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PubMed1981

Histamine provocation of clinical coronary artery spasm: implications concerning pathogenesis of variant angina pectoris.

Twelve patients with nonexertional chest pain and nonobstructive fixed coronary disease (less than 50% luminal diameter narrowing) were given histamine to investigate the potential role (coronary artery H1 receptor agonism) of the endogenous agent in producing coronary artery spasm (CAS). Histamine, at intravenous dose of 0.5 to 1.0 microgram/kg/min, provoked CAS in four patients. In six patients neither histamine nor ergonovine provoked spasm, and these patients were considered by chronic follow-up evaluation to have noncardiac etiology for their chest pain syndrome. In one patient CAS was provoked with ergonovine but not by histamine, and one ergonovine-positive patient had an equivocally positive histamine result. Pretreatment with cimetidine (H2 receptor antagonism) was necessary to avoid unpleasant side effects of histamine. Thus these observations indicate that histamine should be included among the specific agents capable of inducing CAS and provide new insight concerning the mechanism(s) causing variant angina pectoris.

Adult↗
PubMed1990

Magnesium deficiency detected by intravenous loading test in variant angina pectoris.

To study whether magnesium (Mg) deficiency is present in patients with variant angina, 24-hour Mg retention of low dose Mg (0.2 mEq/kg lean body weight) administered intravenously over 4 hours in 20 patients with variant angina was examined. No patient had received calcium antagonists before or during the study. All had attacks of chest pain associated with ST elevation on electrocardiograms. Twenty-one subjects without ischemic heart disease were studied as control subjects. Ten patients with variant angina were restudied 10 to 529 days (mean 235 +/- 30) after the treatment with calcium antagonists (diltiazem 120 to 240 or nifedipine 40 to 80 mg/day), which resulted in complete suppression of anginal attacks. The mean serum Mg concentrations in the patients with variant angina and the control subjects were 2.1 +/- 0.05 and 2.1 +/- 0.03 mg/dl, respectively (difference not significant). However, 24-hour Mg retention in the patients with variant angina was 60 +/- 5%, while that in the control subjects was 36 +/- 3% (p less than 0.001), suggesting that Mg deficiency is present in at least some patients with variant angina. The mean serum Mg concentrations before and after calcium antagonist treatment in 10 patients with variant angina were 2.1 +/- 0.09 and 2.1 +/- 0.07 mg/dl, respectively (difference not significant). However, 24-hour Mg retention decreased significantly (p less than 0.01) from 60 +/- 6 to 34 +/- 7% after the treatment. There is Mg deficiency in many patients with variant angina and it is corrected after treatment with calcium antagonists.

Adult↗
PubMed1991

Prognostic significance of silent myocardial ischemia in variant angina pectoris.

The present study investigates the prognostic significance of silent myocardial ischemia in variant angina. Forty-eight-hour Holter monitoring and coronary angiography were performed in 54 patients with transient ST elevation and no history of myocardial infarction admitted to the coronary care unit for worsening of symptoms. Coronary artery spasm was documented in most of these patients. Over the subsequent month, 20 patients (group 1) had a major coronary event (2 died, 6 had nonfatal myocardial infarction and 12 had urgent coronary revascularization), and the remaining 34 patients (group 2) had a good clinical outcome. From 2,578 hours of recording, 547 ischemic episodes were identified of which only 9% were associated with angina. The mean daily number of ST elevation in group 1 was similar to that in group 2 (4.8 +/- 5.1 vs 4.1 +/- 4.6; p = not significant). Conversely, the mean daily duration of such ischemic episodes was consistently greater in group 1 than in 2 (79 +/- 36 vs 37 +/- 25 minutes; p less than 0.005). The occurrence of greater than or equal to 1 long-lasting (greater than or equal to 10 minutes) episode of ST elevation was observed in 18 of 20 patients in group 1 (sensitivity 90%), but only in 4 of 34 in group 2 (specificity 88%). Significant coronary atherosclerosis (greater than 50% stenoses) was found at angiography in 18 of 20 patients in group 1, and in 18 of 34 in group 2.(ABSTRACT TRUNCATED AT 250 WORDS)

Angina Pectoris, Variant↗
PubMed1989

Comparison of serum lipid values in variant angina pectoris and fixed coronary artery disease with normal subjects.

Lipid and apolipoprotein (apo) levels in patients with variant angina were examined and compared with patients with coronary artery disease (CAD) and normal subjects (control). Cholesterol and triglyceride levels in plasma, lipoprotein fractions and several apolipoproteins were measured in 108 men (90 of whom had undergone coronary angiography): 22 had variant angina, 56 had fixed CAD (effort angina and old myocardial infarction) and 30 were normal subjects. Patients with variant angina showed more severe atherosclerotic lesions than the control group, but less severe lesions than the patients with fixed CAD. In comparison with lipid and apolipoprotein, high density lipoprotein cholesterol, apo AI and apo AII decreased significantly in control, variant angina and fixed CAD groups, respectively. Additionally, stepwise discriminant analysis revealed that apo AI was the best discriminator among the 3 groups or between variant angina or fixed CAD and the control group. Variant angina and fixed CAD patients could be discriminated from the control subjects by an apo AI level of 135 and 126 mg/dl, with 71% (p less than 0.025) and 73% (p less than 0.005) accuracy, respectively. By these criteria 77% of the patients with variant angina and 73% of the patients with fixed CAD were precisely discriminated. Discrimination between variant angina and fixed CAD patients, however, was not practical, even if the best discriminator was used. Thus, the apo AI level is useful in discriminating patients with variant angina and fixed CAD from normal subjects. Therefore, symptomatic patients with low apo AI levels should be aggressively examined.

Adult↗
PubMed1998

A case of variant angina pectoris with similar findings on both rest and matched exercise thallium-201 studies.

A patient with variant angina showed similar findings on both the rest and matched exercise 201Thallium (201Tl) myocardial perfusion scintigrams. The 65-year old man was admitted to hospital because of rest angina. His electrocardiogram during the attack disclosed ST segment elevation on inferior leads. However, emergency coronary arteriogram showed no fixed stenosis. Intracoronary injection of acetylcholine induced a spasm on the distal right coronary artery, but not in the left coronary artery. In the rest 201Tl study, septal perfusion was low on the early image, although partial redistribution of this site was observed on the delayed image without the appearance of chest pain or electrocardiographic ischemic change. Similary, in the 201Tl exercise study undergone 2 weeks later, septal redistribution was diagnosed because the early image had decreased septal perfusion. Both the exercise 123I-metaiodobenzylguanidine study and the rest 123I-betamethyl-p-iodophenyl-pentadecanoic acid study showed inferior abnormalities on the early and delayed images. Although a coronary spasm was not induced in the left anterior descending artery with the acetylcholine test, septal redistribution was observed on the delayed image of both the rest and exercise 201Tl studies. The mechanism of the redistribution on the rest 201Tl study was unclear.

Aged↗
PubMed2001

Impaired endothelium-dependent vasodilation in the brachial artery in variant angina pectoris and the effect of intravenous administration of vitamin C.

UNLABELLED: Endothelial dysfunction in the coronary artery contributes to the pathogenesis of variant angina, and endothelial dysfunction in variant angina may be associated with increased oxidant stress in the systemic arteries. We investigated whether endothelial dysfunction exists in the peripheral artery in patients with variant angina, and also examined the effect of vitamin C, an antioxidant, on endothelium-dependent vasodilation. Using high-resolution ultrasound, both the flow-mediated vasodilation (FMD, endothelium-dependent vasodilation) and sublingual nitroglycerin-induced vasodilation (NTG-D, endothelium-independent vasodilation) in the brachial artery were measured in 28 patients with variant angina and 24 control subjects who had normal coronary arteries. FMD was significantly impaired in patients with variant angina compared with control subjects (1.8 +/- 2.2% vs 6.4 +/- 4.9%, p <0.001). FMD and NTG-D before and after intravenous administration of either vitamin C or placebo were measured in 17 patients with variant angina. FMD significantly improved after the administration of vitamin C (from 2.2 +/- 2.4% to 4.5 +/- 1.6%, p <0.01), but not after administration of the placebo (from 2.0 +/- 2.6% to 1.7 +/- 1.9%). The improved FMD due to vitamin C in patients with variant angina, however, was not significantly different from that in the control subjects. NTG-D was not significantly different between patients with variant angina and control subjects (14.0 +/- 7.8% vs 13.6 +/- 5.0%) and it was also not affected by vitamin C. IN CONCLUSION: (1) FMD in the brachial artery is impaired in patients with variant angina, and (2) the acute administration of the antioxidant, vitamin C, was observed to reverse this endothelial dysfunction. These findings support the theory that the systemic inactivation of nitric oxide due to oxidative stress might exist in patients with variant angina.

Angina Pectoris, Variant↗
PubMed1986

[The effects of medical treatment on the long-term prognosis of variant angina pectoris].

To investigate the changing aspect of the long-term prognosis of patients with medically-treated variant angina, we studied 253 consecutive patients treated from January 1963 to August 1984. The patients were categorized into two groups according to the year of first admission to our hospital; 88 patients hospitalized before January 1975 and mainly treated with nitrates (group I), and 165 patients admitted thereafter and treated with calcium antagonists (group II). The average follow-up period was 63.1 months (ranged from one to 136) in the group I, and 32.4 months (ranged from one to 116) in the group II. Coronary arteriography was performed in 146 patients of the group II. In 82 patients (56%), no fixed coronary artery stenosis of greater than or equal to 75% of the luminal diameter was present; 47 patients (32%) had one-vessel disease, and 17 (12%) had multi-vessel involvement. Seventy-eight patients having both rest and effort angina showed a higher prevalence of fixed coronary artery stenoses (50 of 78 patients) compared with the patients without effort angina (14 of 68 patients) (p less than 0.001). The group II showed a significantly good long-term efficacy of medical treatment for anginal attacks (124 of 165 patients compared with 54 of 88 group I patients: p less than 0.05). Complete remission over three months or more occurred in 56% of the group II compared with 45% of the group I. Fourteen patients (16%) of the group I suffered from myocardial infarction (10 were within six months of onset of angina); whereas, only five (3%) of the group II developed myocardial infarction (two were within six months of initial anginal attack) (p less than 0.001). Cardiac death occurred in five patients (6%) of the group I in contrast to four patients (2%) of the group II. The patients having significantly effective medical treatment for anginal attack were 80%, 62% and 64% in those without significant stenosis, with one-vessel disease, and with multi-vessel disease, respectively. Myocardial infarction occurred in two of 17 patients with multi-vessel disease. Spontaneous remission of angina over at least three years without medical treatment occurred in seven of 32 patients who were followed for more than 10 years. It was concluded that the long-term prognosis of patients with variant angina who received calcium antagonists was reasonably improved compared with patients treated with nitrates.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1989

Hyperventilation and ergonovine tests in Prinzmetal's variant angina pectoris in men.

Hyperventilation and ergonovine tests were carried out in a group of 30 patients with variant angina to assess the sensitivity of the 2 tests and to correlate the response with spontaneous disease activity. Hyperventilation produced a positive response in 83% (25 of 30) and ergonovine in 93% (28 of 30) of the patients. After hyperventilation 22 of 25 showed ST-segment elevation, 2 ST depression and 1 T-wave pseudonormalization; after ergonovine ST-segment elevation developed in 23 patients, ST depression in 4 and T-wave pseudonormalization in 1. In all cases the electrocardiographic changes occurred in the same leads as during the spontaneous attacks. The incidence of chest pain and ventricular arrhythmias was similar during both tests; spontaneous remission of ischemia, however, was more frequent (48 vs 14%) after hyperventilation than after ergonovine. Acute ischemia developed at a mean of 218 +/- 112 seconds after the end of hyperventilation in 19 of 25 positive tests; at that time double product was not significantly different from basal values. The sensitivity of hyperventilation was similar (95 vs 100%) to ergonovine in the patients with greater than or equal to 1 daily attack, while in those with less than 1 daily attack the sensitivity of hyperventilation decreased to 55% compared to 77% with ergonovine. Thus, in variant angina the sensitivity of both tests correlates with disease activity. Hyperventilation is a safe provocative test with a sensitivity similar to ergonovine in patients with active disease; however, in patients with sporadic attacks hyperventilation has a lower sensitivity than ergonovine and therefore a limited diagnostic value.

Adult↗
PubMed1981

Verapamil therapy in variant angina pectoris refractory to nitrates.

Conventional therapy including nitrates, beta blockers, and surgical bypass has proved to be generally unsatisfactory in patients with variant angina of suspected vasospastic etiology. Recent evidence regarding the role of calcium in the pathogenesis of vascular smooth muscle spasm prompted an open study of the clinical effects of verapamil in seven patients with recurrent rest angina refractory to nitrates. The patients studied met strict clinical ECG and angiographic criteria for vasospastic angina. All patients had rapid (within 24 hours) and complete (without recurrence of symptoms) chronic response to oral verapamil therapy. The pharmacology of verapamil relating to the pathogenesis of vasospastic angina is delineated and guidelines for the clinical application of the agent are presented.

Adult↗
PubMed1985

The QRS complex during transient myocardial ischemia: studies in patients with variant angina pectoris and in a canine preparation.

We made continuous electrocardiographic recordings on magnetic tape during 15 episodes of ischemia in five patients with variant angina to determine the characteristics of the QRS changes. Orthogonal leads were used and the electrocardiograms were analyzed visually and by digital computer. Changes were quantified by subtracting baseline electrocardiograms from those obtained during ischemia. Large changes in the QRS occurred during ischemia but the waveform quickly returned to baseline when the episode subsided. In all patients there was prolongation of the QRS duration and an increase in QRS voltage during the terminal 40 msec of the waveform in the lead(s) showing the most marked ST displacement. The increase in the terminal QRS could be represented by a vector directed toward the ischemic zone. In a given patient the amplitude of ST displacement varied between episodes, presumably because of variation in the intensity of ischemia, but the QRS changes were directionally similar in each episode. In two patients there was also a smaller change involving the initial 40 msec of the QRS that could be represented by a vector directed away from the ischemic zone. To determine the possible mechanism for the electrocardiographic changes, ischemic episodes of 120 to 150 sec were produced in seven dogs and electrocardiographic recording and analysis techniques similar to those used in patients were employed. Myocardial conduction velocity was measured in three directions in the ischemic zone and was correlated with simultaneous electrocardiographic recordings from the body surface. The electrocardiographic changes in the dog preparation were virtually identical to those in the patients and strongly correlated with a fall in myocardial conduction velocity. We conclude that the QRS changes during variant angina result from the altered excitation pattern produced by conduction delay in the ischemic zone. The probable cause for the increase in terminal QRS voltage is delayed (and uncancelled) activation of the ischemic zone.

Angina Pectoris, Variant↗
PubMed1991

Efficacy of slow-release nifedipine on myocardial ischemic episodes in variant angina pectoris.

To evaluate the efficacy of slow-release nifedipine (a single dose of 20 mg given at 10 P.M. or 2 doses of 20 mg at 10 P.M. and 6 A.M.) on ischemic episodes in patients with variant angina, a single-blind crossover study with ambulatory electrocardiographic monitoring was performed in 15 patients (13 men and 2 women, mean age 63 years). In all, there were 646 ischemic episodes detected with ambulatory electrocardiographic monitoring during the study period, and 618 episodes of them occurred during placebo periods with a circadian variation. Sixty-nine percent of the episodes in placebo periods were asymptomatic. The number of anginal attacks, nitroglycerin tablets taken, ST-segment elevation and the total ischemic duration significantly decreased during nifedipine therapy compared with results after the placebo therapy period, respectively (p less than 0.01 or 0.05). Twenty-eight ischemic episodes occurred during nifedipine therapy when the plasma level of nifedipine was low. Thus, asymptomatic ischemic episodes more frequently occur than symptomatic episodes and the administration of slow-release nifedipine is highly effective in suppressing not only symptomatic but also asymptomatic myocardial ischemia in patients with variant angina. The timing of the administration of slow-release nifedipine is an important factor in suppressing ischemic episodes.

Aged↗
PubMed1987

Effect of oral levodopa and carbidopa on coronary spasm in variant angina pectoris.

The effect of oral administration of 500 mg of levodopa with 50 mg of carbidopa, a peripheral dopadecarboxylase inhibitor, on coronary vasomotion during vasoconstrictor stimuli was examined in 15 patients with variant angina presenting with hyperventilation-induced myocardial ischemia. Patients were studied during 3 noninvasive sessions and 1 angiographic session. In all sessions the basic protocol consisted of provocation of coronary spasm by hyperventilation before and 2 hours after levodopa and carbidopa administration. During angiography, great cardiac vein blood flow, right atrial and aortic pressures were measured, and coronary angiograms were recorded at baseline and 1 to 4 minutes after each hyperventilation. Samples for dopamine plasma levels were drawn before and throughout the studies. In 3 selected patients, levodopa and carbidopa were associated with 30 mg of domperidone, an antagonist of dopamine peripheral receptors. Levodopa and carbidopa consistently prevented the occurrence of ischemia after hyperventilation in 6 of the 15 patients. This was due to inhibition of local coronary spasm in 2 patients and reduced coronary constriction in 4. Ischemia due to hyperventilation was still prevented despite addition of domperidone with levodopa and carbidopa. Plasma dopamine levels were 23 +/- 15 before and 739 +/- 284 pg/ml 2 hours after administration of levodopa and carbidopa. These findings are consistent with either a decreased central dopaminergic activity and associated disregulation of vasomotor tone, or a peripheral vasodilatory effect of increasing dopamine.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1992

Variant angina pectoris. Role of coronary spasm in the development of fixed coronary obstructions.

BACKGROUND: It has been suggested that recurring coronary artery spasm may lead to the development of fixed atherosclerotic coronary obstructions. METHODS AND RESULTS: We studied 10 patients with typical Prinzmetal's variant angina in whom the disease remained active for years and in whom occlusive coronary spasm occurred reproducibly at the same arterial site during repeat coronary arteriography (25 +/- 12 months after initial angiography). At initial evaluation, four patients had significant (greater than or equal to 50% fixed coronary diameter reduction) one-vessel coronary artery disease, and six had nonsignificant disease. Spasm developed at stenotic sites (20-65% diameter reduction) in nine patients and at an angiographically normal site in one patient. Progression of coronary disease was assessed in 62 segments: 10 spastic (of which nine were stenotic) and 52 nonspastic (eight stenotic and 44 angiographically normal), using computerized arteriography. Mean diameters (millimeters) of spastic segments, nonspastic stenoses, and angiographically normal nonspastic segments were not significantly different at first and second arteriograms (1.52 +/- 0.14 versus 1.43 +/- 0.21, 1.32 +/- 0.17 versus 1.12 +/- 0.23, and 2.40 +/- 0.12 versus 2.42 +/- 0.12, respectively). Stenosis progression (from 65% diameter reduction to total occlusion) occurred in one patient at a spastic site and in two at nonspastic sites (from 34% to 65% and from 84% to 100%). Complicated stenoses suggestive of plaque fissuring were not observed during the study. CONCLUSIONS: In patients with chronic Prinzmetal's variant angina without myocardial infarction, stenosis progression was not frequently observed at spastic sites despite the recurrence of focal coronary spasm over relatively long periods of time.

Adult↗
PubMed1996

Clinical observation of spontaneous anginal attacks and multivessel spasm in variant angina pectoris with normal coronary arteries: evaluation by 24-hour 12-lead electrocardiography with computer analysis.

OBJECTIVES: Using a new, computerized 24-h 12-lead electrocardiographic (ECG) recording and analysis system (the EAGLE system), we sought to evaluate the clinical manifestations of ischemic episodes in patients with variant angina and normal coronary arteries. BACKGROUND: Although the prognosis of variant angina without significant organic stenosis is generally good, the incidence of multivessel spasm, a major prognostic factor, is surprisingly high in provocation tests. METHODS: A total of 122 patients with suspected variant or unstable angina underwent 24-h examination with the EAGLE system and two-channel Holter monitoring. Thirty patients in this group were diagnosed as having variant angina with normal or nearly normal coronary arteries. Twenty-two (73%) of these 30 patients developed anginal attacks with ST segment elevation during monitoring and were enrolled in the study. RESULTS: The 22 patients had a total of 138 episodes of transient ST segment elevation and 13 episodes of ST segment depression. No arrhythmias were observed during ST segment depression, but 26 episodes of ST segment elevation (19%) were associated with arrhythmias: 7 with premature ventricular contractions, 3 with ventricular bigeminy, 3 with complete atrioventricular (AV) block, 1 with complete AV block and couplets of premature ventricular contractions and 12 with marked sinus bradycardia (< 45 beats/min). Ten (45%) of the 22 patients had multivessel spasm. We observed three different patterns of multivessel spasm: 1) spasm at a different site on different occasions (migratory spasm); 2) spasm that sequentially affected two different sites; 3) simultaneous spasm at more than one site. The duration of ST segment elevation was much longer in patients with sequential and simultaneous spasm than in those with single-vessel spasm, and arrhythmias were more frequent during these two types of multivessel spasm. CONCLUSIONS: Although the prognosis of multivessel spasm is believed to be poor, this may not necessarily be so. Anginal attacks due to sequential and simultaneous multivessel spasm seem to be more dangerous than those involving single-vessel spasm or migratory multivessel spasm.

Aged↗
PubMed1975

Variant angina pectoris: Clinical and anatomic spectrum and results of coronary bypass surgery.

Twenty patients are described with the variant angina syndrome (recurrent angina at rest with S-T segment elevations occurring only during pain and no evolution of infarction). In contrast to patients previously reported on, all but one had progressive unstable angina before hospitalization. Angina was frequently associated with arrhythmias, including ventricular fibrillation (2 instances), ventricular tachycardia (4), frequent ventricular premature beats (5), atrioventricular block (4), sinus bradycardia (2), sinoatrial exit block (1) and supraventricular tachycardia (1). Seventeen patients had significant proximal stenosis of one or more coronary arteries with good distal vessels. Bypass surgery in 15 of these patients resulted in one noncardiac postoperative death, one perioperative infarction and relief of pain in all 14 survivors. After a 17 month mean follow-up period (range 4 to 38 months), all survivors are pain-free. Three patients had no significant coronary disease; one of these became asymptomatic with medical therapy, one continues to have angina and one died suddenly. Patients with normal coronary arteries could not be distinguished clinically or by electrocardiogram from those with severe obstructive lesions. This experience suggests that all patients with the variant angina syndrome should be studied by coronary angiography, and that most patients with significant fixed coronary lesions will do well after coronary bypass surgery.

Adult↗
PubMed1982

Efficacy of chronic amiodarone therapy in patients with variant angina pectoris and inhibition of ergonovine coronary constriction.

In three patients with vasospastic angina pectoris, chronic amiodarone administered orally at doses of 800 and 1,000 mg/day totally suppressed spontaneous episodes of ischemic chest pain for 8 to 14 months. Before treatment, ergonovine maleate 0.2 to 0.4 mg intravenously provoked chest pain and similar ischemic ECG changes as those occurring spontaneously. During amiodarone treatment ergonovine vasoconstriction was totally or partially inhibited. In addition to calcium-blocking agents, amiodarone is another spasmolytic drug which effects smooth muscle relaxation by different mechanisms and appears to be useful for the chronic treatment and prevention of variant angina. The vasodilator property of amiodarone is achieved by both direct action and noncompetitive alpha receptor antagonism of coronary vasculature.

Administration, Oral↗