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PubMedDate not supplied

Oculomotor paresis with cyclic spasms. A critical review of the literature and a new case.

Oculomotor paresis with cyclic spasms is a rare syndrome, usually noticeable at birth or developing during the first year of life. On a background of oculomotor paresis, spastic movements occur at regular intervals: about every second minute the lid is raised, the globe wanders toward midline, the pupil contracts, and accomodation increases. These spasms last from 10 to 30 seconds, and then give way again to paresis. Since this phenomenon was first described, opinions were divided about its mechanism and about the site of the responsible defect. Based on a quantitative analysis of a new case, and of all previously published reports, a new theory is proposed which can account for all features of the syndrome.

Adolescent↗

PubMed1986

Human leucocyte antigen and coronary artery spasm.

To elucidate possible genetic links in the pathogenesis of coronary artery spasm, we investigated the frequencies of human leucocyte antigen in 37 patients with variant angina and 236 unrelated healthy controls. We found no significant differences in human leucocyte antigen frequencies between the patients and the controls. These results may suggest that genetic factors in linkage disequilibrium with human leucocyte antigen may not be involved in the pathogenesis of coronary artery spasm.

Angina Pectoris, Variant↗

PubMed1989

Humoral regulation during cold-induced coronary arterial spasm.

Previous attempts to define the etiology of coronary arterial spasm have been focused on mechanisms such as autonomic nervous dysfunction and/or enhanced platelet activation. In the present study, humoral regulation was investigated in patients with vasospastic angina and scintigraphically documented transient myocardial perfusion abnormalities after a peripheral cold pressor test. Serial changes in angiotensin II, epi- and norepinephrine as well as thromboxane B2 (the stable derivate of thromboxane A2), and malondialdehyde were determined at baseline (I), immediately after 5 minutes cold water hand immersion (II), and following 10 minutes recovery (III). Angiotensin II and epinephrine remained unchanged during observation (I vs II, II vs III: P = NS). Norepinephrine was elevated after cold (I vs II: P less than 0.001) and normalized after 10 minutes (I vs III: P = ns). Thromboxane B2 and malondialdehyde increased continuously (I vs III: P less than 0.05 and I vs III: P less than 0.002, respectively). Further radiothin-layer chromatography results indicate an activation of platelet function during myocardial ischemia. Our results do not establish a cause-effect relationship but, together with other evidence, they may suggest that thromboxane A2 is unlikely to be the cause of spasm. It might, however, play an important role in the maintenance of vasoconstriction.

Angiotensin II↗

PubMed1991

Regional sympathetic denervation in von Recklinghausen's disease with coronary spasm and myocarditis.

Two patients with von Recklinghausen's disease presented with coronary artery spasm, transient high concentrations of norepinephrine, catecholamine-induced myocarditis, and regional sympathetic denervation of the heart that was assessed by I-123 metaiodobenzylguanidine scintigram. It is postulated that regional sympathetic denervation of the heart may precipitate both coronary artery spasm and catecholamine-induced myocarditis in susceptible patients with von Recklinghausen's disease.

Autonomic Nervous System Diseases↗

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↗

PubMed1993

Evidence in support of the spasm of resistance vessel concept of ischemic heart disease: an update in 1993.

The goal of this communication is to provide more evidence for the ischemic heart disease (IHD) component of the spasm of resistance vessel (S-RV) concept of IHD and other ischemic diseases. The S-RV concept of IHD is considered to be an alternate paradigm which challenges the accepted understanding of this disorder. The theory asserts that primary S-RV directly induces symptoms in IHD, and this position is in opposition to the accepted view that symptoms are induced directly by primary occlusions of epicardial arteries by coronary artery disease, spasm, and thromboses. The theory, if valid, should be useful in reducing the impact of IHD, as it generally is accepted that the correct appreciation of basic pathophysiological mechanisms helps ensure the most appropriate prevention and treatment of disease.

Angina Pectoris↗

PubMed1991

Progression of coronary atherosclerosis: is coronary spasm related to progression?

A total of 239 patients undergoing serial coronary angiography with a concomitant ergonovine provocation test were studied between July 1974 and June 1987. The progression of coronary artery disease was evaluated in relation to risk factors, especially coronary artery spasm. Patients were classified into three groups: 1) new myocardial infarction group (39 patients); 2) progression without infarction group (90 patients); and 3) nonprogression group (110 patients). To assess how risk factors and coronary spasm are related to the occurrence of new myocardial infarction and progression without infarction, 11 variables in the three groups were examined: age, gender, the time interval between the studies, fasting blood sugar, systolic blood pressure, diastolic blood pressure, smoking, serum cholesterol, triglyceride, uric acid and a positive response to the ergonovine provocation test. Multiple regression analysis selected three independent predictors of progression without infarction: cholesterol (p less than 0.01), systolic blood pressure (p less than 0.05) and a positive response to the ergonovine provocation test (p less than 0.001). Multiple regression analysis also selected three independent predictors of the occurrence of new myocardial infarction: fasting blood sugar (p less than 0.01), systolic blood pressure (p less than 0.05) and a positive response to the ergonovine provocation test (p less than 0.001). A positive response to the ergonovine provocation test was the strongest factor for occurrence of both new myocardial infarction and progression without infarction. To evaluate segmental arterial changes, 3,275 coronary artery segments were analyzed in the 239 patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Catheterization↗

PubMed1996

Basal release of endothelium-derived nitric oxide at site of spasm in patients with variant angina.

OBJECTIVES: The aim of this study was to investigate the basal release of nitric oxide at spastic sites in patients with variant angina. BACKGROUND: We previously reported that endothelium-dependent dilator responses to acetylcholine, substance P and bradykinin are preserved at the site of coronary artery spasm. However, it is not known whether the basal release of endothelium-derived nitric oxide is altered at the spastic site. METHODS: The effects of intracoronary N(G)-monomethyl-L-arginine (L-NMMA, an inhibitor of nitric oxide synthesis) at cumulative doses of 50, 100 and 200 micromol on basal coronary artery tone were investigated in eight patients with variant angina and normal coronary angiograms and in eight control subjects. The lumen diameters of large epicardial coronary arteries were assessed by quantitative coronary arteriography. RESULTS: Coronary spasm was provoked by the intracoronary administration of acetylcholine in all patients with variant angina. L-NMMA did not alter the arterial pressure and heart rate but significantly decreased the coronary artery diameter at spastic and nonspastic sites. Constrictive responses to L-NMMA were significantly greater (p < 0.01) at the spastic site (constriction by 200 micromol, 22+/-7%, mean +/- SD) than at the nonspastic site (10+/-7%). Constrictive responses to L-NMMA at the nonspastic site in patients with variant angina were comparable to those in the control subjects. CONCLUSIONS: These findings support the hypothesis that the basal release of nitric oxide may not be decreased at the spastic site in patients with variant angina.

Aged↗

PubMed1996

Sympathetic nerve activity in the spasm-induced coronary artery region is associated with disease activity of vasospastic angina.

OBJECTIVES: We assessed the relation between sympathetic nerve activity and disease activity of vasospastic angina. BACKGROUND: The autonomic nervous system has been proposed to play a key role in attacks of vasospastic angina. A unique feature of vasospastic angina attacks is periodic fluctuation, which complicates the assessment of disease activity. METHODS: Twenty-five patients with left anterior descending coronary artery (LAD) spasm were studied: 12 with recent onset of chest pain (group 1) and 13 free of angina for more than 3 months after discontinuing medication (group 2). Group 1 underwent iodine-123 metaiodobenzylguanidine (MIBG) imaging (in the active phase) and atropine-stress MIBG imaging early after diagnostic angiography, and repeat MIBG imaging when they were free of angina for more than 3 months with medication (in the stable phase). Group 2 also underwent MIBG imaging (in remission). On a bull's-eye map, quantitative analysis of percent uptake and washout rate of MIBG was performed regionally. RESULTS: In group 1 in the active phase, the washout rate of the LAD territory was significantly lower than the rates in the stable phase, in remission and during atropine-stress MIBG imaging. The regional washout rate of the territories of the right coronary artery and the circumflex artery in the active phase was also significantly lower than that during atropine-stress MIBG imaging. The washout rate of the LAD territory in the active phase was significantly lower than the rates of the other two regions. In contrast, there were no significant differences in the distribution of regional percent uptake in every image. A similar distribution of washout rate was observed among group 1 patients in the stable phase, in group 1 patients during atropine-stress MIBG imaging and in group 2 patients. CONCLUSIONS: The MIBG washout rate of the spasm-induced coronary artery territory changed according to the degree of disease activity. Thus, sympathetic nerve activity could reflect disease activity of vasospastic angina.

3-Iodobenzylguanidine↗

PubMed1990

Coronary artery spasm following coronary artery bypass grafting. Treatment with intracoronary ISDN followed by systemic intravenous nifedipine infusion.

Coronary artery spasm following coronary artery bypass grafting (CABG) has been described previously. The cause and underlying risk factors are mainly speculative and treatment therefore symptomatic. We present the successful management of this condition by administration of an intravenous Nifedipine infusion after intracoronary Isosorbide dinitrate (ISDN) had failed to relieve the spasm.

Angiography↗

PubMed1993

Relaxation responses of the coronary microcirculation after cardiopulmonary bypass and ischemic arrest with cardioplegia: implications for the treatment of postoperative coronary spasm.

Coronary arteriolar spasm may occur following cardiopulmonary bypass and ischemic arrest, resulting in impaired cardiac function. Because myocardial perfusion is principally regulated by the microcirculation, the in vitro effects of various clinically used vasodilating drugs on porcine coronary microvessels less than 200 microns in diameter were examined following cardioplegic arrest and reperfusion. After 1 hour of ischemic arrest using either crystalloid or blood cardioplegia solutions followed by 1 hour of reperfusion, microvessels were studied in a pressurized (40 mmHg), no-flow state, and imaged with a video tracking device. Vessels were preconstricted by 30% to 60% of their resting diameter using acetylcholine, and various vasodilatory agents were applied extraluminally. Responses to the beta-adrenergic receptor agonist isoproterenol and the nitrovasodilator sodium nitroprusside were minimally altered by either cardioplegia solution as compared to control. In contrast, relaxation responses to both the calcium channel antagonist nifedipine and nitroglycerin were diminished after ischemic arrest and reperfusion. Relaxation responses were similar with crystalloid or blood cardioplegia for all drugs tested. Despite its somewhat attenuated response, nifedipine remained the most potent vasodilator of those studied. It is concluded that (1) following ischemic arrest with either crystalloid or blood cardioplegia solutions, responses to sodium nitroprusside and isoproterenol were minimally altered, while responses to nifedipine and nitroglycerin were attenuated; (2) relaxation responses of coronary arterioles were not significantly different with either blood or crystalloid cardioplegia; and (3) despite a slightly decreased response after cardioplegia, nifedipine was the most potent vasodilator of coronary arterioles, and may be the best choice for treating postoperative coronary arteriolar spasm.

Animals↗

PubMed2006

Severe spontaneous three-vessel coronary artery spasm.

Coronary artery spasm is usually defined as a focal constriction of a coronary artery segment, reversible, and causing myocardial ischaemia by coronary blood flow restriction. Sometimes this condition is not focal and can compromise all the coronary tree. This is a very rarely described event. Generally, coronary vasospasm may occur spontaneously or induced, either physically by catheter, physiological manoeuvres (hyperventilation), or by pharmacological agents. It may also occur with or without underlying atheromatous coronary disease. The mechanism of coronary spasm remains unclear but endothelial dysfunction seems to be the main triggering factor in all causes.

Aged↗

PubMed1976

Prinzmetal's variant form of angina as a manifestation of alpha-adrenergic receptor-mediated coronary artery spasm: documentation by coronary arteriography.

In four patients with Prinzmetal's variant form of angina, the attack was induced by the combined administration of epinephrine (0.4 to 0.5 mg, given subcutaneously at 7:30 to 8:00 A.M.) and propranolol (40 mg. given orally at 5:00 A.M.). Selective coronary cinearteriography was done before, during, and after the attack with constant monitoring of the ECG and blood pressure. Severe spasm of the right coronary artery occurred at the proximal portion in association with ST-segment elevation in Lead III during the attack and disappeared with the subsidence of the attack in all of them. These results strongly suggest that severe spasm of a large coronary artery mediated by alpha-adrenergic receptors is responsible for the attack of Prinzmetal's variant form of angina.

Adult↗

PubMed2002

Coronary artery spasm and ventricular fibrillation after off-pump coronary surgery.

Native coronary artery or bypass graft spasm is a rare cause of acute myocardial infarction after coronary artery bypass grafting. This report presents angiographic documentation of native coronary artery spasm following successful multivessel off-pump coronary revascularization, which caused myocardial ischemia leading to inferior wall myocardial infarction and ventricular fibrillatory arrest.

Coronary Angiography↗

PubMed1997

Prevention of internal thoracic artery spasm.

Perioperative spasm of the internal thoracic artery is a common experience in coronary artery bypass grafting. We describe a simple method of harvesting the internal thoracic artery with improved ease of dissection that helps to prevent the arterial spasm.

Coronary Artery Bypass↗

PubMed1987

Calcium antagonist drugs in the treatment of coronary spasm, effort angina and hypertension.

The clinical use of calcium antagonist drugs in coronary artery disease preceded knowledge of the mechanism of their action. Basic research into their pharmacological actions and development of a wide range of compounds which block calcium entry into cells enabled clinicians to greatly expand the indications for their use. Thus the calcium antagonists were rediscovered and found to be potent anti-anginal drugs when used in adequate dosage for effort related angina. Knowledge of their potent relaxing action on vascular smooth muscle led to their use in coronary artery spasm. The exact trigger mechanism/s for spasm and the reason for enhanced vascular reactivity remain unclear, perhaps explaining the failure of specific antagonist therapy. Calcium antagonists acting nonspecifically inhibit both induced and spontaneous attacks of vasospastic angina. They may favourably influence the prognosis and are now drugs of first choice for this condition. The vasodilator action of these drugs has most recently been utilized to treat hypertension, with efficacy confirmed in many controlled trials. Unlike other vasodilators, the calcium antagonists reduce blood pressure without salt and water retention, and with mild or no stimulation of renin, aldosterone, or sympathetic nervous overactivity, and without postural effects. This spectrum of action makes them ideal therapeutic agents, and current guidelines are changing to include calcium antagonists as first or second line therapy.

Angina Pectoris↗

PubMed1999

Ventricular fibrillation induced by coronary spasm during noncardiac surgery.

We report two cases of ventricular fibrillation during noncardiac surgery. Although an emergency coronary angiogram showed no significant coronary stenosis, coronary artery spasm was induced by the intracoronary injection of acetylcholine. It is possible that ventricular fibrillation is caused by coronary artery spasm during noncardiac surgery in patients without overt coronary artery disease.

Aged↗

PubMed2002

[Coronary Spasm after Administration of Propranolol during Dobutamine Stress Echocardiography].

Dobutamine stress echocardiography, a highly useful and safe challenge test for myocardial ischemia, is being used increasingly. We report the case of a 37-year-old man with rest angina, repolarization abnormalities in precordial leads and normal coronary arteries who was referred for dobutamine-atropine stress echocardiography, which was negative for ischemia. However, after testing, upon injection of propranolol, the patient suffered chest pain associated with ST elevation and severe regional systolic abnormalities. After intravenous nitroglycerin administration, chest pain and electrocardiographic abnormalities disappeared quickly, and systolic motion became normal. This complication was interpreted as a coronary spasm. We discuss the causes for the spasm and the role that might have been played by the drugs employed.

Adrenergic beta-Antagonists↗