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

Elevated levels of lipoprotein(a) [Lp(a)] have been associated with an increased risk of ischemic heart disease (IHD), and higher levels of Lp(a) are associated with lesions of significantly greater severity. We have examined Lp(a), total cholesterol (TC) and high density lipoprotein-cholesterol (HDL-C) levels in patients with IHD including those with normal coronary arteries with vasospastic angina. The study population consisted of 206 patients (166 males and 40 females) who underwent diagnostic coronary angiography for known IHD. Twenty-eight patients had effort angina, 36 rest angina, 8 unstable angina and 134 old myocardial infarction. IHD patients were categorized as zero vessel disease (0VD), single vessel disease (SVD) and multi-vessel disease (MVD). To investigate the relationship between atherosclerosis and IHD, these patients were further divided into 3 groups based on angiographic findings. Eighteen patients had entirely normal coronary arteries (normal group), 24 discretely diseased coronary arteries (discrete group) and 80 diffusely diseased coronaries (diffuse group). The results were compared with those obtained from 50 healthy individuals. Lp(a) levels for IHD patients (12.4 mg/dl) were significantly higher than those of controls (7.1 mg/dl, p < 0.05). However, there were no statistical differences between 0VD (13.1 mg/dl) and MVD (12.8 mg/dl). Similarly, no statistical differences of Lp(a) values were found among the normal group (13.3 mg/dl), discrete group (12.0 mg/dl) and diffuse group (12.9 mg/dl). Mean levels of HDL-C in 0VD (51.3 +/- 13.5 mg/dl) were significantly higher than those of SVD (42.9 +/- 11.5 mg/dl, p < 0.05). However, no significant differences were observed between controls (59.5 +/- 15.3 mg/dl) and 0VD (51.3 +/- 13.5 mg/dl).(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Importance of lipoprotein(a) in patients with ischemic heart disease]. 133 90

Traditionally, myocardial ischemia has been viewed as an imbalance in the supply and demand of myocardial oxygen. Stable angina is usually considered to involve a fixed lesion, whereas unstable angina involves a fixed lesion as well as such components as platelet aggregation, thrombotic processes, and vasospasm. Variant angina involves primarily vasospasm. A newer concept holds that most angina results from mixed mechanisms in which both fixed lesions and vasomotor alterations play a role. These mechanisms are responsible for mixed ischemic events, characterized by episodes at varying levels of exertion, with or without anginal pain. This concept would seem to be supported by the occurrence of silent ischemia in the setting of stable, unstable, or variant angina, despite differing pathophysiologic conditions. Ischemic events have important prognostic significance; unfortunately, many are unrecognized by patients. The question whether the treatment of ischemic events will improve prognosis remains a matter of debate.
 ...
PMID:Mechanisms of myocardial ischemia. 144 93

Two cases of angina pectoris, induced by methylergometrine (Methergin) and by an association of ergotamine tartrate (Gynergene) and methysergide (Desernil) respectively, are reported. In both patients, angiography revealed spontaneous spasm in a coronary system free from any significant atheromatous stenosis. In the second case, a test administration of i.v. Methergin, administered during calcium-channel antagonist treatment a few days after the "guilty" drugs had been stopped was found to be negative. The outcome was favorable in both cases: the angina disappeared and the base-line and exercise ECG returned to normal. The hypothesis of coronary spasm induced by the treatment was adopted in both cases. In this context, the major iatrogenic etiologies of vasospastic angina are recalled, together with the prophylactic and therapeutic measures they call for.
 ...
PMID:[Vasospastic angina with angiographically normal coronary vessels of iatrogenic origin. Apropos of 2 cases]. 155 64

To investigate the mechanism of coronary spasm, we compared the action of acetylcholine with that of ergonovine in 11 patients with vasospastic angina (group 1) and in 15 patients with chest pain (group 2). Coronary arteriography was performed immediately after the patients received intracoronary injections of titrated increments of each agent. In the patients in group 1 occlusive or near-occlusive (99% luminal narrowing) coronary spasm associated with angina and ischemic electrocardiographic ST changes was noted in nine of 11 patients receiving acetylcholine and in all 11 patients receiving ergonovine. The region and the degree of the most severe coronary spasm on coronary arteriograms evoked by the two agents were the same in nine of the 11 patients in group 1. In the other two patients in group 1, spontaneous focal coronary spastic stenosis in the baseline coronary arteriogram was relieved by the intracoronary injection of acetylcholine, and a focal coronary occlusive spasm in the same region was induced repeatedly by the subsequent intracoronary injection of ergonovine (paradoxic phenomenon). In contrast, occlusive or near-occlusive coronary spasm was not induced by either agent in any patient in group 2. These results suggest that the two provocative tests for coronary spasm that involve acetylcholine and ergonovine are clinically useful in the diagnosis of vasospastic angina, but testing with intracoronary ergonovine is needed when a spontaneous focal coronary spasm is relieved by the intracoronary injection of acetylcholine. The results also indicate that in many patients with vasospastic angina, nonspecific hypersensitivity to acetylcholine or ergonovine in a definite region of the coronary arteries generally plays an important role in the induction of coronary spasm.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Induction of coronary artery spasm by intracoronary acetylcholine: comparison with intracoronary ergonovine. 161 26

We report a patient with Prinzmetal's angina with nearly normal coronary angiogram who not only developed severe myocardial ischemia during exercise, documented both electrocardiographically (ST elevation) and scintigraphically (with thallium-201), but also did so intermittently as the graded exercise progressed. Diagnostic coronary angiography showed spontaneous focal spasm of the proximal left anterior descending coronary artery. This unique response to exercise in a patient with variant angina suggests that factors other than catecholamine stimulation alone are active and rapidly attenuated in some patients. This phenomenon could be overlooked without appropriate electrocardiographic monitoring.
 ...
PMID:Intermittent coronary spasm during graded exercise. 162 62

A 60-year-old man with atypical chest pain not submitted to adequate diagnostic procedures was treated on an empirical basis with nifedipine 20 mg b.i.d. The patient was referred to our institution where a first symptom-limited exercise stress-test during treatment was performed; neither S-T alterations nor clinical symptoms were induced at the maximal tolerated work load. Therefore we suggested a short period of hospital stay to repeat the stress-test after a progressive tapering off of the drug with the aim of obtaining a more definite diagnosis. However the patient refused and an at-home nifedipine withdrawal was planned. Some days later a second test showed marked S-T segment elevation in leads V4 to V6; concomitant high-grade ventricular arrhythmias and anginal pain occurred. Both the ECG alterations and the clinical symptom promptly regressed interrupting the test and administering sublingual isosorbide dinitrate. A coronary angiography performed few days later showed only a single and no significant stenosis of the left anterior descending artery (60%). The clinical and electrocardiographic pictures were therefore attributed to stress-induced vasospastic ischemia. A week later a third maximal stress-test during further treatment with nifedipine was totally negative. The pathophysiological mechanisms of rest and stress-induced vasospastic angina and the usefulness of Ca-blocking agents are discussed.
 ...
PMID:[A clinical case: coronary vasospasm induced by exercise after stopping nifedipine therapy]. 163 Jun 75

Nitrates, molsidomin, betablockers, calcium antagonists, inhibitors of platelet aggregation and anticoagulants are the most important drugs for the management of the different forms of angina pectoris. Their use in chronic stable, unstable and vasospastic angina pectoris and for secondary prophylaxis are discussed.
 ...
PMID:[Anti-ischemia drug therapy]. 168 96

Nifedipine antagonises influx of calcium through cell membrane slow channels, and sustained release formulations of the calcium channel blocker have been shown to be effective in the treatment of mild to moderate hypertension and both stable and variant angina pectoris. Preliminary findings also indicate that these formulations are effective in the treatment of Raynaud's phenomenon and hypertension in pregnancy, and that they reduce the frequency of ischaemic episodes in some patients with silent myocardial ischaemia. The exact mechanism of action of nifedipine in all of these disorders has not been defined. However, its potent peripheral and coronary arterial dilator properties, together with improvements in oxygen supply/demand, are of particular importance. A major goal of sustained release therapy is to permit reductions in the frequency of nifedipine administration, preferably to once daily, and thus improve patient compliance. Two new once-daily formulations--the nifedipine gastrointestinal therapeutic system (GITS) and a fixed combination capsule comprising sustained release nifedipine 20 mg and atenolol 50 mg--have exhibited marked antihypertensive efficacy. The GITS preparation has also been used effectively in the treatment of stable angina pectoris, and both formulations appear to be well tolerated. Sustained release nifedipine formulations are generally better tolerated than their conventionally formulated counterparts, particularly with regard to reflex tachycardia. Adverse effects seem to be dose related, are mainly associated with the drug's potent vasodilatory action, and include headache, flushing and dizziness. Generally, these effects are mild to moderate in severity and transient, usually diminishing with continued treatment. Thus, sustained release nifedipine formulations are useful and established cardiovascular therapeutic agents which have demonstrable efficacy in various forms of angina, mild to moderate hypertension and Raynaud's phenomenon. Further, promising results shown by the nifedipine GITS formulation, with its advantage of once daily administration suggest that it is likely to become one of the preferred nifedipine formulations for the treatment of hypertension and the various forms of angina.
 ...
PMID:Sustained release nifedipine formulations. An appraisal of their current uses and prospective roles in the treatment of hypertension, ischaemic heart disease and peripheral vascular disorders. 171 8

We examined whether recurrent transient ischemia may effect left ventricular systolic and diastolic function or not. Left ventricular systolic and diastolic function during the asymptomatic period was studied by gated radionuclide ventriculography (RNV) in 25 patients with vasospastic angina (VA) who had no significant coronary stenosis, in 25 patients with effort angina (EA), and in 20 controls (C). There was no significant difference among patients in all three groups in regards to systolic indices (Ejection Fraction, Peak Ejection Rate). But diastolic indices (Peak Filling Rate, Time to Peak Filling Rate, 1/3 Mean Filling Rate, 1/3 Filling Fraction) were impaired not only in patients with EA but also in patients with VA. The treatment with nitrates and/or Ca antagonist for 6-24 months did not bring about any changes in these data concerning systolic and diastolic function in patients with VA. Thus, it is suggested that the diastolic function is impaired in patients with VA even during the asymptomatic period, though systolic function remains normal. Recurrent transient ischemia may cause irreversible myocardial injury.
 ...
PMID:[Impairment of left ventricular diastolic function during the asymptomatic period in vasospastic angina patients without significant coronary stenosis]. 174 68

The pathogenesis, clinical manifestations and diagnosis, and drug and nondrug therapies of unstable angina pectoris are reviewed. Coronary-artery plaque fissure and rupture, with subsequent platelet aggregation and thrombosis, are the primary underlying stimuli for unstable angina. Unstable angina has been defined as consisting of new-onset angina; angina that is increasing in frequency, intensity, or duration (crescendo angina); or angina at rest. The diagnosis of unstable angina is based on the clinical presentation, electrocardiographic findings, the lack of evidence of myocardial infarction (MI), exercise testing, and coronary angiography. I.V. nitroglycerin is the cornerstone of medical therapy for unstable angina, it relieves chest pain and has a short onset of action. I.V. nitroglycerin, however, has not been shown to reduce the occurrence of MI or death, and its beneficial effects may decrease over time. Aspirin reduces the occurrence of MI and death in patients with unstable angina, but the ideal dosage has not been established. Heparin may reduce the frequency of angina and MI, but its effect on mortality is unknown. Nifedipine has produced beneficial effects in small trials, whereas larger trials have suggested that the drug has deleterious effects when used in the treatment of unstable angina. Verapamil and diltiazem may be effective in relieving chest pain. Calcium-channel blockers have generally not been proved to reduce the risk of MI and death. Data evaluating the efficacy of beta-adrenergic blockers as monotherapy for unstable angina are lacking; these drugs should not be used in patients with vasospastic or Prinzmetal's angina. Thrombolytic therapy has produced mixed results when used in the treatment of unstable angina. Nondrug therapies for unstable angina include intra-aortic balloon counterpulsation, percutaneous transluminal coronary angioplasty, and coronary-artery bypass surgery. Numerous drug and nondrug therapies may be employed in the treatment of unstable angina pectoris.
 ...
PMID:Advances in the treatment of unstable angina pectoris. 179 19


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>