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PubMed1991

Clinical effects of nitrendipine on variant angina pectoris.

The clinical effects of nitrendipine, a new calcium antagonist, were investigated in a single-blind test on 21 patients with variant angina pectoris. The efficacy of the drug was evaluated on the basis of frequency of anginal attacks and Holter electrocardiographic findings during different treatment periods at doses of 10 mg once a day (period I) and 20 mg once a day (period II). The number of anginal attacks decreased significantly from a pretreatment level of 2.1 +/- 0.3 per day to 0.7 +/- 0.2 per day in treatment period I and 0.3 +/- 0.1 per day in treatment period II (p less than 0.01, p less than 0.001, respectively). The consumption of sublingual nitroglycerin tablets decreased significantly in both treatment periods in comparison with the observation period before treatment (p less than 0.01, p less than 0.001, respectively). In 20 patients with continuous ECG monitoring, the frequency of ST-segment elevation was 4.5 +/- 1.0 per day during the pretreatment period; it decreased significantly to 0.9 +/- 0.6 per day in treatment period I and 0.5 +/- 0.3 per day in treatment period II (p less than 0.01, p less than 0.001, respectively). The duration and the maximum magnitude of ST-segment elevation also improved significantly in both treatment periods. These results demonstrate the efficacy of nitrendipine in the treatment of variant angina at a single daily dose of 10 mg.

Angina Pectoris, Variant↗
PubMed1976

Variant angina pectoris. Pain and arrhythmias controlled after postoperative myocardial infarction.

A 30-year-old man with variant angina pectoris and ventricular arrhythmias had an angiographically demonstrable 60% obstructive lesion of the proximal left anterior descending coronary artery that was observed to progress to 100% during spasm. Control of pain and arrhythmia by pharmacologic means was unsuccessful. Aortocoronary saphenous vein-internal mammary coronary bypass was associated with an anteroseptal wall myocardial infarction and relief from both angina pectoris and arrhythmias. It is suggested that infarction of the ischemic myocardium played a role in the successful management of this case.

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↗
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↗
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↗
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↗
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↗
PubMed1976

Ventricular reciprocal rhythm occurring in succession in a patient with a variant angina pectoris.

A clinical surface electrocardiogram (ECG) in which ventricular reciprocal rhythm occurred occasionally three times and probably seven times in succession together with paroxysmal ventricular tachycardia and ventricular extrasystoles in competition with sinus rhythm causing incomplete A-V dissociation is described. An ECG tracing of ventricular reciprocal rhythm occurring in succession has never been reported previously as far as can be ascertained from published reports.

Angina Pectoris↗
PubMed1990

[Inhibition of vasospastic angina by alcohol ingestion].

A 66-year-old man having a long history of angina on effort has started to show frequent episodes of angina at rest since 6 months ago. He noticed that chest pain was uncommon after taking alcohol. A variant form of angina pectoris (variant angina) was diagnosed by documentation of typical ST elevation during anginal attack and also by inducing coronary arterial spasm with intracoronary administration of ergonovine maleate. Ambulatory ECG monitoring revealed frequent ST elevation during sleep. Since the history suggested that alcohol ingestion could be effective for preventing variant angina, this effect was examined by giving 540 ml of "sake" in the evening. Variant angina was inhibited, while plasma ethanol was detected. The plasma ethanol reached its peak value as 152 mg/dl at 10 o'clock pm and returned to zero after 12 hours. When ethanol disappeared in the plasma, variant angina recurred again. Although the precise mechanism for inhibition of variant angina by alcohol ingestion is not clear, alcohol or its metabolite such as acetaldehyde seems to be able to inhibit coronary arterial spasm.

Aged↗