measured in 32 patients with SAH who underwent aneurysmal clipping within 48 h of onset. CSF and blood samples were obtained from these patients during the early period (days 1-3, day 0 being regarded as the day of SAH onset) and the late period (days 8-10).. In all patients, AM concentration during the early and late periods was significantly higher in the CSF than in the plasma (p = 0.0028 and p < 0.0001). In addition, CSF AM concentration was significantly higher during the late period than during the early period (p < 0.0001). Hyponatremia (plasma sodium <135 mmol/l) was present in 11 patients (34.4%) during the late period, and DIND developed in 6 patients (19%) between day 5 and day 13. Logistic regression analysis demonstrated that late-period CSF AM concentration correlated with hyponatremia and DIND (95% CI: 1.003-1.069, p = 0.0074 and 95% CI: 1.003-1.052, p = 0.0108).. The present study demonstrated that CSF AM during the late period following SAH correlates with hyponatremia and DIND.

Topics: Adrenomedullin; Aged; Atrial Natriuretic Factor; Brain Ischemia; Case-Control Studies; Cohort Studies; Female; Humans; Hyponatremia; Intracranial Aneurysm; Male; Middle Aged; Natriuretic Peptide, Brain; Subarachnoid Hemorrhage; Time Factors

To determine whether serum N-terminal pro-B-type natriuretic peptide (N-BNP), a biomarker of myocardial wall stress, is specific to acute heart failure (HF) in patients hospitalized with stroke.. Case-control study.. Tertiary hospital, Neurosciences Critical Care Unit and Stroke Unit.. Consecutive patients with acute ischemic or hemorrhagic stroke who were evaluated for HF.. None.. Cases and controls were classified, respectively, as patients with or without HF, defined according to modified Framingham criteria. Seventy-two patients were evaluated, 39 with ischemic stroke, 22 with aneurysmal subarachnoid hemorrhage (SAH), and 11 with intracerebral hemorrhage (ICH). Thirty-four patients (47%) met criteria for HF, and 47 patients (65%) had systolic or diastolic left ventricular (LV) dysfunction on echocardiogram. Serum N-BNP was measured a median of 48 h following the onset of stroke and was increased (> 900 pg/ml) in 56 patients (78%), with higher levels in non-survivors (11898 +/- 12741 vs 4073 +/-5691; p = 0.001). In a multiple regression model, N-BNP elevation was not independently associated with HF (OR 5.4, 95% CI 0.8-36.0, p = 0.084). At a cut-off of 900 pg/ml, the sensitivity of N-BNP for HF was 94%, specificity 37%, positive predictive value (PPV) 57%, and negative predictive value (NPV) 88%. For systolic or diastolic LV dysfunction, the sensitivity of N-BNP was 89%, specificity 44%, PPV 75%, and NPV 69%.. These results demonstrate that N-BNP elevation is not specific to HF or LV dysfunction in patients with acute ischemic stroke, SAH, and ICH.

Topics: Biomarkers; Case-Control Studies; Cerebral Hemorrhage; Female; Heart Failure; Humans; Male; Middle Aged; Natriuretic Peptide, Brain; Peptide Fragments; Predictive Value of Tests; ROC Curve; Sensitivity and Specificity; Stroke; Subarachnoid Hemorrhage; Ultrasonography; Ventricular Dysfunction, Left

Cerebral salt wasting (CSW) frequently occurs concomitantly with aneurysmal subarachnoid hemorrhage (SAH). CSW induces excessive natriuresis and osmotic diuresis, and reduces total blood volume. As a result, the risk of symptomatic cerebral vasospasm may be elevated. Therefore, it is important to determine the mechanism of CSW. The purpose of this study was to evaluate whether the rat SAH model exhibits CSW and to investigate the relationship between CSW and natriuretic peptides. A SAH model was produced in 24 rats by perforating a cerebral artery with a nylon thread up through the common carotid artery. To evaluate CSW, urine was cumulatively collected from SAH onset to 12 hours and sodium (Na) excretion was analyzed. Body weight and hematocrit were analyzed before and after SAH onset. Concentrations of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) in plasma were also analyzed. Urine volume and total Na excretion of SAH rats were significantly higher than those of sham rats (p<0.05). Body weight of SAH rats significantly decreased and hematocrit significantly increased (p < 0.05). ANP concentration was significantly decreased in SAH rats (p<0.05). However, BNP concentrations did not change. This study demonstrated for the first time that a rat SAH model exhibited CSW. It was suggested that the cause of CSW was neither ANP nor BNP. In addition, this rat SAH model will be useful for study of CSW after SAH.

Topics: Animals; Atrial Natriuretic Factor; Carotid Artery, Common; Cerebral Arteries; Disease Models, Animal; Emaciation; Hematocrit; Male; Natriuretic Peptide, Brain; Rats; Rats, Wistar; Sodium Chloride; Subarachnoid Hemorrhage; Vasospasm, Intracranial; Wasting Syndrome

Topics: Biomarkers; Humans; Natriuretic Peptide, Brain; Prognosis; Subarachnoid Hemorrhage; Ventricular Dysfunction, Left

Serum B-type natriuretic peptide (BNP) is elevated after subarachnoid hemorrhage (SAH), as well as in the setting of congestive heart failure and myocardial infarction. The aim of this study was to prospectively quantify the relationship between BNP levels and cardiac outcomes after SAH.. Plasma was collected for BNP measurements as soon as possible after enrollment; a mean of 5+/-4 days after SAH symptom onset. On days 1, 3, and 6 after enrollment, troponin I (cTi) was measured and 2-dimensional echocardiography was performed. The following cardiac variables were collected and treated dichotomously: left ventricular ejection fraction (LVEF), regional wall motion abnormalities (RWMA), diastolic dysfunction, pulmonary edema, and cTi.. There were 57 subjects. The median BNP level was 141 pg/mL (range, 0.8 to 3330 pg/mL). Higher mean BNP levels were present in those with RWMA (550 versus 261 pg/mL; P=0.012), diastolic dysfunction (360 versus 44; P=0.011), pulmonary edema (719 versus 204; P=0.016), elevated cTi (662 versus 240; P=0.004), and LVEF <50% (644 versus 281; P=0.015).. Early after SAH, elevated BNP levels are associated with myocardial necrosis, pulmonary edema, and both systolic and diastolic dysfunction of the left ventricle. These findings support the hypothesis that the heart releases BNP into the systemic circulation early after SAH.

Topics: Aged; Cohort Studies; Diastole; Echocardiography; Female; Humans; Male; Middle Aged; Natriuretic Peptide, Brain; Prognosis; Prospective Studies; Pulmonary Edema; Subarachnoid Hemorrhage; Systole; Time Factors; Treatment Outcome; Troponin I; Ventricular Dysfunction, Left; Ventricular Function, Left

Serum brain natriuretic peptide (BNP) is elevated after subarachnoid hemorrhage (SAH), causes diuresis and natriuresis (cerebral salt wasting), and may exacerbate delayed ischemic neurological deficits. We examined the temporal relationship between serum BNP elevation, hyponatremia, and the onset of delayed ischemic neurological deficits and determined whether serum BNP levels correlated with the 2-week outcome after SAH.. Serum BNP and sodium were measured prospectively every 12 hours for 14 days in 40 consecutive patients admitted with SAH. All patients remained euvolemic, underwent transcranial Doppler assessment every 48 hours, and underwent angiography at the onset of delayed neurological deficits. New-onset neurological deficits were attributed to vasospasm only in the absence of other causes and when supported by transcranial Doppler or cerebral angiography.. Sixteen patients (40%) experienced symptomatic cerebral vasospasm after SAH. A more than threefold increase in admission serum BNP was associated with the onset of hyponatremia (P < 0.05). Mean BNP levels were similar between vasospasm and nonvasospasm patients fewer than 3 days after SAH (126 +/- 39 pg/ml versus 154 +/- 40 pg/ml; P = 0.61) but were elevated in the vasospasm cohort 4 to 6 days after SAH (285 +/- 67 pg/ml versus 116 +/- 30 pg/ml; P < 0.01), 7 to 9 days after SAH (278 +/- 72 pg/ml versus 166 +/- 45 pg/ml; P < 0.01), and 9 to 12 days after SAH (297 +/- 83 pg/ml versus 106 +/- 30 pg/ml; P < 0.01). BNP level remained independently associated with vasospasm adjusting for Fisher grade and Hunt and Hess grade (odds ratio, 1.28; 95% confidence interval, 1.1-1.6). In patients in whom vasospasm developed, mean serum BNP increased 5.4-fold within 24 hours after vasospasm onset and 11.2-fold the first 3 days after vasospasm onset. Patients with increasing BNP levels from admission demonstrated no change (0 +/- 3) in Glasgow Coma Scale score 2 weeks after SAH versus a 3.0 +/- 2 (P < 0.05) improvement in Glasgow Coma Scale score in patients without increasing serum BNP levels.. Increasing serum BNP levels independently were associated with hyponatremia, significantly increased the first 24 hours after onset of delayed ischemic neurological deficits, and predicted the 2-week Glasgow Coma Scale score.

Topics: Adult; Aged; Brain Ischemia; Female; Glasgow Coma Scale; Humans; Hyponatremia; Male; Middle Aged; Natriuretic Peptide, Brain; Predictive Value of Tests; Subarachnoid Hemorrhage; Time Factors; Treatment Outcome

The present study was designed to assess the relationship between the presence of focal brain aedema and serum concentrations of atrial natriuretic peptide (ANP) or brain natriuretic peptide (BNP) in patients with subarachnoid haemorrhage (SAH). Serum levels of ANP and BNP were measured at six different time periods (Day 1, 2, 3, 4 to 7, 8 to 14, and 15 to 25) in 61 SAH-patients. Focal brain aedema, which was caused by an intracerebral haematoma associated with SAH or surgical complications, was found in eight SAH-patients by means of consecutive CT scans. The mean serum ANP and BNP levels in patients with focal brain aedema were significantly higher than those in patients without focal brain aedema between Days 4 and 14. These findings suggest that focal brain aedema may have some role in the pathogenesis of an excessive secretion of ANP and BNP during the subacute phase of SAH.

Topics: Adult; Aged; Aged, 80 and over; Atrial Natriuretic Factor; Brain Edema; Female; Humans; Male; Middle Aged; Natriuretic Peptide, Brain; Retrospective Studies; Statistics, Nonparametric; Subarachnoid Hemorrhage; Time Factors

We report two cases of neurogenic pulmonary oedema following subarachnoid haemorrhage. A 58-year-old woman became increasingly dyspneic and needed oxygen support during a few days. A 53-year-old woman rapidly developed clinical and laboratory signs of respiratory failure, recovering in 48 hours. In both cases, chest radiography showed bilateral diffuse infiltrates, electrocardiogram revealed ST abnormalities, and cardiac troponin I level was elevated. In both patients, pro brain natriuretic peptide level was increased whereas global cardiac function was normal. The factors initiating its secretion are discussed.

Topics: Biomarkers; Electrocardiography; Female; Heart; Heart Function Tests; Humans; Middle Aged; Natriuresis; Natriuretic Peptide, Brain; Pulmonary Edema; Sodium; Subarachnoid Hemorrhage; Troponin I

The purpose of this study is to investigate the mechanism of increased atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) in patients with subarachnoid hemorrhage due to ruptured aneurysms. ANP and BNP plasma concentrations were measured by immunoradiometoric assay in 53 patients at the day of onset of ruptured aneurysm, the correlation between values of increased ANP or BNP, and sex, age, location of ruptured aneurysm, degree of SAH, and severity of WFNS were statistically studied. The concentration of BNP in ruptured anterior communicating artery aneurysm (A-com) shows a significant elevation compared with other site aneurysms (p = 0.0007). The patients classified as WFNS Grade V, show a significantly higher concentration of BNP, compared with the patients classified as Grade I-IV (p =0.01). It is concluded that the hypersecretion of BNP, but not ANP, is caused by direct mechanical damage at the anterior hypothalamus by ruptured A-com aneurysm and a higher increase of BNP is also observed in cases suffering from severe neurological deficit.

Topics: Adult; Aged; Aged, 80 and over; Aneurysm, Ruptured; Female; Humans; Intracranial Aneurysm; Male; Middle Aged; Natriuretic Peptide, Brain; Neurologic Examination; Radioimmunoassay; Subarachnoid Hemorrhage

Brain natriuretic peptide (BNP) is a potent natriuretic factor responsible for hyponatremia observed in patients with SAH. Through its systemic effects (reduction of blood volume and blood pressure) BNP may augment cerebral blood flow reduction and ischemia secondary to vasospasm. The purpose of the present study was to evaluate the relationship between BNP plasma concentration during the first 12 days following SAH and the development of cerebral vasospasm (CVS). The authors propose a hypothesis for the role played by natriuretic peptides in the pathophysiology of cerebral vasospasm based on the present findings and review the literature.. Thirty eight patients with spontaneous SAH were prospectively included in the present study. BNP plasma concentrations were assessed at four different time periods following SAH (day 1-3, 4-6, 7-9, 10-12). TCD evidence of CVS was found in 26 patients (68.5%), fourteen patients (36.8%) had delayed ischemic neurological deficits (DIND).. Initial BNP plasma concentrations were significantly more elevated in patients who eventually did not develop DIND (95.07+/-107.65 pg/ml vs. 25.81+/-22.57 pg/ml, p=0.0053). However, in patients with DIND, the BNP plasma concentration increased by 3.69 ( p<0.05), 5.89 ( p<0.001) and 4.54 fold ( p<0.001) between days 1-3 to days 4-6, 7-9 and 10-12 respectively (day 1 was regarded as the day of hemorrhage). In patients without CVS or asymptomatic CVS the BNP plasma concentration decreased between days 1-3 to day 10-12. A similar trend in BNP plasma concentration was found in patients with severe SAH (Fisher's score 3-4) as compared with patients with non visible or moderate SAH (BNP concentration ratio day 7-9/1-3: 4.37 vs. 0.75, p=0.015; day 10-12/1-3: 3.37 vs. 0.3, p=0.0144). The trend in BNP plasma concentration between day 1-3 to day 7-9 was found to correlate with CVS severity with an average increase of 2.01, 3.8 and 5.44 fold for mild, moderate and severe VS respectively ( p<0.01, r=0.4174).. These results suggest that BNP secretion in SAH patients is closely related to the bleeding intensity and vasospasm severity as well as to development of DIND with a progressive and marked increase during the clinical course in patients who eventually develop cerebral ischemia. Taken together the local and systemic effects of BNP on CBF suggest that BNP might play a role in the pathophysiology of CVS through its systemic effects on blood pressure and plasma volume BNP leading to an aggravation of brain ischemia secondary to vasospasm.

Topics: Adult; Aged; Brain; Brain Ischemia; Female; Humans; Male; Middle Aged; Natriuretic Peptide, Brain; Regional Blood Flow; Subarachnoid Hemorrhage; Vasospasm, Intracranial

Hyponatremia and hypovolemia following aneurysmal subarachnoid hemorrhage (SAH) might be speculated by exaggerated secretion of natriuretic peptides and resulted ischemic sequela caused by cerebral vasospasm. We measured serum concentration of natriuretic peptides and investigated their influence on post-SAH hyponatremia. Among 49 patients of SAH, their plasma concentration of the natriuretic peptides (atrial natriuretic peptide: ANP and brain natriuretic peptide: BNP) were measured at the day of ictus and 7th day of SAH. The correlation between concentration of natriuretic peptides and location of aneurysm, severity of SAH, incidence of hyponatremia and symptomatic vasospasm were elucidated. The plasma concentration of ANP did not alter on admission and 7th day post SAH, whereas that of BNP increased in the patients with moribund SAH and those with ruptured A-com aneurysm. The initial increase of BNP following SAH could be attributed to direct damage of SAH on the hypothalamus. Hyponatremia and symptomatic vasospasm tended to occur in the patients who had persistent increase of plasma BNP concentration during one week post SAH. Therapeutic intervention to maintain normonatremia by fluid-management decreased occurrence of symptomatic vasospasm, even though patients with increased plasma BNP concentration. It might be concluded that increased secretion of BNP following SAH is caused by direct effect to the hypothalamus and prolonged hyper secretion of BNP resulted hyponatremia, hypovolemia and exaggerated symptomatic vasospasm.

Topics: Aneurysm, Ruptured; Atrial Natriuretic Factor; Female; Humans; Hyponatremia; Intracranial Aneurysm; Male; Middle Aged; Natriuretic Peptide, Brain; Natriuretic Peptides; Subarachnoid Hemorrhage; Vasospasm, Intracranial

Central salt wasting syndrome may be caused by pathological increases in serum natriuretic peptides after subarachnoid hemorrhage (SAH). However, it is unclear as to why the serum concentration of atrial natriuretic peptide (ANP) or brain natriuretic peptide (BNP) increases in the subacute phase of SAH. The present study was designed to assess the correlation between focal brain edema and serum concentration of ANP or BNP in patients with SAH. Focal brain edema was found in 8 SAH-patients and peaked between days 4 and 7 of SAH. The mean serum ANP and BNP levels in patients with focal brain edema were significantly higher than those in patients without focal brain edema between days 4 and 14 of SAH. These results suggest that focal brain edema might correlate with increased levels of ANP and BNP in the subacute phase of SAH.

Topics: Atrial Natriuretic Factor; Brain Edema; Humans; Natriuretic Peptide, Brain; Retrospective Studies; Subarachnoid Hemorrhage; Tomography, X-Ray Computed; Vasopressins

Whereas cardiac hormones increase after subarachnoid haemorrhage (SAH), and may contribute to sodium wastage and hyponatraemia, there is controversy concerning the relative roles of atrial natriuretic peptide (ANP) vs. brain natriuretic peptide (BNP) and the factors initiating their secretion. Noting previous work linking stress hormone responses with cardiac injury after SAH, we have studied responses in stress hormones, markers of cardiac injury and the temporal changes in ANP and BNP and related them to changes in sodium status post ictus and during recovery from acute SAH.. Eighteen patients with verified SAH of variable severity were studied in a single unit for a 14-day period post ictus under controlled conditions of sodium and fluid intake. All received a standardized protocol of daily dexamethasone and nimodipine throughout the study. Severity was graded using criteria of Hess and Hunt at admission. Stress hormones (AVP, catecholamines and admission plasma cortisol), markers of cardiac injury (ECG and daily plasma troponin T) and cardiac hormones (ANP and BNP) were measured daily and related to severity, plasma sodium and renin-aldosterone activity. Hormone levels (ANP, BNP and endothelin) in cerebrospinal fluid (CSF) were also measured in nine patients.. Intense neurohormonal activation (AVP, cortisol and catecholamines) at admission was associated with increased levels of both plasma ANP and BNP whereas levels in CSF were unaffected. In individual patients plasma levels of ANP and BNP were strongly correlated (P < 0.001). Cardiac events (abnormal ECG and/or elevated troponin) occurred in six of seven patients graded severe but neither stress hormones nor cardiac peptides differed significantly in patients with mild (n = 11) vs. severe (n = 7) SAH. During the course of a progressive fall in plasma sodium concentration (P = 0.001), there was a delayed activation of renin-aldosterone which was inversely correlated with declining levels of plasma ANP/BNP (P < 0.002).. Excessive secretion of both ANP and BNP occurs in all patients after acute subarachnoid haemorrhage and is unrelated to severity, stress hormone activation or markers of cardiac injury. Inhibition of renin-aldosterone by cardiac hormones may impair renal sodium conservation and contribute to developing hyponatraemia. In the absence of evidence for activation of natriuretic peptides within the brain, the prompt and consistent increase in both ANP and BNP strongly supports the view that the heart is the source of increased natriuretic peptide secretion after acute subarachnoid haemorrhage.

Topics: Acute Disease; Adult; Aged; Aldosterone; Arginine Vasopressin; Atrial Natriuretic Factor; Creatine; Electrocardiography; Endothelins; Epinephrine; Female; Humans; Hydrocortisone; Male; Middle Aged; Natriuretic Peptide, Brain; Norepinephrine; Sodium; Subarachnoid Hemorrhage; Time Factors; Troponin T

Hyponatremia after subarachnoid hemorrhage has been linked to high plasma concentration of atrial natriuretic peptide and brain natriuretic peptide. Volume expansion therapy to prevent symptomatic vasospasm, such as intensive hypertensive and hypervoremic therapy, may alter systemic concentration of these peptides. We therefore examine brain natriuretic peptide secretion in rats in response to acute volume expansion, infusing to 10 ml of saline over 1 h. In the 10 ml group, brain natriuretic peptide concentrations showed a significant increase from pre-infusion concentrations 1 h after initiation of infusion, but had begun to fall 1 h later. We suspect that high plasma concentration of brain natriuretic peptide after subarachnoid hemorrhage is partly caused by hypervoremic therapy.

Topics: Animals; Blood Volume; Brain; Disease Models, Animal; Hyponatremia; Male; Natriuretic Peptide, Brain; Plasma Substitutes; Rats; Rats, Wistar; Sodium Chloride; Subarachnoid Hemorrhage; Vasospasm, Intracranial; Water-Electrolyte Balance

Topics: Adult; Aged; Female; Humans; Male; Middle Aged; Natriuretic Peptide, Brain; Osmolar Concentration; Subarachnoid Hemorrhage; Ultrasonography, Doppler, Transcranial; Vasospasm, Intracranial

Hyponatremia has been shown in association with cerebral vasospasm (CVS) following aneurysmal subarachnoid hemorrhage (SAH). In the past few years there has been increasing evidence that brain natriuretic peptide (BNP) is responsible for natriuresis after SAH. The purpose of the present study was to investigate the relationship between BNP plasma concentrations and CVS after aneurysmal SAH.. BNP plasma concentrations were assessed at 4 different time periods (1 to 3 days, 4 to 6 days, 7 to 9 days, and 10 to 12 days) in 19 patients with spontaneous SAH. BNP plasma levels were investigated with respect to neurological condition, SAH severity on CT, and flow velocities measured by means of transcranial Doppler.. Thirteen patients had Doppler evidence of CVS; 7 of these had nonsymptomatic CVS. In 6 patients, CVS was severe and symptomatic, with delayed ischemic lesion on CT in 5 of these. CVS was severe and symptomatic in 6 patients, and delayed ischemic lesions were revealed on CT in 5 of these. BNP levels were found to be significantly elevated in SAH patients compared with control subjects (P=0.024). However, in patients without CVS or with nonsymptomatic CVS, BNP concentrations decreased throughout the 4 time periods, whereas a 6-fold increase was observed in patients with severe symptomatic CVS between the first and the third periods (P=0.0096). A similar trend in BNP plasma levels was found in patients with severe SAH compared with those with nonvisible or moderate SAH (P=0.015).. In conclusion, our results show that BNP plasma levels are elevated shortly after SAH, although they increase markedly during the first week in patients with symptomatic CVS. The present findings suggest that secretion of BNP secretion after spontaneous SAH may exacerbate blood flow reduction due to arterial vasospasm.

Topics: Adult; Aged; Female; Humans; Male; Middle Aged; Natriuretic Peptide, Brain; Subarachnoid Hemorrhage; Ultrasonography, Doppler, Transcranial; Vasospasm, Intracranial

Topics: Diagnosis, Differential; Humans; Hyponatremia; Inappropriate ADH Syndrome; Kidney Concentrating Ability; Natriuretic Peptide, Brain; Subarachnoid Hemorrhage

Several authors described elevated natriuretic peptides, atrial natriuretic peptide(ANP) and brain natriuretic peptide (BNP), in patients with subarachnoid hemorrhage(SAH), which were account for inappropriate antidiuretic hormone(SIADH) or cerebral salt wasting syndrome(CSW). Although the secretion of natriuretic peptide depends on the total blood volume, central venous pressure, and cardiac output volume, the volume of fluid intake in patients with SAH had not been taken in consideration in previous report. We here examined the relationship between fluid intake and the natriuretic peptides in two cases without cardiac failure. ANP elevated 2 or 3 days after SAH and remained in normal range for 2 weeks. BNP elevated when the volume of fluid intake was increased, and BNP did not elevate during the periods with lower fluid intake. Several authors proposed the possibility of iatrogenic factor in natriuresis after SAH and these results supported this opinion.

Topics: Adult; Atrial Natriuretic Factor; Female; Fluid Therapy; Humans; Male; Middle Aged; Natriuretic Peptide, Brain; Subarachnoid Hemorrhage

Hyponatremia after subarachnoid hemorrhage (SAH) is commonly associated with diuresis and natriuresis, but the causes are still controversial. We investigated whether brain natriuretic peptide (BNP) was related to such hyponatremia.. Plasma BNP concentrations were measured by immunoradiometric assay in 18 patients at 0 to 2 days (period 1), 7 to 9 days (period 2), and > 14 days (period 3) after SAH. Plasma concentrations of antidiuretic hormone (ADH), atrial natriuretic peptide (ANP), and noradrenaline were also measured during period 2.. The 11 patients with hyponatremia (serum sodium concentration of < 135 mEq/L) had much higher plasma BNP concentrations during each period than did healthy controls (P < 0.05), whereas the 7 patients with normonatremia did not show statistically higher values. In the patients with hyponatremia, the plasma BNP concentration during period 2 was statistically higher than that during periods 1 and 3 (P < 0.05). The plasma noradrenaline concentration during period 2 was higher in patients with hyponatremia than in those with normonatremia (P < 0.05), whereas the plasma concentrations of ADH and ANP during period 2 were not statistically different between the hyponatremic and normonatremic patients.. We conclude that BNP may be related to hyponatremia associated with natriuresis following SAH. The increase of noradrenaline may promote the secretion of BNP.

Topics: Acute Disease; Aged; Female; Humans; Hyponatremia; Male; Middle Aged; Natriuretic Peptide, Brain; Nerve Tissue Proteins; Norepinephrine; Radioimmunoassay; Sodium; Subarachnoid Hemorrhage; Vasopressins

Subarachnoid haemorrhage is commonly associated with natriuresis and hyponatraemia. One possible explanation for these features is a defect in the central regulation of renal sodium reabsorption with increased secretion of a natriuretic factor. We investigated whether excess sodium secretion in patients with subarachnoid haemorrhage is related to increased secretion of natriuretic peptides or to the presence of digoxin-like immunoreactive substances.. We measured the plasma concentrations of digoxin-like immunoreactive substances (by a fluorescence polarisation immunoassay) and natriuretic peptides, aldosterone, renin, and antidiuretic hormone (by radioimmunoassay) in ten patients with aneurysmal subarachnoid haemorrhage, ten patients undergoing elective craniotomy for cerebral tumours, and 40 healthy controls of similar age and sex distribution. Samples were collected before surgery, 1 h, 4 h, and 12 h after surgery, then daily until 7 days postoperatively in the two groups of patients.. All patients with subarachnoid haemorrhage, but none of the tumour patients, showed increased urine output and urinary excretion of sodium (p = 0.018 for comparison of means of curves to 7 days). The patients with subarachnoid haemorrhage had much higher plasma concentrations of brain natriuretic peptide (BNP) than controls, on admission (mean 15.1 [SE 3.8] vs 1.6 [1.0] pmol/L, p < 0.001) and throughout the study period, accompanied by lower than normal aldosterone concentrations and normal plasma concentrations of atrial and C-type natriuretic peptides (ANP, CNP). The patients with tumours had similar plasma concentrations of ANP, BNP, and CNP to the controls. We did not detect digoxin-like immunoreactive substances in either group of patients.. Salt-wasting of central origin may induce hyponatraemia in patients with aneurysmal subarachnoid haemorrhage, possibly as a result of increased secretion of BNP with subsequent suppression of aldosterone synthesis.

Topics: Brain Neoplasms; Cardenolides; Digoxin; Enzyme Inhibitors; Female; Fluorescence Polarization Immunoassay; Humans; Hyponatremia; Intracranial Aneurysm; Male; Middle Aged; Natriuretic Agents; Natriuretic Peptide, Brain; Nerve Tissue Proteins; Saponins; Sodium; Sodium-Potassium-Exchanging ATPase; Subarachnoid Hemorrhage

The natriuretic peptide system consists of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and C-type natriuretic peptide (CNP). The system is implicated in the control of body fluid homeostasis, causes natriuresis and diuresis (ANP and BNP), and regulates vascular tone (CNP). A reciprocal relationship between ANP and endothelin (ET) has been suggested, and earlier studies have documented a possible role of ET in cerebral vasospasm after aneurysmal subarachnoid hemorrhage (SAH). The authors studied plasma ANP, BNP, CNP, and ET for 6 consecutive days in 13 patients with SAH by using radioimmunoassay. The median admission values for ANP were 31.5 pg/ml (range 16.8-323 pg/ml [normal 15 +/- 7 pg/ml]); for BNP, 45.3 pg/ml (range 2.2-80.2 pg/ml [normal 12 +/- 9 pg/ml]); for CNP, 7.7 pg/ml (range < 2-20 pg/ml [normal 5.2 +/- 3 pg/ml]); and for ET, 11 pg/ml (range 6.5-25.1 pg/ml [normal 7.2 +/- 4 pg/ml]). Additional increases (defined as > 100% increase on two consecutive measurements) were noted in ANP (11 patients), BNP (10 patients), and CNP (three patients), and resulted in a negative fluid balance in 10 of the 13 patients. The CNP increased in three of four patients with cerebral vasospasm and in one of nine patients without cerebral vasospasm (Fisher's exact test, p = 0.2). No major fluctuations in plasma ET were noted. In seven patients, the plasma ET level did not increase beyond 10 pg/ml during the days of measurement. In six patients, only an occasional sample showed an increase to a maximum of 25 pg/ml. Changes in BNP, ANP, and CNP were independent of each other. The authors conclude that both plasma ANP and BNP increase after SAH and often result in a negative fluid balance. Plasma ANP and BNP seem differentially regulated in the presence of SAH but not by the level of the plasma ET. The possible role of CNP as a regulatory response to cerebral vasospasm needs further exploration.

Topics: Adult; Aged; Atrial Natriuretic Factor; Endothelium; Female; Humans; Intracranial Aneurysm; Male; Middle Aged; Natriuretic Peptide, Brain; Natriuretic Peptide, C-Type; Nerve Tissue Proteins; Proteins; Radioimmunoassay; Subarachnoid Hemorrhage

Hyponatremia is a common complication after subarachnoid hemorrhage. In this study we investigated the relations among hyponatremia, plasma natriuretic peptides, and antidiuretic hormone concentrations after subarachnoid hemorrhage.. Blood samples for radioimmunoassay measurement of plasma brain natriuretic peptide-like immunoreactivity, atrial natriuretic peptide-like immunoreactivity, and antidiuretic hormone were obtained every 2 to 4 days until day 14 after subarachnoid hemorrhage.. Eleven of 20 patients with verified subarachnoid hemorrhage demonstrated mild hyponatremia (126 mEq/L < serum sodium < 135 mEq/L) during their clinical course. Atrial natriuretic peptide and antidiuretic hormone concentrations were significantly elevated on days 0 to 2 after onset of subarachnoid hemorrhage. Atrial natriuretic peptide concentrations remained high in patients who developed mild hyponatremia on days 6 to 14 after onset of subarachnoid hemorrhage. In contrast, antidiuretic hormone concentrations became significantly lower during the second week in these patients.. Mild hyponatremia after subarachnoid hemorrhage may be attributable not to the syndrome of inappropriate secretion of antidiuretic hormone but to cerebral salt-wasting syndrome. Atrial natriuretic peptide may be a causal natriuretic factor in cerebral salt-wasting syndrome.

Topics: Adult; Aged; Atrial Natriuretic Factor; Body Water; Female; Humans; Male; Middle Aged; Natriuretic Agents; Natriuretic Peptide, Brain; Nerve Tissue Proteins; Osmolar Concentration; Sodium; Subarachnoid Hemorrhage; Vasopressins