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 physician today is presented with a plethora of possibilities in the therapy of each of the aspects of ischemic heart disease (Fig. 15-5). There is the temptation to recommend complex and impossible dietary prescriptions coupled with several pharmaceutical agents for control of anginal pain, hypertension, arrhythmias, hypercholesterolemia, and clinical congestive heart failure. While each of the objectives may be in part valid, the burden on the patient of following such a constraining and difficult life may make it virtually impossible either to enjoy life or to follow the physician's recommendations explicitly. Often a compromise must be reached between theoretically optimal therapy and that which is reasonable and acceptable to the patient. Again, a review of each aspect of the program with the patient may aid in establishing that which is possible rather than that which is ideal.
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PMID:Principles in selection of therapy. 1 Apr 91

The short-acting nitrite sublingual nitroglycerin is the cornerstone of drug treatment of angina pectoris. It is most useful when given two to three minutes before activity that may precipitate an anginal attack. If disabling angina persists despite medical management and there is no contraindication, the beta-adrenergic blocking agent propranolol should be tried before coronary artery surgery is considered. Newer bera-adrenergic blocking agents do not appear to be more effective than propranolol. Digitalis may be beneficial in patients with congestive heart failure or with cardiac arrhythmias responsive to digitalis and in some patients with radiographic evidence of left ventricular enlargement or with nocturnal angina resulting from increased left ventricular end-diastolic volume. If bypass graft surgery is done, medical management must be continued postoperatively.
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PMID:Treatment of angina pectoris. Pharmacologic approaches. 1 May 62

Some of the symptoms and signs of hypothyroidism and hyperthyroidism in elderly patients may be mistakenly attributed to "old age." Weight loss, muscle weakness, tremor, angina, congestive heart failure--all signs of hyperthyroidism--are also concomitants of aging. Fatigue, sluggishness, withdrawal behavior, senile atrophic skin changes--all signs of hypothroidism--are also a part of the normal aging process. Although screening elderly people for thyroid disease is economically unsound, the physician should maintain a high index of suspicion of its presence. Laboratory tests must be interpreted with extra care. Values of 131I uptake, serum T4 and T3, thyroid-stimulating hormone, and thyrotropin-releasing hormone are all helpful in diagnosis. Thyroid disease is easily treated in elderly patients, and results often are dramatic. Propranolol is effective in thyrotoxic patients when symptoms require prompt relief. The definitive treatment, however, is 131I; antithyroid drugs are difficult to manage. Hypothyroidism is easily treated with T4.
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PMID:How thyroid disease presents in the elderly. 2 76

The efficacy and toleration of a new beta1-selective beta-blocker, H 87/07, was compared with placebo in 33 patients with angina pectoris. The efficacy was evaluated using subjective assessments of attack rate and nitroglycerin consumption as well as objective assessments of exercise tolerance on a bicycle ergometer. H 87/07 significantly reduced the attack rate and the nitroglycerin consumption compared with placebo. The mean reduction amounted to 13 and 36% respectively. No significant differences were found between H 87/07 and placebo with regard to exercise tolerance. Due to high intrinsic stimulating activity (I.S.A.) H 87/07 altered the heart rate and blood pressure only slightly at rest but during exercise significant reductions were seen. Except for one patient who had cardiac decompensation on H 87/07 no side-effects of clinical importance were seen. No significant changes were seen with regard to the laboratory tests performed.
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PMID:Effects of a new beta1-selective beta-blocker H 87/07 in angina pectoris. 2 87

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.
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PMID:[Gamma-glutamyl transpeptidase activity in ischemic heart disease]. 2 82

Digitalis and diuretics constitute conventional therapy of congestive heart failure, but systemic vasodilators offer an innovative approach in acute and chronic heart failure of decreasing increased left ventricular systolic wall tension (ventricular afterload) by reducing aortic impedance and/or by reducing cardiac venous return. Thus, vasodilators increase cardiac output (CO) by diminishing peripheral vascular resistance (PVR) and/or decrease increased left ventricular end-diastolic pressure (LVEDP) (ventricular preload) by diminishing venous tone. Concomitantly, there is reduction of myocardial oxygen demand, thereby reliably reducing angina pectoris in coronary disease, and potentially limiting infarct size and ischemia provided systemic arterial pressure remains normal. The vasodilators produce disparate modifications of cardiac function depending upon their differing alterations of preload versus impedance: nitrates principally cause venodilation (decrease LVEDP); nitroprusside, phentolamine and prazosin produce balanced arterial and venous dilation (decrease LVEDP and increase CO) provided left ventricular filling pressure is maintained at the upper limit of normal; whereas hydralazine predominantly effects arteriolar dilation (increases CO). With depressed CO plus highly increased LVEDP and increased PVR, nitrates also induce some increase of CO by reducing PVR. Combined nitroprusside and dopamine synergistically enhance CO and decrease LVEDP. Mechanical counterpulsation aids nitroprusside in acute myocardial infarction. The 30-minute venodilator action of sublingual nitroglycerin is extended for 4 to 6 hours by cutaneous nitroglycerin ointment, by sublingual and oral isosorbide dintrate, and by oral pentaerythritol tetranitrate and sustained-release nitroglycerin capsules. Ambulatory oral vasodilator therapy is provided by long-acting nitrates (relieve pulmonary congestion); hydralazine (improves fatigue); prazosin alone, combined nitrate-hydralazine combined prazosin-hydralazine (improve both dyspnea and fatigue).
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PMID:Afterload reduction and cardiac performance. Physiologic basis of systemic vasodilators as a new approach in treatment of congestive heart failure. 9 30

The expanding applications of nitroglycerin and nitrate esters--in congestive heart failure, in the reduction of infarct size in myocardial infarction and in the long-term prophylaxis of angina--have enhanced the clinical importance of these drugs. This article reviews some of the significant recent investigations of the nitrates and makes specific recommendations regarding clinical use.
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PMID:Nitroglycerin and nitrate esters. 9 32

A multicentre retrospective study of 467 cases of operated aortic valve disease was undertaken to define the indications of coronary arteriography in the pre-operative work-up. Significant coronary artery disease was present in 15% of all cases or, more precisely, in 17% of cases with angina and in 8% when investigation was only routine. Coronary artery disease was more frequent in males, in patients with clinical or electrical evidence of previous myocardial infarction, in patients with ST-T wave changes, and when angina was severe (more than one attack per day). None of these factors was specific. It is therefore difficult to limit coronary arteriography to these patients or there would be a risk of missing significant lesions in a small number of cases. It is important to give the surgeon all the necessary information before aortic valve replacement and so coronary arteriography should be widely practiced in this context. However exceptions may be made for young patients and also those in congestive cardiac failure in whom coronary arteriography represents an unnecessary risk before surgery.
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PMID:[Coronary lesions due to aortic valve disease. I -- Occurrence and clinical prognosis]. 12 Jul 16

The prognosis of 141 patients with obstructive left main coronary artery disease was studied. The patients were followed up for 5 to 10 years from the date of coronary arteriography. The 5 year cardiac mortality rate was 51 percent. During the first 3 years after diagnosis, the mortality rate was especially high, 21.9, 34.7 and 43 percent, respectively. Among patients who died in the 1st year after diagnosis, evidence of left ventricular hypertrophy or conduction delay in the electrocardiogram and multiple vessel involvement indicated poor prognosis. Severe angina pectoris, evidence of congestive heart failure and generalized decrease in left ventricular contractility increased the 5 year mortality rate. More than 97 percent of the total patient population had additional lesions elsewhere in the coronary arteries.
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PMID:Left main coronary arterial obstruction: Long-term follow-up of 141 nonsurgical cases. 12 39

Certain clinical and morphologic observations are described in 27 patients with severe isolated angina pectoris of either the stable (five patients) or the unstable form (22 patients). Twenty-four patients died during or shortly after cardiac operations designed to relieve angina pectoris and three died during cardiac catheterization. During life none had had clinical evidence of acute myocardial infarction or congestive cardiac failure. At necropsy, each had diffuse, extensive coronary atherosclerosis with severe luminal narrowing: the lumens of at least two, an average of three, of the four major epicardial coronary arteries were narrowed greater than 75% in cross-sectional area by old atherosclerotic plaques. Despite the severe coronary narrowing, there was little myocardial damage. Left ventricular scarring (excluding papillary muscle) was observed grossly in only 14 (52%) of the 27 patients and in each it involved only a small portion of myocardial wall. The left ventricular cavity was of normal size in all except two patients. The hearts were of normal weight in 15 (56%) patients, and the average increase above the upper range of normal for the other 12 hearts was 19%. Thus, clinically isolated, severe angina pectoris is associated with severe, diffuse luminal narrowing but relatively little myocardial damage.
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PMID:The coronary arteries and left ventricle in clinically isolated angina pectoris: a necropsy analysis. 13


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