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PubMed1983

Diurnal distribution of ST-segment elevation and related arrhythmias in patients with variant angina: a study by ambulatory ECG monitoring.

Twenty-four-hour ambulatory ECG recording was performed in 26 patients with variant angina to evaluate the diurnal distribution of ST-segment elevation in relation to chest pain and the incidence of arrhythmias during the episodes. During a recording period of 52 days, 364 ST-segment elevations of 1 mm or greater were observed and 79% were asymptomatic. ST-segment elevation frequently occurred between 0:00 and 9:00 hours (72%) and most frequently between 5:00 and 6:00 hours (13%). Only a few episodes occurred between 10:00 and 18:00 hours. Premature atrial contractions, premature ventricular contractions (PVCs), ventricular tachycardia (VT) and complete atrioventricular block occurred during 12% of the episodes and were more common during painful episodes (32%) than during painless ones (6%). However, VT and severe forms of PVCs (couplets and bigeminy) appeared eight times during painless episodes and nine times during painful ones. Arrhythmias occurred more frequently when the elevated ST segment started to return or was returning to the control level (n = 38) than when the ST segment was rising (n = 8). The incidence of arrhythmias was lower when the daily frequency of ischemic episodes was high. This study shows that episodes of asymptomatic coronary artery spasm predominantly occur early in the morning as symptomatic episodes; complex dysrhythmias appear during the asymptomatic episodes; arrhythmias occur predominantly during a "reperfusion period;" and more arrhythmias accompany infrequent daily episodes of ischemia than frequent ones.

Adult↗
PubMed1991

Effect of H1 receptor stimulation on coronary artery diameter in patients with variant angina: comparison with effect of acetylcholine.

It has been suggested that histamine is involved in the pathogenesis of coronary spasm but its exact role remains unclear. H1 receptor stimulation of the coronary artery was performed with a selective intracoronary infusion of histamine (2 micrograms/min) in 21 patients with variant angina after blockade of the H2 receptor with cimetidine (25 mg/kg) and its effect on the coronary artery diameter was examined. Intracoronary injection of acetylcholine was also performed in 19 of the 21 patients. Ergonovine (0.2 mg) was intravenously administered in one patient. The coronary artery diameter was measured with cinevideodensitometric analysis. A mean plasma histamine concentration in the coronary sinus increased from 4 x 10(-9) to 7 x 10(-8) M 5 min after histamine infusion into the left coronary artery (n = 18). Coronary spasm was induced in 6 patients (29%) with histamine, in 18 (95%) with acetylcholine and in 1 with ergonovine. The effect of histamine on the luminal diameter was analyzed at the site of spasm in the 26 coronary arteries in which spasm was induced by acetylcholine or ergonovine. Of the 20 coronary arteries with a normal arteriogram or a fixed stenosis less than or equal to 50% of luminal diameter, histamine decreased the diameter in 4, increased it in 14 (70%) and caused no change in 2; of the 6 coronary arteries with a fixed stenosis greater than or equal to 75%, histamine decreased the diameter in 5 and increased it in 1. In the coronary arteries in which spasm was not induced by either acetylcholine or ergonovine, histamine increased the diameter, especially in those without advanced atherosclerosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1989

[Psychological background as a risk factor of variant angina].

In this study, the role of psychological make-up was assessed as a risk factor in the etiology of vasospasm in variant angina (VA) using the Cornell Medical Index (CMI). Study subjects consisted of 15 patients with VA; 32 with effort angina or old myocardial infarction having no vasospasm (EA + OMI); and 34 healthy men. For a neurosis discriminative diagram, the areas I and II were judged as normal and the areas III and IV were judged compatible with a neurotic disorder. Correlation of serum lipid levels with psychological factors was attempted. 1. Among the VA patients, 46.7% belonged to the areas III and IV, as compared to 18% of the patients with EA + OMI, and 2.6% of the healthy subjects. 2. Seventy-three percent of the VA group showed anxiety states indicating a correlation with a psychological disorder. 3. A majority of the VA patients had a variety of psychological symptoms unrelated to myocardial ischemia. 4. Total cholesterol, triglycerides, LDL cholesterol, serum uric acid and the atherogenic index were all lower in the VA group than in the EA + OMI group. 5. In the EA + OMI group, triglycerides, serum uric acid and the atherogenic index were higher in the psychological group than in the non-psychological group. However, total cholesterol, LDL cholesterol and HDL cholesterol were lower in the former than in the latter group. It was concluded that an anxiety state constitutes a contributing background for developing VA and it was speculated that such an anxiety state may lead to an exaggerated secretion of stress hormones, resulting in vasospasm of the coronary arteries.

Aged↗
PubMed1994

Once daily felodipine in preventing ergonovine-induced myocardial ischaemia in Prinzmetal's variant angina.

The efficacy of extended-release felodipine in preventing ergonovine-induced myocardial ischaemia was assessed in 14 patients (12 male, two female, aged 56 +/- 7 years) with Prinzmetal's variant angina. Four of the patients had normal coronary arteries, eight had one-vessel and two had two-vessel disease. The ergonovine test was performed once in basal conditions and twice 5 days after beginning the oral administration of felodipine 20 mg o.d., 4 and 24 h after the last administration. During a continuous 6-lead ECG recording, ergonovine was injected at doses of 25, 50, 100, 200, and 400 micrograms at 5 min intervals. Blood samples for felodipine plasma concentrations were drawn at the time of the tests. The basal ergonovine test was positive in all 14 patients (seven with anterior and seven with inferior ST segment elevation > 0.1 mV) at a mean ergonovine dose of 162 +/- 138 micrograms. The test was repeated 4 h after the last felodipine administration and was negative in 13 patients (93%), but 24 h after the last drug administration, eight patients (57%) had a positive test response (five with anterior, three with inferior ST segment elevation) at a higher ergonovine dose than at baseline (150 vs 97 micrograms, P = 0.042). The only differences between patients with a negative and a positive test were the mean values of the left ventricular end-diastolic pressure (9.3 vs 14.9 mmHg, P = 0.002) and the ergonovine doses used in the baseline tests (250 vs 97 micrograms, P = 0.034).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed2002

Endothelial function fluctuates with diurnal variation in the frequency of ischemic episodes in patients with variant angina.

OBJECTIVES: The aim of the present study was to investigate whether there is diurnal fluctuation in the endothelial function of patients with variant angina (VA). BACKGROUND: Coronary spasm is induced by acetylcholine and is promptly relieved by nitroglycerin. Thus, it is possible that endothelial dysfunction is involved in the pathogenesis of coronary spasm. Furthermore, the frequency of ischemic episodes is known to display diurnal variation. METHODS: Flow-mediated, endothelium-dependent vasodilation of the brachial arteries was measured in the early morning (6 AM), afternoon (2 PM) and evening (8 PM) in 20 patients with VA (mean age 54.5 years; 10 men and 10 women) and in 20 control subjects (mean age 54.2 years; 10 men and 10 women). All patients underwent 24-h ambulatory electrocardiographic monitoring during the study. RESULTS: Flow-mediated vasodilation in patients with VA was deteriorated by the early morning and improved by the afternoon (patients with VA at 8 PM vs. 6 AM vs. 2 PM: 7.8 +/- 2.1% (p < 0.01 vs. VA at 6 AM) vs. 5.4 +/- 2.3% vs. 8.8 +/- 1.9% (p < 0.01 vs. VA at 6 AM); control subjects: 9.5 +/- 2.8% vs. 9.0 +/- 2.2% vs. 9.9 +/- 1.9%, respectively). The frequency of spontaneous ischemic episodes was highest from midnight to morning and was lowest from morning to late afternoon (4 PM to midnight: 7 episodes; midnight to 8 AM: 25 episodes; 8 AM to 4 PM: 3 episodes). CONCLUSION: There is diurnal fluctuation in endothelial function, which is associated with variation in the frequency of ischemic episodes.

Aged↗
PubMed1983

Potentiation of coronary vasoconstriction by beta-adrenergic blockade in patients with coronary artery disease.

Although beta-adrenergic blocking agents reduce myocardial oxygen consumption and symptoms of myocardial ischemia in patients with coronary artery disease (CAD), propranolol has been reported to exacerbate coronary artery spasm in some patients with variant angina. To determine whether increased coronary vasomotor tone can be induced by beta-adrenergic blockade, we measured the changes in coronary vascular resistance (CVR) during cold pressor testing (CPT) in 15 patients, nine with severe CAD and six with normal left coronary anatomy, before and after i.v. propranolol (0.1 mg/kg). Coronary blood flow was measured by coronary sinus thermodilution. CVR was calculated as mean arterial pressure divided by coronary sinus blood flow. Heart rate was maintained constant at a paced subanginal rate of 95 +/- 5 beats/min. Before propranolol, CPT induced significant increases in coronary vascular resistance in patients with CAD (15.0 +/- 2.2%, p less than 0.02), but no increase in CVR in the normal patients. After propranolol, the CVR change during CPT was augmented for patients with CAD (29 +/- 6%, p less than 0.01) and for the normal population (9 +/- 5%, NS). The potentiated increase in CVR occurred without significant changes in resting CVR or in the magnitude of the hypertensive response to CPT. We conclude that beta-adrenergic blockade with propranolol can potentiate coronary artery vasoconstriction in some patients with CAD, possibly mediated by unopposed alpha-adrenergic vasomotor tone. These changes may be important in patients in whom intense adrenergic stimulation may increase coronary artery tone and adversely influence the balance between myocardial oxygen supply and demand.

Adrenergic beta-Antagonists↗
PubMed1987

Efficacy of diltiazem in variant angina. Results of a double-blind crossover study in CCU by Holter monitoring. The possible occurrence of a withdrawal syndrome.

The short and long term efficacy of diltiazem, a calcium-entry blocker, has been evaluated in a group of ten patients with Prinzmetal's variant angina admitted to a CCU. In the short term part of the study, after a run-in period, diltiazem 60 mg tid and placebo were administered alternatively during 4 randomized 72 hour periods. Response was assessed using continuous Holter monitoring, measuring the frequency of transient ischemic attacks. During the run-in period the number of episodes/day/patient was 16.1. No episodes of transient ST segment elevation were recorded during both periods of diltiazem treatment in 3 patients and during one of the two periods in 4. For the group as a whole the number of episodes during the first placebo period was not statistically different from that during the run-in period (208 versus 161). No statistically significant difference was also found in 8 patients comparing the number of episodes during the second placebo period and the run-in period (166 versus 101). During each period of diltiazem treatment an highly significant reduction in the number of episodes was observed (43 and 5, p = .006 and p = .02). Two patients did not complete the study protocol. Both patients had a worsening of angina during the first placebo period following diltiazem treatment. One of them developed an acute myocardial infarction. The possible occurrence of a rebound phenomenon after withdrawal of diltiazem seems to be indicated, in 6 patients, by a significant increase in the number of ischemic episodes recorded during the placebo period following active treatment in respect to the number during the first placebo period (159 versus 73, p = .04).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed2006

Sumatriptan provokes coronary artery spasm in patients with variant angina: possible involvement of serotonin 1B receptor.

BACKGROUND: Serotonin (5HT) can induce coronary artery spasm (CAS) in patients with variant angina (VA). We have previously reported that 5HT(1B) and 5HT(2A) receptors gene were expressed in human coronary arterial smooth muscle cells and that isolated coronary artery from a patient with VA showed the supersensitivity to sumatriptan (SMT), a 5HT(1B/1D) receptor agonist. The aim of the present study was to determine whether SMT can provoke CAS directly or indirectly through platelet aggregation in patients with VA. METHODS: We evaluated the effects of intracoronary infusion of graded concentrations of SMT on coronary arteries in 9 patients, including 5 documented VA and 4 participants with atypical chest pain as control. RESULTS: SMT provoked CAS in all patients with VA. SMT could not induce CAS in control. SMT (10(-4) M) caused significant contractions (%diameter of baseline; median [interquartile range], 0 [0-18.4]% in VA, as compared with control (proximal segments; 92.6 [77.9-118.9]%, p<0.05 vs. VA, distal segments; 92.9 [65.3-158.5]%, p<0.01 vs. VA). In control, minor dilation occurred at SMT concentration up to 10(-5) M. SMT could induce in vitro platelet aggregation neither in healthy subjects nor in patients with VA. CONCLUSIONS: These findings suggest that activation of 5HT(1B) receptor by SMT can induce CAS directly in patients with VA without platelet activation. This is the first report directly demonstrating the effect of 5HT(1B) receptor activation on human coronary arteries in vivo.

Adult↗
PubMed1995

Correlation between isolated negative U waves and the grade of coronary artery spasm.

The relation between isolated negative U waves and the severity of induced coronary artery spasm was investigated in 24 patients with variant angina to determine the grade of myocardial ischemia during the appearance of isolated negative U waves. Coronary artery spasm was induced by injections of either incremental doses of acetylcholine or ergonovine into the left coronary artery. Coronary spasm was quantified into 4 grades: Grade 0 = complete perfusion, Grade 1 = partial perfusion, Grade 2 = penetration without perfusion, and Grade 3 = no perfusion. Induction with acetylcholine was discontinued when a coronary spasm of Grade > or = 2 was induced. Electrocardiogram in leads V1 to V6 and systemic blood pressure were recorded continuously. Provocations of coronary spasm with at least 2 doses of acetylcholine could be performed in 15 patients. All acetylcholine-induced coronary spasms of Grade < or = 1 disappeared spontaneously within 3 min. Negative U waves developed in 19 (79%) patients, in whom 37 trials with acetylcholine or ergonovine injection were performed. Isolated negative U waves were detected in 10 trials, negative U waves and ST depression in 8 trials, and negative U waves and ST elevation in 14 trials. The induced coronary spasms associated with isolated negative U waves were of Grade 1 in 9 of the 10 trials. In contrast, all of the coronary spasms associated with negative U waves and ST elevation had a Grade of > or = 2. In conclusion, the coronary angiographic finding associated with isolated negative U waves is coronary spasm with delayed filling of the distal coronary artery, with opacification of the entire coronary bed.

Acetylcholine↗
PubMed1988

Multivessel coronary spasm in patients with variant angina: a study with intracoronary injection of acetylcholine.

Multivessel coronary spasm has been described but its incidence in patients with variant angina still remains unclear. Thirty-three patients with variant angina were studied during coronary angiographic examination with selective intracoronary injection of acetylcholine (ACh). In all but three patients, the location of ischemia during attack was determined by the electrocardiographic findings, by exercise 201Tl myocardial scintigraphy, and by two-dimensional echocardiography during a hyperventilation test, and the coronary artery (or arteries) responsible for the attack was predicted before the study. ACh induced spasm of at least one coronary artery in all but one patient. ACh induced spasm of both the left and right coronary arteries (i.e., multivessel coronary spasm) in 24 patients: in two of the four patients who were predicted to have spasm of the left coronary artery, in six of the 11 predicted to have spasm of the right coronary artery, in 13 of the 15 predicted to have spasm of both the left and right coronary arteries, and in three of the three in whom coronary artery responsible for attack had not been predicted. This ACh-induced spasm of the left and right coronary arteries occurred separately and no patients showed hemodynamic instability during attack. In one patient in whom multivessel coronary spasm had been predicted and ACh failed to induice coronary spasm, ergonovine maleate (0.2 mg) induced spasm of both the left and right coronary arteries simultaneously, resulting in severe prolonged hypotension. Nineteen of the 25 patients in whom multivessel coronary spasm was documented showed angiographically normal or nearly normal coronary arteries after administration of nitroglycerin.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1984

[Characterization and therapy of ventricular arrhythmias due to transient myocardial ischemic attacks in variant angina].

Forty-two patients with variant angina were studied by ambulatory ECG monitoring to determine the incidence and the characteristics of ventricular arrhythmias during ischemic attacks. Twenty-six patients had no ventricular arrhythmias in 633 ischemic attacks; 16 patients had ventricular arrhythmias in 116/586 ischemic attacks. The number of ischemic attacks per day and the magnitude of ST elevation were significantly (p less than 0.05) greater in patients with ventricular arrhythmias. Ventricular arrhythmias appeared at the onset or at the peak of ST elevation (first phase) in 17 ischemic attacks, during the resolution of ST elevation (second phase) in 43 attacks, during both the phases in 9 attacks. ST alternans appeared during 6 ischemic attacks with arrhythmias. Two episodes of ventricular fibrillation and 22 runs of ventricular tachycardia occurred during the first phase, 17 episodes of ventricular tachycardia were recorded during the second phase. Ventricular tachycardia of the second phase compared with ventricular tachycardias of the first phase were significantly (p less than 0.01) slower, uniform and initiated by a late premature beat. Incidence of arrhythmias of the second phase was strictly correlated with the duration of ischemic attacks. Nine patients who showed ventricular arrhythmias during the second phase of ischemic attacks were enrolled in a cross-over study to assess the antiarrhythmic effects of nifedipine (120 mg/day) and verapamil (480 mg/day). During treatment with nifedipine, the frequency of ischemic attacks declined by 85%, while the frequency of attacks with arrhythmias declined by 97% (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1996

Diffuse disorder of coronary artery vasomotility in patients with coronary spastic angina. Hyperreactivity to the constrictor effects of acetylcholine and the dilator effects of nitroglycerin.

OBJECTIVES: We examined the vasomotility of the entire epicardial coronary artery system in patients with and without coronary spastic angina. BACKGROUND: The coronary arteries of patients with variant angina are hyperreactive to diverse constrictor stimuli. It is unclear whether the abnormal responses to constrictive or dilative stimuli, or both, result from a localized or diffuse disorder in the coronary artery tree. METHODS: Coronary artery diameter responses to intracoronary acetylcholine and nitroglycerin were examined at the proximal, middle and distal segments of three principal coronary arteries in 36 patients with coronary spastic angina without significant stenosis and in 12 young (< or = 30 years old) and 20 older control subjects (> 30 years old) with normal coronary arteriographic findings. In 10 patients with significant coronary stenosis, the responses of the prestenotic segments were also examined. RESULTS: In patients with coronary spastic angina, coronary spasm was induced in 23 left anterior descending, 13 left circumflex and 17 right coronary arteries by acetylcholine. Multivessel spasm was observed in 15 patients. Acetylcholine had a dilator effect on most segments in young control subjects and a mild constrictor effect in older control subjects and in patients with significant stenosis. Comparison of the responses to acetylcholine among groups demonstrated that the constrictor response of the artery with spasm was enhanced significantly and diffusely. That of the artery without spasm also tended to be enhanced. Coronary artery diameters after nitroglycerin did not differ in any segment among patients with coronary spastic angina and both control groups. In patients with coronary spastic angina, nitroglycerin significantly enhanced dilation in all segments of the artery with spasm compared with that observed in both control groups and in most segments of the artery without spasm. Patients with significant coronary stenosis had a reduced response compared with that in control subjects. CONCLUSIONS: Hyperreactive responses not only to the constrictor effects of acetylcholine, but also the dilator effects of nitroglycerin were detected diffusely in the epicardial coronary arteries of patients with coronary spastic angina. This finding indicates that a diffuse, not localized, disorder in vasomotility is involved in the pathogenesis of coronary spastic angina.

Acetylcholine↗
PubMed2004

Prinzmetal's angina.

Prinzmetal's angina, often referred to as "variant" angina, is a temporary increase in coronary vascular tone (vasospasm) causing a marked, but transient reduction in luminal diameter. This coronary vasospastic state is usually focal at a single site and can occur in either a normal or diseased vessel. Patients are predominantly younger women who may not have the classical cardiovascular risk factors (except for cigarette use). PVA has been associated with vasospastic disorders such as Raynaud's phenomenon and migraine headaches. Arrhythmias are common and may be life threatening especially when the effects of vasospasm are seen in those ECG leads that reflect the potential variations of the epicardial surface of the left ventricle. Endothelial dysfunction has been considered as primarily responsible for PVA. The diagnosis is made by observing transient ST-segment elevation during the attack of angina. Since PVA is not a "demand"- induced symptom, but rather a supply (vasospastic) abnormality, exercise treadmill stress testing is of no value in the diagnosis of PVA. The most sensitive and specific test for PVA is the administration of ergonovine intravenously. Fifty micrograms at 5-minute intervals is given until a positive result or a maximum dose of 400 microg has been administered. When positive, the symptoms and associated ST-segment elevation should be present. Nitroglycerin rapidly reverses the effects of ergonovine if refractory spasm occurs. Medical therapy classically employs vasodilator drugs, which include nitrates and calcium channel blockers. The prognosis is good when there is no significant coronary artery stenosis. Treatment of associated coronary atherosclerosis in elderly patients with PVA is advised. When PVA is associated with coronary atherosclerosis, the prognosis is determined by the severity of the underlying disease. beta-Blockers and large doses of aspirin are contraindicated in PVA.

Aged↗
PubMed1987

Findings from long-term electrocardiographic monitoring of patients with variant angina in a coronary care unit.

Eleven patients with frequent episodes of variant angina underwent 24-hour electrocardiographic monitoring in a coronary care unit for a total of 70 days to assess circadian variation in ischemic episodes and its correlation with circadian heart rate (HR) rhythm. In each patient a series of 4 to 13 consecutive days, in the absence of therapy, with 8 or more ischemic episodes per day were analyzed. Harmonic regression models were fitted to the hourly number of ischemic episodes and the hourly values of HR. Out of 54 days, with 8 or more episodes per day for a total of 1,357 episodes, a circadian rhythm was observed for 34 days (64%), in at least 1 day in all patients and during the entire period of observation in only 3. Its presence was independent of the number of episodes; the peak of periodic functions occurred at 2.9 +/- 2.7 AM. A cadian rhythm for HR was observed in 61 of the 70 days (87%), consistently in 7 patients; the nadir occurred at 2.4 +/- 1.5 AM; simultaneous cycling in HR and transient ischemia was found on 32 days. The intrapatient difference between the peak and the nadir of the ischemic and the HR function was, on average, 2.6 +/- 3.3 hours. Thus, a circadian rhythm of ischemic episodes was present in all patients although it was not consistently present; simultaneous occurrence of circadian variation in ischemic episodes and HR was observed only in 60% of the days with a sufficiently high number of attacks and when this occurred, a significant phase shift was observed; occasional loss of HR cycling was observed in some patients, without an apparent cause.

Adult↗
PubMedDate not supplied

Diagnosis and treatment of Prinzmetal's variant angina.

The presentation, diagnosis (including provocative testing), and therapy of Prinzmetal's variant angina are reviewed. Prinzmetal's variant angina (PVA) is a form of angina caused by coronary-artery vasospasm (CAS) and is not associated with exertion. It is diagnosed by history, electrocardiogram, or coronary-artery angiography. Provocative tests, such as the cold-pressor test or intravenous ergonovine maleate, are sometimes used to aid diagnosis of PVA. Nitrates, adrenergic - blocking agents, and calcium-channel blocking agents can be used in treating PVA. Nitroglycerin and isosorbide dinitrate effectively relieve CAS. However, long-term prospective studies on the use of these drugs for PVA are lacking in the literature. Studies on treating PVA with adrenergic-blocking agents have been equivocol, with some studies reporting improvement and some reporting worsening. Calcium-channel blocking agents are promising drugs for PVA. Nifedipine is generally considered the prototype of this class for antianginal activity. It is administered orally in PVA patients and is effective. Side effects are mild and do not usually require termination of therapy. Verapamil hydrochloride, the prototype calcium-channel blocking agent for arrhythmias, is effective for PVA, but only 10-20% of an orally administered dose reaches systemic circulation because of the first-pass effect. Other calcium-channel blockers, including perhexilene maleate, diltiazem hydrochloride, prenylamine, and lidoflazine, have been tested in a few CAS patients with some success; adverse effects and toxicities limit the use of some of them, especially perhexilene. Therapy, using combinations of nitrates, adrenergic-blocking agents, and calcium-channel blocking agents, is needed in some patients. Dosing guidelines for all drugs are given in the paper. Treatment of PVA should begin with oral nitrates. Calcium-channel blocking agents are indicated in the patient who has failed to respond or is intolerant to maximum doses of nitrates given in various forms.

Angina Pectoris, Variant↗
PubMed2003

Did the widespread use of long-acting calcium antagonists decrease the occurrence of variant angina?

BACKGROUND: We have not often encountered variant angina (VA) since the use of long-acting calcium antagonists (L-CAs) became widespread. OBJECTIVES: This study examined the frequency of VA retrospectively. METHODS: and results: We diagnosed angiographically confirmed coronary spastic angina (CSA) in 349 consecutive patients using selective spasm provocation tests from January 1991 to December 2002. During this period, 3,148 diagnostic cardiac catheterizations and 1,515 selective spasm provocation tests were performed. Seventy-four of these 349 patients (21.2%) had VA. Coronary spasms were defined as transient luminal narrowings of > 99%, and VA was defined as an ST elevation during spontaneous attacks or noninvasive stress tests. We classified the 12 years of the study into four periods of 3 years each. No tendency to decrease for the ratio of the number of patients with CSA and the number of selective spasm provocation tests was observed among the four time periods (18%, 24%, 32%, and 23%, respectively). However, the number of patients with VA (28, 33, 9, and 4) and the VA/CSA ratio (32%, 28%, 14%, and 5%, respectively) in the four group significantly decreased. The frequency of administration of calcium antagonists (CAs) before hospital admission (49% vs 33%, respectively; p < 0.05) was significantly higher in the last time period (from 2000 to 2002) than in the first period (from 1991 to 1993). L-CAs were administered in > 90% of CSA patients who had been medicated with CAs before hospital admission in the last period (from 2000 to 2002), while L-CAs were administered in only 20% in the former period (from 1991 to 1993). The administration of statins and angiotensin-converting enzyme inhibitors/angiotensin receptor blockers before hospital admission gradually increased according to the period passed, but not significantly. CONCLUSION: The frequency of VA has decreased in Japan, possibly due to the widespread use of therapy with L-CAs.

Angina Pectoris, Variant↗
PubMed1996

Autonomic changes associated with spontaneous coronary spasm in patients with variant angina.

OBJECTIVES: This study sought to investigate whether changes in nervous autonomic tone may have a role in the mechanisms triggering spontaneous coronary spasm in variant angina. BACKGROUND: Previous studies have suggested that both sympathetic and vagal activation may act as a trigger of epicardial artery spasm in patients with variant angina, but the actual role of autonomic changes in spontaneous coronary spasm remains unknown. METHODS: We analyzed the changes in heart rate variability associated with episodes of ST segment elevation detected on Holter monitoring in 23 patients with variant angina (18 men, 5 women; mean [+/-SD] age 59 +/- 12 years). For study purposes, episodes of transmural ischemia lasting > or = 3 min and without any ST segment changes in the previous 40 min were selected for analysis. Heart rate variability indexes were calculated at 2-min intervals, at 30,15,5 and 1 min before ST elevation and at peak ST segment elevation. Ninety-three of 239 total ischemic episodes (39%) fulfilled the inclusion criteria. RESULTS: The results showed that 1) high frequency (HF) (0.04 to 0.15 Hz), a heart rate variability index specific for vagal activity, decreased in the 2 min preceding ST segment elevation (p < 0.001) and returned to basal levels at peak ST segment elevation; 2) heart rate and low frequency (0.04 to 0.15 Hz), which are partially correlated with sympathetic activity, showed a significant increase at peak ST segment elevation (p < 0.001 for both); 3) the pattern of the HF reduction before ST segment elevation was consistently confirmed in several subgroups of ischemic episodes, including those of patients with or without coronary stenoses, those of patients with anterior or inferior ST segment elevation, those occurring during daily or nightly hours and silent episodes. There were no significant variations in heart rate variability in control periods selected from Holter tapes of patients and before ST segment elevation induced by balloon inflation in 20 patients undergoing coronary angioplasty. CONCLUSIONS: Our data show that changes in autonomic tone are likely to contribute to trigger or predispose to epicardial spasm. In particular, although not excluding an active role for adrenergic mechanisms, our data suggest that a vagal withdrawal may often be a component of the mechanisms leading to spontaneous coronary vasospasm.

Aged↗
PubMed1996

Ergonovine echocardiography as a screening test for diagnosis of vasospastic angina before coronary angiography.

OBJECTIVES: In patients with chest pain suggestive of variant angina, we performed this prospective study to test the specificity and diagnostic validity of ergonovine echocardiography (detection of regional wall motion abnormality during bedside ergonovine challenge) as a screening procedure before coronary angiography. BACKGROUND: Spasm provocation test outside the catheterization room has generally not been accepted as a safe diagnostic method. METHODS: Ergonovine echocardiography was performed in 80 consecutive patients with chest pain syndrome after confirmation of negative treadmill or normal stress myocardial perfusion scan results using thallium-201. A bolus of ergonovine maleate was injected at 5-min intervals up to a total cumulative dosage of 0.35 mg with echocardiographic monitoring of left ventricular wall motion. A 12-lead electrocardiogram (ECG) was also recorded every 3 min after each ergonovine injection. Positive test results were development of regional wall motion abnormalities or transient ST segment elevation or depression >0.1 mV in any single lead of the 12-lead ECG. Coronary angiography was undertaken within 2 +/- 4 days (mean +/- SD) after ergonovine echocardiography, and the spasm provocation test with acetylcholine or ergonovine was performed in patients with normal angiographic findings or lumen diameter narrowing <70%. RESULTS: On the basis of angiographic criteria, 56 patients had coronary vasospasm; this finding was later ruled out in 19 patients with near-normal angiographic results by a negative response on the spasm provocation test. In the remaining five patients, coronary spasm provocation was not performed because they revealed a high degree of fixed stenosis (lumen diameter narrowing 97 +/- 4%). Ergonovine echocardiography could diagnose coronary vasospasm before angiography, with a sensitivity of 91% (51 of 56 patients, 95% confidence interval [CI] 84% TO 98%) and specificity of 88% (21 of 24 patients, 95% CI 75% to 100%). Of 53 patients showing regional wall motion abnormalities during ergonovine echocardiography, characteristic ST segment elevation in the simultaneously recorded ECG was observed in only 20 (38%). There were no complications, including myocardial infarction or fatal arrhythmia, during the test. CONCLUSIONS: Ergonovine echocardiography before coronary angiography is safe and can be used as a reliable diagnostic screening test for coronary vasospasm in patients with negative treadmill or normal stress myocardial perfusion scan results. These findings suggest that invasive coronary angiography can be avoided in selected patients for the diagnosis of vasospastic angina.

Adult↗