atrial-natriuretic-factor and Angina--Unstable

The natriuretic peptide system (atrial natriuretic peptide, brain natriuretic peptide, BNP, and C natriuretic peptide) is an important marker of cardiac failure. These peptides are synthesized in atrial or ventricular myocytes in response to wall tension. In several studies the correlation between high BNP levels and mortality, in patients with acute coronary syndrome and heart failure, has been demonstrated. On the other hand, plasma levels of BNP could be considered as independent predictors of mortality in patients with heart failure. BNP could be used, for instance, as an early diagnostic marker for the differential diagnosis between cardiogenic and non cardiogenic dyspnea. In the Emergency Department its use will be important in the diagnosis of thoracic pain origin since it may help in the diagnostic and therapeutic course of this patient and to define the modality of hospitalization. Moreover, it can be used as a marker of heart failure severity and as an important negative prognostic factor. Some studies have confirmed that plasma BNP reflects the degree of left ventricular dysfunction and the prognostic significance after acute myocardial infarction and chronic heart failure.

Topics: Angina, Unstable; Atrial Natriuretic Factor; Biomarkers; Diagnosis, Differential; Humans; Myocardial Infarction; Natriuretic Peptide, Brain; Prognosis; Protein Precursors; Syndrome; Ventricular Dysfunction, Left

Topics: Adrenergic beta-Antagonists; Aged; Aged, 80 and over; Angina, Unstable; Angiotensin-Converting Enzyme Inhibitors; Atrial Natriuretic Factor; Diagnosis, Differential; Electrocardiography; Female; Heart Failure; Humans; Male; Myocardial Infarction; Natriuretic Peptide, Brain; Prognosis; Randomized Controlled Trials as Topic; Sensitivity and Specificity; Syndrome; Ventricular Dysfunction, Left

Topics: Angina, Unstable; Angiotensin II; Angiotensin-Converting Enzyme Inhibitors; Atrial Natriuretic Factor; Biomarkers; Cytokines; Humans; Inflammation Mediators; Myocardial Infarction; Natriuretic Peptide, Brain; Ventricular Remodeling

B-type natriuretic peptide (BNP) and the N-terminal fragment of its prohormone (N-proBNP) are released from the heart in response to increased wall stress. Assays for these peptides are now commercially available, and measurement of BNP and N-proBNP is becoming commonplace in patients with suspected heart failure. BNP and N-proBNP facilitate diagnosis and risk stratification in patients with heart failure, and may help guide response to therapy. This review focuses on the emerging role of BNP and N-proBNP measurement in patients with acute coronary syndromes (ACS). Although experimental studies demonstrate rapid BNP release in response to cardiac ischemia, it is unlikely that BNP will be used to diagnose cardiac ischemia, because many other conditions are also associated with modest BNP elevation. In contrast, BNP holds tremendous promise as a prognostic marker in patients with ACS. Studies to date have shown consistently that higher BNP levels are associated with worse clinical outcomes, and that BNP provides unique information to clinical variables, other biomarkers, and left ventricular ejection fraction. Future studies are needed to identify the therapeutic implications of BNP elevation in patients with ACS.

Topics: Acute Disease; Angina, Unstable; Atrial Natriuretic Factor; Cardiotonic Agents; Humans; Myocardial Infarction; Myocardial Ischemia; Natriuretic Peptide, Brain; Protein Precursors; Syndrome

This study was designed to evaluate B-type natriuretic peptide (BNP) for risk assessment and clinical decision making over a range of cut points, alone and with cardiac troponin I (cTnI), in patients with non-ST-elevation acute coronary syndromes (ACS).. B-type natriuretic peptide holds promise for risk stratification. Additional evidence regarding optimal decision limits, use in combination with troponin, and use in targeting therapy is needed before acceptance into clinical use for ACS.. We evaluated BNP at baseline in 1,676 patients with non-ST-elevation ACS randomized to early invasive versus conservative management.. Patients with elevated BNP (>80 pg/ml; n = 320) were at higher risk of death at seven days (2.5% vs. 0.7%, p = 0.006) and six months (8.4% vs. 1.8%, p < 0.0001). The association between BNP and mortality at six months (adjusted odds ratio [OR] 3.3; 95% confidence interval [CI] 1.7 to 6.3) was independent of important clinical predictors, including cTnI and congestive heart failure (CHF). Patients with elevated BNP had a fivefold higher risk of developing new CHF by 30 days (5.9% vs. 1.0%, p < 0.0001). B-type natriuretic peptide added prognostic information to cTnI, discriminating patients at higher mortality risk among those with negative (OR 6.9; 95% CI 1.9 to 25.8) and positive (OR 4.1; 95% CI 1.9 to 9.0) baseline cTnI results. No difference was observed in the effect of invasive versus conservative management when stratified by baseline levels of BNP (p(interaction) > or = 0.6).. Elevated BNP (>80 pg/ml) at presentation identifies patients with non-ST-elevation ACS who are at higher risk of death and CHF and adds incremental information to cTnI. Additional work is needed to identify therapies that may reduce the risk associated with increased BNP.

Topics: Adult; Aged; Angina, Unstable; Atrial Natriuretic Factor; Biomarkers; Cardiotonic Agents; Female; Heart Conduction System; Humans; Male; Middle Aged; Myocardial Infarction; Natriuretic Peptide, Brain; Predictive Value of Tests; Randomized Controlled Trials as Topic; Research Design; Risk Assessment

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

The role of C2238/atrial natriuretic peptide (ANP) minor allele, at the T2238C ANP gene variant, as a predisposing risk factor for acute cardiovascular events, has been previously reported. We aimed at evaluating, by a retrospective approach, the long-term impact of C2238/ANP-minor allele carrier status toward the risk of recurrent acute coronary syndromes (re-ACS) in an Italian cohort of ischemic heart disease patients.. A total of 379 patients (males = 80.5%; mean age = 62.5 ± 9.2 years) presenting with ACS were retrospectively analyzed. Mean follow-up was 5.1 ± 3.5 years (range 1-26 years). Occurrence of new episodes of unstable angina, non-ST-segment elevation myocardial infarction and STE myocardial infarction over the years was recorded and compared between subjects not carrying and carrying C2238/ANP-minor allele.. At univariate analysis, C2238/ANP-minor allele carrier status and treatment with beta-blocker, aspirin and statin were associated with risk of re-ACS. Multivariate analysis confirmed that hypercholesterolemia (P < 0.0001) and C2238/ANP-minor allele carrier status (P < 0.05) were both significantly and independently associated with increased risk of re-ACS. Both treatments with beta-blocker and with statin were significantly associated with reduced risk of re-ACS (P = 0.01 and P < 0.01, respectively). Age above 55 years was associated with recurrence of ACS in C2238/ANP-minor allele carriers (hazard ratio 1.427, 95% confidence interval 1.066-1.911, P = 0.017). Kaplan-Meier curves confirmed highest risk of new events occurrence in C2238/ANP-minor allele carriers (P = 0.035).. The present results demonstrate that C2238/ANP-minor allele carrier status is an independent risk factor for ACS recurrence in an Italian cohort of ischemic heart disease patients over the long term, and they support the role of C2238/ANP-minor allele as a negative prognostic factor in coronary artery disease patients.

Topics: Acute Coronary Syndrome; Aged; Alleles; Angina, Unstable; Aspirin; Atrial Natriuretic Factor; Female; Humans; Italy; Kaplan-Meier Estimate; Male; Middle Aged; Multivariate Analysis; Myocardial Infarction; Proportional Hazards Models; Recurrence; Retrospective Studies; Risk Factors

To compare the accuracy of the N-terminal fragment of its pro-hormone (Nt-proBNP) and N-terminal pro-atrial natriuretic peptide (Nt-proANP) in the prediction of the 2 year mortality and to investigate whether additional measurement of Nt-proANP to troponin I (TnI) could improve risk assessment in the subgroups of patients with unstable coronary artery disease (UCAD) and normal Nt-proBNP.. Plasma levels of the TnI, Nt-proANP, and Nt-proBNP were determined in 120 consecutive patients with UCAD without ST-segment elevations and normal left ventricular function. In multivariable logistic regression analysis, TnI and Nt-proBNP were independent predictors of mortality (P=0.01 and P=0.02, respectively). However, in the group of patients with normal Nt-proBNP levels, only Nt-proANP and TnI were independently associated with mortality (P=0.007 and P=0.03, respectively). Accordingly, patients with elevated Nt-proANP levels in this group of patients had significantly higher mortality rate than patients with normal Nt-proANP levels (P=0.003).. Our results suggest that determination of Nt-proANP might improve risk assessment in patients with UCAD, especially when Nt-proBNP is in the normal range.

Topics: Adult; Aged; Angina, Unstable; Atrial Natriuretic Factor; Female; Humans; Male; Middle Aged; Myocardial Infarction; Natriuretic Peptide, Brain; Nerve Tissue Proteins; Peptide Fragments; Protein Precursors; Regression Analysis; Risk Assessment; Risk Factors; Sensitivity and Specificity; Statistics, Nonparametric; Troponin I

Topics: Adult; Aged; Aged, 80 and over; Angina, Unstable; Atrial Natriuretic Factor; Biomarkers; Female; Humans; Male; Middle Aged; Multicenter Studies as Topic; Myocardial Infarction; Prognosis; Prospective Studies; Protein Precursors; Randomized Controlled Trials as Topic; Survival Analysis; Sweden

Topics: Angina, Unstable; Atrial Natriuretic Factor; Biomarkers; C-Reactive Protein; Confounding Factors, Epidemiologic; Humans; Logistic Models; Multivariate Analysis; Myocardial Infarction; Natriuretic Peptide, Brain; Prognosis

Topics: Aged; Angina, Unstable; Atrial Natriuretic Factor; Case-Control Studies; Female; Humans; Male; Myocardial Infarction; Natriuresis; Natriuretic Peptide, Brain; Peptide Fragments; Prognosis; Protein Precursors; Randomized Controlled Trials as Topic; Syndrome

Topics: Angina, Unstable; Atrial Natriuretic Factor; Coronary Stenosis; Humans; Myocardial Infarction; Natriuretic Peptide, Brain; Prognosis

Brain (B-type) natriuretic peptide is a neurohormone synthesized predominantly in ventricular myocardium. Although the circulating level of this neurohormone has been shown to provide independent prognostic information in patients with transmural myocardial infarction, few data are available for patients with acute coronary syndromes in the absence of ST-segment elevation.. We measured B-type natriuretic peptide in plasma specimens obtained a mean (+/-SD) of 40+/-20 hours after the onset of ischemic symptoms in 2525 patients from the Orbofiban in Patients with Unstable Coronary Syndromes-Thrombolysis in Myocardial Infarction 16 study.. The base-line level of B-type natriuretic peptide was correlated with the risk of death, heart failure, and myocardial infarction at 30 days and 10 months. The unadjusted rate of death increased in a stepwise fashion among patients in increasing quartiles of base-line B-type natriuretic peptide levels (P< 0.001). This association remained significant in subgroups of patients who had myocardial infarction with ST-segment elevation (P=0.02), patients who had myocardial infarction without ST-segment elevation (P<0.001), and patients who had unstable angina (P<0.001). After adjustment for independent predictors of the long-term risk of death, the odds ratios for death at 10 months in the second, third, and fourth quartiles of B-type natriuretic peptide were 3.8 (95 percent confidence interval, 1.1 to 13.3), 4.0 (95 percent confidence interval, 1.2 to 13.7), and 5.8 (95 percent confidence interval, 1.7 to 19.7). The level of B-type natriuretic peptide was also associated with the risk of new or recurrent myocardial infarction (P=0.01) and new or worsening heart failure (P<0.001) at 10 months.. A single measurement of B-type natriuretic peptide, obtained in the first few days after the onset of ischemic symptoms, provides powerful information for use in risk stratification across the spectrum of acute coronary syndromes. This finding suggests that cardiac neurohormonal activation may be a unifying feature among patients at high risk for death after acute coronary syndromes.

Topics: Acute Disease; Aged; Angina, Unstable; Atrial Natriuretic Factor; C-Reactive Protein; Female; Heart Failure; Humans; Male; Middle Aged; Myocardial Infarction; Natriuretic Peptide, Brain; Prognosis; Randomized Controlled Trials as Topic; Regression Analysis; Risk Assessment; Statistics, Nonparametric

Topics: Acute Disease; Angina, Unstable; Atrial Natriuretic Factor; Biomarkers; Coronary Artery Disease; Humans; Myocardial Infarction; Myocardium; Natriuretic Peptide, Brain; Necrosis; Pregnancy-Associated Plasma Protein-A; Prognosis; Risk Assessment

Effects were studied of diltiazem on parameters characterizing cardiohemodynamics, peripheral bloodflow, condition of atrial natriuretic peptide (ANUP), of cyclic nucleotides (cGMP), the renin-angiotensin system in patients with various manifestations of stenocardia. An inhibitory action of diltiazem on ANUP and cGMP secretion in a VEM-test was recordable but changes were not significant at the height of the drug action in rest. Improvement in myocardial contractility after the course treatment with the drug was accompanied by reduction in blood plasma levels of ANUP and cGMP. It is suggested that changes in ANUP concentration might be traced to improvement in the anginal course and to the drug effects such as lowering of myocardial oxygen demand, of pre- and afterload, improvement in the indices for myocardial contractility.

Topics: Adult; Aged; Angina Pectoris; Angina, Unstable; Atrial Natriuretic Factor; Calcium Channel Blockers; Diltiazem; Exercise Tolerance; Female; Hemodynamics; Humans; Male; Middle Aged; Myocardial Ischemia; Neurotransmitter Agents; Renin-Angiotensin System

This study was designed to examine the plasma levels of B-type or brain natriuretic peptide (BNP), as well as A-type or atrial natriuretic peptide (ANP) in patients with unstable angina as compared with those in patients with stable exertional angina and control subjects. We measured the plasma levels of BNP and ANP in 33 patients with unstable angina, 20 patients with stable exertional angina, and 20 control subjects. The plasma levels of BNP were significantly increased in patients with unstable angina compared with those in patients with stable exertional angina and control subjects, respectively (39.5 +/- 29.4 pg/ml vs 15.1 +/- 8.0 pg/ml; p < 0.01 and 39.5 +/- 29.4 pg/ml vs 10.3 +/- 6.4 pg/ml; p < 0.01, respectively). On the other hand, there was no significant difference in the plasma levels of ANP among the three groups. Furthermore, in patients with unstable angina, the plasma levels of BNP decreased significantly after the medical treatment (from 39.5 +/- 29.4 pg/ml to 15.8 +/- 11.0 pg/ ml; p < 0.01), whereas the plasma levels of ANP did not change. We conclude that the plasma levels of BNP are increased in the majority of patients with unstable angina and that the increased levels decrease toward normal after treatment.

Topics: Adult; Aged; Angina Pectoris; Angina, Unstable; Atrial Natriuretic Factor; Cardiovascular Agents; Echocardiography; Electrocardiography; Electrocardiography, Ambulatory; Female; Humans; Male; Middle Aged; Myocardial Ischemia; Natriuretic Peptide, Brain; Nerve Tissue Proteins; Physical Exertion

Endothelin is an extremely potent vasoconstrictor that may have a role in the pathogenesis of acute myocardial ischaemia. Atrial natriuretic factor is an endogenous antagonist of endothelin. To find the pattern and possible importance of circulating endothelin in ischaemic heart disease, concentrations in normal controls and those in patients with stable and unstable angina, acute myocardial infarction, and chronic cardiac failure were compared. The relation between circulating concentrations of endothelin and atrial natriuretic factor in the aftermath of myocardial infarction was also examined.. Eighteen patients with acute myocardial infarction, 10 with unstable angina, 10 with stable angina, 12 with chronic cardiac failure, and 10 normal controls were studied. Endothelin concentration was measured in venous plasma by radioimmunoassay. In patients with acute myocardial infarction simultaneous concentrations of endothelin and atrial natriuretic factor were measured on admission and at one, four, and 24 hours.. Mean concentrations (SEM) of endothelin were 5.72 (0.19) fmol/ml in controls, 6.56 (0.48) fmol/ml in stable angina, 6.41 (0.48) fmol/ml in unstable angina, and 13.83 (0.95) fmol/ml in chronic cardiac failure. In acute myocardial infarction concentrations were 8.81 (0.69) fmol/ml on admission, 11.85 (1.02) fmol/ml at one hour, 11.88 (1.10) fmol/ml at four hours, and 7.30 (0.49) fmol/ml at 24 hours. Concentrations of atrial natriuretic factor at the same times were 68.1 (13.1) pg/ml, 8.4 (1.5) pg/ml, 24.4 (4.1) pg/ml, and 42.0 (6.9) pg/ml.. Plasma endothelin is raised in chronic heart failure and in the aftermath of acute myocardial infarction but not in stable or unstable angina. After myocardial infarction endothelin concentrations are raised whereas concentrations of atrial natriuretic factor are relatively low. The role of endothelin in the pathogenesis of acute myocardial infarction and its interactions with other humoral factors require further investigation.

Topics: Angina Pectoris; Angina, Unstable; Atrial Natriuretic Factor; Chronic Disease; Endothelins; Heart Failure; Humans; Myocardial Infarction; Time Factors

This investigation was designed to determine if acute ischemic cardiac injury causes the release of the 98 amino acid (aa) N-terminus of the 126 aa atrial natriuretic factor prohormone (pro ANF). Seventeen patients with acute myocardial infarction, but without clinical evidence of congestive heart failure, had their circulating concentrations of the whole N-terminus (ie, pro ANF 1-98), the midportion of the N-terminus of the ANF prohormone (consisting of aa 31-67; pro ANF 31-67) and creatine phosphokinase (CPK) monitored daily for 14 days. All seventeen patients had elevated plasma pro ANF 1-98 and pro ANF 31-67 concentrations at the time of presentation. Maximal increase on day three post-infarction correlated with the size of infarction estimated by the maximal CPK (r = 0.675; p less than 0.05) but did not correlate with the amount of left ventricular dysfunction. Another three patients with acute myocardial infarction were treated with tissue plasminogen activator (tPA). The measured pro ANF 1-98 and pro ANF 31-67 levels in these patients were within our normal range and significantly lower (p less than 0.001) than seen in patients with acute myocardial infarction not given thrombolytic therapy. Six patients with unstable angina, likewise, had normal circulating pro ANFs 1-98 and 31-67 concentrations during prolonged episodes of chest pain. These data suggest that myocardial necrosis but not ischemia triggers the release of the entire 126 aa prohormone.

Topics: Adult; Aged; Angina, Unstable; Atrial Natriuretic Factor; Creatine Kinase; Female; Fibrinolytic Agents; Humans; Male; Middle Aged; Myocardial Infarction; Peptide Fragments; Protein Precursors

The present investigation was designed to determine if acute ischemic cardiac injury causes the release of atrial natriuretic factor (ANF). Seventeen patients with acute myocardial infarction but without clinical evidence of congestive heart failure had their circulating concentration of ANF and creatine phosphokinase monitored daily for 14 days. All 17 patients had an elevated plasma ANF concentration at time of presentation. Maximal increase in ANF was on day 2 and 3 post-infarction. This maximal increase correlated with the size of infarction estimated by the maximal creatine phosphokinase concentration (r = 0.475; p less than 0.05), but did not correlate with the amount of left ventricular dysfunction. ANF began to decrease by day 4 post-infarction and was normal at 10 days post-infarction in 14 of the 17 (82%) patients. At 12 days post-infarction, all 17 patients had normal ANF levels. Another three patients with acute myocardial infarction were treated with tissue plasminogen activator (tPA). The measured ANF levels in these patients were within our normal range and were significantly lower (p less than 0.001) than those seen in patients with acute myocardial infarction not given thrombolytic therapy. Six patients with unstable angina likewise had normal circulating ANF concentrations during prolonged episodes of chest pain. These levels were also significantly lower (p less than 0.001) than the 17 patients with acute infarcts not given tPA. The distinct pattern of release of ANF may be useful as an adjunct to serum cardiac enzymes in determining if a myocardial infarction has occurred.

Topics: Adult; Aged; Angina, Unstable; Atrial Natriuretic Factor; Creatine Kinase; Fibrinolytic Agents; Humans; Middle Aged; Myocardial Infarction; Reference Values; Time Factors