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At least 487 records · Page 27Linked to original sources
PubMed1998

Inappropriate microvascular constriction produced transient ST-segment elevation in patients with syndrome X.

OBJECTIVES: The aim of this project was to study the responsible site(s) and underlying cardiac disease(s) of patients with transient ST-segment elevation and normal coronary angiograms. BACKGROUND: Transient ST-segment elevation has been demonstrated in patients with variant angina or unstable angina. In those patients, epicardial coronary arteries, not microvessels, are always the responsible site for the transient ST-segment elevation. METHODS: This study consisted of three cases with a transient ST-segment elevation and normal coronary angiograms. Treadmill testings were performed before coronary angiography in all cases. Coronary angiography was undertaken during the control state and during ST-segment elevation and, when possible, a Doppler guide wire was positioned in the left anterior descending artery (LAD). Coronary responses to vasodilators were observed. Finally, cardiac biopsy was performed and pathologic observation was conducted. RESULTS: All three cases had significant ST-segment depression during treadmill testing in II, III, aVF and V4-6 leads; however, no angiographic coronary stenosis was demonstrated and vasospasm was not provoked. A transient ST-segment elevation associated with chest pain was observed in V1-5 leads, but normal coronary angiograms during ST-segment elevation were observed in every case. Coronary blood flow (CBF) velocity profile remained normal during ST-segment elevation. In one case, vasodilator responses to the LAD during ST-segment elevation were also measured. A 0.5 mg intracoronary injection of nitroglycerin increased CBF velocity (220%), but ST-segment elevation was not normalized and chest pain persisted. A 10 mg intracoronary injection of papaverine (PVN) further increased CBF velocity up to 340%, and this normalized ST-segment elevation and relieved chest pain quickly. Either endothelium-dependent coronary flow reserve (CFR) measured with a 100 microg intracoronary infusion of acetylcholine, or flow-dependent CFR by a 10 mg intracoronary injection of PVN was reduced in one of two cases measured. Pathologic findings supported syndrome X as the underlying cardiac disease in all cases. CONCLUSIONS: These findings suggested a new clinical implication involving transient ST-segment elevation mimicking variant angina and normal coronary angiograms in patients with syndrome X. The major responsible site for this phenomenon was suggested to be coronary arterioles of less than 200 microm in diameter.

Acetylcholine↗
PubMed1984

Variant angina induced by alcohol ingestion.

We gave alcohol to 15 patients with variant angina to induce the attacks at the hospital. Anginal attacks were repeatedly induced in seven of them. Although the time lag between alcohol ingestion and the attacks varied widely among patients, from 1.5 to 12 hours, it was fairly constant in each patient. We carefully examined the histories of 101 patients with variant angina to become familiar with the relationship between alcohol ingestion and the attacks of angina. Seventy-one patients took alcohol in their daily lives. Nineteen of the 71 patients (26.8%) who took alcohol had a definite relationship between alcohol ingestion and the attacks. We conclude that alcohol induces anginal attacks or coronary artery spasm in not a small number of patients with variant angina.

Aged↗
PubMed2006

Variations in presentation and various options in management of variant angina.

Patients with variant angina represent a diagnostic and therapeutic dilemma. Variant angina is a disease with various causes, variations in treatment guidelines and variable prognosis. In an era of robotic cardiac surgery and automatic cardioverter defibrillators, it is regrettable that we lack enough information on the optimal management of this entity. Lack of randomised trials and a tendency for spontaneous remissions makes interpretation of results difficult. We review the pathophysiology, presentation and recent developments in medical and surgical management of variant angina. Literature is full of conflicting data and it is difficult to make specific recommendations.

Angina Pectoris, Variant↗
PubMed1996

Heart period variability in patients with variant angina.

To clarify how cardiac autonomic control is affected in variant angina, we analyzed heart period variability in 35 patients with variant angina and in 19 control subjects. Patients with variant angina were divided into 1-vessel (group S, n = 17) and multivessel spasm groups (group M, n = 18) according to the site(s) of ST elevation on the electrocardiogram during attacks. The 24-hour Holter electrocardiogram recorded 6 +/- 3 days after the treatment with calcium antagonist was analyzed to avoid the possible influence of spontaneous attacks. In 5 group M patients, the electrocardiogram recorded 1 month after the treatment was also analyzed. There was no difference in the number of spontaneous attacks between groups S and M. The standard deviation of all normal RR intervals (SDNN) and the percentage of differences between adjacent normal RR intervals >50 (pNN50) in variant angina were slightly but significantly lower than those in controls. There were no differences in other indexes between variant angina and controls. When the data were analyzed separately in groups S and M, averaged RR intervals (MN), SDNN, pNN50, high-frequency power, and low-frequency power in group M were significantly lower than those in group S and controls, and the ratio of low- to high-frequency power in group M was significantly higher than that in group S and controls. There was no difference in any index between group S and controls. All abnormal indexes in group M recovered to levels similar to those in controls 1 month after the treatment. In conclusion, depressed cardiac vagal control and sympathetic-dominant sympathovagal interaction were present in patients with variant angina, especially in those with multivessel spasm.

Aged↗
PubMed1984

Abnormal reflex vasoconstriction to cold stimulation in forearm of patients with variant angina.

The responses of the blood vessels of the forearm to cold pressor test and mental stress were examined in patients with variant angina and in control subjects. In response to cold pressor test, blood pressure, heart rate and forearm vascular resistance increased with statistical significance in both groups. Percentage changes in blood pressure and heart rate were not significantly different in patients and control subjects. Percentage change in forearm vascular resistance in patients with variant angina (120 +/- 101%) was significantly greater (p less than 0.05) than that in control subjects (47 +/- 26%). In response to mental stress, percentage change in forearm vascular resistance was -20 +/- 19% in patients with variant angina and -24 +/- 18% in control subjects and there was no significant difference in the two groups. We conclude that, in some patients with variant angina, not only the coronary artery but the forearm vessels show the abnormal reflex vasoconstriction and it may be postulated that it represents the generalized abnormality of vascular smooth muscle or of their neural control which exists in some patients with variant angina.

Adult↗
PubMed1999

Prognostic significance of the pattern of multivessel spasm in patients with variant angina.

Multivessel spasm in variant angina is believed to be a major prognostic factor. Three patterns of multivessel spasm have been detected: (1) spasm at different sites on different occasions (migratory spasm); (2) spasm sequentially affecting 2 different sites (sequential spasm); and (3) simultaneous spasm at more than 1 site (simultaneous spasm). The present study investigated the prognosis based on this factor for variant angina without fixed coronary stenosis and examined the influence of multivessel spasm on cardiac events. Twenty-six patients were diagnosed as having variant angina without fixed coronary stenosis using 12-lead 24-h ECG recording system and coronary cineangiography. These patients were followed up prospectively for 57.1+/-7.6 months. Of the 26 patients 13 had single-vessel spasm, 6 had migratory multivessel spasm angina, and 7 showed sequential and/or simultaneous multivessel spasm angina. The survival free of serious cardiac events and of all cardiac events was significantly lower for patients with sequential and/or simultaneous multivessel spasm than for those with migratory multivessel spasm (p<0.05, p<0.05), whereas for patients with migratory multivessel spasm the difference comparison with single-vessel spasm did not attain statistical significance (p = ns, p = ns). The results of this study suggest that there seems to be a high-risk subgroup (i.e., sequential and/or simultaneous multivessel spasm) among patients with variant angina.

Aged↗
PubMed1996

Sudden death during Holter electrocardiogram monitoring in a patient with variant angina.

We report a case of sudden death due to variant angina during Holter electrocardiogram (ECG) monitoring. The patient, a 60-year-old man, had been aware of chest discomfort lasting less than one minute at midnight 2 days earlier. Because variant angina or arrhythmia was suspected, Holter ECG monitoring was performed. The patient spent a whole day without a recurrence of chest pain before going to bed, but at midnight he developed sudden chest pain, and died immediately after taking a sublingual tablet of isosorbide-dinitrite. Analysis of the Holter ECG revealed ventricular fibrillation after several ventricular premature beats following ST-segment elevation in both the CM5 and NASA leads. This case shows that sudden death from variant angina may occur within a few days after the first onset, and also highlights whether priority should be given to making a definite diagnosis or giving treatment when variant angina is strongly suspected.

Angina Pectoris, Variant↗
PubMed1983

Pathogenesis of angina pectoris and role of nitrates in relief of myocardial ischemia.

The pathophysiologic mechanism of angina of effort has been understood for one and three-quarter centuries. However, the mechanisms underlying angina at rest are still largely unknown. Coronary spasm, whatever its mechanism, clearly causes Prinzmetal's variant angina. However, evidence that spasm is the cause of all angina at rest is wanting. Rather than spasm, it is suggested that most attacks may be the result of normal fluctuations in the tone of conductive coronary arteries in the presence of critical levels of organic obstruction. The nitrates both relieve coronary spasm and diminish normal coronary tone. They also affect the systemic circulation, so as to favorably influence the level of energy demand.

Angina Pectoris↗
PubMed1985

Catheter-induced spasm during spontaneous attack of variant angina.

The simultaneous occurrences of spontaneous spasm and catheter-induced spasm during coronary angiography were obtained in 3 patients. Catheter-induced spasm was seen in the right coronary artery in 3 patients: 1 patient had spontaneous spasm in the distal right coronary artery and 2 patients had spontaneous spasm in the proximal left anterior descending coronary artery. These findings suggest that patients with variant angina may be susceptible to mechanical induction of spasm.

Angina Pectoris, Variant↗
PubMedDate not supplied

Variant angina in an adolescent.

We describe a case of variant angina associated with acute myocardial ischemia in an adolescent presenting with severe chest pain and transient ST elevation. Subsequent cardiac catheterization revealed normal coronary anatomy, and the patient has been asymptomatic since discharge on calcium channel blockers. Variant angina is a rare cause of chest pain in adolescents.

Adolescent↗
PubMed2001

Increased QT dispersion in patients with Prinzmetal's variant angina and cardiac arrest.

OBJECTIVES: We sought to compare QT dispersion in patients presenting with Prinzmetal's variant angina complicated by cardiac arrest or syncope and patients with uncomplicated variant angina. BACKGROUND: Despite the usually benign course of treated Prinzmetal's variant angina, a proportion of vasospastic angina patients develop ventricular arrhythmias and sudden death in association with coronary spasm. Increased QT dispersion has been suggested to increase susceptibility to ventricular arrhythmias in patients with coronary artery spasm. METHODS: We studied 25 consecutive patients (mean age 58 years; 14 men) with classical Prinzmetal's variant angina and documented coronary artery spasm. None of the patients had coronary artery stenoses < or =40%. Five patients had suffered a documented cardiac arrest, two had recurrent syncope and 18 had no arrhythmic events or syncopal episodes. In all patients QT dispersion (QT maximum-QT minimum in every ECG lead) was measured on the baseline 12-lead electrocardiogram at study entry using a digitising board. RESULTS: Mean (+/-S.D.) QT dispersion of study patients was 62.3+/-19.5 ms. QT dispersion in patients with cardiac arrest and syncope (79.4+/-17.3 ms) was significantly higher compared to patients with no such events (56.3+/-16.9 ms), (95% CI 7.5-38.8, P=0.005). No significant clinical, biochemical or angiographic differences were found between patients with and those without cardiac arrest or syncope. CONCLUSION: QT dispersion is increased in patients with Prinzmetal's variant angina complicated by cardiac arrest and syncope compared to patients without such events. Increased QT dispersion may be both a substrate for sudden cardiac death and a marker of risk in patients with Prinzmetal's variant angina.

Adult↗