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At least 19 recordsLinked to original sources
PubMed1976

The variant form of angina pectoris.

Variant angina pectoris, usually not precipitated by exertion or emotional stress, often is more severe and lasts longer than classic angina. The pain tends to recur at about the same time each day. Arrhythmias, usually ventricular, occur in about 50% of cases during the peak of pain. Electrocardiograms show a characteristic ST segment elevation during pain, which is in contrast to the ST segment depression of classic angina pectoris. Pain may be due, at least in some cases, to a temporary increase in tonus of a single, large, narrowed coronary artery. Chemical changes in the myocardium and plasma catecholamine changes differ from those occurring in classic angina pectoris. The course of the disease is highly variable but the prognosis must be regarded as grave, since single large vessel disease, present in most cases, is associated with severe myocardial ischemia. Patients with variant angina pectoris should be studied early with coronary arteriography and considered for coronary artery bypass surgery if appropriate.

Angina Pectoris↗
PubMed1998

[Clinical differences between variant and non-variant angina pectoris].

The differences in clinical characteristics were studied between variant angina pectoris with ST segment elevation during ischemic attacks and non-variant angina pectoris without ST segment elevation. Spasm provocation test was performed with either acetylcholine or ergonovine in 192 consecutive patients with vasospastic angina from January 1991 to June 1997. Thirteen patients were excluded because of insufficient data. Fifty-five patients had variant angina and 124 patients had non-variant angina. Coronary risk factors, serum cholesterol level, triglyceride level, high-density lipoprotein cholesterol level, history of syncope, the rates of second or third atrioventricular block and ventricular tachycardia or fibrillation, the incidence of organic stenosis (> or = 50%), the number of vessels with provoked spasm, the dose of acetylcholine and ergonovine used, and duration from the first appearance of chest pain were compared between the 2 groups. Patients with variant angina had more fixed stenosis (p < 0.01), required more percutaneous transluminal coronary angioplasty procedures, lower doses of intracoronary administration of acetylcholine for the induction of coronary arterial spasm and shorter duration from the first appearance of chest pains (p < 0.01) than patients with non-variant angina. However, there were no differences in other factors between the 2 groups. Variant angina pectoris has the same clinical characteristics as non-variant angina pectoris, although variant angina tends to cause higher spasmophilic activity and more fixed stenosis.

Acetylcholine↗
PubMed1975

Variant angina pectoris.

A patient with variant angina pectoris due to a pedunculated calcific mass extending from the aortic valve and resulting in intermittent obstruction of the left coronary ostia is reported. No atherosclerotic disease was demonstrated by coronary angiography. During attacks, marked ST segment elevation and episodes of tachycardia were associated with a moderate rise in pulmonary artery pressure. Replacement of the calcified aortic valve resulted in total relief of symptomatology.

Angina Pectoris↗
PubMed1979

Treatment of variant angina pectoris with perhexilene maleate.

Three patients with variant angina pectoris resistant to therapy with nitrates and propranolol were treated with perhexilene maleate. Two patients had normal coronary arteries with documented coronary artery spasm, while the third patient had a fixed coronary artery obstruction. In all three patients, attacks of variant angina pectoris disappeared following institution of therapy with perhexilene maleate. When the dose of this drug was decreased to 100 mg per day or less, symptoms reappeared in all patients. Reinstitution of therapeutic doses of perhexilene maleate once again resulted in complete control of symptoms. Perhexilene maleate is therefore a useful agent for the treatment of variant angina pectoris.

Angina Pectoris↗
PubMed1985

Echocardiographic versus hemodynamic monitoring during attacks of variant angina pectoris.

Six attacks of variant angina (2 spontaneous, 4 induced by ergonovine) were studied in 6 patients by combined echocardiographic and hemodynamic monitoring. A decrease of percent systolic thickening of the ischemic wall, which occurred as early as the decrease in peak dP/dt of contraction, was detected before the onset of ST-segment elevation ("pre-electrocardiographic phase"). At this stage, no significant change in left ventricular (LV) end-diastolic pressure or end-diastolic diameter was observed. Subsequently, in the presence of clear-cut ST-segment elevation ("electrocardiographic phase"), percent systolic thickening (an index of regional function) reached its nadir, while dP/dt of contraction (an index of global function) was almost back to preischemic values. In this phase, a significant increase in LV end-diastolic diameter and end-diastolic pressure could be also detected. In the recovery phase, when the ST segment had returned to the isoelectric line ("post-electrocardiographic phase"), percent systolic thickening and dP/dt of contraction showed supernormal values, while LV end-diastolic pressure and end-diastolic diameter decreased below basal values. Thus, echocardiographic signs of impairment in LV mechanics are as early and sensitive as hemodynamic indexes during attacks of variant angina. Furthermore, information on morphologic characteristics and regional LV function, not available with hemodynamic monitoring, can be obtained by echocardiography.

Adult↗
PubMed2005

Comparison of plasma serotonin levels in patients with variant angina pectoris versus healed myocardial infarction.

Patients with variant angina pectoris showed greater serotonin plasma levels than did control subjects and patients with healed myocardial infarction. The levels also tended to be greater in those with >1 episode/month than in those with fewer episodes. Moreover, patients with variant angina pectoris also had greater levels of nitrite and nitrate plasma levels than did control subjects or patients with healed myocardial infarction, partly, perhaps, as a compensatory mechanism.

Aged↗
PubMed1983

The mechanism of dysrhythmias in variant angina pectoris: occlusive versus reperfusion.

Thirty-six patients with variant angina pectoris (VAP) were analyzed to investigate whether the mechanism underlying dysrhythmia is related to coronary occlusion or reperfusion. Fifteen of the 36 patients demonstrated dysrhythmias (42%). Twelve of 15 patients (80%) experienced dysrhythmia prior to the acme of ST-segment elevation (occlusive dysrhythmia), and those of tachyarrhythmia type were characterized by the presence of ventricular premature beats initially isolated, increasing in frequency, and preceding the more malignant forms of dysrhythmias, such as ventricular tachycardia or ventricular fibrillation. The occlusive dysrhythmias included ventricular dysrhythmia (ventricular premature beats, ventricular tachycardia, slow ventricular tachycardia, ventricular fibrillation) in eight patients and conduction abnormalities (second- and third-degree AV block, left posterior fascicular block) in four patients. Thirteen episodes of VAP were fully recorded electrocardiographically. The average time to onset of dysrhythmia, after the beginning of ST-segment elevation, was 4.94 minutes +/- 1.52. The duration of the episodes without dysrhythmia was 0.86 minute +/- 0.53. The "reperfusion dysrhythmia" occurred in three patients (20%) and was characterized by the appearance of isolated couplets of ventricular premature beats, ventricular tachycardia, or ventricular fibrillation without prodromal ectopic activity. The dysrhythmia occurred in one patient during the resolution of ST-segment elevation and in two patients within seconds of ST-segment normalization. We conclude that the occlusive related dysrhythmias are the most important mechanism in VAP. They are dependent on the duration of the ischemic episode.

Adult↗
PubMedDate not supplied

Surgical treatment of Wolff-Parkinson-White syndrome combined with variant angina pectoris.

Seven patients with coexistent Wolff-Parkinson-White (WPW) syndrome and variant angina pectoris underwent surgical interruption of an accessory atrioventricular conduction pathway. In two of these patients, perioperative coronary artery spasm occurred. One patient had a perioperative myocardial infarction and the other patient treated successfully had no infarction. Nitroglycerin and nifedipine were administered during and following operation in the other 5 patients without perioperative coronary artery spasm. No adverse effect was observed in the intraoperative electrophysiological study. Combined therapy of intravenous nitroglycerin administration and sublingual nifedipine administration are useful in the perioperative management of patients with coexistent WPW syndrome and variant angina pectoris.

Adult↗
PubMed1985

Prominent negative U wave in variant angina pectoris.

The extremely prominent negative U wave occasionally appears during a cardiac attack in variant angina pectoris. The clinical profile of the negative U wave was therefore studied in 80 patients with variant angina pectoris (VA) and 33 controls with resting angina pectoris (RA). The prominent negative U wave appeared in 55 of the patients with VA (68.8% of patients) and in 10 of the patients with RA (30.3%); thus, there was a significant difference in the appearance of the wave between the 2 groups of patients (p less than 0.001). The leads in which the negative U wave appeared were mostly consistent with those in which the ST segment was elevated. The negative U wave began to appear at about the time when ST-segment elevation began to improve; the wave then gradually became very prominent and then eventually disappeared. The patients with VA and also those with RA on whose ECGs the negative U wave appeared during exercise testing also had negative U waves during spontaneous episodes of angina. An investigation of the frequency of appearance of ST deviation and negative U waves during exercise testing, regardless of the type of angina pectoris, disclosed that the negative U wave appeared in 14 of 20 patients with ST-segment elevation (70% of patients), while the negative U wave appeared in only 52 of 519 patients with either no ST change or ST-segment depression (10.4%); thus, there was a significant difference in the appearance of the negative U wave between these 2 groups (p less than 0.001). Coronary cinearteriography failed to disclose any apparent difference between the appearance of the negative U wave and the presence of stenosis. The prognosis of VA and RA in patients with negative U waves was less favorable compared to those without negative U waves. In particular, we noted that of the 10 patients with RA associated with negative U waves, 4 died. Although the mechanism of the negative U wave is not yet known, we believe that the above findings contribute to its elucidation.

Adult↗
PubMed1999

[Effect of tongxinluo capsule in treating variant angina pectoris patients and its influence on endothelial function].

OBJECTIVE: To assess the efficacy of Tongxinluo capsule (TXLC) in treating variant angina pectoris and its effect on endothelial function. METHODS: Sixty-four patients with variant angina pectoris were enrolled in the study for four weeks by a randomized clinical trial treatment with TXLC or isosorbide mononitrate. RESULTS: (1) The symptoms of both groups were significantly improved, the total effective rate of TXLC and isosorbide were 86.67% and 87.10% respectively; (2) The level of serum nitric oxide was increased, and the serum endothelin was decreased after treatment, there was no significant difference between these two groups. CONCLUSION: TXLC could effectively improve the symptoms of variant angina pectoris, the mechanism of which may likely be mediated by nitric oxide and endothelin.

Adult↗
PubMed1993

Suppression of hyperventilation-induced attacks with infusion of atrial natriuretic peptide in patients with variant angina pectoris.

Atrial natriuretic peptide (ANP) is reported to dilate a major coronary artery in both experimental animals and humans. Spasm of a major coronary artery is the cause of variant angina pectoris and can be induced by hyperventilation. The effect of the ANP infusion on anginal attack induced by hyperventilation was studied in patients with variant angina pectoris. The study was performed in the early morning on 3 consecutive days in 11 patients with variant angina pectoris in whom the attacks were reproducibly induced by hyperventilation. On days 1 and 3 (saline solution infusion), and day 2 (ANP infusion), hyperventilation was started 14 minutes after beginning infusion of ANP (0.1 microgram/kg/min) or saline solution for 6 minutes. The attacks were induced in all 11 patients by hyperventilation on days 1 and 3. However, the attacks were not induced in any patient on day 2 of the ANP infusion. The plasma ANP level increased from 33 +/- 7 pg/ml to the peak level of 2,973 +/- 479 pg/ml (p < 0.01) at the end of the ANP infusion, and the plasma level of cyclic guanosine monophosphate (cGMP) increased from 5 +/- 1 pmol/ml to the peak level of 58 +/- 6 pmol/ml (p < 0.01) 5 minutes after the ANP infusion. The plasma levels of ANP and cGMP did not change after hyperventilation on days 1 and 3. It is concluded that the ANP infusion suppresses the attacks induced by hyperventilation in patients with variant angina pectoris, and cGMP is related to the mechanisms of suppression of the attacks.

Adult↗
PubMed1987

Effect of a new coronary vasodilator, nicorandil, on variant angina pectoris.

The effect of nicorandil, a new coronary vasodilator, was evaluated in 32 patients with variant angina pectoris in a single-blind trial. The study was comprised of a pretreatment period of 2 days with a placebo, a 3-day nicorandil medication period (20 mg/day), and a 2-day posttreatment period with the placebo. Anginal attacks disappeared completely in 24 of the 32 patients. The number of attacks during the pretreatment period, 3.6 +/- 0.4 per day, became significantly reduced to 0.7 +/- 0.2 per day during nicorandil therapy (P less than 0.001) and significantly increased to 1.3 +/- 0.3 per day after withdrawal of the drug (P less than 0.05). In 17 patients with continuous ECG monitoring, the frequency of occurrence of ST-segment elevation was 8.6 +/- 2.7 per day during the preobservation period, significantly decreased to 0.4 +/- 0.2 per day during nicorandil therapy (P less than 0.01), and significantly increased to 1.9 +/- 0.7 per day after withdrawal of the drug (P less than 0.05). The results demonstrate the effectiveness of nicorandil in the treatment of variant angina pectoris.

Angina Pectoris, Variant↗
PubMed1989

[Comparison of isosorbide dinitrate and nifedipine in the treatment of variant angina pectoris. Randomized study].

The effects of isosorbide dinitrate single dose 120 mg daily and nifedipine 20 mg twice daily were studied in 17 patients with variant angina pectoris due to coronary artery spasm. After a placebo phase the patients were randomized to treatment with either isosorbide dinitrate or nifedipine. After six weeks the patients were crossovered for another six weeks period of treatment. There was significant decrease of number of angina attacks during both treatment regimens. Using 24 hours Holter monitoring we also proved significant decrease of number of ST segment elevation or depression, either symptomatic or asymptomatic. There was increase of performed work during exercise tests after both treatment periods. The efficacy of Isoket 120 mg and Adalat Retard 2 x 20 mg daily in the treatment of patients with active variant angina pectoris was comparable in our study. 3 patients suffered untolerable headache during isosorbide dinitrate phase and had to terminate treatment after first day only.

Adult↗
PubMed1971

Left ventricular performance and related haemodynamic changes in Prinzmetal's variant angina pectoris.

Attacks of Prinzmetal's variant form of angina pectoris are spontaneous, recur cyclically, and present unequivocal electrocardiographic alterations: they are ideal for a detailed haemodynamic study.Four patients with this form of angina were investigated. In each of them episodes occurred of electrocardiographic abnormalities either accompanied or unaccompanied by pain. During the same session, the cardiogram, heart rate, arterial pressure, and right atrial pressure were continuously recorded during periods ranging from 5 to 7 hours in each patient. Cardiac output was measured at selected times. Left ventricular ejection time, isovolumic contraction time, mean rate of isovolumic pressure development, and mean systolic ejection rate were also determined. In the 38 recorded anginal episodes, no circulatory change preceded the cardiographic modifications. From the onset of the electrocardiographic abnormalities to the beginning of their reversion, the following circulatory events were observed: (1) obvious reduction of cardiac output; (2) arterial hypotension; (3) lengthening of isovolumic contraction time and mean rate of isovolumic pressure development; (5) reduction of mean systolic ejection rate. It is concluded: (1) that no circulatory factor interfering with work or oxygen consumption of the heart is responsible for eliciting these anginal episodes; (2) that conspicuous left ventricular impairment occurs during the increasing and steady period of the electrocardiographic abnormalities. As the electrocardiogram started reverting to the pre-attack aspect, cardiac performance rapidly improved and, after a ;supernormal' phase, returned in about 2 minutes to basal levels. It is possible that this phase is dependent on a temporary sympathetic compensatory mechanism. No significant qualitative differences were detected between the circulatory pattern of various anginal episodes. The difference was mainly quantitative and the magnitude of the haemodynamic changes correlated well with the degree of the electrocardiographic abnormalities. Pain, when present, seemed just a concomitant symptom not significantly interfering with the circulatory changes associated with the episodes of this form of angina pectoris.

Angina Pectoris↗
PubMed1990

Randomized double-blind comparison of isosorbide dinitrate and nifedipine in variant angina pectoris.

The antianginal and anti-ischemic effect of isosorbide dinitrate (ISDN), 120 mg once daily, and nifedipine, 20 mg twice daily, both in slow-release formulations, were compared in 17 patients with variant angina pectoris in a randomized, double-blind trial. The design included a placebo run-in period and two 6-week crossover periods of active treatment. Mean frequency of angina decreased significantly from 43 attacks per week during the placebo period to 4 per week with ISDN and 8 with nifedipine (p less than 0.001). Sublingual nitroglycerin consumption decreased significantly from 37 tablets per week with placebo to 3 tablets per week with ISDN and 7 with nifedipine (p less than 0.001). Both drugs reduced the silent and symptomatic ST-segment deviations on ambulatory electrocardiographic recording and increased maximal exercise tolerance. Episodes of coronary spasm could be provoked, by hyperventilation, in all patients during the placebo phase but in no patient during therapy with either active drug. Thus, both ISDN and nifedipine, in their slow-release formulations, are effective in the treatment of variant angina pectoris.

Adult↗
PubMed1982

Methacholine provocation of Prinzmetal's variant angina pectoris: a revised perspective.

We report 13 patient with unequivocal Prinzmetal's variant angina pectoris as the entire experience with this syndrome during a 7-year period in a single institution. The clinical diagnosis of this relatively uncommon disorder is emphasized. Five patients were given 10 mg of methacholine subcutaneously. Three demonstrated subsequent delayed appearance of chest pain, ECG change, and coronary vasospasm following early appearance of muscarinic effects. Two Prinzmetal patients had no provocation of variant angina following methacholine, though they did experience significantly less blood pressure fall in response to muscarinic provocation. Another 23 subjects with incompletely explained chest pain given methacholine had neither ECG change nor spasm. Methacholine provocation of variant angina need not necessarily implicated a parasympathomimetic mechanism for otherwise spontaneous episodes. Rather, provocation would appear to occur via the customary reflex adrenergic response to drug-induced hypotension. Methacholine is probably safe though unreliable as an agent to be used for spasm provocation.

Adult↗