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At least 595 records · Page 33Linked to original sources
PubMed1999

Limited efficacy of magnesium for the treatment of variant angina.

Some patients with variant angina show both ST segment elevation at rest and exercise-induced ST segment elevation. Magnesium deficiency has also been observed in patients with variant angina. This study investigated the correlation between the degree of magnesium deficiency and the efficacy of intravenous administration of magnesium in patients with variant angina. Fifteen patients with angiographically confirmed variant angina were assessed for magnesium deficiency and whether intravenous administration of magnesium (19.2 mEq/l) suppressed exercise-induced ST segment elevation. All 15 patients were studied with a magnesium retention test (0.2 mEq/kg over 4 hr) to analyze magnesium deficiency. In our study, magnesium retention rate in patients with variant angina was not higher than that of controls (57 +/- 24% vs 45 +/- 10%, NS). All 15 patients had anginal attacks during accelerated exercise combined with hyperventilation after placebo infusion, whereas only 8 patients had anginal attacks after magnesium administration. ST segment elevation occurred in 14 patients after placebo infusion, but in only 4 patients after magnesium administration. There were no correlations between disease activity, degree of magnesium deficiency or failure of suppression of ST elevation by the intravenous administration of magnesium. Intravenous administration of magnesium can suppress exercise-induced coronary spasms in some patients with variant angina, but the degree of magnesium deficiency did not correlate with the suppressions of exercise-induced ST elevation after magnesium administration. Intravenous administration of magnesium had limited efficacy in patients with variant angina and exercise-induced ST segment elevation.

Acetylcholine↗
PubMed1991

Experimental induction of spasm, sudden progression of organic stenosis and intramural hemorrhage in the epicardial coronary arteries.

Pathogenesis of the so-called "heart attack" still remains to be elucidated. The links between stable effort angina and unstable or acute myocardial infarction, and between asymptomatic and spontaneous angina are all missing. In medicine presently, pathophysiology of ischemic heart disease is considered a consequence of i) the progression of atherosclerotic narrowing of the coronary artery, and ii) dynamic and transient obstruction (coronary spasm), but these mechanisms are traditionally believed to be unrelated. This article demonstrates various experimental evidence indicating that these two mechanisms are related. And, this review article describes how to produce experimental coronary spasm in the presence of atherosclerosis, similar to that seen in patients with variant angina, and that coronary spasm can produce sudden progression of coronary atherosclerotic obstruction due to intramural hemorrhage. Establishment of various animal models to elucidate mechanisms related to various stages of ischemic heart disease are needed.

Angina Pectoris, Variant↗
PubMed2001

Menstrual cyclic variation of myocardial ischemia in premenopausal women with variant angina.

BACKGROUND: An abundance of ovarian hormones is assumed to be a major contributor to the low incidence of ischemic heart disease in premenopausal women. However, the effects of ovarian hormones remain undetermined. OBJECTIVE: To examine whether the variation in ovarian hormone levels throughout a menstrual cycle affects myocardial ischemia in women with variant angina. DESIGN: Prospective, observational study. SETTING: University medical center in Japan. PARTICIPANTS: 10 premenopausal women with variant angina. MEASUREMENTS: Frequency of spontaneous ischemic episodes, flow-mediated dilation of brachial artery, and serum levels of estradiol and progesterone. RESULTS: Frequency of ischemic episodes was highest from the end of the luteal phase to the beginning of the menstrual phase and was lowest in the follicular phase. Flow-mediated vasodilation and estradiol levels were lowest from the end of the luteal phase to the beginning of the menstrual phase and were highest in the follicular phase. CONCLUSIONS: In premenopausal women with variant angina, we documented a cyclic variation in endothelial function and the frequency of myocardial ischemia that was associated with the variation in estrogen levels.

Adult↗
PubMed2002

Coronary vasospasm-induced ventricular tachyarrhythmias.

Coronary artery spasm has been shown to play an important role in the pathogenesis of not only variant angina but also various arrhythmias. We present a case report of coronary vasospasm-induced arrhythmia and review the prevalence, mechanism, prognosis and management of this problem.

Aged↗
PubMed2004

"Torsade de pointes" in a patient with variant angina.

Ventricular tachyarrhythmias have been well documented in patients with variant angina. Episodes of torsade de pointes have been described infrequently. We report a case of a 60-year-old male with a previous history of one vessel artery disease and a successful coronary angioplasty with stenting of the left anterior descending artery, who experienced an episode of angina at rest and electrocardiographic evidence of self-terminating torsade de pointes. After a negative coronary angiography and a positive hyperventilation test, the diagnosis of variant angina was considered and beta-blockers discontinued and calcium channel antagonists prescribed. No other episodes of angina were documented during the following 6 months of follow-up.

Angina Pectoris, Variant↗
PubMed1987

A case of variant angina exacerbated by administration of rifampicin.

Rifampicin, an antituberculosis agent, is known to be a potent inducer of microsomal drug-metabolizing enzymes in the liver. Elimination or clearance of many drugs has been reported to be enhanced, and their effectiveness reduced; however, no report in the literature has dealt with the interaction between rifampicin and dihydropiridine calcium entry-blocking drugs such as nifedipine. We present here evidence for the possible interaction between rifampicin and nifedipine in a patient with angina pectoris, which was exacerbated during coadministration or rechallenge with rifampicin. The peak plasma level and area under the curve were reduced and the apparent oral clearance of nifedipine was increased by rifampicin, suggesting that rifampicin enhanced the elimination of nifedipine via induction of a hepatic microsomal drug-metabolizing enzyme, as has been reported on other drugs widely metabolized in the liver.

Aged↗
PubMed1987

Coronary vasoconstrictor response to cold pressor test in variant angina: lack of relation to intracoronary thromboxane concentrations.

To test the hypothesis that intracoronary concentrations of thromboxane (Tx)A2 could influence the response to cold pressor test (CPT) in variant angina, great cardiac vein blood flow (by thermodilution) and the concentration of TxB2 (the stable metabolite of TxA2) in the great cardiac vein and aorta were measured under control conditions and during CPT in 14 patients with angina at rest associated with transient ST-segment elevation in the anterior leads. In seven patients pretreated with aspirin (intravenous administration of 3.6 mg/kg lysine salt of acetylsalicylic acid, corresponding to 2 mg/kg aspirin), TxB2 baseline concentrations were lower in both the great cardiac vein (47 +/- 19 vs 176 +/- 88 pg/ml; p less than 0.005) and the aorta (45 +/- 16 vs 109 +/- 56 pg/ml, p less than 0.02) than in seven patients who were not taking cyclooxygenase inhibitors. In the two groups, great cardiac vein flow and anterior region coronary resistance were similar under control conditions. During CPT anterior region coronary resistance increased in patients pretreated with aspirin (from 1.97 +/- 0.99 to 2.22 +/- 1.11 mm Hg/ml/min; p less than 0.02) and in patients without aspirin pretreatment (from 1.94 +/- 0.43 to 2.06 +/- 0.34 mm Hg/ml/min; p less than 0.05), and the difference between the two groups was not statistically significant. Therefore the vasoconstrictor response of coronary vessels to CPT in variant angina is not influenced by the intracoronary TxB2 concentrations and is not modified by aspirin pretreatment.

Adult↗
PubMed1982

Clinical characteristics associated with sudden death in patients with variant angina.

After hospital discharge, 114 patients with variant angina were followed for a mean period of 26 months. Six died suddenly and 13 others were resuscitated from sudden cardiac death. The extent of coronary disease and the prevalence of left ventricular dysfunction in these 19 "sudden death" patients were similar to those in the patients who did not experience sudden death ("survivors"). During spontaneous episodes of ST elevation recorded in hospital, 56 of the 114 patients had serious arrhythmias: ventricular fibrillation in two, ventricular tachycardia in 28, ventricular couplets or bigeminy in 17, second- or third-degree atrioventricular block in six and asystole in three. Patients with and those without these arrhythmias during attacks were similar with respect to extent of coronary disease, left ventricular function and most other clinical variables. The maximal ST elevation, however, was higher in the arrhythmia group (7.5 +/- 5.7 vs 3.3 +/- 2.3 mm, p less than 0.01). Serious arrhythmias were detected in 16 of the 19 sudden death patients, compared with 36 of the 86 survivors (p less than 0.01). Sudden death occurred during follow-up in 15 of the 36 patients (42%) with ventricular fibrillation, ventricular tachycardia, high-degree atrioventricular block or asystole during attacks, compared with only four of 69 (6%) without these arrhythmias (p less than 0.001). We conclude that variant angina patients with serious arrhythmias during spontaneous attacks differ from other variant angina patient only in the degree of ischemia during attacks, as reflected by maximal ST elevation, but are at a much higher risk for sudden death.

Adult↗
PubMed2002

Episodic coronary artery vasospasm and hypertension develop in the absence of Sur2 K(ATP) channels.

K(ATP) channels couple the intracellular energy state to membrane excitability and regulate a wide array of biologic activities. K(ATP) channels contain a pore-forming inwardly rectifying potassium channel and a sulfonylurea receptor regulatory subunit (SUR1 or SUR2). To clarify the role of K(ATP) channels in vascular smooth muscle, we studied Sur2 gene-targeted mice (Sur2(-/-)) and found significantly elevated resting blood pressures and sudden death. Using in vivo monitoring, we detected transient, repeated episodes of coronary artery vasospasm in Sur2(-/-) mice. Focal narrowings in the coronary arteries were present in Sur2(-/-) mice consistent with vascular spasm. We treated Sur2(-/-) mice with a calcium channel antagonist and successfully reduced vasospastic episodes. The intermittent coronary artery vasospasm seen in Sur2(-/-) mice provides a model for the human disorder Prinzmetal variant angina and demonstrates that the SUR2 K(ATP) channel is a critical regulator of episodic vasomotor activity.

Adenosine Triphosphate↗
PubMed1979

Prinzmetal's variant angina associated with subarachnoid hemorrhage: A case report.

Prinzmetal's variant of angina occurred in a 48-year-old man who sustained two attacks of subarachnoid hemorrhage within 10 days. The first anginal pain started at the same time that the second cerebrovascular accident developed, but subsequent anginal episodes were not accompanied by other symptoms or signs that indicated new development of subarachnoid hemorrhage. Twelve days later, when nuchal rigidity was fairly improved, the episodes of chest pain ended. A vasospasm of the large coronary arteries--probably due to the derangement of the autonomic nervous system caused by subarachnoid hemorrhage--was presumed to contribute to the occurrence of the variant angina. Based on this case and on review of the literature, we propose that coronary arterial spasm is one of several causes of the cardiac changes seen in subarachnoid hemorrhage.

Angina Pectoris↗
PubMed2000

Heart rate variability in patients with variant angina: effect of the presence of significant coronary stenosis.

BACKGROUND: The syndrome of variant angina occurs in patients with a wide spectrum of coronary disease ranging from angiographically normal coronary arteries to severe three-vessel disease. Survival and choice of therapy for these patients are determined by the extent of underlying fixed coronary obstruction. We examined whether heart rate variability (HRV) due to reduced vagal outflow may correlate with the severity of coronary stenoses in such patients. METHODS: Fifteen men and 2 women with clinically unstable variant angina underwent 24-hour Holter monitoring from which low and high-frequency power, standard deviation of mean 24-hour RR interval, proportion of adjacent RR intervals that differed by more than 50 ms, and mean root square of differences between successive RR intervals were extracted by power spectral analysis. Coronary angiography was later performed to determine coronary pathology and verify variant angina. As controls we studied an age-matched control group of 8 subjects (5 men, 3 women) with no clinical and/or electrocardiographic evidence of coronary heart disease or spasm as shown by negative treadmill exercise and hyperventilation tests. RESULTS: All measured components of HRV were significantly lower in the 9 patients with severe coronary artery disease compared to the 8 patients with normal coronary arteries or < 40% stenosis. The two groups were otherwise similar in terms of age and clinical parameters. CONCLUSIONS: These preliminary findings on a small but carefully selected group of patients with variant angina indicate that the analysis of HRV can select patients with severe disease for a more intensive approach. These findings require confirmation on a larger patient series.

Angina Pectoris, Variant↗
PubMedDate not supplied

Failure of ketanserin, a serotonin inhibitor, to prevent spontaneous or ergonovine-induced attacks of variant angina.

Six patients hospitalized with active variant angina were treated for 3 days with the serotonin antagonist ketanserin after a 3 day control period on no medication. The number of variant angina episodes per patient per day was 1.52 +/- 1.42 during the control period and 2.05 +/- 2.30 during ketanserin therapy (p = NS). Ergonovine was administered in incremental doses of 0.0125 mg to 0.4 mg in the control period, during intravenous ketanserin administration and after 3 days of oral treatment. All 6 patients developed ST elevation during all 3 ergonovine tests. The ergonovine dose at which ST elevation developed was similar in each of the 3 periods. It is concluded that ketanserin is of no value in the treatment of variant angina and that both spontaneous and ergonovine-induced coronary spasm in man are unlikely to be mediated by a serotonergic mechanism.

Aged↗
PubMed1994

[Prevention of coronary spasm during and shortly after coronary revascularization in patients with variant angina].

From June 1990 to March 1993, 9 patients undergoing coronary artery bypass grafting (CABG), 4.4% of all CABG cases at our hospital during this period, had significant perioperative coronary spasm. For 4 patients who underwent CABG before May 1992 (Group 1), preventive and suppressive procedures for the coronary spasm were the addition of diltiazem in the cardioplegic solution and the continuous intravenous infusion of nitroglycerin. Perioperative myocardial infarction (PMI) occurred in all 4 patients in Group 1, with the mean peak MB-CPK of 356 +/- 197 IU/l. One patient had delayed sternal closure because of his unstable hemodynamic status. Thereafter, we changed our protocol as follows: 1) Ergometrine loading (intracoronary infusion) test was performed in all candidates for CABG, aiming at finding out patients with a high risk. And for the high-risk patients, in addition to the measures done in Group 1, 2) intraaortic balloon pumping was performed through the perioperative period, and 3) a pig-tail catheter was dwelled in the Valsalva sinus, through which bolus doses of isosorbide dinitrate were injected frequently in this period. 4) Additionally nifedipine was periodically administered through the nasogastric tube. With these intensive preventive/suppressive measures, the perioperative spasm in 5 patients (Group 2) with variant angina were successfully managed, with no resultant PMI nor operative death (The occurrence of PMI was significantly less frequent in Group 2 than in Group 1, with the p value < 0.05). For patients with variant angina undergoing CABG, combined intensive preventive/suppressive measures for perioperative coronary spasm as listed above proved effective.

Adult↗
PubMed1982

Verapamil therapy for Prinzmetal's variant angina: comparison with placebo and nifedipine.

This study was performed (1) to assess the efficacy and safety of verapamil in patients with variant angina, and (2) to compare verapamil and nifedipine in patients with this clinical syndrome. In 27 patients, placebo and verapamil were administered in a long-term randomized, and double-blind study of 9 months' duration. In comparison to placebo, verapamil reduced the frequency of angina, nitroglycerin usage, transient episodes of electrocardiographic S-T segment deviation (as assessed by 2-channel Holter monitoring), and hospitalizations required for clinical instability. Subsequently, 23 patients were treated with nifedipine in a nonblind fashion for 2 months, and this agent exerted a beneficial effect similar to that of verapamil. Finally, gated equilibrium blood pool scintigraphy, performed in 10 patients at rest and during exercise during treatment with placebo, verapamil, and nifedipine, demonstrated that neither calcium antagonist caused a deterioration of left ventricular performance. Thus, (1) long-term oral verapamil and nifedipine are each superior to placebo and are of similar efficacy in patients with variant angina, and (2) neither agent adversely influences left ventricular performance in patients with relatively normal left ventricular function.

Angina Pectoris, Variant↗
PubMed1999

Refractory coronary artery spasm with superimposed thrombosis: successful treatment with Palmaz-Schatz stent.

Prinzmetal variant angina due to epicardial coronary artery spasm is a disease usually treated with drug therapy with successful results. A case of variant angina, refractory to conventional pharmacological treatment, and complicated by coronary artery thrombosis, was treated with percutaneous transluminal coronary angioplasty and stenting with good immediate and late clinical results.

Aged↗
PubMed2006

[Recurrent cardiac arrest due to electro-mechanical dissociation in a patient with variant angina -- a case report].

We present a case of a 44-year-old male with recurrent episodes of cardiac arrest in the course of Prinzmetal's angina. Episodes of variant angina can be life threatening due to episodes of advanced atrioventricular block, asystole, ventricular tachycardia or ventricular fibrillation. It has been suggested to implant an ICD in all patients with variant angina after cardiac arrest. This patient received an ICD, however, he died suddenly 6 months later. The possible mechanism of cardiac arrest was an electromechanical dissociation.

Adult↗