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At least 739 records · Page 41Linked to original sources
PubMed2005

Autonomic antecedents to variant angina exacerbation after beta-blockade withdrawal.

We describe a patient with nonsignificant coronary artery disease who experienced variant angina after beta -blockade withdrawal. Standard therapy with nifedipine and nitrates aimed at suppressing symptoms and typical transient ST-segment elevations was superseded by the reinstitution of metoprolol. The autonomic alternations before and after readministration of metoprolol were analyzed by time and spectral indices of heart rate variability (HRV). Metoprolol reduced the HRV and reversed the low-frequency/high-frequency power ratio toward a more physiological autonomic balance. We conclude that the reinstitution of beta -blocker acted protectively by preventing surges of sympathetic activity on an underlying basis of parasympathetic predominance.

Adrenergic beta-Antagonists↗
PubMed1993

Transient terminal U wave inversion as a more specific marker for myocardial ischemia.

Transient U wave inversion can be caused either by regional myocardial ischemia or by an elevation of systemic blood pressure. The characteristics of U wave inversion during chest pain attacks in 21 patients with variant angina were compared with those observed in 38 patients with hypertension without apparent ischemic heart disease. Differentiation was possible according to the ECG phase in which U wave inversion appeared. U wave inversion was considered to be significant if there was a discrete negative deflection of more than 0.05 mV within the TP segment. U wave inversion proceeded to positive deflection of U wave in patients with hypertension without ischemic heart disease (initial U wave inversion). In contrast, inverted U wave occurred after positive U wave deflection during attacks in patients with variant angina (terminal U wave inversion). When cold pressor test was performed in patients with variant angina during treatment with calcium entry blockers, no patient had either anginal attacks or ischemic ST-segment deviation, but 9 of 21 patients (43%) had transient initial U wave inversion, which was followed by positive U wave deflection. U wave inversion can be classified as initial U wave inversion and terminal U wave inversion according to the phasic relationship to positive U wave deflection; the latter is observed in association with regional myocardial ischemia. The former seems to be related to elevated blood pressure rather than to myocardial ischemia.

Adult↗
PubMed2006

Coronary artery stent placement as a treatment of acute coronary syndrome in course of variant angina.

High doses of calcium antagonists and nitrates are the treatment of choice in vasospasm angina when no stenosis or mild stenosis is present. In ca. 5-30% patients this kind of treatment is not effective. We present five cases of variant angina with acute coronary syndrome in patients despite standard pharmacological treatment. These patients also did not respond for intracoronary nitroglycerine injection. They were successfully treated with stent implantation in place of vasospasm. Our observations indicate that early enough interventional treatment prevent myocardial infarction. In one case in which stent placement was performed 12 h after clinical manifestation myocardial infarction with Q waves and enzymes release occurred. In others, accurately treated with stent implantation, coronary spasm did not produce myocardial damage. We did not see any clinical and biochemical evidence of myocardial infarction.

Angina Pectoris, Variant↗
PubMed1977

Sympathetic denervation in association with coronary artery grafting in patients with Prinzmetals' angina.

Myocardial revascularization in patients with Prinzmetal's angina has yielded variable results. Two patients are presented who underwent partial cardiac sympathectomy in combination with coronary artery grafting for typical variant angina associated with severe organic obstructive coronary artery disease. Late results 12 and 18 months postoperatively have been excellent in both instances as shown by clinical and angiographic evaluation. Although the exact mechanism responsible for Prinzmetal's angina is not known, it is believed that spasm through increased activity of vasomotor tone or of the autonomic nervous system plays a major role. Since this variant form of angina encompasses a whole spectrum at angiography, ranging from normal arteries to severely narrowed ones, including those with spasm, it is suggested that surgical treatment be planned accordingly. Thus, in patients who have organic stenoses with and without spasm, operative treatment may consist of removal of the preaortic or pretracheal plexus in association with conventional coronary artery grafting. In patients who have intractable episodes of ventricular arrhythmia or angina and who angiogram is normal or shows isolated spasm, coronary artery grafting should be abandoned, in view of the poor results reported in the literature in these circumstances, and cervicothoracic sympathectomy should be considered.

Adult↗
PubMed1989

Angiographic demonstration of spontaneous diffuse three vessel coronary artery spasm.

The spontaneous occurrence of diffuse three vessel coronary artery spasm was documented during routine coronary angiography in three patients with a history of variant angina. Quantitative angiographic analysis of 18 arterial segments demonstrated that the mean luminal diameter of 1.47 mm during spasm increased to 2.47 mm after the administration of nitroglycerin (p less than 0.0001). The underlying coronary arteries were normal or near normal. Although multivessel spasm has previously been considered to be uncommon and its spontaneous occurrence during angiography only rarely documented, these cases suggest that it may be more common than previously recognized. In addition to important diagnostic considerations, this phenomenon may have important implications regarding the pathophysiologic role of endothelium in coronary artery spasm.

Aged↗
PubMed1993

Correlation of basal coronary artery tone with constrictive response to ergonovine in patients with variant angina.

OBJECTIVES: This study was conducted to examine whether basal coronary artery tone is elevated at the spastic site in patients with variant angina and to determine the significance of basal artery tone in predicting provocation of coronary artery spasm. BACKGROUND: Previous data have been conflicting on whether basal coronary artery tone is elevated in patients with variant angina. METHODS: We assessed basal coronary artery tone by obtaining the percent increase in coronary artery diameter induced by nitroglycerin in 20 patients with variant angina and 24 control subjects. We also examined the correlation between basal coronary artery tone and the constrictive response to ergonovine. RESULTS: In the patients with variant angina in whom spasm was provoked by the lower doses (1 or 5 micrograms) of ergonovine, basal coronary artery tone was greater (p < 0.05) at the spastic site (54 +/- 15% or 36 +/- 16%, respectively) than at the nonspastic site (40 +/- 25% or 25 +/- 15%, respectively). Basal coronary tone at the nonspastic site in these patients was greater (p < 0.01) than that in control subjects (15 +/- 6%). In the patients with variant angina in whom spasm was provoked only by the higher doses (15 or 50 micrograms) of ergonovine, basal coronary artery tone was comparable at the spastic and nonspastic sites and was not different from that in control subjects. The diagnostic sensitivity and specificity of elevated basal coronary artery tone (> or = 40%) in predicting provocation of spasm were 26% and 98%, respectively. CONCLUSIONS: These results indicate that elevated basal coronary artery tone may be useful in predicting provocation of coronary spasm, but the normal level of basal coronary artery tone does not exclude such provocation.

Adult↗
PubMed1988

Increase of pulmonary vascular resistance during cold provocation in patients with variant angina.

This study was performed to evaluate pulmonary vascular reactivity in patients with angiographically documented coronary vasospasm. Right heart catheterization was performed in 8 subjects with vasospastic angina without evidence of Raynaud's phenomenon: heart rate, systemic and pulmonary arterial pressure as well as cardiac output were determined at rest, during cold provocation and after 20 minutes recovery. Data were obtained both before and during treatment with nifedipine. During cold provocation pulmonary vascular resistance was elevated significantly (P less than 0.02 compared with baseline); systemic vascular resistance tended to increase; nifedipine blunted both vasoconstrictor effects. Our results indicate an abnormal vascular response of the pulmonary arteries to cold provocation in patients with symptomatic coronary artery spasm and suggest a primary vasospastic disorder with coronary and pulmonary manifestation.

Adult↗
PubMedDate not supplied

Prevention of coronary spasms during aorto-coronary (A-C) bypass surgery for variant angina and effort angina with ST-elevation.

Aorto-coronary (A-C) bypass surgery was carried out in 15 cases of Prinzmetal's angina and effort angina with ST-elevation, commonly ascribed to coronary vasospasms. A-C bypass surgery is usually indicated for vasospastic angina when there are significant organic lesions of the coronary arteries. Fifty mg of verapamil was added to the priming solution for cardiopulmonary bypass, and A-C bypass surgery was successfully performed without the occurrence of perioperative coronary spasms even though severe episodes of spasm had been documented before surgery. However, four cases of vasospastic angina not receiving verapamil developed coronary spasms during or after A-C bypass surgery. It was concluded that administration of verapamil, a potent calcium entry blocking agent, is effective in preventing perioperative coronary vasospasms. Patency of the saphenous vein grafts bypassing the spasm-related coronary arteries was satisfactory.

Adult↗
PubMed1999

[An adrenaline-induced vasospasm as the form of presentation of variant angina].

A 41-year-old-man without previous ischemic heart disease, developed a severe anaphylactic reaction. After administration of epinephrine (0.5 mg) the patient complained of chest pain. The electrocardiogram showed an elevation of ST segment in inferior leads. Myocardial necrosis was ruled out. Coronary arteriography disclosed normal coronary arteries. Eight months later, the patient developed severe chest pain during physical activity. ST elevation was again seen in inferior leads. ECG changes disappeared, when sublingual nitroglycerin was administered. A diagnosis of vasospastic angina was made. Exercise test was negative, during treatment with calcium-blocking agents. The patient subsequently remain free of symptoms taking medication. The physiological mechanisms of vasospastic angina and precipitating factors are discussed.

Adult↗
PubMed1993

Vasotonic angina: a spectrum of ischemic syndromes involving functional abnormalities of the epicardial and microvascular coronary circulation.

OBJECTIVES: The present study was undertaken to investigate the response of large and small coronary arteries in a subgroup of patients with no or minimal coronary artery disease found to have objective signs of myocardial ischemia. BACKGROUND: Many patients apparently have normal coronary arteries despite abnormal electrocardiographic (ECG) changes during spontaneous anginal attacks or exercise stress testing. METHODS: Twenty-five patients with no or minimal (< 30% stenosis) coronary artery disease were chosen from a pool initially selected on the basis of spontaneous anginal attacks and ST segment shifts in the anterior leads. Of these, 10 were grouped as having variant angina (at least one episode of ST elevation) and the remaining 15 as having syndrome X (exercise-induced anginal pain, ST depression and reversible thallium abnormalities). Data were compared with those obtained in 10 patients with stable angina and documented coronary artery disease. Eighteen patients with supraventricular arrhythmias and normal coronary arteries served as control patients. Patients showing focal spasm during ergonovine testing were not included in the subsequent angiographic analysis. Great cardiac vein blood flow, aortic pressure and changes in coronary artery diameter were measured at rest and 2 to 4 min after hyperventilation in the remaining study group. The same procedure was repeated after sublingual administration of 0.3 mg of nitroglycerin in eight patients (four with syndrome X and four with variant angina). RESULTS: Hyperventilation induced diffuse epicardial coronary diameter reduction, which was marginal in control patients (9 +/- 4%) and those with coronary artery disease (5 +/- 3%) but severe (p < 0.001) in those with variant angina (28 +/- 14%) or syndrome X (25 +/- 13%). Concomitant determination of coronary blood flow showed significant (p < 0.001) decreases in those with variant angina (25 +/- 11%) and syndrome X (28 +/- 10%) but not in control patients (5 +/- 8%) or those with coronary artery disease (4 +/- 5%). Changes in great cardiac vein blood flow during hyperventilation were similar before and after nitroglycerin. CONCLUSIONS: These findings indicate that vasoconstrictor stimuli may trigger a diffuse abnormal response of both epicardial and resistance vessels in some patients with chest pain and angiographically normal coronary arteries. Patients showing such diffuse vasoconstrictor abnormalities are suggested to have a single pathogenetic entity with a spectrum of ECG manifestations ranging from ST depression to ST elevation.

Adult↗
PubMedDate not supplied

Physiopathological considerations on the arterial coronary spasm. Some diagnostic and therapeutical conclusions.

Starting from the cyclicity of the anginal attack in variant angina, the authors point out the role of alkalosis, besides the richness in alfa-adrenoceptors of the great coronary trunks. At the level of the muscular cell there is a competition between H+-ions and Ca++-ions. The diminution of H+-ions as a result of alkalosis brings about the penetration of Ca++ into the cell and the appearance of the coronary spasm. So, we worked out an original method for the provocation of the spasm (the cold and hiperpneea test) and an original therapeutical procedure (by acetozolamid). We present, herein the first results scored in 16 patients.

Angina Pectoris, Variant↗
PubMed1986

Problems related to the detection of myocardial ischemia caused by coronary vasospasm.

We compared the sensitivity of three commonly used provocative tests, exercise, ergonovine and the cold pressor test, in a series of 34 hospitalized patients with well-documented, active variant angina. All tests were performed off medication at the same time of day, usually on 3 consecutive days. Angina was provoked by ergonovine in all 34 patients, by exercise in 17 and by the cold pressor test in only 5 (p less than 0.005). ST elevation developed during the ergonovine test in 32 (94%), during exercise in 10 (29%) and during the cold pressor test in only 3 (9%). With ergonovine one patient had ST depression only and one had no ECG changes. During the cold pressor test two patients had pseudonormalization of abnormally negative T waves and 29 had no ECG changes. Exercise induced T wave pseudonormalization in 4 patients, ST depression in 9 others and no ECG changes in 11. Thus, in patients with active variant angina, the sensitivity of the cold pressor test and exercise are too low to be useful clinically. Other studies suggest that the sensitivity of hyperventilation or provoked alkalosis is higher, but not as high as ergonovine administration. In patients who have become asymptomatic, either with treatment or spontaneously, the sensitivity of all tests decreases markedly. If such patients no longer have coronary spasm, the test is not a 'false negative' but a 'true negative'. Deaths have been reported following ergonovine administration and for this reason the test is not universally accepted.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Increased plasma plasminogen activator inhibitor activity after coronary spasm.

To examine whether ischemic attack induced by coronary spasm changes fibrinolytic activity, we examined plasma levels of tissue-plasminogen activator antigen and plasminogen activator inhibitor activity before and after hyperventilation test in patients with variant angina and in control subjects. In 12 patients with variant angina, ischemic attack associated with ST-segment elevation on the electrocardiogram was induced by hyperventilation and plasma plasminogen activator inhibitor activity levels increased significantly 15 min after the attacks (pre, 5.1 +/- 0.8; immediately after, 5.8 +/- 1.1; and 15 min after, 7.2 +/- 0.9 IU/ml, P < 0.01). In 12 control subjects, plasminogen activator inhibitor activity levels did not change. Plasma tissue-plasminogen activator antigen levels did not change in both two groups. We conclude that coronary artery spasm increases plasma plasminogen activator inhibitor activity and that it may thereby lead to the coronary thrombus formation.

Adult↗
PubMed1980

Pathophysiology and treatment of coronary arterial spasm.

Spasm of a large coronary artery occurs most often from midnight to early morning and least often in the afternoon, due to the circadian variation of the tone of the large coronary artery in most patients with variant angina. Alpha adrenergic stimulation induces coronary spasm most easily in the early morning and least easily in the afternoon. Coronary spasm is due to strong contraction of coronary vascular smooth muscle cells which is triggered by an increase of intracellular calcium ions; hyperventilation plus TRIS-buffer infusion induces coronary spasm by decreasing hydrogen ions which antagonize the action of calcium ions. Administration of nitroglycerin promptly relieves the acute attack of coronary spasm, and calcium antagonists such as diltiazem, nifedipine and verapamil, which block the entry of calcium ions into coronary vascular smooth muscle cells and dilate large coronary arteries, prevent the occurrence of coronary spasm.

Adult↗
PubMed1993

Preserved endothelial function in the spastic segment of the human epicardial coronary artery in patients with variant angina--role of substance P in evaluating endothelial function.

This study aimed to determine whether or not endothelium-dependent vasodilation is preserved in spastic segments of human epicardial coronary arteries. Segmental responses of coronary arteries to substance P were examined in 30 patients with variant angina and in 10 patients with atypical chest pain using a quantitative angiographic technique. Coronary diameter at the basal state was matched between spastic and non-spastic segments in patients with variant angina, normal coronary arteries and with atypical chest pain (2.3 +/- 0.2 mm, 2.3 +/- 0.4 mm, 2.4 +/- 0.3 mm, respectively). In segments where vasospasm was induced by ergonovine and/or acetylcholine, changes in diameter in response to substance P did not differ from those in non-spastic segments; maximal dilation averaged 27.1 +/- 9.5% in the spastic segments and 24.4 +/- 9.6% in the non-spastic segments (expressed as a percent increase over the value before drug administration). It would appear that the potential of the endothelium to release endothelium-dependent relaxant factor (EDRF) and the vasodilator response to EDRF are preserved, even in spastic segments.

Acetylcholine↗
PubMed1981

Treatment of variant angina with drugs: a survey of 11 cardiology institutes in Japan.

Data from 11 cardiology institutes in Japan were examined to determine the effectiveness of drug therapy, especially with calcium antagonists, on variant angina. The subjects were 243 males and 43 females, most of whom were 40-59 years old. Coronary artery lesions were found in 92 of 162 patients (56.7%) in whom cinecoronary arteriograms were done. The efficacy rates of nifedipine, diltiazem and verapamil were 94.0%, 90.8% and 85.7%, respectively. Regardless of the presence or absence of organic coronary artery lesions, the drugs were effective in 92.3% of the patients with normal or nearly normal coronary arteries and in 82.6% of those with stenosis of more than 50% of the luminal diameter. These findings suggest that the drugs are effective through their antispasmodic actions.

Adrenergic beta-Antagonists↗
PubMed1995

Improvement of coronary vasomotion with eicosapentaenoic acid does not inhibit acetylcholine-induced coronary vasospasm in patients with variant angina.

Impaired function of the endothelium may be a mechanism of the coronary vasospasm induced by acetylcholine. We examined whether purified eicosapentaenoic acid (EPA), a major component of fish oil, improves the coronary vasomotion in response to acetylcholine, and the effect of purified EPA on acetylcholine (ACh)-induced coronary vasospasm in 22 patients with variant angina. ACh was infused into the coronary artery both before and after 4 months of EPA treatment (EPA 1.8 g/day, n = 12). In the control group (n = 10) that did not receive EPA, the response of the coronary diameter to ACh did not change over time. In the EPA-treated group, the cholinergic response in non-spastic sites changed from vasoconstriction to vasodilation, while ACh-induced coronary vasospasm persisted at the spastic sites. Therefore, EPA treatment improved the coronary vasomotor responsiveness to ACh, but did not inhibit ACh-induced coronary vasospasm.

Acetylcholine↗
PubMed1979

Prinzmetal's angina:reflex cardiovascular response during episode of pain.

Previous angiographic studies have shown that coronary spasm occurs in association with the variant angina described by Prinzmetal, confirming his original hypothesis. In this work we recorded the heart rate changes and the incidence of arrhythmias during variant angina. The patients were divided into two groups: anterior, with electrocardiographic signs of anterior ischaemia, and inferior, with changes in the inferior leads. There was a significant increase of heart rate during pain in anterior myocardial ischaemia and a significant decrease when the ischaemia was inferior. The incidence of ectopic arrhythmias during pain was significantly greater in patients with anterior ischaemia, but there was a high incidence of atrioventricular block in patients with inferior ischaemia. We suggest that these findings can be explained by different responses of the automatic nervous system to anterior and inferior acute myocardial ischaemia.

Adult↗