natriuretic-peptide--brain and Intracranial-Aneurysm

B-type natriuretic peptide (BNP) levels increase with an increase in intracranial pressure. A decrease in BNP levels has been found to be associated with patient positive prognosis. Brain-derived neurotrophic factor (BDNF) levels decrease in patients with acute stroke.. To compare the BNP and BDNF values in serum before and after elective endovascular cerebral aneurysm treatment (ECAT).. A total of 50 patients who underwent elective ECAT were included in the study. Exclusion criteria were determined to be history of heart failure or heart attack (n = 8), renal failure (n = 5), subarachnoid hemorrhage (n = 4), or previous aneurysm clip procedure (n = 3). Intravenous blood samples were obtained from 30 patients who underwent elective ECAT before and after treatment. After centrifugation, the BNP and BDNF values in serum were obtained with the ELISA method and compared.. This study included 19 female and 11 male patients, aged between 24 and 75 years. The average age of the patients was 51.27 ± 13.31 years. The median BDNF values did not change significantly after ECAT (before the endovascular procedure: 3.1 ± 1.3 pg/dl; after the endovascular procedure: 2.8 ± 0.9 pg/dl, p = 0.16). Median BNP levels decreased significantly after ECAT (before the endovascular procedure: 617.50 ± 483.11 pg/ml; after the endovascular procedure: 395.00 ± 352.15 pg/ml, p < 0.001).. After elective endovascular cerebral aneurysm treatment, the BNP values in serum decreased significantly, and the BDNF values in serum did not change significantly.

Topics: Adult; Aged; Biomarkers; Brain-Derived Neurotrophic Factor; Female; Heart Failure; Humans; Intracranial Aneurysm; Male; Middle Aged; Natriuretic Peptide, Brain; Predictive Value of Tests; Young Adult

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

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

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

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

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

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