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At least 775 records · Page 43Linked to original sources
PubMed1980

Medical therapy of Prinzmetal's variant angina.

Medical therapy for Prinzmetal's variant angina has been treatment of the acute attack with sublingual nitroglycerin. Prophylactic therapy has been more difficult, utilizing long-acting vasodilators that are limited because of their short half-life and side effects when therapeutic doses are used. Alpha-adrenergic blockade has been effective in some patients but is frequently associated with intolerable side effects or apparent development of tolerance to the drug. Preliminary experience from a randomized double-blind trial of diltiazem, a new calcium antagonist, has demonstrated a 90% reduction in pain episodes, with many patients becoming pain-free on the 240-mg daily dose. These data and the lack of adverse side effects demonstrate a dramatically effective therapy for patients with coronary artery spasm.

Angina Pectoris↗
PubMed1989

[Variant angina due to deficiency of intracellular magnesium by anorexia nervosa].

A 51-year-old man who had a past history of gastric resection for medically uncontrollable gastric ulcer has loss of appetite that recurs periodically. And he has frequently presented spontaneous angina early in the morning since 1984. He was diagnosed as having variant angina by the documentation of typical ST elevation during anginal attack and also by showing coronary artery spasm (#2 and #12) during hyperventilation on coronary arteriography. A large quantity of calcium blocking agents and nitrates could not improve his symptoms. Lack of intracellular magnesium by loss of appetite was suspected from a daily excretion of urine magnesium (5.3 mEq) and magnesium tolerance test (56.7%). To confirm the effect of magnesium administration, the second coronary arteriography was performed. After magnesium sulphate (80 mEq, hourly) was injected, coronary artery spasm could not be induced by ergonovine. And orally magnesium oxide, calcium blocking agents and nitrates were started. Anginal attack disappeared with increasing urine magnesium.

Angina Pectoris, Variant↗
PubMed1993

[Successful documentation by coronary angiography of spontaneous simultaneous multivessel coronary spasm in a variant angina patient: a case report].

A 59-year old female who complained of chest discomfort was admitted to our hospital. Electrocardiogram (ECG) on admission and treadmill exercise test showed negative for ischemia. She underwent coronary arteriography. Initial angiography showed there was no significant coronary arterial stenosis. However, when we were preparing the spasm provocation test, she complained of the same kind of chest discomfort as she had felt before. We found that ST segment was elevated in both the anterior and inferior leads on the ECG. Coronary arteriography showed that severe spasm occurred in both the left anterior descending artery (Seg. 6) and the right coronary artery (Seg. 1). Heart rate decreased and electromechanical dissociation occurred. She temporarily lost consciousness. After cardiopulmonary resuscitation, she recovered and the elevation of ST segment returned on the ECG. This is the first case report which has documented spontaneous simultaneous multivessel coronary spasm by coronary arteriography.

Angina Pectoris, Variant↗
PubMed1982

Effects of calcium antagonists, especially nifedipine, on variant angina, resting angina, and unstable angina.

The effects of drugs were evaluated in 47 cases with variant angina (VA), 19 with resting angina showing ST depression (RA), and 84 with unstable angina (UA). In VA patients, calcium antagonists were effective in 87.1% of the cases, while other drugs were effective in 56.3%. The difference was statistically significant. In RA patients, calcium antagonists were effective in 80.0% of the cases and other drugs in 44.4%. Nifedipine was effective in all 5 cases with coronary stenosis of more than 75.0%. All cases of RA had multiple vessel disease and nifedipine was effective in 80.0% of the patients. Nifedipine was effective in 83.3% of VA cases showing ST elevation during an exercise test, and was particularly effective in all patients having attacks only at rest. The effects of nifedipine were confirmed in 83.3% of UA cases. These results indicate that calcium antagonists are effective in VA, RA, and UA.

Aged↗
PubMed1993

[A case of dual origin of the left anterior descending coronary artery from the left and right coronary arteries with variant angina].

We present a case of a 68-year-old male inflicted with a rare anomaly of the coronary artery. He had been suspected to have worsening effort angina and underwent urgent cardiac catheterization. The coronary angiography revealed 75% stenosis in the first diagonal branch. The left anterior descending artery was terminated in the mid portion and did not reach the apex. Instead, an anomalous coronary artery from the portion just proximal to the right coronary artery reached the apex. After cardiac catheterization, nocturnal chest pain at rest started to occur frequently. We suspected that vasospasm may have occurred because ST segment elevations in leads II, III, aVF were recorded on the electrocardiogram. Administration of diltiazem (120 mg per day) suppressed angina. Exercise stress electrocardiogram and thallium-201 myocardial scintigram did not show apparent ischemia. This case suggests that we must consider the presence of coronary vasospasm even in patients with clinically-supposed effort angina, to be possibly due to vasospasm occurring in anomalous coronary arteries.

Aged↗
PubMed1981

[Echocardiographic findings of variant angina (author's transl)].

Two-dimensional echocardiographic studies of left ventricular wall motion were performed in three patients with ergonovine induced variant angina, who were diagnosed by electrocardiography and/or coronary angiography. The two-dimensional echocardiogram during anginal attack demonstrated hypokinesis or akinesis of the left ventricular wall where ischemia was suspected by the electrocardiogram. This change in the wall motion occurred earlier than that of the electrocardiogram, and the abnormal wall motion in ischemic region returned to normal earlier than the electrocardiographic recovery after the attack. In some cases non-ischemic region showed hypokinesis probably because ergonovine caused coronary artery narrowing in a whole region including spastic region. With relief of the chest pain and restoration of ST segment elevation in the electrocardiogram following nitroglycerin administration, the left ventricular wall tended to be hyperkinetic on the echocardiogram.

Aged↗
PubMed1990

Anginal attack following a sodium bicarbonate and hydrocortisone injection.

A case of a 73-year-old man with variant angina who developed chest pain and shock following an injection of sodium bicarbonate and hydrocortisone is reported. The electrocardiogram (ECG) during the chest pain attack revealed ST elevation in leads II, III and aVF. It returned to a normal pattern 10 min later. Coronary angiography, performed 2 hours after the anginal attack, showed no significant coronary arterial stenosis. One month later, an injection of ergonovine (16 micrograms) into the right and left coronary arteries induced spasms in segments 4 and 13, with ischemic ECG changes. Possible causes of the anginal attack are a coronary arterial spasm induced by the allergic reaction to hydrocortisone and/or serum alkalosis due to the sodium bicarbonate injection triggered by hyperventilation.

Aged↗
PubMed1980

TQ segment (baseline) alternans during Prinzmetal's variant angina.

In a study of 93 patients who met criteria for Prinzmetal's angina, alternans of the ST segment was observed in 28 of 93 patients (30%). In 8 of these 28 patients, a hitherto undescribed variant of alternans, namely alternation (larger than or equal to 1 mm shift in 2:1 pattern) in the amplitude of the baseline or TQ segment (TQ Alt) was observed. In all eight patients serious ventricular arrhythmias were noted, namely, ventricular fibrillation in two, ventricular tachycardia in four, and multiform or advanced ventricular ectopic activity in eight. The TQ Alt developed only after ST segment alternans occurred. It is postulated that the alternations of the ST and TQ segments are due to differences in current flows due to inhomogeneity of depolarization and repolarization of the action potential caused by ischemia. Furthermore, the associated arrhythmias observed are related to the inhomogeneous state initiated by the ischemia.

Action Potentials↗
PubMed2004

Exercise-triggered transient R-wave enhancement and ST-segment elevation in II, III, and aVF ECG leads: a testament to the "plasticity" of the QRS complex during ischemia.

We describe a patient with coronary artery disease who showed transiently augmented R-waves in his electrocardiogram (ECG) during the course of an exercise treadmill test (ETT), an ECG pattern occasionally associated with the hyperacute phase of myocardial infarction and variant angina. This change in the R-waves was noted in II, III, and aVF ECG leads and was associated with ST-segment elevation; both changed gradually and were normalized during the recovery period. Cardiac enzymes after ETT were negative, and arteriography revealed 3-vessel coronary artery disease, with a completely occluded right coronary artery. The ventriculogram showed very mild hypokinesis of the inferior left ventricular wall, while the global ejection fraction was 75%. These ECG changes, noted previously during ETT in precordial ECG leads, are herein reported to occur also in II, III, and aVF ECG leads. The generation of these ECG changes, which hinges upon a late unopposed depolarization occurring in the course and at the site of severe ischemic injury, constitutes a transient focal ventricular conduction abnormality.

Adult↗
PubMed1992

[An analysis of the variability in the heart rate in relation to the presence of transient ischemia and to its physiopathological mechanism].

To assess the differences in the pathogenesis of cardiac ischemic events and the role of the autonomic nervous system, we studied the electrocardiographic measures of tonic vagal activity during 24-hour Holter monitoring. We tested the circadian rhythm of the power in the high frequency energy (HF: 0.15-0.40 Hz) of the normal R-R interval power spectrum, the daily percent of successive normal R-R greater than 50 ms (pNN50) and the roots mean square of successive difference of normal R-R intervals (MMSD) in patients with coronary artery disease of comparable angiographic severity. Group A consisted of 5 patients (mean age 62 +/- 8) with chronic stable angina and Group B of 5 patients (mean age 61 +/- 8) with variant angina. Characteristic anginal pattern, typical ST changes during ischemic events on Holter monitoring and angiographic evidence of vasoconstriction induced by hyperventilation distinguished the 2 groups. Mean Cosinor analysis showed the presence of a significant circadian rhythm of HF only in Group A with a peak in the early morning hours (phi at 03.45, % rhythm 50.0, p less than 0.03); a significant reduction of parasympathetic activation was also found in Group B (MSSD: 27.8 vs 15.4, p less than 0.05; pNN50: 2.9 vs 0.6, p less than 0.05). These results suggest a different pattern in circadian variation of HF and lower degree of time and frequency domain of heart rate variability, as a marker of vagal tone in patients with high susceptibility to coronary vasospasm.

Angina Pectoris, Variant↗
PubMed1981

Surgical therapy of variant angina associated with nonobstructive coronary disease.

Patients with variant angina refractory to medical therapy pose a difficult management problem. We report two patients with variant angina who had focal spasm in coronary arteries with fixed obstructions of less than 20% of the luminal diameter. Ischemic episodes were accompanied by malignant ventricular arrhythmias and third degree atrioventricular block. Symptoms were refractory to intensive medical management with nitrates and calcium blocking agents in one patient and with nitrates in the other who was treated before calcium blockers were available. Surgery was done; a bypass graft was placed distal to the area of focal spasm and the native artery was ligated proximally. Both patients are asymptomatic 24 and 66 months after surgery and neither takes anginal medication regularly. The surgical procedure outlined should be considered only if therapy to control life threatening ischemic symptoms with nitrates and calcium blocking agents fails.

Angina Pectoris↗
PubMed1983

Pre-infarction Prinzmetal's angina. A case report and review of the literature.

A 45-year-old White man presented with the classic history of Prinzmetal's variant angina, culminating in a transmural inferior myocardial infarction despite intensive treatment with continuous nitroglycerin infusion and the oral calcium antagonist nifedipine. During the frequent episodes of 'pre-infarction' Prinzmetal's variant angina intermittent second-degree atrioventricular heart block as well as ventricular tachycardia was witnessed, necessitating the insertion of a temporary transvenous right ventricular pacemaker. Selective coronary angiography performed approximately 1 week after the infarction in an attempt to elucidate the cause of continuing chest pain unresponsive to medication showed subtotal occlusion of the distal part of the dominant right coronary artery proximal to the origin of the artery to the atrioventricular node, while only very minor narrowings of the internal lumen were evident in the left coronary artery. The well-known angiographic features of a resolving intracoronary thrombus were visualized without any superimposed reversible coronary vasospasm. After catheterization the angina settled down and the patient was discharged on oral nifedipine and isosorbide dinitrate treatment. The place of coronary artery spasm in the pathophysiology of acute myocardial infarction, one facet of the clinical spectrum of ischaemic heart disease, is reviewed.

Angina Pectoris, Variant↗
PubMed1983

Exercise-induced cyclic episodes of S-T segment elevation in a patient with variant angina.

A unique case of variant angina is described in which cyclic S-T segment elevation was reproducibly induced by exercise. The treadmill test revealed cyclic S-T segment elevation to occur from the first minute onward, recurring with a cycle length of 2 min throughout the exercise while the work load was being increased. Similar cyclic episodes were also induced by the cold pressor test, and the ambulatory electrocardiogram demonstrated spontaneous episodes of S-T segment elevation with a similar cycle length in early mornings. Coronary arteriography revealed a fixed lesion in the mid-portion of right coronary artery with a 90% narrowing associated with coronary spasm leading to subtotal occlusion. The cyclic episodes were abolished by the administration of the calcium antagonist diltiazem. The spontaneous phasic activity of coronary arterial muscle is discussed as a possible cause or mechanism.

Angina Pectoris, Variant↗
PubMed1998

[Absence of induced spasm by intracoronary injection of 50 micrograms acetylcholine in the right coronary artery: usefulness of 80 micrograms of acetylcholine as a spasm provocation test].

This study investigated whether the maximal dose of 50 micrograms acetylcholine for the induction of coronary spasm in the right coronary artery is adequate. The acetylcholine test was performed in 388 consecutive patients to evaluate spasm from January 1994 to December 1997. Coronary spasm in the right coronary artery was induced in 43 patients, 37 men and 6 women with a mean age of 63 +/- 8 years by intracoronary injection of 80 micrograms of acetylcholine rather than 50 micrograms. These included 15 patients (35%) with rest angina, 23 patients with ischemic heart disease other than rest angina and 5 patients (12%) with non-ischemic heart disease. Acetylcholine was injected in incremental doses of 20, 50 and 80 micrograms into the right coronary artery. Positive spasm was defined as induction of more than 90% reversible narrowing associated with either usual chest pain or ischemic electrocardiographic changes. Clinical and angiographical characteristics was studied in these patients. Fifteen (35%) patients had rest angina and 4 patients had variant angina with ST elevation in the inferior leads. Two thirds of the patients had coronary spasm in the distal portion of the right coronary artery and one third of those disclosed spasm focally. Coronary spasm was induced in 38 (15%) of 246 patients with ischemic heart disease and in 5 (4%) of 142 patients with non-ischemic heart disease. The prevalence of positive spasm in patients with ischemic heart disease was significantly higher (p < 0.01) than in patients with non-ischemic heart disease. A dose of 80 micrograms of acetylcholine, more than the maximal standard dose, might be clinically useful for the induction of spasm in the right coronary artery if coronary spasm of this artery is strongly suspected.

Acetylcholine↗
PubMed1991

[A case of vasospastic angina: development of transient collateral circulation lessen the degree of myocardial ischemia during coronary artery spasm].

A 57-year-old man was admitted to our hospital because he had had attacks of chest pain at rest for more than a year, in spite of daily oral diltiazem (90 mg/day) and isosorbide dinitrate (15 m/day). The diagnosis of variant angina was made for him based on ST elevation in chest leads of the electrocardiogram during his first attack. However, one year later, the electrocardiograms during attacks showed only ST depression or T wave inversion in chest leads. The coronary arteriogram during spontaneous chest pain revealed that the left anterior descending artery was totally occluded at its middle portion, and that its peripheral portion was perfused by collateral circulation from the right coronary artery. The coronary arteriograms after administration of nitroglycerin were apparently normal, and no signs of collateral circulation were observed. These findings indicated that the transient collateral circulation could develop after repetitive coronary artery spasms even in the absence of significant coronary stenosis, and that it could lessen the degree of myocardial ischemia during coronary artery spasm.

Angina Pectoris, Variant↗
PubMed1979

The syndrome of variant angina culminating in acute myocardial infarction.

Ten patients 28-54 years old with recurrent attacks of variant angina (chest pain associated with transient ST-segment elevation) culminating in acute myocardial infarction were studied. Systemic blood pressure and heart rate remained unchanged or decreased during chest pain. Diagnosis of myocardial infarction was made on the basis of pathognomonic enzyme changes and T-wave inversions persisting for several weeks (seven patients) or development of Q waves (three patients). Complications were similar to the ones previously observed in conventional myocardial infarction. None of these patients died. Past history was characterized by absence of effort angina. Exercise stress testing after infarction was normal, and coronary arteriography revealed a spectrum of pathology, ranging from normal arteriograms to three-vessel disease. Intraaortic balloon pumping was ineffective in two patients, but subsequent coronary bypass surgery shortly after myocardial infarction was not followed by further attacks of chest pain. Follow-up of these patients revealed a benign course. Alcohol drinking and cigarette smoking appeared to be very prevalent in this group.

Acute Disease↗
PubMed1979

Inappropriate coronary vasoconstriction in patients with coronary artery disease: a role for nifedipine?

Coronary arterial vasoconstriction, well recognized in Prinzmetal's variant angina, may participate in the pathogenesis of classic angina as well. Several recent studies in patients with obstructive coronary artery disease suggest that apparently spontaneous reductions in coronary blood flow can result in myocardial ischemia and even infarction. Evidence supporting the alpha adrenergic nervous system as a cause of such coronary vasoconstriction is reviewed, particularly the results of provocative testing with the cold pressor stimulus. Upon exposure of the skin to cold, patients with coronary artery disease demonstrate an inappropriate coronary vasoconstrictor response, often sufficient to produce angina. Normal patients, by contrast, show no change in coronary vascular resistance. In patients with a diseases coronary circulation, inappropriate vasoconstriction further restricts myocardial perfusion and appears to be little affected by beta adrenergic blocking agents or nitrates in the usual dosages. Nifedipine has proved effective in preventing coronary arterial spasm in patients with Prinzmetal's angina. Studies currently in progress suggest that it is also effective in blocking inappropriate coronary vasoconstriction in patients with typical angina. Nifedipine may thus be a useful addition to the treatment of ischemic heart disease.

Angina Pectoris, Variant↗
PubMed1990

The dynamic changes of plasma tissue-type plasminogen activator level and the activity of its inhibitor during coronary vasospasm.

This study aimed to examine the dynamic changes of the fibrinolytic system during coronary vasospasm. Tissue-type plasminogen activator (t-PA), plasminogen activator inhibitor (PAI) and fibrinopeptide A (FPA) levels were measured in the great cardiac venous and arterial blood of 9 patients with clinically and angiographically proven vasospastic angina and 11 controls. Before ergonovine provocation, although there was no difference between the above 2 groups in t-PA levels in the aorta or the great cardiac vein, the PAI level in patients with variant angina was lower than in the controls both in the aorta (4.2 +/- 3.5 IU/ml vs 10.9 +/- 5.2 IU/ml) and in the great cardiac vein (2.3 +/- 2.9 IU/ml vs. 11.9 +/- 4.9 IU/ml). During ergonovine-induced coronary vasospasm in patients with variant angina, the t-PA level in the great cardiac vein significantly increased from 3.4 +/- 0.7 ng/ml to 4.4 +/- 0.5 ng/ml (p less than 0.05), but it did not change in the aorta. The maximal dose of ergonovine (0.4 mg) induced mild diffuse coronary vasoconstriction in the controls, and this diffuse coronary vasoconstriction induced a reduction of PAI levels in the great cardiac vein from 11.9 +/- 4.9 IU/ml to 9.5 +/- 4.8 IU/ml (p less than 0.05). FPA levels in the great cardiac vein did not change during ergonovine-induced coronary vasospasm in either group. Thus, the coronary vasospasm induced the release of t-PA from endothelial cells of coronary vessels and resulted in the reduction in the PAI activity in the great cardiac vein.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗