Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002962 (angina)
 21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. This study was conducted to assess the role of artrial and brain natriuretic peptides during acute myocardial ischaemia associated with dynamic exercise. 2. Study subjects consisted of 35 angiographically proven patients with angina pectoris and 35 angiographically normal control subjects. All subjects underwent 201Tl dynamic exercise testing. The presence and localization of the exercise-induced acute myocardial perfusion defect were assessed by 201Tl single-photon emission computed tomography. The severity score was calculated using the early image for quantitative assessment of the acute myocardial perfusion defect. 3. Plasma levels of atrial natriuretic peptide increased from 21.3 +/- 3.8 to 72.2 +/- 26.7 pg/ml (P < 0.01) in the angina pectoris group, and increased from 19.4 +/- 2.4 to 36.4 +/- 17.4 pg/ml (P < 0.01) in the control group during dynamic exercise. Plasma levels of brain natriuretic peptide increased from 2.8 +/- 0.8 to 6.9 +/- 2.6 pg/ml (P < 0.01) in the angina pectoris group, but did not change significantly in the control group (from 2.7 +/- 0.7 to 2.9 +/- 1.0 pg/ml) during dynamic exercise. At peak exercise, plasma levels of these natriuretic peptides in the angina pectoris group were significantly higher than those in the control group (P < 0.01). 4. At peak exercise, there were correlations between the plasma level of atrial natriuretic peptide and heart rate in both the angina pectoris and control groups (P < 0.01, r = 0.46; P < 0.01, r = 0.51, respectively), but no significant correlations between the plasma level of brain natriuretic peptide and heart rate in either group. The plasma levels of these peptides at peak exercise correlated well with the severity score in the angina pectoris group (atrial natriuretic peptide, r = 0.71, P < 0.01; brain natriuretic peptide, r = 0.69, P < 0.01).
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PMID:Increased secretion of atrial and brain natriuretic peptides during acute myocardial ischaemia induced by dynamic exercise in patients with angina pectoris. 761 14

B-type (brain) natriuretic peptide (BNP) forms a peptide family with A-type (atrial) natriuretic peptide (ANP), which is involved in the regulation of blood pressure and fluid volume. We have demonstrated that BNP is a novel cardiac hormone secreted predominantly from the ventricle and that plasma levels of BNP markedly increase in proportion to the severity of congestive heart failure. Spasm of a major coronary artery (coronary spasm) is the cause of variant angina and can be induced by hyperventilation. We examined whether BNP infusion suppresses coronary spasm in patients with variant angina. The effect of BNP infusion on anginal attacks induced by hyperventilation was studied in 11 patients with variant angina in whom the attacks were reproducibly induced by hyperventilation. This study was performed in the early morning on 3 consecutive days. Fourteen minutes after infusion of BNP was begun (day 2, 0.05 micrograms/kg/min) or saline (days 1 and 3), hyperventilation was started and continued for 6 minutes. Anginal attacks were induced in all 11 patients by hyperventilation on days 1 and 3, respectively. Anginal attacks were not induced in any patient on day 2 (BNP infusion). Fourteen minutes after BNP infusion was begun, plasma BNP levels increased from 23.7 +/- 6.7 pg/ml to peak levels of 2591 +/- 255 pg/ml (p < 0.01) and plasma ANP levels increased from 28.9 +/- 7.5 pg/ml to peak levels of 69.2 +/- 13.2 pg/ml. Five minutes after BNP infusion was finished, plasma levels of cyclic guanosine monophosphate (cGMP) increased from 20.3 +/- 7.4 pg/ml to peak levels of 63.5 +/- 13.7 pg/ml (p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Suppression of hyperventilation-induced attacks with infusion of B-type (brain) natriuretic peptide in patients with variant angina. 798 89

Interleukin-6 (IL-6), a proinflammatory cytokine, plays a key role in the pathogenesis of coronary artery disease (CAD). We investigated circulating IL-6 and its receptors in patients with CAD. We evaluated 39 Japanese patients with CAD (30 males and 9 females aged 36-79 years), measuring their plasma levels of IL-6 and IL-6 receptors alpha and beta (IL-6R alpha, IL-6R beta). Circulating levels of IL-6, IL-6R alpha and IL-6R beta were measured by an enzyme-linked immunosorbent assay. Blood was sampled immediately after admission and again after 1, 2, 3, 6 and 9 h, then every 12 h for 5 days. Atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) were measured on day 3 after symptom onset. Plasma levels of IL-6 and IL-6Rs were significantly increased in 28 patients with acute myocardial infarction (AMI) compared with 15 normal controls. However, neither IL-6 nor IL-6Rs showed an increase in 6 patients with angina pectoris. We observed two peaks for circulating IL-6 in AMI, the first of which showed a significant correlation with ANP as well as BNP. These results may help to explain why the amount of IL-6 produced is closely related to the severity of myocardial dysfunction in patients with CAD.
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PMID:Circulating interleukin-6 and interleukin-6 receptors in patients with acute and recent myocardial infarction. 1096 91

From the clinical standpoint a cardiomyopathy can be classified as primitive when other causes, i.e. ischemic, infiltrative, systemic diseases, can be ruled out. Initial symptoms usually include a progressive dyspnea and fatigue with tachycardia in a patient previously healthy. Congestive heart failure may be the initial manifestation. Angina is often present, not only because of coronary heart disease. Auscultatory findings usually include a gallop rhythm with a third heart sound, not rarely a four-sound gallop. Blood test to evaluate renal and liver function should be performed. The dosage of troponin I and/or troponin T, plasma renin activity, brain natriuretic peptide or endothelins has recently gained some reputation to indicate prognosis, but there is no reason to believe that these measures are superior to cardiopulmonary stress test.
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PMID:[Dilated cardiomyopathy: role of clinical and laboratory evaluation]. 1202 82

The results of several large therapeutic cardiovascular trials were reported in 2002. The LIFE study concluded that losartan is superior compared to atenolol in terms of prevention of cardiovascular morbidity and mortality, the benefit being for CVA without changing the incidence of myocardial infarction. The OPTIMAAL study stated the disappointing results of post-infarct losartan. The IONA study represents a first demonstration with nicorandil of benefit not only in angina crises but equally on cardiac morbidity and mortality. The HPS study confirms the benefit of a statin in secondary prevention but for the first time, no matter what the initial level of LDL-cholesterol. Finally in the LIPS study, it is reported that statins reduce major cardiovascular events after coronary angioplasty. The year 2002 was marked elsewhere by imagination after the publication of the RAVEL study on coated stents delivering anti-proliferative drugs in order to avoid coronary restenosis. Three drugs were the subject of work confirming their potential significance in cardiovascular pathology: a) ezetimibe, representing a new class of cholesterol lowering drugs with which the association with statins seems especially synergic, b) nesiritide recombinant type B natriuretic peptide, whose significance was confirmed in acute cardiac insufficiency. c) levosimendan (calcium sensitisor) which moreover can be a significant treatment in cardiac decompensation as suggested by the LIDO study with a follow up of 180 days. By contrast, omapatrilate did not confirm its potential superiority over ACE inhibitors in the treatment of cardiac insufficiency. Some encouraging data were reported in 2002 in the field of therapeutic angiogenesis as much at the myocardial level as in lower limb arteritis. Finally, 2002 was marked by the publication of the WHI study which intensified suspicions regarding hormonal substitution treatment, confirming the advantage of not only secondary but perhaps primary cardiovascular prevention.
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PMID:[The best of clinical pharmacology in 2002]. 1261 62

Since B-type natriuretic peptide (BNP) concentration has been shown by recent studies to be elevated in patients presenting acute coronary syndrome (ACS) even in the absence of overt heart failure, other mechanisms for elevating plasma BNP (p-BNP) concentrations may be suggested to exist. We have studied the correlation between p-BNP level and the extent of myocardial ischemia (EMI) in non-ST elevation (NSTE) ACS and evaluated the BNP level as an objective marker of EMI. In 204 patients with NSTE ACS, we estimated the EMI by the echocardiographic wall motion score index (WMSI) and the coronary angiographic Gensini score. As the positive control group, 44 patients with stable angina were enrolled into the study. We compared their initial p-BNP levels with WMSI and the Gensini score. Additionally, peak troponin-T level was compared with p-BNP level in NSTE myocardial infarction (MI) patients. Using the multiple regression analysis, adjustments for age, left ventricle (LV) wall stress, LV mass amount and ejection fraction (EF) were made. Patients with LVEF < 45% or age > 75 years or underlying diseases that could elevate BNP levels were excluded from the study. P-BNP level was increased in NSTE ACS patients compared with stable angina patients (133.9 +/- 87.4 vs. 12.2 +/- 9.2 pg/ml, p < 0.05). P-BNP levels were found to correlate with WMSI and the Gensini score in unstable angina (r=0.519, p < 0.01; r=0.680, p < 0.01) and NSTEMI (r=0.716, p < 0.01; r=0.684, p < 0.01) patients, respectively. Additionally, p-BNP levels correlated with the peak troponin-T level in patients with NSTEMI (r=0.700, p < 0.01). P-BNP level might be a useful marker in the assessment of EMI.
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PMID:Assessment of extent of myocardial ischemia in patients with non-ST elevation acute coronary syndrome using serum B-type natriuretic peptide level. 1511 97

Brain natriuretic peptide (BNP) levels were measured in 100 patients with coronary heart disease (CHD) who underwent myocardial stress thallium-201 single-photon emission computed tomography (30 with stable angina without basal electrocardiographic ischemia and no perfusion defects, 31 with angina with electrocardiographic ischemia and reversible perfusion defects, and 39 with myocardial infarction and irreversible defects) and in 42 controls. BNP levels progressively increased in patients with CHD and were significantly greater in patients with ischemia (p <0.01) and infarction (p <0.001) compared with controls and subjects with angina. BNP concentration was correlated positively (r = 0.923, p <0.001) with perfusion defect extent and inversely (r = -0.690, p <0.001) with the left ventricle ejection fraction (not different in the subjects examined).
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PMID:Usefulness of brain natriuretic peptide levels to discriminate patients with stable angina pectoris without and with electrocardiographic myocardial ischemia and patients with healed myocardial infarction. 1537 88

We evaluated the circulating levels of brain natriuretic peptide (BNP) in stable angina, unstable angina, and myocardial infarction relating hormone levels to extension of coronary disease and number of vessels involved after angiographic examination. We studied 86 patients consecutively undergoing angiographic coronary examination and echocardiographic evaluation for coronary heart disease. These included 15 control subjects (group 0), 21 with stable angina (group I), 26 with unstable angina (group II), and 24 with non-Q myocardial infarction (group III). Patients with heart failure, a history of myocardial infarction, or recent myocardial damage with electrocardiographic S-T elevation were excluded. BNP levels in patients with unstable angina and myocardial infarction were significantly increased with respect to the group with stable angina (P<0.01). There were no differences between the groups with unstable angina and myocardial infarction. Analysis of peptide levels in relation to the number of involved vessels demonstrated a significant increase in patients with three-vessel disease compared with subjects with one or two vessels involved (P<0.03); among subjects with mono-vessel disease, patients with left descendent anterior stenosis had a more-marked BNP elevation than subjects with stenosis in other regions (P<0.01). Hence, BNP levels appear to be elevated in coronary disease, especially in acute coronary syndromes, even in the absence of systolic dysfunction. BNP levels also seem to be related to the severity of coronary atherosclerosis and number of vessels involved. BNP could prove a novel marker for risk stratification, not only in heart failure but also in coronary heart disease.
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PMID:Plasma brain natriuretic peptide levels in coronary heart disease with preserved systolic function. 1559 85

Circulating B-type natriuretic peptide (BNP) is a strong predictor of survival in patients with acute coronary syndromes and in patients with congestive heart failure. Whether circulating BNP levels are predictive of long-term survival in patients with angiographically documented, clinically stable coronary artery disease is unknown. We studied 186 patients with stable angina pectoris and angiographic evidence of significant coronary artery disease. Patients with a recent myocardial infarction, electrocardiographic evidence of ongoing ischemia, anginal pain at rest, or symptomatic congestive heart failure were excluded from the study. During a follow-up of 7.4 years, 23 patients died. By Cox proportional-hazards regression, patient age (p = 0.031), pathologic Q waves on the electrocardiogram (p = 0.037), left ventricular ejection fraction (p = 0.016), and plasma BNP (p = 0.008) were significantly associated with long-term survival. In a stepwise forward multivariate model, BNP (p = 0.005) provided prognostic information above and beyond conventional risk markers. In patients with clinically stable, angiographically documented coronary artery disease, plasma BNP levels are independently related to long-term survival.
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PMID:B-type natriuretic peptide and long-term survival in patients with stable coronary artery disease. 1561 89

Comparative assessment of N-terminal pro-brain natriuretic peptide (NT-pro-BNP) across a wide spectrum of angiographic and clinical coronary artery disease (CAD) in a consecutive series of patients has not been reported. This study examined 879 subjects (684 patients who had angiographically proved CAD and 195 controls who did not have CAD). NT-pro-BNP concentrations were measured before an angiographic procedure that allowed diagnosis of CAD and measurements of left ventricular ejection fraction and end-diastolic blood pressure. Median values (25th and 75th percentiles) of NT-pro-BNP in patients and controls were 474.5 pg/ml (162.3 and 1,542.8) and 117.0 pg/ml (60.1 and 230.6), respectively (p <0.001). In patients who had stable angina, unstable angina, and acute myocardial infarction, NT-pro-BNP concentrations were 327.7 pg/ml (129.2 and 973.2), 660.6 pg/ml (201.2 and 1,563.5), and 1,045.0 pg/ml (323.8 and 2,486.0, p <0.001). NT-pro-BNP concentrations in subgroups with 1-, 2-, and 3-vessel CAD were 385.5 pg/ml (117.2 and 1,266.0), 463.0 pg/ml (135.0 and 1,480.5), and 533.8 pg/ml (221.8 and 1,809.4), respectively (p = 0.005). Multivariable analysis showed that NT-pro-BNP was an independent correlate of the presence of CAD (chi-square 10.8, odds ratio 1.08, 95% confidence interval 1.03 to 1.13 for 100-pg/ml increase in concentration; p <0.001), acute coronary syndromes (chi-square 6.3, odds ratio 1.01, 95% confidence interval 1.00 to 1.02 for 100-pg/ml increase in concentration, p = 0.01) and a strong trend that was independently associated with angiographic severity (chi-square 3.68, p = 0.055). This study shows that NT-pro-BNP concentrations are high across the entire spectrum of CAD and parallel the clinical or angiographic severity of CAD.
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PMID:Plasma levels of N-terminal pro-brain natriuretic peptide in patients with coronary artery disease and relation to clinical presentation, angiographic severity, and left ventricular ejection fraction. 1572 Oct 90


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