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 effects of nitroglycerin ointment (15 mg nitroglycerin) on hemodynamics at rest and during exercise were studied in 12 patients with coronary artery disease and exertional angina (angina group) and in 8 patients with normal coronary arteriograms or with nonsignificant arteriographic abnormalities who did not have exertional chest pain (nonangina group). In both groups at rest nitroglycerin ointment induced within 15 minutes a significant decrease in left ventricular end-diastolic pressure that was sustained for at least 60 minutes; systemic arterial pressure also decreased within 15 minutes and continued to decrease during the 60 minutes of observation. By 30 to 60 minutes there were significant decreases in cardiac index, stroke index, left ventricular stroke work index and tension-time index. During exercise performed 60 minutes after receiving nitroglycerin ointment, 10 of the 12 patients in the angina group had no pain, whereas 2 had delayed and less severe symptoms. Hemodynamic observations during this exercise period revealed significant decreases in left ventricular end-diastolic pressure, systemic pressure and tension-time index from values in the initial exercise period; heart rate remained unchanged. These data document the protective effect of nitroglycerin ointment for a period of at least 60 minutes and also suggest that the beneficial effects are related to a reduction in myocardial oxygen requirements.
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PMID:Effect of nitroglycerin ointment on the clinical and hemodynamic response to exercise. 82 28

140 patients underwent atrial stimulation and a triangular exercise test on the bicycle ergometer; coronary arteriography was carried out on 80 of them. Atrial stimulation is slightly more sensitive (74% compared with 68%) and significantly less specific (57% compared with 74%) than bicycle ergometry. It is valuable to combine the two tests as at least one of them is positive in 84% of subjects with a significant coronary lesion (larger than or equal 70%). "False positive" responses during the stimulation test occur especially where the ECG at rest shows evidence of the non-specific repolarisation disorders of coronary insufficiency; but these "false positives" are accompanied by angina during the test significantly less frequently than the true positives. It may be possible, on the basis of the accounts in the literature and on the present analysis, to establish a methodology for the atrial stimulation test which will increase its sensitivity slightly, but which will also increase, more importantly, its specificity. It may also be possible to reach, by progressive 2-minute steps, a rate which is slightly greater than the maximum rate according to Astrand's law, and to take less account of ST depression as a positive criterioe, and more of the appearance of pain; the fact that this pain is angina could be confirmed by a dual test using placebo and trinitrin.
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PMID:[Diagnostic significance of atrial stimulation in coronary insufficiency. Correlation with the exercise test and/or coronary angiography]. 82 85

The effect of 10 mg of sublingual isosorbide dinitrate were studied using exercise test in 10 patients with stable angina pectoris. First the reproducibility of angina threshold of each patient was controlled. then the effects after 30, 90, 150 minutes of the administration of the drug and a placebo, administered in random sequence, were studied. No significant changes of the parameters examined were observed after the placebo. Significant increase of duration of exercise and total amount of work performed before angina were observed after the drugs. Also, the appearance of electrocardiographic alterations was retarded, and disappearance of pain after exercise interruption was quicker. These changes were maximal in the tests made 30 minutes after administration of the drug, declining therafter; nevertheless, statistically significant differences from placebo were also observed in tests after 90 and 150 minutes.
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PMID:[Long-term effects of sublingual isosorbide dinitrate (author's transl)]. 82 72

We studied the effects of coronary artery spasm on perfusion of the microvasculature in a patient with Prinzmetal's angina. Intracoronary injections of 99mTc and 131I-labelled macroaggregated human serum albumin were performed (1) at rest, (2) during spontaneous angina, (3) after the administration of nitroglycerin and (4) during pacing-induced spasm and the resultant scans compared. The resting scan was normal. Pain and spasm were associated with a perfusion defect that was localized to the anterior and inferior walls of the left ventricle. The localization of the perfusion defect corresponded with angiographically demonstrated spasm involving left anterior descending and distal circumflex coronary arteries. A subsequent myocardial infarction was localized by 43K scanning to the same perfusion area. Metabolic and parasympathetic stimulation studies were performed but were inconclusive. The patient's recurrent pains were ultimately controlled with large oral doses of isosorbide dinitrate.
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PMID:Prinzmetal's angina with coronary artery spasm. Angiographic, pharmacologic, metabolic and radionuclide perfusion studies. 82 56

Six new cases of acute myocardial infarction with normal coronary arteriogram are presented and supplemented by 19 collected cases (group I). These are compared with 16 cases of myocardial infarction caused by occlusive coronary artery disease in a comparable population (group ii). The following significant differences between the two groups are established: patients in group I were younger (27.5 years vs 33.7 years, P less than 0.005); at least one risk factor was present in all patients in group II, but in only 40% of group I (P less than 0.0001). effort angina preceded the attack in ten patients of group II, but in none of group I (P less than 0.0001). The attack was unheralded in 24 of the 25 patients in group I, but was preceded by prodromes in 11 of 16 in group II (P less than 0.0001). Attacks of pain following myocardial infarction occurred in five patients of group 2 and II of group II) (P less than 0.001). Results are discussed in the light of the nature of myocardial infarction in group I. No support is found for the coronary spasm theory. The most likely mechanism for development of myocardial infarction in group I is thought to be a thromboembolic "accident." This accident is not necessarily related to atherosclerotic coronary disease and is presumed to be benign in nature.
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PMID:The nature and clinical features of myocardial infarction with normal coronary arteriogram. 83 99

To evaluate the usefulness of routine coronary arteriography in patients undergoing cardiac catheterization for the evaluation of valvular heart disease, we performed coronary arteriographic studies routinely in a series of 201 patients primarily catheterized for such evaluation. Coronary artery obstructive lesions in excess of 50% of the lumen were present in 45 of the 201 patients. In 18 of the 45 there was no history of chest pain. Three of the 18 had three vessels involved while 2 had two vessels involved. A total of 27 patients (13.4%) had luminal obstruction greater than 70%, and 9 of these had no pain. In 35 of the 201 patients, classic angina pectoris existed in the absence of radiographically significant disease. Severe coronary disease was found to coexist with hemodynamically severe valvular heart disease and was not predictable noninvasively.
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PMID:Coronary atherosclerosis in valvular heart disease. 85 80

In vitro experiments employing the polarographic technique of in-rush currents have demonstrated that adrenalin and noradrenaline in concentrations approaching those found in blood of myocardial infarction patients during the early days of the disease inhibit the tissue respiration of the cardiac muscle by 10--50%. A 10-minute intensive pain stimulation was found to inhibit the aerobic processes in the myocardium by 20--24%. Hypercatecholaminemia observed in the acute period of myocardial infarction is suggested to play an important role in the pathogenesis of cardiac insufficiency during myocardial infarction, since it causes histotoxic hypoxia of the intact portions of the cardiac muscle. The importance of eliminating the pain syndrome in patients with myocardial infarction and angina pectoris is emphasized.
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PMID:[Effect of exogenous catecholamines and pain action on the tissue respiration of the myocardium]. 85 43

To determine the origin of angina pectoris at rest hemodynamic monitoring was performed for 24 to 72 hours in 25 patients with unstable angina who had pacing-induced angina during cardiac catheterization. During the monitoring period, seven patients had spontaneous epidsodes of angina at rest that could be compared with the pain-free periods and periods of pacing-induced angina. At the onset of spontaneous angina, the patients had a significantly lower mean double product (P is less than 0.005) and triple product (P is less than 0.025) than at the onset of pacing-induced angina. The mean double product (heart rate x systolic blood pressure) was 9,411 +/- 2,815 mm Hg/min during pain-free rest, 10,635 +/- 2,587 at the onset of spontaneous angina and 16,623 +/- 3,904 during pacing-induced angina. The mean resting pain-free triple product (heart rate x systolic blood pressure x ejection time) was 3,023 +/- 703 and 3,536 +/- 931 mm Hg/sec per min during, respectively, pain-free rest and spontaneous angina, and 4,350 +/- 938 mm Hg/sec per min during pacing-induced angina. These marked differences in the double and triple products were associated with a mean increase in pulmonary arterial diastolic pressure (from 10.7 mm Hg at rest to 14 mm Hg) at the onset of both spontaneous and pacing-induced angina. Although indirect, these data suggest that transient changes in coronary blood flow, rather than changes in myocardial work, may be primarily responsible for spontaneous angina at rest in certain patients with the syndrome of unstable angina.
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PMID:Hemodynamic changes at the onset of spontaneous versus pacing-induced angina. 86 Jun 91

Forty-six patients admitted with acute coronary insufficiency are reviewed. All were investigated by coronary angiography; 4 had normal coronary arteries and are included in this study; the remainder had a distribution of coronary artery disease similar to other angina patients. The clinical and angiographic findings, management, and subsequent course of the other 42 patients are presented. Fourteen patients (33%) in whom rest pain persisted after 48 hours underwent emergency coronary angiography, with 3 deaths; of the surviving 11 who had acute saphenous vein bypass grafting, 2 died at operation and 3 had perioperative myocardial infarctions. Seventeen patients (41%) who initially improved required surgery within 6 months because of symptoms. Eleven patients (26%) were not operated on. It is concluded that acute coronary insufficiency is best managed initially by intensive medical therapy but a high proportion will require surgery later because of disabling angina. Early investigation and surgery are associated with a high mortality and incidence of myocardial infarction. Survivors of surgery are symptomatically improved and there is a low incidence of late infarction and death.
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PMID:Acute coronary insufficiency. Review of 46 patients. 86 73

The instable angina pectoris belongs to the prodromes of an acute transmural my ocardial infarction, to which we refer every fresh angina pectoris, increase and prolongation of the anginous pain after stress and the appearance of pain in rest. Retrospectively we established the instable angina pectoris in 45% of the cases of a transmural myocardial infarction. Prospectively the syndrome of the instable angina pectoris was followed by a transmural myocardial infarction in 18%. In 14% of the cases with instable angina pectoris without provable transmural myocardial infarction a sudden heart death took place. In the discussion the author deals with questions of the not clarifyed pathogenesis and therapy. The instable angina pectoris is, indeed, an important clinical syndrome, but from the point of view of the short-time prognosis in our opinion it has not the presumed significance for the development of the transmural myocardial infarction and the sudden heart death.
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PMID:[Instable angina pectoris and the pre-infarct condition]. 90 97


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