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)

To investigate the potential anti-ischaemic effects of benazepril (10 mg bid) in comparison to placebo, this new ACE-inhibitor was given to 11 patients with chronic stable angina, reproducible exercise-induced ST-segment depression and angiographically verified coronary artery disease. Blood pressure at rest, plasma renin activity, and plasma concentration of atrial natriuretic peptide were measured after treatment periods of two weeks. Bicycle exercise tests at the same time should evaluate ST-segment depression at comparable maximal workload, work capacity, blood pressure, and heart rate at exercise. In comparison to placebo, benazepril reduced arterial blood pressure significantly from 140 +/- 14/90 +/- 11 mm Hg to 125 +/- 16/84 +/- 10 mm Hg (p less than 0.05) and increased plasma renin activity from 2.19 +/- 3.76 ng/ml/h to 9.62 +/- 8.49 ng/ml/h (p less than 0.005). In contrast, ST-segment depression decreased only slightly and not significantly from 2.09 +/- 1.22 mm to 1.91 +/- 1.00 mm. Benazepril had neither an effect on the frequency of episodes of angina pectoris nor did it reduce the amount of GTN-consumption. Also, work capacity and plasma concentration of atrial natriuretic peptide were not changed in comparison to placebo. Although the significant reduction of blood pressure and the highly significant increase of plasma renin activity demonstrate the specific action of benazepril, a significant anti-ischaemic effect could not be established.
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PMID:[Treatment of chronic stable angina pectoris with angiotensin converting enzyme inhibition--a randomized, placebo-controlled, double-blind cross-over study]. 192 85

Plasma levels of atrial natriuretic peptide (ANP) were determined in 34 male patients undergoing diagnostic right heart catheterization. Patients with effort angina exhibited significant higher ANP levels at rest (259 +/- 42 pg/ml; n = 7) than patients without signs of coronary heart disease (78 +/- 30 pg/ml; n = 8). Patients with effort angina also had higher ANP levels at rest than patients exhibiting impaired cardiac function on exertion without signs of ischemia (105 +/- 15 pg/ml; n = 4), patients with only minimal functional alterations due to infarction residues (95 +/- 27 pg/ml; n = 7), or patients with only borderline changes of ST-segments during exertion (61 +/- 19 pg/ml; n = 8). In contrast, mean pulmonary capillary or right atrial pressures were not significantly different between the various groups of patients. The patients with effort angina also exhibited the highest ANP levels during bicycle exercise (846 +/- 238 pg/ml). There was only a weak to moderate linear correlation between ANP levels and pulmonary or right atrial pressures in the whole group of patients (r = 0.1-0.6). The plasma levels of epinephrine and norepinephrine and of ANP were not significantly correlated, with the exception of norepinephrine levels during exercise (r = 0.54). Our observations suggest that in patients with effort angina there may exist additional stretch-independent factors stimulating the release of ANP, possibly associated with repetitive myocardial ischemia.
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PMID:[Increased plasma level of atrial natriuretic peptide in patients with stress-induced coronary insufficiency: stretch-independent release of atrial natriuretic peptide?]. 214 Dec 8

At rest, during cardiac catheterization, aortic plasma levels of immunoreactive atrial natriuretic peptide did not differ between 10 controls with atypical chest pains and normal coronary arteries and 9 patients with stable angina pectoris and coronary arterial disease (55.2 +/- 19.8 vs. 64.8 +/- 19.8 pg/ml, NS). Nor did atrial natriuretic peptide values differ between the two groups during or after atrial pacing (150 beats/minute), which induced electrocardiographic and metabolic signs of acute myocardial ischaemia in the patients with coronary arterial disease but in none of the controls. Pacing, when carried out for more than 300 seconds, induced an increase of plasma atrial natriuretic peptide that correlated with duration of pacing (r = 0.80, P less than 0.001), and similarly in controls and patients with coronary arterial disease. In a second part of the study, which included 2 controls and 2 patients with coronary arterial disease, post-pacing coronary sinus concentrations of atrial natriuretic peptide were 10-20 times higher than peripheral levels (415- greater than 890 pg/ml). The concentration of atrial natriuretic peptide rose as blood from the caval veins (34 +/- 7 pg/ml) entered the right atrium (56 +/- 24 pg/ml), but thereafter was unchanged in the pulmonary artery (51 +/- 3 pg/ml) and the aorta (46 +/- 9 pg/ml). In conclusion, the results gave no evidence for ischaemic heart disease without congestive cardiac failure to be associated with altered levels of atrial natriuretic peptide. It was confirmed that atrial pacing stimulates the secretion of atrial natriuretic peptide which is produced by the heart and released via the coronary sinus into the circulation.
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PMID:Atrial natriuretic peptide during pacing in controls and patients with coronary arterial disease. 296 Jun 26

The relation of dyspnea of presumed cardiac origin to regional and global left ventricular (LV) function was evaluated among 67-year old men sampled from the general population of Gothenburg, Sweden. From a screened cohort of 644 men, 42 men with cardiac dyspnea and without obstructive pulmonary disease, and 45 controls were sampled. Dyspnea was measured and graded according to the World Health Organization standard. Two-dimensional and M-mode echocardiography, carotid pulse tracing, apexcardiography and phonocardiography were used to evaluate regional wall motion, systolic time intervals, LV ejection indices, wall stress, diastolic time intervals, direct and indirect indices of LV filling properties, and indices of pulmonary hypertension. The plasma concentrations of immunoreactive atrial natriuretic peptide (IrANP) and catecholamines were also assessed. The dyspneic men had more regional wall motion abnormalities than the controls. Systolic, as well as diastolic LV impairment, and increased LV mass were more abundant. Dyspnea grade was significantly related to either of these abnormalities in univariate analyses, and also in multivariate analyses when clinical information, such as chest X-ray, electrocardiogram, and clinical history were taken into account. Multivariate analyses of all the studied indices of cardiac function, together with clinical information, showed dyspnea grade to be significantly and independently related to mitral valve E-point to septal separation (EPSS), presence of akinetic segments, a history of angina pectoris, exercise capacity, and left atrial dimension. Taken together these variables explained 74% of dyspnea grade variance. There was also a relation between dyspnea grade and IrANP, which was independent of clinical findings, but only appeared under conditions of severe dyspnea. It is concluded that the degree of dyspnea is associated with a fairly similar progressive impairment of diastolic, regional and systolic function. In mild heart failure LV hypertrophy and diastolic abnormalities are more prevalent than systolic dysfunction. In severe dyspnea a mixture of regional, systolic, and diastolic abnormalities are present. A decrease of fractional shortening and increased levels of IrANP are late phenomena. EPSS may be a useful indicator of LV dysfunction in population studies.
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PMID:Relation between cardiac dyspnea and left ventricular function. A non-invasive study of 67-year-old men. 296 21

The elevation of cardiac filling pressure induces the release of atrial natriuretic peptide into the circulation. Ischemia during exercise in patients with coronary artery disease may manifest itself with elevation of cardiac filling pressure before the onset of electrocardiographic changes or chest pain. Thus, patients with ischemic heart disease might have an elevated circulating atrial natriuretic peptide after exercise. The present study investigated the effect of exercise on circulating atrial natriuretic peptide in patients with and without ischemic heart diseases. Group 1 was composed of five patients who had ischemic heart disease by clinical history, previous myocardial infarction, angina or angiographically proven coronary artery disease and positive electrocardiogram during exercise. Group 2 was composed of five patients without ischemic heart disease and negative electrocardiogram response. Heart rate, blood pressure, and atrial natriuretic peptide were measured during routine treadmill exercise testing using the Bruce protocol. Our results indicate that the rate of rise of heart rate (12.3 +/- 1.8 vs. 8.5 +/- 0.7 beats/min/min), blood pressure (7.1 +/- 1 vs. 4.2 +/- 0.8 mm Hg/minute), and atrial natriuretic peptide (4.1 +/- 1 vs. 1.4 +/- 0.3 pg/ml/min) was significantly elevated in patients with ischemic heart disease compared to the group 2 patients. These findings suggest that the disproportionate elevation of atrial natriuretic peptide after exercise in ischemia may be caused by elevation of cardiac filling pressure, which may provide a noninvasive method for the diagnosis of ischemic heart disease.
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PMID:The differential response in atrial natriuretic peptide release during exercise in patients with and without ischemic heart disease. 296 77

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

Cardiac amyloidosis is caused by amyloid deposits derived from different human plasma proteins. It can lead to cardiac conduction disturbances, restrictive cardiomyopathy, and low output heart failure. The heart is variably involved during the development of systemic amyloidosis and seems to be more frequently affected in immunoglobulin (primary) than in reactive (secondary) amyloidosis. Amyloid is common in the elderly. Isolated atrial amyloid, for which a major subunit is the atrial natriuretic peptide, seems to be three times more frequent than senile cardiac amyloid, which is derived from normal prealbumin (transthyretin). Like polyneuropathy, cardiac amyloidosis is a prominent clinical feature of hereditary amyloidosis, namely of the autosomal dominant transthyretin (TTR) type. All 28 cases of TTR amyloidoses reported so far were heterozygotes for a single nucleotide change in the gene for TTR that resulted in amino acid substitutions in the mature protein. A new TTR genetic variant is reported in a German family where the index patient presented at the age of 63 with anginal pain and arrhythmia. Electrocardiography was suggestive of a pseudoinfarction pattern, and echocardiography and cardiac catheterisation showed signs of hypertrophic nonobstructive cardiomyopathy with increased ventricular filling pressures and a prominent "a" wave. Amyloid of the TTR type was identified by immunohistochemistry in the endomyocardial biopsy specimen. Hybrid isoelectric focusing established heterozygosity by showing normal TTR protein and an electrically neutral TTR variant differing from all known TTR variants so far. The patient died in an accident before investigations were complete. Electrophoretic analysis of the plasma from his first degree relatives (son, daughter, brother, and mother) identified the asymptomatic 22 year old son as an apparently heterozygous carrier of the mutant TTR protein. Comparative tryptic peptide mapping and sequencing showed that isoleucine at position 68 of the amino acid sequence was replaced by leucine.
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PMID:Cardiac amyloidosis: a review and report of a new transthyretin (prealbumin) variant. 803 17

The effects of epanolol (200 mg once daily) and diltiazem (60 mg three times daily) on the response of atrial natriuretic peptide (ANP) to exercise were investigated in a double-blind placebo-controlled crossover study in 16 patients with angina pectoris. Exercise tolerance as assessed by peak oxygen consumption was similar with all treatments. Peak heart rate (mean and 95% confidence intervals) was lower (P < 0.05) with epanolol (121 (115-130) beats min-1) than with diltiazem (137 (126-148) beats min-1) or placebo (141 (130-152) beats min-1). ANP did not change from resting values with placebo or diltiazem, but rose significantly (P < 0.05) with epanolol from 19.7 (13.0-29.8) pg ml-1 (geometric mean and 95% confidence intervals) during supine rest to 49.6 (33.7-73.0) pg ml-1 at peak exercise. Since ANP release is stimulated by atrial distension, patients with untreated angina may stop exercise before atrial dilatation occurs. With beta-adrenoceptor blockade, a reduction in peak heart rate may necessitate increased chamber volumes to maintain cardiac output, accounting for the rise in ANP.
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PMID:Effect of beta-adrenoceptor blockade on atrial natriuretic peptide levels during exercise in angina pectoris. 809 50

Plasma atrial natriuretic peptide (ANP) and the N-terminal (NT) fragment of the 126-amino acid prohormone of ANP (proANP; NT-proANP) were correlated with clinical findings in 41 patients with acute myocardial infarction and in 19 patients with angina pectoris. On admission to the hospital, the 39 patients with nonfatal infarction who subsequently had overt heart failure (n = 8) had plasma NT-proANP (2374 +/- 1038 pmol/L) and ANP (54 +/- 43 pmol/L) concentrations that were higher (p < 0.01) than those in the patients who remained without or who presented with minor signs of failure. In contrast to the relatively stable NT-proANP levels, ANP decreased markedly during the first 24 hours in the patients who had any signs of failure. Hence the plasma levels of NT-proANP and ANP did not go hand in hand in acute myocardial infarction, and NT-proANP appeared to be a better marker of cardiac dysfunction than ANP.
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PMID:Plasma N-terminal atrial natriuretic peptide in acute myocardial infarction. 819 67

Coronary angioplasty has been the favoured model in studying ischemic preconditioning in humans, but results have remained controversial, possibly due to some artefacts related to coronary balloon angioplasty as an ischemia model. We examined this issue by monitoring the sequential metabolic, functional and neurohumoral changes during repeated vessel occlusion in coronary angioplasty performed in patients with chronic angina pectoris. Two groups of patients undergoing two successive balloon inflations of approximately 2 min duration were studied. These balloon inflations were preceded by a short inflation performed immediately after introduction of the balloon into the stenosis. The aim of this primary inflation was to establish adequate coronary blood flow with the deflated balloon in the stenosis and to guarantee that the subsequent two balloon inflations were truly comparable in time. Group I consisted of 23 patients, in whom the changes in the degree of angina, pulmonary capillary wedge pressure (PCWP), atrial natriuretic peptide (ANP) and circulating catecholamines during the procedure were studied. The sequential changes in myocardial metabolism were monitored in group II of nine patients by determining the lactate extraction ratios and femoroarterial coronary sinus (Fa-CS) differences in pH and pCO2 before and after each balloon inflation. In group I, PCWP and total catecholamines increased similarly during both balloon inflations, but ANP remained unchanged. In group II patients the lactate extraction ratios turned negative, the Fa-CS pH-differences increased and the pCO2-differences decreased during vessel occlusions, the changes being somewhat more prominent during the second balloon inflation. To study adaptation to ischemia, the group I patients were divided into two subgroups with and without signs of ischemic dysfunction during balloon inflations (PCWP increase > 5 mmHg and < 5 mmHg, respectively), and the group II patients were divided into two subgroups with and without metabolic ischemia (lactate-producers and non-producers). The ANP levels were constantly higher in the patients demonstrating ischemic dysfunction during balloon inflations, but catecholamine levels increased only after the second balloon inflation. The anginal pain experienced by the patients and the signs of metabolic ischemia were identical during both balloon inflations. We conclude that acute ischemic preconditioning does not occur in patients with repeated vessel occlusions of approximately 2 min duration. The patients without ischemia during the procedure had more critical stenoses and pre-existing collaterals. However, other protective mechanisms, such as chronic adaptation at the cellular level or recruitment of new collaterals, cannot be excluded.
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PMID:No evidence for ischemic preconditioning during repeated vessel occlusion in coronary angioplasty. 887 22


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