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At least 433 records · Page 24Linked to original sources
PubMed1998

Alterations of autonomic nervous activity preceding nocturnal variant angina: sympathetic augmentation with parasympathetic impairment.

BACKGROUND: Autonomic nervous discharge has been implicated in the pathogenesis of coronary artery spasm. METHODS: Cardiac autonomic nervous activities were evaluated from the power of the low-frequency and the high-frequency spectral components of heart rate variability with Holter monitoring in 18 patients with nocturnal variant angina. Samples during the first 512 seconds of each 10-minute period from 60 minutes before to immediately before an anginal attack occurring during the night or at dawn (2:00 to 7:00 AM) were analyzed by fast Fourier transformation. RESULTS: The R-R interval during the 10- to 0-minute period was significantly shorter than those during the other 10-minute periods. The coefficient of variance of the high-frequency component (0.15 to 0.40 Hz) (CVHF) from the 10- to 0-minute period was not significantly different from the other 10-minute periods. However, both the coefficient of variance of the low-frequency component (0.04 to 0.15 Hz) (CVLF) and the ratio of CVLF and CVHF (CVLF/CVHF) were significantly greater during the 10- to 0-minute period than those during the 30- to 20-minute period, respectively. A significant nighttime fluctuation in the spectral components of heart rate variability with a peak in the CVHF and a nadir in both the CVLF and CVLF/CVHF observed in the control group was blunted in the patients during the attack-free periods while they were medicated with calcium entry blockers. CONCLUSION: Sympathovagal imbalance, sympathetic activation without parasympathetic augmentation, enhanced in the early morning may play an important role in the genesis of coronary artery spasm in patients with nocturnal variant angina.

Adult↗
PubMed1986

Diagnosis of important fixed coronary stenosis in patients with variant angina by exercise tests after treatment with calcium antagonists.

A 12 lead electrocardiogram was recorded during treadmill exercise in 57 patients with variant angina in whom coronary angiography was performed. Thirty six patients performed exercise tests with and without calcium antagonists, and 21 performed them only with calcium antagonists. In 55 patients calcium antagonists had prevented spontaneous attacks of variant angina for more than two days before the test. The other two patients were given a single dose of diltiazem (90 mg) two hours before the test. Exercise testing without calcium antagonists induced ST segment elevation with chest pain in nine patients, ST segment depression in 10 (nine with chest pain), and no important shift of the ST segment in 17. Five patients had severe coronary stenosis (greater than or equal to 75%) and all of them showed positive response. Thirty one patients had no important coronary stenosis and 14 of them showed positive response. The sensitivity of the exercise test in detecting a coronary stenosis greater than or equal to 75% was 100% without calcium antagonists but the specificity was low (55%). When the exercise test was done in patients taking calcium antagonists, only two (specificity 96%) of 48 patients without severe coronary stenosis showed positive response (elevation of ST segment in one and depression in another) whereas all nine patients with severe coronary stenosis had a positive response (depression of ST segment in six and elevation in three (sensitivity 100%). It is concluded that exercise testing with calcium antagonists may be a useful method for detecting severe coronary stenosis in patients with variant angina.

Adult↗
PubMed1986

An unusual presentation of variant angina.

A previously well 46-year-old man presented with ventricular fibrillation as an initial complication of Prinzmetals variant angina. Coronary angiography subsequently demonstrated normal coronary arteries.

Angina Pectoris, Variant↗
PubMed2005

[Variant angina mimicking right ventricular infarction--a case report].

A case of a 59-year-old man with recurrent angina associated with ST-segment elevation in leads II, III, aVF and V4R-V6R, cardiogenic shock and complete atrio-ventricular block, is presented. Coronary angiography was normal. Therapy with calcium channel blockers was effective. Difficulties in the treatment of patients with variant angina are discussed.

Angina Pectoris, Variant↗
PubMed1989

Local cooling test for clinical capillaroscopy in Raynaud's phenomenon, unstable angina, and vasospastic visual disorders.

A local cooling test produces a typical flow stop reaction in nailfold capillaries in 88% of patients with Raynaud's phenomenon, but only in 15% of healthy controls. A stop reaction occurred in 9 of 12 patients with Prinzmetal variant angina, exceeding significantly that in 2 of 12 matched control subjects. Also in patients with reversible visual disorders presumably due to vasospasm, the test resulted in a stop reaction in 16 of 25 cases exceeding that in control. In both of these patient groups the cooling test as well as the symptoms reacted favorably to nifedipine. Thus, the local cold exposure test appears to be useful for objective clinical examination not only of patients with Raynaud's phenomenon but also of patients with vasospastic syndromes such as variant angina and visual disorders.

Adult↗
PubMed1995

Effect of calcium antagonists in variant or Prinzmetal angina.

Variant angina, first described by Prinzmetal in 1959, is a syndrome of recurrent ischemic-type chest pain that occurs at rest and is associated with ST segment elevation. The syndrome has been convincingly demonstrated to be caused by temporary occlusion at a site of local spasm. The objectives of this article are to review treatment of the patient with variant angina and to address the important role of calcium antagonists.

Angina Pectoris, Variant↗
PubMed1979

Transient left anterior hemiblock during angina pectoris: coronarographic aspects and clinical significance.

The data of 6 patients in whom a left anterior hemiblock appeared in the course of angina pectoris attacks were reviewed. All 6 patients were found to fulfill the criteria for unstable angina. 1 patient who presented the features of Prinzmetal variant angina was included in this group. Coronary arteriography showed significant coronary artery disease in all 6 patients involving 3 vessels in 2 patients, 2 vessels in 1 and 1 vessel in 3. A severe lesion (70--100%) of the left anterior descending artery in the vicinity of the first perforator was demonstrated in every case. The 2 patients with 3-vessel disease were not operable and died 4 and 5 days after the hemodynamic study. These deaths were caused by myocardial infarction with cardiogenic shock in one case and intractable ventricular arrhythmias in the other case. 4 patients were operable and underwent aortocoronary saphenous bypass surgery. There were 2 operative deaths. The 2 survivors are asymptomatic 7 and 16 mth after surgery. This study suggest that transient left anterior hemiblock during an attack of angina pectoris may be a feature of impending myocardial infarction and may be indicative of a severe obstruction of the left anterior descending coronary artery.

Adult↗
PubMed1982

Effects of oral calcium-antagonists in spontaneous angina. Verapamil and nifedipine in a double-blind cross-over trial.

Verapamil and nifedipine, two calcium-antagonist drugs, were evaluated in a double-blind cross-over trial. The study was performed in 15 patients admitted to our Coronary Care Unit for spontaneous angina. Before and after a 24 hours placebo period, oral verapamil 480 mg daily and oral nifedipine 60 mg daily were administered alternatively. Symptomatic as well as asymptomatic ischemic episodes with ST segment elevation or depression and ventricular and supraventricular ectopic beats were documented by continuous electrocardiographic Holter monitoring. The average number of attacks during the placebo periods was 243; the number of attacks decreased to 129 during verapamil treatment (P less than 0.05) and to 57 during nifedipine treatment (P less than 0.01). Ventricular ectopic beats decreased with both drugs while supraventricular ectopic beats decreased only during verapamil treatment. The difference was not statistically significant because of a small number of observations. In conclusion the two drugs appear to be effective in the management of patients with unstable angina at rest, especially in the variant form.

Angina Pectoris↗
PubMed1983

Prazosin therapy for refractory variant angina.

The selective alpha, blocker prazosin was used to abolish Prinzmetal's variant angina in six patients. All had had an acute transmural myocardial infarction, after which the anginal attacks with transient ST segment elevation developed, and three of them had already suffered from variant angina prior to the infarction. Therapeutic trials with high doses of nifedipine, verapamil, nitrates, beta blockers, and (in one case) phenoxybenzamine were ineffective in all six patients. Prazosin, 8 to 30 mg/day combined with low-dose nitrates or nifedipine completely abolished the attacks in four patients, markedly reduced their frequency and intensity in one patient, and had to be stopped in the sixth one because of hypotension and dizziness. Except for this last patient, the drug was well tolerated by all the others, and no changes in blood pressure were observed. In four patients discontinuation or reduction of prazosin resulted in exacerbation of symptoms, but its renewal was followed by disappearance of the attacks. Since the mean follow-up period in this study was 4 to 6 months, further evaluation appears necessary concerning the long-term effects of this drug in Prinzmetal's variant angina.

Aged↗
PubMed1983

Influence of partial sympathetic denervation on the results of myocardial revascularization in variant angina.

Poor results of the aortocoronary bypass graft operation in the treatment of variant angina have been ascribed to recurrent vasospastic activity due to autonomic imbalance. Cardiac sympathetic denervation (plexectomy) may represent a rational approach in the prevention of vasospasm. To test the value of plexectomy in the treatment of variant angina, 31 patients were studied, 17 of whom (Group 1) underwent conventional coronary artery grafting whereas the remaining 14 (Group 2) underwent cardiac sympathetic denervation also. The 2 groups were similar with respect to age (54 +/- 8 versus 50 +/- 7 years), sex distribution (male/female ratio 12/5 versus 9/5), prevalence of coexisting effort angina (10 versus 12 patients), previous myocardial infarction (7 versus 4 patients), and duration of variant angina (3.3 +/- 5.4 versus 2.4 +/- 2.7 months). The left ventricular ejection fraction was comparable in both groups (60 +/- 11 versus 60 +/- 4%) as were left ventricular end-diastolic pressure (15 +/- 4 versus 13 +/- 5 mm Hg) and extent of coronary artery disease (65 versus 71% prevalence of multivessel disease). The average duration of follow-up was 23 +/- 15 months in Group 1 and 22 +/- 18 months in Group 2 (p = not significant [NS]). There were no operative deaths. Four patients, 2 in each group, had a perioperative myocardial infarction. Seven patients in Group 1 and 1 patient in Group 2 had recurrent variant angina. There was sudden death and 2 infarcts in Group 1. Actuarial curves showed the cumulative probability of recurrent variant angina to be significantly lower (p less than 0.05 and p less than 0.001 at 6 and 10 months, respectively) in Group 2. This study suggests that cardiac sympathetic denervation may prevent recurrent vasospastic activity in variant angina.

Adult↗
PubMed1985

Variant angina in an 11 year old boy.

Variant angina is a syndrome in which ischemic cardiac pain occurs with ST segment elevation. The syndrome is due at least in part to coronary vasospasm. Although well documented in adults, there are no known reports of this syndrome in children. The clinical, electrocardiographic and echocardiographic findings in an 11 year old boy with variant angina are reported.

Age Factors↗
PubMed1983

Alpha-adrenergic blockade for variant angina: a long-term, double-blind, randomized trial.

Recent reports have shown that beta-adrenergic blockade may exacerbate variant angina. On theoretical grounds, alpha-adrenergic blockade may be beneficial in these patients. To test this hypothesis, we assessed the efficacy of prazosin, an alpha-adrenergic blocking agent, in six men, mean age 49 years, with variant angina. Prazosin, 14.0 +/- 2.4 mg/day (mean +/- SD) in three equal doses, was compared with placebo in a double-blind, randomized, double-crossover trial lasting 4 1/2 months: 2 weeks of open-label prazosin followed by four 1-month periods of blinded alternating therapy. No other vasoactive medications were administered during the study. Prazosin reduced sitting systolic arterial pressure from 145 +/- 18 to 127 +/- 16 mm Hg (p = 0.02), but exerted no effect on diastolic arterial pressure or heart rate. Prazosin did not change the weekly number of episodes of chest pain (2.5 +/- 2.3 with placebo vs 3.1 +/- 3.0 with prazosin, NS), nitroglycerin tablets used (3.9 +/- 3.7 with placebo vs 4.6 +/- 4.2 with prazosin, NS), or transient ST-segment deviations (by calibrated two-channel Holter monitoring for 24 hours/week throughout the study) (6.5 +/- 10.1 with placebo vs 11.8 +/- 17.4 with prazosin, NS). During prazosin therapy, three patients had orthostatic dizziness and one patient had headache. Thus, in a long-term, randomized, double-blind trial, prazosin exerted no obvious beneficial effect in patients with variant angina.

Adrenergic alpha-Antagonists↗