atrial-natriuretic-factor has been researched along with Chest-Pain* in 5 studies
1 trial(s) available for atrial-natriuretic-factor and Chest-Pain
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Albuminuria in ischemic heart disease.
Proteinuria associated with acute heart disease was studied prospectively in 160 patients admitted to the coronary care unit with suspected AMI. Series 1 comprised 150 patients, divided into the following groups: AMI, 27 UAP, 43 AP, 22 NIP and 18 excluded. Albumin and creatinine were measured in the first urine passed after admission (sample 1) and the first morning urine the following 2 days (samples 2 and 3). The ACR was significantly higher in the AMI and UAP groups than in the other patient groups (p < 0.0001). There was no significant difference of ACR between the AMI and UAP in sample 1 (p = 0.31). In the AMI, UAP and AP groups ACR was significantly higher in sample 1 than in samples 2 and 3 (p < 0.005). In the NIP group there were no significant differences between sample 1 versus samples 2 and 3 (p = 0.06). Series 2 comprised 10 patients: 8 AMI, 1 UAP and 1 AMYO. ACR were measured in all specimens voided during the period of observation. ACR can oscillate within hours between normal concentrations and concentrations well into or above the microalbuminuric range. We propose the term episodic albuminuria for this reversible, switch-like change in renal function. The albuminuric episodes lasted 90-600 minutes. Maximum values for ACR were between 133-790 mumol/mol or 78-466 mg/g. In healthy, resting individuals ACR is < 50 mumol/mol (< 30 mg/g). The rapid changes in glomerular permeability may reflect systemic changes in endothelial permeability in the affected individuals. We speculate that atrial natriuretic peptide (ANP) may be a mediator of this type of albuminuria. Topics: Adult; Aged; Albuminuria; Angina, Unstable; Atrial Natriuretic Factor; Biomarkers; Chest Pain; Creatinine; Female; Humans; Kidney Function Tests; Male; Middle Aged; Myocardial Infarction; Myocardial Ischemia; Myocarditis; Prospective Studies | 1999 |
4 other study(ies) available for atrial-natriuretic-factor and Chest-Pain
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MR-proANP and MR-proADM for risk stratification of patients with acute chest pain.
To evaluate mid-regional pro-adrenomedullin (MR-proADM) and mid-regional pro-atrial natriuretic peptide (MR-proANP) as prognostic biomarkers in a representative 'real world' cohort of patients with suspected acute coronary syndrome (ACS).. Prospective observational multicentre cohort study.. Chest pain units of three major hospitals in Germany from 2007 to 2008.. Patients presenting with signs and symptoms suggestive of an ACS.. Primary end point was death or non-fatal myocardial infarction (MI), and secondary end point was death, non-fatal MI, stroke, need for coronary revascularisation, and hospital admission for cardiovascular cause or acute heart failure within 6 months after enrolment.. 1386 patients (male/female = 920/466) were enrolled. Follow-up information was available for 97.8% of patients (median follow-up time 183 days). Forty-three patients reached the primary end point, and 132 the secondary end point. Patients who reached a primary end point had significantly higher MR-proANP (271 vs 101 pmol/l, p < 0.001) and MR-proADM (0.86 vs 0.59 nmol/l, p < 0.001) concentrations than those who did not. Cox regression analysis revealed a 2.55-fold risk of death or non fatal MI (95% CI 1.48 to 2.46, p < 0.001) for an increment of the log-transformed MR-proANP concentration by 1 SD after adjustment for cardiovascular risk factors, and a 1.91-fold risk (95% CI 1.48 to 2.46, p < 0.001) for MR-proADM. Both peptides could result in significant reclassification of patients when added to the Global Registry of Acute Coronary Events risk score, with an overall net reclassification improvement of 41.2% for MR-proADM and 35.7% for MR-proANP.. MR-proADM and MR-proANP are predictors of future cardiovascular events in patients presenting with acute chest pain and might facilitate the choice of treatment in those patients complementary to established risk scores. Topics: Acute Disease; Adrenomedullin; Atrial Natriuretic Factor; Biomarkers; Chest Pain; Follow-Up Studies; Germany; Humans; Incidence; Myocardial Infarction; Peptide Fragments; Prognosis; Prospective Studies; Protein Precursors; Risk Assessment; Survival Rate | 2013 |
Tako-Tsubo cardiomyopathy caused immediately following cesarean section delivery of triplets: a case report.
The name 'tako-tsubo' cardiomyopathy was initially used to describe a unique 'short-neck round-flask'-shaped form of left ventricular apical ballooning, resembling a Japanese tako-tsubo, a jar (tsubo) used for capturing octopus (tako). Tako-tsubo cardiomyopathy exhibits acute onset, transient left ventricular apical wall motion abnormalities with chest symptoms and minimal myocardial enzymatic release, mimicking acute myocardial infarction in patients without angiographic stenosis on coronary angiography. There have been few case reports on tako-tsubo cardiomyopathy, and this disorder is especially rare in pregnant women. A 30-year-old woman who was pregnant with triplets, and had been treated with ritodrine hydrochloride for 12 weeks for threatened premature delivery, underwent cesarean section with spinal anesthesia at 30 weeks' gestation. Three hours later, she complained of acute chest pain, dyspnea and episodes of unconsciousness. She was transferred to the intensive care unit and intubated for ventilatory support. We diagnosed heart failure due to tako-tsubo cardiomyopathy based on heart ultrasonography, blood tests, chest X-ray, electrocardiogram and myocardial scintigraphy. She was extubated from the ventilator after 3 days of catecholamine, furosemide and carperitide administration. She was discharged from the hospital on day 53 without symptoms. Topics: Adult; Atrial Natriuretic Factor; Catecholamines; Cesarean Section; Chest Pain; Female; Furosemide; Heart Failure; Humans; Infant, Newborn; Pregnancy; Premature Birth; Respiration, Artificial; Ritodrine; Sodium Potassium Chloride Symporter Inhibitors; Takotsubo Cardiomyopathy; Tocolytic Agents; Triplets | 2012 |
Multi-marker strategy of natriuretic peptide with either conventional or high-sensitivity troponin-T for acute coronary syndrome diagnosis in emergency department patients with chest pain: from the "Rule Out Myocardial Infarction using Computer Assisted T
Compared to troponin alone, a dual-marker strategy with natriuretic peptides may improve acute coronary syndrome (ACS) diagnosis with a single blood draw and provide physiologic information regarding underlying heart disease. We evaluate the value of adding natriuretic peptides (myocyte stress markers) to troponins (myocardial injury markers) for diagnosing ACS in emergency department patients with chest pain.. In 328 patients (53 ± 12 years, 63% men) with an initially negative conventional troponin and nonischemic electrocardiogram who underwent 64-slice cardiac computed tomography (CT), we measured conventional troponin-T (cTnT), high-sensitivity troponin-T (hsTnT), N-terminal pro-B type natriuretic peptide, and mid-regional pro-atrial natriuretic peptide. ACS was defined as myocardial infarction or unstable angina. CT was evaluated for coronary plaque, stenosis, and regional wall motion abnormality.. Patients with ACS (n = 29, 9%) had higher concentrations of each biomarker compared to those without (all P < .01). Adding natriuretic peptides, especially N-terminal pro-B type natriuretic peptide, to both cTnT or hsTnT improved the C-statistics and net reclassification index for ACS, largely driven by correctly reclassifying events. Dual-negative marker results improved sensitivity (cTnT 38% to 83%-86%, hsTnT 59% to 86%-90%; all P < .01) and negative predictive value (cTnT 94% to 97%-98%, hsTnT 96% to 97%-98%) for ACS. Patients with dual-negative markers had the lowest percentage of CT coronary plaque, stenosis, and regional wall motion abnormality (all P-trend <.001).. Among emergency department patients with low-intermediate likelihood of ACS, combining natriuretic peptides with either conventional or highly-sensitive troponin improved discriminatory capacity and allowed for better reclassification of ACS, findings supported by structural and functional CT results. Topics: Acute Coronary Syndrome; Adult; Atrial Natriuretic Factor; Biomarkers; Chest Pain; Emergency Service, Hospital; Female; Humans; Male; Middle Aged; Myocardial Infarction; Natriuretic Peptide, Brain; Natriuretic Peptides; Peptide Fragments; Sensitivity and Specificity; Tomography, X-Ray Computed; Troponin T | 2012 |
Plasma atrial natriuretic peptide in patients with acute myocardial infarction: effects of streptokinase.
Plasma concentrations of immunoreactive atrial natriuretic peptide (mean (SEM] were measured in 135 patients admitted to two coronary care units with myocardial infarction, ischaemic chest pain, or non-ischaemic chest pain. Concentrations were significantly higher in patients with acute myocardial infarction not treated with systemic thrombolysis (60.4 (14.3) pg/ml) than in patients with non-ischaemic chest pain (21.1 (4.3) pg/ml). Patients with ischaemic chest pain had intermediate values (39.3 (7.1) pg/ml). Patients with acute myocardial infarction treated with intravenous streptokinase had normal concentrations of plasma atrial natriuretic peptide (20.2 (3.6) pg/mg), which were significantly lower than those in patients with myocardial infarction not given streptokinase. These changes could not be explained by factors such as age, pre-existing hypertension, renal dysfunction, or cardiac failure, nor treatment other than streptokinase. Raised plasma concentrations of atrial natriuretic peptide in acute myocardial infarction may be a homoeostatic response acting to reduce atrial pressures by natriuresis, diuresis, and venodilatation. The lower concentrations of atrial natriuretic peptide in patients with acute myocardial infarction treated with streptokinase may reflect a short term beneficial haemodynamic effect of streptokinase. Topics: Angina Pectoris; Atrial Natriuretic Factor; Chest Pain; Female; Humans; Male; Middle Aged; Myocardial Infarction; Streptokinase | 1989 |