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At least 685 records · Page 38Linked to original sources
PubMed1991

Refractory variant angina relieved by denopamine--a case report.

A 48-year-old man with severe variant angina refractory to conventional treatment with calcium antagonists and nitrates, or prazosin, or trihexyphenidyl hydrochloride, became symptom free rapidly when treated with denopamine, a adrenergic beta-1 agonist. Denopamine may prove to be an additional therapeutic agent in the management of severe variant angina. Therefore the response to denopamine and the lack of response to prazosin in this patient suggests that not only the adrenergic alpha receptor but also the adrenergic beta-1 receptor plays an important role in the production of coronary spasm, at least in some patients.

Adrenergic beta-Agonists↗
PubMed1998

Intracoronary ST-segment alternans during coronary balloon angioplasty.

ST-segment alternans has been described in experimental coronary artery occlusion and in patients with variant angina. It is also seen during coronary angioplasty. This report describes a patient who on balloon inflation during coronary angioplasty demonstrated ST-segment alternans only on intracoronary electrocardiogram but did not on surface 12 lead electrocardiogram. Hemodynamic pulsus alternans of the aortic pressure tracing was not observed during electrical alternans.

Adult↗
PubMed1982

Transient bifascicular block during Prinzmetal's variant angina.

A 49-year-old man had bradycardia-hypotension syndrome and transient right bundle branch block with left anterior fascicular block during an attack of Prinzmetal's angina. Coronary arteriography showed 50 percent obstruction of the proximal left anterior descending artery; subsequently, he had subtotal occlusion at the stenotic portion with ergonovine administration. The occurrence of this conduction abnormality with Prinz metal's angina suggests that diminished blood supply of the proximal His-Purkinje system is the probable mechanism.

Angina Pectoris, Variant↗
PubMed1999

Coronary artery stent placement in patients with variant angina refractory to medical treatment.

We performed a prospective study to establish the efficacy of coronary stent placement in a highly selected group of patients with focal coronary artery spasm in whom anginal attacks could not be prevented by full medical therapy. The results of this study indicate that intracoronary stent placement may represent an alternative and feasible treatment for patients with vasospastic angina refractory to aggressive medical therapy.

Angina Pectoris, Variant↗
PubMed1985

Coronary spasm, prostaglandin and HLA factors.

To elucidate the contribution of prostanoids in coronary spasm, plasma levels of thromboxane B2 (TXB2) and 6-keto PGF1 alpha at the coronary sinus and ascending aorta in 21 patients with variant angina were measured, as compared with findings in 20 with effort angina and 13 subjects with normal coronaries. In the coronary sinus blood, plasma TXB2 in patients with effort angina exhibited statistically significant high levels, as compared with data in the controls. On the contrary, the data obtained from patients with variant angina were not statistically significant. However, eight patients whose coronary angiogram revealed more than 50% of coronary stenoses had statistically significant high levels of TXB2 and other patients with normal coronaries or less than 50% of narrowing showed almost the same levels of TXB2 as the controls. In contrast to TXB2, the plasma levels of 6-keto PGF1 alpha in patients with variant angina were very low in both groups with variant angina. These data suggest that high levels of TXB2 observed in patients with atherosclerotic coronaries may be an accelerating factor while low levels of prostacyclin may be an essential factor leading to spasm. HLA analysis of 23 patients with variant angina was performed to search for genetic factors, under the hypothesis that such may contribute to the low levels in prostacyclin. This preliminary study revealed statistically significant high frequencies of Bw52 and B-40 in the patients, as compared with frequencies among 152 normal Japanese. Genetic studies are ongoing in our clinic.

6-Ketoprostaglandin F1 alpha↗
PubMed1989

Perivascular nerve lesion of the coronary artery involved in spasm in a patient with variant angina.

An autopsy case of a 52-year-old man with typical variant angina is reported. He had recurrent attacks of chest pain at rest, particularly from midnight to early morning, associated with ST segment elevation in the electrocardiogram. At autopsy, degenerative changes and fibrosis were confirmed light microscopically in the perivascular nerves of the coronary artery involved in spasm. This finding indicates an intimate relationship between coronary spasm and the autonomic nervous system.

Angina Pectoris, Variant↗
PubMed1978

Prinzmetal's variant angina--response to verapamil.

A patient with frequent attacks of Prinzmetal's variant angina complicated by ventricular tachycardia and ventricular fibrillation is described in whom these episodes persisted daily during 4 weeks of hospital observation in spite of treatment with nitrates, alpha-adrenergic-blocking drugs, and anticholinergic agents. The oral administration of verapamil, an investigational vasodilator drug, led to prompt and complete resolution of the attacks.

Adult↗
PubMed1999

An uncommon case of variant angina.

This case report describes a 48-year-old woman patient with variant angina who died because of severe myocardial ischemia and cardiogenic shock, in spite of chronic therapy with nitrates and calcium-antagonists and acute intravenous administration of nitrates, calcium-antagonists and tissue-type plasminogen activator. Her Holter monitoring showed a reduction of time domain measures of heart rate variability. The hemodynamic study exhibited a normal ventriculography and angiographically normal epicardial coronary arteries. The provocative testing, performed (during intravenous therapy with nitrates and diltiazem) by intracoronary injection of progressively increasing doses of ergonovine, induced only a mild vasoconstriction of proximal left anterior descending artery, without symptoms or ST-T segment changes. This case reminds us that variant angina can be a lethal disease, confirms that a negative result of intracoronary ergonovine testing performed during intravenous therapy with nitrates and calcium-antagonists does not assure the prevention of new episodes during chronic oral therapy with the same drugs, suggests a possible prognostic value of the reduction of heart rate variability indexes and shows an unusual response to nitrate administration.

Angina Pectoris, Variant↗
PubMed1989

Time-related decrease in sensitivity to ergonovine in patients with variant angina.

Eighteen patients with variant angina, a positive ergonovine test, and a favorable response to calcium antagonists were studied by serial ergonovine tests and Holter monitoring to assess the long-term changes in response to ergonovine and the relationship with the spontaneous activity of the disease. The number of patients with a positive test decreased from 18 of 18 in the acute phase to 12 of 18 (66%) at 3 months, 10 of 17 (59%) at 6 months, and five of 17 (29%) at 12 months. The mean dose level of ergonovine associated with a positive response and the percentage of positive tests with ST segment depression increased progressively during follow-up. The results of the ergonovine test were well correlated with the spontaneous activity of the disease in 94%, 83%, 76%, and 71% of the patients at initial observation and at 3, 6 and 12 months, respectively. Thus in patients with variant angina and a favorable response to calcium antagonists, a time-related decrease in sensitivity to ergonovine develops during follow-up. In most patients the response to ergonovine is well correlated with the spontaneous activity of the disease; thus the ergonovine test may be a useful tool in the assessment of the natural evolution of vasospastic angina.

Adult↗
PubMed1998

5-HT1Dbeta receptor mediates the supersensitivity of isolated coronary artery to serotonin in variant angina.

Although serotonin (5-hydroxytryptamine; 5-HT) is used for provocation of coronary spasm, 5-HT receptor subtypes in spastic coronary arteries remain undetermined. We demonstrated the supersensitivity of isolated coronary artery to ergonovine, 5-HT, and sumatriptan, a 5-HT1D receptor agonist, in a patient with variant angina. Furthermore, we detected gene expression of 5-HT1Dbeta and 5-HT2A receptors in spastic coronary artery using RNase protection assay. These findings suggest that the leftward shift of the dose-response curve for 5-HT, which plays an important role in the pathogenesis of coronary spasm, is mediated by activation of 5-HT1Dbeta receptor.

Angina Pectoris, Variant↗
PubMed2004

[Myocardial infarction in patient with variant angina].

We present a case of a 49-year-old male with myocardial infarction in a course of variant angina. He was treated successfully with streptokinase, calcium antagonist and nitrates. Coronary angiography showed spasm of the left coronary artery, proximal spasm of the right coronary artery and myocardial bridging of the left anterior descending artery. He has been stable and symptom-free on a treatment with long acting calcium antagonist, nitrates and statin for 3-years.

Angina Pectoris, Variant↗
PubMed1982

The role of coronary artery spasm in anginal syndromes.

The role of coronary artery spasm in the production of angina at rest is emphasized. Three case reports of variant angina are presented to illustrate the spectrum of presentation and to stress the principles underlying the therapy of coronary artery spasm. This entity should be suspected and diagnosed more frequently in order that patients may derive the benefit of relatively specific therapy which consists of calcium antagonists and long-acting nitrates.

Adrenergic alpha-Antagonists↗
PubMed1998

Coronary stent for variant angina: atypical presentation.

Pharmacological therapy remains the treatment of choice for Prinzmetal angina. We report an unconventional approach of coronary artery stenting to treat coronary artery spasm in variant angina refractory to triple drug therapy. Favorable clinical and angiographic results and a negative Ergonovine test, under less aggressive medical therapy, are valuable arguments for stenting. Four-month angiographic follow-up showed absence of intrastent restenosis with a negative Ergonovine test. However, long-term follow-up is necessary before advocating this as a systematic approach.

Adult↗
PubMed1984

Ventricular arrhythmias during ergonovine-induced episodes of variant angina.

Of 95 consecutive patients with active variant angina who underwent ergonovine testing in the coronary care unit while off treatment, 24 (25%) developed serious ventricular arrhythmias: ventricular tachycardia in eight, bigeminy in seven, pairs in five, and frequent ventricular extrasystoles in four. Ergonovine-induced arrhythmias were observed more often in patients with anterior than inferior ST segment elevation (p less than 0.05). ST segment elevation was significantly higher (10.3 +/- 8.1 vs 3.1 +/- 2.1 mm) in patients who developed arrhythmias. All ventricular arrhythmias began within 3 minutes after the onset of ST segment elevation. The intravenous administration of nitroglycerin eliminated arrhythmias in 22 of 24 cases; in only two patients did ventricular arrhythmias develop after the administration of nitroglycerin. Serious ventricular arrhythmias were found during spontaneous variant angina attacks in 14 of 24 patients with ergonovine-induced arrhythmias compared to 16 of 71 patients without ergonovine-induced arrhythmias (p less than 0.001). We conclude that arrhythmias during ergonovine testing are most often caused by ischemia and not reperfusion. Patients with arrhythmias during ergonovine-induced attacks are more likely to have arrhythmias during spontaneous attacks.

Adult↗
PubMed1983

Ventricular tachyarrhythmias in Prinzmetal's variant angina: clinical significance and relation to the degree and time course of S-T segment elevation.

Fifty-six patients with active Prinzmetal's variant angina were studied to determine the incidence and clinical significance of ventricular tachyarrhythmias and the correlation between arrhythmias and degree and time course of S-T segment changes during the ischemic attacks. Twenty-nine patients (Group I) had no ventricular arrhythmias in any of the 1,083 recorded episodes, while 27 patients (Group II) developed arrhythmias in 18% of the attacks. No significant differences in clinical, electrocardiographic, angiographic, or hemodynamic findings could be found between the 2 groups. In 23 of the 27 Group II patients, ventricular arrhythmias developed during maximal S-T segment elevation (occlusion arrhythmias), while in 10 they occurred during resolution of S-T segment changes (reperfusion arrhythmias); 6 of the latter patients also had occlusion arrhythmias. Eight of the 23 patients with occlusion arrhythmias and 6 of the 10 with reperfusion arrhythmias had ventricular fibrillation or ventricular tachycardia. Maximal S-T segment elevation was significantly greater (p less than 0.001) in patients with occlusion arrhythmias than in those without arrhythmias. The episodes with reperfusion arrhythmias were significantly longer (p less than 0.001) and showed a significantly greater S-T segment elevation (p less than 0.001) than those without arrhythmias in Group I patients. This study shows that significant ventricular tachyarrhythmias develop during ischemic attacks in about 50% of patients with active variant angina; clinical and angiographic features are not useful in distinguishing patients with arrhythmias from the others. Our findings suggest that in variant angina ventricular arrhythmias may be due to the effects of both coronary artery occlusion and reperfusion; both types of arrhythmias are correlated with the severity of ischemia, as measured by the degree of S-T segment elevation. Reperfusion arrhythmias also appear to be correlated with the duration of ischemia.

Adult↗
PubMed1985

Coronary spasm and allergy. Retrospective study of the incidence of allergic history in patients with variant angina.

Despite a large number of papers concerning coronary spasm, its mechanism still remains unsolved. Several cases have been reported in which coronary spasm was triggered by allergy. Since histamine is one of the causative substances released in allergic reactions, we speculated on some involvement of an allergic mechanism in the pathogenesis of coronary spasm. We retrospectively examined by questionnaire the incidence of allergic history in patients with variant angina (n = 47) and compared it with that in patients with non-ischemic heart diseases (n = 83). We could not find any relationship between coronary spasm and allergy. Furthermore, we have not experienced any case in which myocardial ischemia was provoked by an allergic reaction. Accordingly, allergy could not be a major cause of coronary spasm in our present experience.

Adult↗
PubMed1986

Clinical evidence suggesting vasospastic cause of myocardial infarction.

To examine the vasospastic cause of myocardial infarction (MI) we studied 1) the incidence of rest angina before MI, 2) clinical features of postinfarction angina and 3) the occurrence of MI in variant angina. 1) Of 178 patients with MI, 60 (34%) experienced rest angina for 1 day to 10 years before the onset of MI. The incidence of rest angina was significantly higher in patients having milder coronary stenosis of 75% or less (15/30, 50%) than in others having severe stenosis of 90% or more (45/148, 30%), p less than 0.05. 2) Postinfarction angina with ST elevation was observed in 16 patients (9%) and ST elevation developed in leads with pathological Q waves in all patients. The incidence of postinfarction angina was significantly higher in those having milder coronary stenosis than in others having severe stenosis, (27% versus 5%, p less than 0.005). Patients with postinfarction angina experienced rest angina before MI more frequently (81%) than others (29%, p less than 0.005). Sublingual nitroglycerin was effective in relieving postinfarction angina attacks and oral calcium antagonist prevented attacks in all patients. 3) MI developed in 9 of 97 patients with variant angina. Six patients had transmural and 3, non-transmural MI. Pathological Q waves and/or coronary T waves appeared in leads where ST elevation was observed during anginal attack. In 7 patients MI developed when antispastic agents were not used and in 2, when angina persisted even under treatment with calcium antagonist. These data strongly suggest that the coronary spasm can be a cause of MI in some patients.

Adult↗
PubMed2002

[Prinzmetal's variant angina with transient complete atrio-ventricular block--case report].

A case of 44-year-old women with episodes of chest pain with ST-T segment elevation and paroxysmal atrioventricular complete block with syncopal episodes is presented. Coronary angiography did not reveal atheromatous lesions. A patient was treated with nitrates and calcium channel blockers. However syncopal episodes with A-V block reoccurred. A single-chamber (ventricular demand) pacemaker was implanted. A six month follow-up was uneventful.

Adult↗