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)

The beta-receptor blocker Timolol was investigated for 28 weeks in a double blind trial and then for up to 100 weeks in an open trial in patients with angina pectoris. In both phases of the investigation. Timolol caused a quite marked regression in the frequency of attacks and in the pulse rate at rest. The evaluation of therapeutic success by doctor and patient was positive for Timolol.
MMW Munch Med Wochenschr 1976 Sep 03
PMID:[Longterm therapy of angina pectoris patients with a new beta-receptor blocker (author's transl)]. 0 83

The findings in a patient with an angiographically proven aneurysm of the coronary artery are described. The case is reviewed in the light of 115 similar cases reported in the literature. The patient had had numerous episodes of variant angina, a feature not previously described in coronary arterial aneurysms, which may be related to embolic showers originating from the aneurysm.
Chest 1977 Sep
PMID:Arteriosclerotic aneurysm of the coronary artery. 1 8

The blood plasma gamma-glutamyltranspeptidase (GGTP) activity was studied in 133 patients with macrofocal myocardial infarction, in 40 patients with microfocal myocardial infarction, in 30 patients with angina pectoris, and in 75 patients with cardiosclerosis and congestive cardiac failure. The activity of the enzyme increased in most patients with macrofocal myocardial infarction and in less than half of those with microfocal myocardial infarction beginning with the 3rd or 4th day, reached maximum by the 6th to 8th day of the disease, and then returned to normal levels in various lengths of time. In all patients with angina pectoris and acute left-ventricular failure the activity of the enzyme remained normal. It may be assumed from the results of the study that determination of GGTP activity in dynamics may be mainly employed in the diagnosis of macrofocal myocardial infarction, particularly after the first days of the disease. The enzyme test is hardly suitable for differential diagnosis between microfocal myocardial infarction and angina pectoris.
Kardiologiia 1978 Sep
PMID:[Gamma-glutamyl transpeptidase activity in ischemic heart disease]. 2 82

The aim of this study based on a series of 200 patients, was to define the outcome and the prognostic factors of patients presenting with unstable angina, according to Bertolazi's criteria [3] and at least one stenosis greater than 80% on a proximal segment of a main coronary trunc, and to determine which factors should eventually be taken into consideration in the discussion of surgical indications. 70 out of 200 patients (35%) were turned down for direct revascularisation surgery because of an ejection fraction less than 0,35 and/or a poor arterial run off. Coronary arteriography showed 30% patients with a menacing stenosis (greater than 80%) on all three vessels, 36% on two vessels and 22% on a single vessel. The distribution and the extent of the lesions was about the same as in the operated patients. 20% patients had an ejection fraction less than 0,35, 24% between 0,34 and 0,50, and 56% greater than 0,50. At patient, the follow up period ranges from 22 to 66 months (average 32 months). In this group, the hospital mortality was 2,9%, the secondary cardiac deaths 16% and the global mortality 19% compared to 12,6% for the operated patients in the same period. The incidence of secondary non-fatal infarction was low (9%). 52% of survivors have persistent angina, 39% severe (Class II or III). Two prognostic factors were detected from this study: the type of angina: the intermediary syndrome had a bad prognosis, 38,5% mortality compared to 13% for aggravated chronic angina; and the ventriculography: patients with ejection fractions less than 0,35 had 64% mortality compared to 7,3% for those with ejection fractions greater than 0,40. The number of menacing lesions, the extent of the lesions of the artery involved did not affect the prognosis when severe abnormalities of left ventricular function were absent.
Arch Mal Coeur Vaiss 1979 Sep
PMID:[Unstable angina with threatening coronary lesions turned down for surgery. Outcome and prognostic factors]. 4

Twelve patients aged 33--70 years (mean 49.5) underwent nightly recordings in the ICU and subsequently on the ward following acute myocardial infarction. Sleep patterns were analyzed according to night after infarct and ICU versus ward environment. Significant differences in nocturnal sleep patterns from matched controls initially after infarction included greater wakefulness, low REM sleep per cent, long REM latency, fewer REM periods, more awakenings, more stage shifts and decreased sleep efficiency. The usual circadian variation in HR was absent, and there was an estimated 8--10 h of unrecorded daytime sleep, which together suggested a quite generalized disruption of biological rhythms. With time, there was loss of daytime sleep, lowered nocturnal wakefulness and increased REM sleep. Slow-wave sleep (sometimes with very long duration delta waves) increased above normal over post-infarction nights 3--9, and sleep was otherwise renormalized by post-infarction night 9. No sudden sleep changes occurred with transfer from ICU to ward. The altered sleep patterns appeared mainly attributable to infarction itself. Twelve nocturnal anginal attacks occurred. Ten began in NREM sleep and two in REM periods without particularly intense phasic activity. Post-infarction nocturnal angina therefore appears to differ in pathogenesis from angina outside this period, which usually occurs in REM sleep. ECG changes could occur during sleep before awakening with pain, and overall decrease in ECG amplitude sometimes accompanied angina. Most attacks (10 of 12) occurred on post-infarction nights 4 and 5, indicating that undetermined that undetermined factors produce a secondary period of heightened risk at that time.
Electroencephalogr Clin Neurophysiol 1978 Sep
PMID:Sleep patterns in the intensive care unit and on the ward after acute myocardial infarction. 7 74

Cardiovascular mortality and morbidity were assessed, after a mean follow-up period of 5 years, in an unselected series of 159 adults presenting with the nephrotic syndrome between 1972 and 1975. 60% of the deaths were attributed to terminal renal failure, and the incidence of deaths from ischaemic heart-disease (IHD) was not significantly above normal. The proportion of patients experiencing angina and intermittent claudication and the prevalence of ischaemic electrocardiographic changes did not differ significantly from those of a London control population. At follow-up, hypertension was significantly more common (p less than 0.001) in male nephrotic patients than in controls. Earlier reports of a greatly increased incidence of IHD in unselected patients with the nephrotic syndrome were not confirmed. Routine treatment of hyperlipidaemia in the nephrotic syndrome is not, therefore, recommended.
Lancet 1979 Sep 29
PMID:Does the nephrotic syndrome increase the risk of cardiovascular disease? 9 Jul 59

The patient with unstable angina (angina of recent onset, of changing pattern or occurring at rest) is at high risk of myocardial infarction and sudden death. Patients with simple angina of recent onset can generally be managed out of hospital. Those with progressive angina or angina at rest should be admitted to a coronary care unit, kept at bed-rest, and given propranolol and long-acting nitrates when such therapy is indicated. With these approaches the rate of infarction within 1 to 3 months after the onset of unstable angina is about 12% (as compared with 40% before 1970); the mortality in the same period is less than 2% (as compared with 17% before 1970), though during the first year it is about 17%, much higher than in patients with stable angina and in survivors of acute myocardial infarction.Urgent aortocoronary bypass grafting has proven to be unnecessary and probably undesirable for most patients with unstable angina, and is now generally reserved for patients who continue to have angina in hospital while receiving full medical therapy. The ongoing management of patients whose angina is controlled during the acute phase remains controversial. The main options are to operate on every possible patient, to operate only on those with certain distributions of coronary artery lesions, and to operate only on those who have recurrent symptoms. Further studies are required to delineate the etiology and the Optimal management of unstable angina.
Can Med Assoc J 1978 Sep 09
PMID:Current management of unstable angina. 9 24

Fourteen patients with angina pectoris completed a double blind trial of atenolol 25 mg, 50 mg, and 100 mg twice daily and propranolol 80 mg thrice daily. In comparison with placebo, all active treatments significantly reduced anginal attacks, consumption of glyceryl trinitrate, resting and exercise heart rate, resting and exercise systolic blood pressure, and significantly prolonged exercise time. There was no significant difference between the effects of propranolol and atenolol. Nine patients completed a further trial comparing atenolol given once or twice daily. Both regimens were effective and there was no significant difference between the reductions in anginal attacks, glyceryl trinitrate consumption, systolic blood pressure, or heart rate. Twenty-four-hour ambulatory electrocardiograms showed that atenolol consistently reduced heart rate throughout the 24-hour period whether given once or twice daily. Atenolol is a potent antianginal agent which, in most patients, is likely to be effective once daily.
Br Heart J 1978 Sep
PMID:Comparison of atenolol with propranolol in the treatment of angina pectoris with special reference to once daily administration of atenolol. 10 Dec 23

One hundred and fifty-three men with angina were studied to determine the risk of death over a 5-year period. Multivariate analysis using age, systolic and diastolic pressure, and six electrocardiographic variables (QRS axis, PR interval, the sum of S in V1 and R in V5, T-wave and ST segment anomalies and incomplete left bundle branch block) identified sub-groups having very different prognoses. An analysis using only six variables (omitting diastolic pressure, ST segment anomalies and PR interval) retained a good discriminatory value, and this same discriminant function calculated from half of the sample had good prognostic value in the other half. A prognostic index based on this function (designed to simplify the calculations in clinical use) identified a sub-group (24% of the total group) in which no mortality occurred, while another sub-group (16% of the total group) suffered a mortality of 67%. The logical use of the blood pressure and ECG leads to a more precise prognosis in angina and should help in determining the indications for myocardial revascularisation.
Arch Mal Coeur Vaiss 1978 Sep
PMID:[Prognosis of adult angina pectoris by means of blood pressure and the electrocardiogram]. 10 94

Changes in left ventricular size may be of importance in the development of angina and in its amelioration by glyceryl trinitrate, but left ventricular dimensions have not been measured during exercise in the upright position, the circumstance in which angina most often occurs. To assess changes in left ventricular end-systolic and end-diastolic dimensions, echocardiograms were obtained from 5 normal subjects and 6 patients with angina during rest and exercise upright, both before and after glyceryl trinitrate. The end-systolic dimension was considered an index of regional performance rather than an estimate of overall left ventricular behaviour. During exercise the end-diastolic dimension rose both in the normal subjects and in the patients. The end-systolic dimension fell progressively with exercise in the normal subjects but changed inconsistently in the patients. Glyceryl trinitrate lowered the end-diastolic dimension during exercise below comparable pretreatment values in both groups; the glyceryl trinitrate-induced decrease in end-diastolic dimension in the patients diminished at higher exercise levels. In all normal subjects and in 4 of the 6 patients with normal systolic shortening (= end-diastolic--end-systolic dimension) glyceryl trinitrate caused relatively small changes in the end-systolic dimension and systolic shortening on exercise. In contrast, in the 2 patients with hypokinetic ventricles glyceryl trinitrate conspicuously decreased the end-systolic dimension and increased systolic shortening. Thus, during exercise, in the normal subjects and in the patients with normally functioning left ventricles on echocardiography, glyceryl trinitrate caused a modest fall in the end-diastolic dimension and little change in the end-systolic dimension, but in patients with ventricular hypokinesia it greatly improved regional contractile performance. Alleviation of ischaemic hypokinesia during exercise may be an important part of the benefit of glyceryl trinitrate.
Br Heart J 1979 Sep
PMID:Effect of glyceryl trinitrate on echocardiographic left ventricular dimensions during exercise in the upright position. 11 68


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