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PubMed2001

An anaphylactic reaction possibly associated with an intraoperative coronary artery spasm during general anesthesia.

We report a case of anaphylactic reaction occurring during general anesthesia that may have been accompanied by a coronary artery spasm. The present case and a review of the medical literature suggest that coronary artery spasm is evoked by common vasoactive mediators with anaphylactic reactions. Coronary artery spasm should be counted as a symptom of the cardiovascular manifestation of anaphylaxis. Clinicians should be aware of this possible complication when treating an anaphylactic reaction, especially in patients at risk for atherosclerosis. Early recognition of ST segment elevation is essential for diagnosis and treatment of coronary artery spasm.

Aged↗
PubMed2003

Wavelet transform analysis of heart rate variability to assess the autonomic changes associated with spontaneous coronary spasm of variant angina.

We used Wavelet transform (WT) to investigate whether variation in autonomic tone was associated with spontaneous coronary spasm in patients with variant angina by analysis of heart rate variability (HRV). Twenty-one episodes preceding ST-segment elevation were selected under Holter monitoring in 12 men and 3 women with variant angina. HRV indices were calculated at 10 second intervals with the continuous WT, and analyzed within 30 minutes preceding ST-segment elevation. High frequency (HF; 0.15 approximately 2.00 Hz) increased significantly during the 4 minutes prior to ST-segment elevation, low frequency (LF; 0.04 approximately 0.15 Hz) decreased significantly during the period from 10 to 5 minutes and increased significantly during the 2 minutes prior to ST-segment elevation, the LF/HF ratio decreased significantly during the period from 10 to 3 minutes and increased significantly during the 2 minutes prior to ST-segment elevation. The RR interval decreased significantly during the 2 minutes prior to ST-segment elevation. These results suggest that the acute variation in autonomic tone was associated with spontaneous coronary spasm in patients with variant angina. A reduction in sympathetic activity, then enhancement of vagal activity may play a key role in triggering the spontaneous coronary spasm, and the secondary activation of sympathetic activity may worsen the coronary spasm resulting in the attack.

Adult↗
PubMed2000

Hemifacial spasm due to a large distant ipsilateral posterior fossa meningioma.

A rare case of hemifacial spasm due to an ipsilateral foramen magnum/clival meningioma is described. Magnetic resonance imaging demonstrated that the tumor was located distant to the cranial nerve VII/VIII complex. Resolution of the ipsilateral hemifacial spasm was noted after complete resection of the tumor. The mechanism of hemifacial spasm was likely due to displacement and distortion of the brain stem from the lesion distant to the cranial nerve VII/VIII complex. In our review of the literature this is the first reported case of an ipsilateral posterior fossa meningioma causing hemifacial spasm from indirect mass effect.

Case Reports↗
PubMed1990

[Variant (Prinzmetal's) angina with diffuse coronary spasm without coronary sclerosis].

A 49-year-old man developed, over a period of three years, progressively more frequent nocturnal attacks of angina and palpitations. Exercise electrocardiogram was negative. 24-hour Holter monitoring revealed ventricular extrasystoles and tachycardia with ST segment elevations. The dominant left coronary artery, which was free of atherotic changes, went into diffuse spasm after ergonovine administration, accompanied by angina and ventricular extrasystoles. Registration of spontaneous ischaemia confirmed the diagnosis of variant (Prinzmetal) angina. Administration of twice daily 90 mg diltiazem retard and once daily 120 mg isosorbide dinitrate retard at night ended the spasms and with it the attacks of angina and the arrhythmias. This case illustrates that typical angina and ventricular tachyarrhythmias can be caused by spontaneous coronary spasms, even in the presence of normal exercise ECGs and coronary angiograms. If coronary artery spasms are not detectable by ECG, the ergonovine test may further the diagnosis.

Angina Pectoris, Variant↗
PubMed1981

Coronary-artery spasm immediately after myocardial revascularization: recognition and management.

We investigated coronary-artery spasm in six patents who had had unexpected hemodynamic collapse within two hours after cardiopulmonary bypass for myocardial revascularization. All six had profound hypotension and recurrent ST-segment elevation in electrocardiographic Leads II, III, and aVF. All had either normal or noncritical luminal irregularities of dominant right coronary arteries and more than 75 per cent occlusions in the left coronary circulation. Right-coronary-artery spasm, which was reversed after intracoronary nitroglycerin, was demonstrated angiographically in one patient; a patent right coronary artery was found at autopsy in another patient. Three patients died despite large intravenous doses of nitroglycerin. Two patients who had been unresponsive to intravenous nitroglycerin recovered after direct infusion of nitroglycerin into the right coronary artery. Coronary-artery spasm immediately after myocardial revascularization may cause circulatory collapse and death; although the spasm may be refractory to usual therapy, it may respond to intracoronary nitroglycerin.

Adult↗
PubMed1983

Cerebral arterial spasm--a controlled trial of nimodipine in patients with subarachnoid hemorrhage.

We enrolled 125 neurologically normal patients with intracranial aneurysms in a multi-institution, prospective, double-blind, randomized, placebo-controlled trial within 96 hours of their subarachnoid hemorrhage, to determine whether treatment with the calcium blocker nimodipine would prevent or reduce the severity of ischemic neurologic deficits from arterial spasm. A deficit from cerebral arterial spasm that persisted and was severe or caused death by the end of the 21-day treatment period occurred in 8 of 60 patients given placebo and in 1 of 56 given nimodipine (P = 0.03, Fisher's exact test). Analysis of the amount of basal subarachnoid blood on pre-entry CAT scans in patients with deficits from spasm showed that an increase in subarachnoid blood was not associated with a worse neurologic outcome among patients who received nimodipine, unlike the situation in patients given a placebo. There were no side effects from nimodipine. We conclude that nimodipine should be given to patients who are neurologically normal after subarachnoid hemorrhage in order to reduce the occurrence of severe neurologic deficits due to cerebral arterial spasm.

Adolescent↗
PubMed1988

Serotonin, atherosclerosis, and collateral vessel spasm.

Studies on animal models demonstrate that platelet products contribute to vascular spasm in ischemic syndromes and that this is reversible with administration of ketanserin and thromboxane synthesis inhibitors. Laboratory animals (dogs, rabbits, and rats) that had femoral artery ligations exhibited supersensitivity to serotonin within days in their collateral blood vessels. This supersensitivity lasted at least 6 months. The response to serotonin was reversed by ketanserin, but not by 5HT-1 antagonists. Supersensitivity does not extend to norepinephrine, and alpha blockers do not influence the response to serotonin. It appears that platelet activation by endothelial injury contributes to ischemia through blood vessel occlusion and vascular spasm. When platelet activation occurs in vivo, blood vessel occlusion and vascular spasm are reversible in part by using ketanserin or agents that block thromboxane synthesis or its action. Combining both classes of agents reverses spasm completely. These findings support existing evidence that platelet products contribute to vascular disease, and provide an approach to improved management with currently available pharmacologic agents.

Animals↗
PubMed1988

Coronary artery spasm in a transplant patient.

The mechanism of coronary spasm is poorly understood. We report a case of coronary artery spasm in a cardiac transplant patient. Pharmacologic testing indicated denervation of the patient's heart. Therefore coronary artery spasm may occur despite cardiac denervation. This case demonstrates that intact autonomic nervous system and cardiac innervation are not essential for coronary artery spasm.

Adult↗
PubMed2003

Cocaine-induced endothelin-1-dependent spasm in rabbit basilar artery in vivo.

Although cocaine-induced constriction of cerebral vessels may play an important negative role in the pathogenesis of cocaine-related stroke, the mechanism underlying the vasospasm remains unclear. This study investigated the role of endothelin-1 in mediating the spasm. Intracisternal cocaine infusion (10 microl/h via osmotic pump) into the cisterna magna of rabbits induced time- and concentration-dependent spasm. Maximal spasm was achieved with 100 microM cocaine infusate, and was observed as early as 0.5 days and reached a maximum at 2 days. Coinfusion of 100 microM cocaine with the endothelin receptor antagonist PD145065 (100 microM) prevented the spasm. Cerebral spinal fluid levels of cocaine and benzoylecgonine, a major cocaine metabolite, were below the limit of assay detection. This study demonstrates the novel finding that endothelin-1 mediates cocaine-induced cerebral vasospasm.

Animals↗
PubMed1993

Coronary artery spasm is a major cause of sudden cardiac arrest in survivors without underlying heart disease.

BACKGROUND: The role of coronary spasm in underlying disease-free patients who were resuscitated from sudden cardiac arrest remained uncertain. This study investigated the cause of cardiac arrest, and the etiologic and prognostic differences were compared between patients with underlying heart disease (group I) and those patients without underlying heart disease (group II). METHODS: Twenty-five survivors of sudden cardiac arrest were classified into two groups according to the presence or absence of underlying heart disease. To investigate the cause of cardiac arrest, we performed ergonovine testing and electrophysiologic study. Fifteen of the patients had underlying heart disease, while 10 did not. RESULTS: Electrophysiologic abnormalities were found in 13 of the 15 patients in group I. In group II, spontaneous attack of coronary spasm occurred in four patients during the observation period, and coronary spasm was induced in three of the remaining six period of 32 +/- 23 months, whereas no patients in group II had recurrence of sudden cardiac arrest at a median follow-up of 32 months (range, 10 to 72 months). CONCLUSIONS: Electrophysiologic study identified a potential cause in 13 of 15 patients with underlying heart disease. Coronary spasm was involved in the pathogenesis of sudden cardiac arrest in survivors without identifiable underlying heart disease.

Adolescent↗
PubMed1993

Platelet-derived growth factor is released into the coronary circulation after coronary spasm.

BACKGROUND: Platelet-derived growth factor (PDGF) is a potent mitogen for vascular smooth muscle cells and is implicated in the vascular response to injury and the pathogenesis of atherosclerosis. It is also a potent vasoconstrictor. METHODS: To examine whether acute myocardial ischemia increases the level of PDGF in the coronary circulation, we measured plasma levels of PDGF in the coronary sinus and the aortic root simultaneously in 14 patients with coronary spastic angina. These measurements were performed before and after the left coronary artery spasm induced by intracoronary injection of acetylcholine, and measurements were also taken in 15 patients with stable exertional angina before and after acute myocardial ischemia induced by rapid atrial pacing. Eleven patients with chest pain but normal coronary arteries and no coronary spasm served as controls. RESULTS: Plasma PDGF levels increased significantly (P < 0.01) from 274 +/- 28 pg/mL to 364 +/- 27 pg/mL only in coronary sinus after anginal attacks in the patients with coronary spastic angina. However, plasma PDGF levels in coronary sinus remained unchanged after these attacks in the patients with stable exertional angina (from 230 +/- 27 pg/ml to 247 +/- 28 pg/mL) and after intracoronary injection of acetylcholine in the control subjects. Plasma PDGF levels in aortic root remained unchanged in all three patient groups. CONCLUSIONS: PDGF is released into the coronary circulation after coronary artery spasm, and this may exacerbate coronary artery spasm.

Aged↗
PubMed2004

Repeated epicardial coronary artery endothelial injuries lead to a global spontaneous coronary artery spasm.

OBJECTIVES: This study was conducted to develop a spontaneous coronary spasm model. MATERIALS AND METHODS: Balloon endothelial denudation was carried out in the epicardial left anterior descending coronary artery (LAD) every 2 weeks, for a total of four times, in 12 pigs. Changes in the denuded site diameter and LAD blood flow caused by acetylcholine or serotonin were assessed before each denudation and at week 8. Blood pressure, electrocardiogram (ECG) from the LAD area and LAD blood flow were monitored continuously in conscious and unrestrained pigs. RESULTS: Spontaneous ECG ST depression with a decrease in LAD blood flow appeared at around 2 weeks. In accordance with this, 0.5 microg/kg acetylcholine induced similar ECG and LAD blood flow changes without denuded site narrowing, suggesting microvascular spasm. Thereafter, ECG ST depression or elevation by serotonin via a denuded site spasm was found after 6 weeks and spontaneous ECG ST changes due to epicardial coronary artery spasm were observed. CONCLUSION: Epicardial coronary artery endothelial injury may induce spontaneous vasospasticity in the downstream coronary microvessels as well as in the denuded portion, suggesting functional abnormality through the entire coronary arterial tree.

Acetylcholine↗
PubMed1991

Coronary artery spasm and vascular biology. Cholinergic constriction.

Coronary artery spasm is undoubtedly one of the causative factors of ischemic heart disease, particularly variant-type angina pectoris and myocardial infarction, but the disease mechanisms involved are still unclear. The present review describes the clinical background of coronary artery spasm in relation to ischemic heart disease, including a brief history of studies in this field, and also suggests future guidelines for experimental investigations based on the characteristics of coronary artery spasm, focusing particularly on data we have obtained in our laboratory from studies of cholinergic constriction. The pig may be a suitable animal in which coronary artery spasm could be provoked with cholinergic agents following endothelial denudation. The use of such large animals would allow the study of spastic arterial segments by various methods with angiographic confirmation. After endothelial denudation it is possible that phenotypic changes in cholinergic receptors might occur in smooth muscle cells, and that such changes might remain even after endothelial repair.

Acetylcholine↗
PubMed1981

Coronary and peripheral arterial responses to ergometrine in patients susceptible to coronary and oesophageal spasm.

Vascular responses to ergometrine were compared in groups of patients subject to coronary artery spasm, or oesophageal spasm, or neither. We measured the degree of diffuse narrowing at different coronary artery sites (not in spasm), and the rise in blood pressure. The data provide no evidence for a generalised sensitivity to alpha-adrenergic stimulation underlying either of these two clinical entities. The left main stem was narrowed significantly less than the three main branches of the coronary artery tree. The degree of diffuse coronary artery narrowing was not influenced by the presence or absence of minor (less than or equal to 50%) fixed stenotic lesions, nor by the initial calibre of the arteries. Ergometrine did not alter arterial lactate concentration or lactate extraction in the absence of coronary spasm.

Adult↗
PubMed1984

Unusual vasomotor coronary arterial responses after reversal of ergonovine induced spasm with glyceryl trinitrate.

Unusual vasomotor responses in the coronary arteries occurred in two patients after the administration of glyceryl trinitrate to relieve spasm induced by ergonovine maleate. In one patient after treatment with glyceryl trinitrate and despite dilatation of the adjoining segments a new severe reduction in diameter occurred distally to the segments of the right coronary artery where the ergonovine induced spasm developed. In the other patient the left anterior descending artery filled very slowly after the completely occlusive spasm of the right coronary artery had resolved with glyceryl trinitrate though the circumflex did not. These vasomotor changes were associated with chest discomfort and electrocardiographic abnormalities in both cases. These findings indicate that caution is needed when performing provocative tests even after the ergonovine induced spasm has been reversed with glyceryl trinitrate.

Adult↗
PubMed1985

Morphology of ambulatory ST segment changes in patients with varying severity of coronary artery disease. Investigation of the frequency of nocturnal ischaemia and coronary spasm.

The frequency and magnitude of objectively determined myocardial ischaemia during normal daily activities of patients with varying severity of coronary artery disease are unknown. Furthermore, the incidence of nocturnal resting myocardial ischaemia and frequency of coronary spasm in patients with normal coronary arteries and chest pain are also not known. One hundred consecutive patients with chest pain referred for coronary angiography were therefore investigated with exercise testing and ambulatory ST segment monitoring. Fifty two of 74 patients with significant coronary artery disease and six of 26 with no significant coronary narrowing had episodes of ST segment change during 48 hours of ambulatory monitoring. Two patients, one with normal coronary arteries and localised spasm and one with three vessel disease, had episodes of ST segment elevation, whereas all other patients had episodes of ST segment depression. The frequency, duration, and magnitude of ST segment changes were greater in patients with more severe types of coronary artery disease. Thus more than six episodes of ST segment change per day occurred in patients with two or three vessel disease or left main stem stenosis and in the only patient with coronary spasm and normal coronary arteries. Nocturnal ischaemia occurred in 15% of patients with coronary artery disease and was almost an invariable indicator of two or three vessel coronary artery disease or left main stem stenosis. Episodes of ST segment change occurred most commonly during the morning hours and least commonly during the night, in parallel with changes in basal hourly heart rates. The heart rate at the onset of ST segment change tended to be lower in patients with coronary artery disease than in those with normal coronary arteries. The duration of exercise to ST segment depression tended to be shorter in patients with more severe disease, but it could not predict patients with nocturnal myocardial ischaemia, left main stem stenosis, or coronary spasm, whereas ambulatory ST segment monitoring was able to identify most of these patients.

Activities of Daily Living↗
PubMed1986

Incidence of spasm at the site of previous successful transluminal coronary angioplasty: effect of ergometrine maleate in consecutive patients.

The incidence of coronary artery spasm at the site of previous successful angioplasty and its importance in leading to subsequent restenosis or recurrence of symptoms are unknown. Fourteen consecutive patients with single vessel coronary artery disease who had undergone successful percutaneous transluminal angioplasty were studied. All patients were given ergometrine maleate (ergonovine maleate) intravenously during repeat cardiac catheterisation six weeks to three months after angioplasty. Five patients demonstrated excessive luminal reduction (spasm) at the site of previous angioplasty that led to luminal stenoses ranging from 50% to 79%. Two of these patients developed chest pain and ST segment changes during ergometrine maleate provocation and they also showed maximal vasoconstriction. The remaining nine patients did not develop important luminal change at the site of angioplasty after ergometrine maleate. Ergometrine maleate administration resulted in less than or equal to 20% reduction in lumen diameter of adjacent apparently normal sections of the coronary arteries in all but two patients. At the site of previous angioplasty in the five patients with spasm, however, the lumen was constricted by a mean (SD) of 51 (12)%, whereas in the nine patients not demonstrating spasm mean reduction was 12 (7)%. Thus hypersensitivity to ergometrine maleate at the site of previous successful angioplasty was demonstrated in over a third of consecutive patients with single vessel coronary artery disease. The importance of this finding to long term results of coronary angioplasty needs to be investigated further.

Angioplasty, Balloon↗
PubMed1997

Distinct patterns of motor unit behavior during muscle spasms in spinal cord injured subjects.

Surface electromyograms (EMG) and force were recorded during repeated involuntary spasms of paralyzed triceps surae muscles of four men with chronic cervical spinal cord injury. The firing rates of 78 medial gastrocnemius (MG) motor units also were recorded intramuscularly with tungsten microelectrodes. Spasms typically involved a relatively rapid rise, then a more gradual fall in triceps surae EMG and torque. Motor unit firing rates either increased and then decreased with the spasm intensity (54%) or were relatively constant (26%), firing mainly at 2-10 Hz. The remaining units (20%) produced trains that included one or several doublets. Mean peak spasm firing rates were 18 +/- 9 Hz (mean +/- SD) for rate modulated units and 11 +/- 10 Hz for units with little or no rate modulation. Some motor units fired at rates comparable with those recorded previously during maximum voluntary contractions performed by intact subjects. Others fired at rates below the minimum usually seen when normal units are first recruited (< 6 Hz). Doublets (interspike interval < 10 ms) often repeated every 123-333 ms, or were interspersed in trains firing at low steady rates (< 11 Hz). This study shows that rate coding for many motor units appears to be similar whether descending motor input is intact or whether it has been reduced severely by spinal cord injury. In contrast, rate modulation in other units appears to depend mainly on voluntary motor commands.

Adult↗