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PubMed1982

Role of coronary arterial spasm in sudden coronary ischemic death.

Sudden coronary death is a syndrome caused by different mechanisms, all of which should be separately considered with respect to preventive measures. Ventricular fibrillation, tachycardia, and complete atrioventricular block were repeatedly observed during ischemic episodes caused by spasm in both the presence and absence of anginal pain. Spasm is, therefore, a potential cause of sudden coronary death. In "variant" angina, which is a reasonably reliable indicator of coronary spasm, arrhythmias occur in about 25% of patients and tend to recur in the same patient. The severity of coronary atherosclerosis in patients who develop severe arrhythmias is quite variable and not dissimilar from patient who do not. Mortality is considerably higher in patients with severe disease, but fibrillation and death can occur also in patients with angiographically normal arteries. In these patients acute and long-term treatment with nitrates and slow channel blockers appears to give remarkable results. Prevention of arrhythmias in patients in whom arrhythmias are secondary to acute ischemic episodes caused by vasospasm should be attempted by preventing vasospasm.

Arrhythmias, Cardiac↗

PubMed1983

Coronary artery spasm induced in atherosclerotic miniature swine.

Angiographically demonstrable coronary artery spasm could be provoked repeatedly by giving intracoronary or intravenous injections of histamine to miniature swine with experimentally induced atherosclerotic lesions of the coronary artery. The spasm induced in this way subsided either spontaneously or after the administration of nitroglycerin and was prevented by a calcium antagonist or an agent that blocks histamine H1 receptors. This model, which suggests that atherosclerotic changes may be one of the primary factors in the occurrence of coronary artery spasm, should facilitate studies on the pathogenesis of this condition.

Animals↗

PubMed2004

Failure of intravascular ultrasound to identify the site of recurrent focal coronary spasm during stenting.

Focal coronary spasm is often associated with an area of mural plaque disease. This report describes a patient with recurrent severe coronary spasm unresponsive to medical treatment. Coronary arteriography and intravascular ultrasound identified a candidate area of minor coronary atheromatous disease but ergonovine provocation testing showed the spastic coronary segment to be distal to and distinct from this area. Coronary stenting of the site identified by ergonovine provocation testing was effective in relieving provoked and spontaneous spasm.

Chest Pain↗

PubMed1973

Arterial spasm and slowing of the cerebral circulation in the ischaemia of head injury.

Carotid angiograms of 33 patients who had died during 1968 and 1969 from blunt head injury were reviewed and assessed for evidence of arterial spasm and slowing of the cerebral circulation. Spasm was found in 57·5%, a prolonged circulation time in 57·5%, and a combination of both features in 42·4% of cases. In the same group of patients there was also a high incidence of ischaemic brain damage. There appeared to be some correlation between arterial spasm and ischaemic damage in the cerebral cortex, but none in the basal ganglia or in the white matter. There was no apparent correlation between a prolonged cerebral circulation time and ischaemic brain damage.

Adolescent↗

PubMed1994

Pathophysiology of hemimasticatory spasm.

Two patients aged 21 and 50 years presented with facial hemiatrophy and unilateral spasms of the masticatory muscles. Masticatory muscle biopsy showed normal findings in both patients and facial skin biopsy specimens only showed atrophy, although morphoea (localised facial scleroderma) had been diagnosed nine years previously in the second patient. The involuntary movements consisted of brief twitches and prolonged contractions clinically and electromyographically similar to those of hemifacial spasm and cramps. The jaw jerk and the silent periods were absent in the affected muscles. Direct stimulation of the muscle nerve and transcranial stimulation of the trigeminal root demonstrated slowing of conduction and after-activity due to autoexcitation. Observations in other reported cases and these two patients suggest that hemimasticatory spasm is produced by ectopic activity secondary to focal demyelination of the trigeminal motor nerve fibres. The proposed cause of the neuropathy is focal damage to the masticatory nerves caused by compression, possibly resulting from the deep tissue changes that occur in facial hemiatrophy.

Adolescent↗

PubMed1999

Cold pressure test producing coronary spasm, coronary thrombosis and myocardial infarction in a patient with IgM antibodies against Coxsackie B virus.

Several lines of evidence have shown that viral infections are capable of causing coronary spasm and precipitating or mimicking clinical myocardial infarction. Here we report the case of a 41-year-old woman with recurrent angina who was admitted to our hospital because of ventricular tachycardia. Laboratory examination revealed positive IgM titers against Coxsackie B virus. Coronary angiography showed normal coronary arteries, but following a cold pressure test severe spasm of all coronaries with thrombotic occlusion of the second marginal branch of the circumflex artery occurred. We conclude that coronary spasm should be clinically suspected in patients with chest pain and ventricular arrhythmia in combination with IgM antibodies against Coxsackie B virus. In these patients, a cold pressure test should be avoided, and antithrombotic and antispastic therapy is recommended.

Adult↗

PubMed1975

Effect of pentagastrin and gastric alkalinization on lower esophageal sphincter pressure in diffuse esophageal spasm.

The purpose of this study was to evaluate the effect of intravenous pentagastrin and gastric alkalinization on the lower esophageal sphincter (LES) pressure in seven patients with diffuse esophageal spasm as compared to nine normal controls. Intravenous injections of 0.2 and 0.4 mug pentagastrin/kg body weight increased LES pressure significantly more in patients than in control subjects (p less than 0.05, p less than 0.01). Following gastric alkalinization both groups showed increases in LES pressure, but these were significantly greater for patients with diffuse esophageal spasm (p less than 0.05) than for controls. The results of our study indicate that the LES in patients with diffuse esophageal spasm is supersensitive to pentagastrin and gastric alkalinization.

Esophageal Achalasia↗

PubMed2003

Evidence for protein kinase C-mediated activation of Rho-kinase in a porcine model of coronary artery spasm.

OBJECTIVE: We have recently demonstrated that protein kinase C (PKC) and Rho-kinase play important roles in coronary vasospasm in a porcine model. However, it remains to be examined whether there is an interaction between the two molecules to cause the spasm. METHODS AND RESULTS: A segment of left porcine coronary artery was chronically treated with IL-1beta-bound microbeads in vivo. Two weeks after the operation, phorbol ester caused coronary spasm in vivo and coronary hypercontractions in vitro at the IL-1beta-treated segment; both were significantly inhibited by hydroxyfasudil, a specific Rho-kinase inhibitor. Guanosine 5'-[gamma-thio]triphosphate (GTPgammaS), which activates Rho with a resultant activation of Rho-kinase, enhanced Ca2+ sensitization of permeabilized vascular smooth muscle cells, which were resistant to the blockade of PKC by calphostin C. The GTPgammaS-induced Ca2+ sensitization was greater in the spastic segment than in the control segment. Western blot analysis revealed that only PKCdelta isoform was activated during the hypercontraction. CONCLUSIONS: These results demonstrate that PKC and Rho-kinase coexist on the same intracellular signaling pathway, with PKC located upstream on Rho-kinase, and that among the PKC isoforms, only PKCdelta may be involved. Thus, the strategy to inhibit Rho-kinase rather than PKC may be a more specific and useful treatment for coronary spasm.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗

PubMed1981

Coronary arterial spasm in single coronary artery.

A 48-year-old man developed severe chest pain and became unconscious. Coronary cineangiography revealed single coronary artery of the type L2b by Sharbaugh and White. Ergonovine, 0.2 mg i.v., produced coronary arterial spasm in the right coronary artery. This case suggests that coronary arterial spasm might be a cause of sudden death in patients with single coronary artery. However, an association of single coronary artery and coronary arterial spasm might be coincidental.

Coronary Angiography↗

PubMed1990

Fibrinopeptide A is released into the coronary circulation after coronary spasm.

To examine whether acute myocardial ischemia activates the coagulation system and platelet activation in the coronary circulation, we measured plasma levels of fibrinopeptide A and beta-thromboglobulin in the coronary sinus and the aortic root simultaneously in 15 patients with coronary spastic angina before and after the left coronary spasm induced by intracoronary injection of acetylcholine and in 15 patients with stable exertional angina before and after acute myocardial ischemia induced by rapid atrial pacing. Fifteen patients with chest pain but normal coronary arteries and no coronary spasm served as controls. The coronary sinus-arterial difference of fibrinopeptide A increased markedly (p less than 0.001) from 0.1 +/- 0.2 to 4.3 +/- 0.7 ng/ml after the anginal attacks in the coronary spastic angina group. However, fibrinopeptide A levels remained unchanged after the attacks in the stable exertional angina group and after intracoronary injection of acetylcholine in the control group. Plasma beta-thromboglobulin levels remained unchanged after the attacks in both patient groups and after acetylcholine in the control group. Our data indicate that coronary spasm induces thrombin generation and may lead to thrombus formation in the coronary artery involved, but pacing-induced ischemia does not activate the coagulation system.

Angina Pectoris↗

PubMed1997

Enhanced myosin light chain phosphorylations as a central mechanism for coronary artery spasm in a swine model with interleukin-1beta.

BACKGROUND: Although coronary artery spasm plays an important role in a wide variety of ischemic heart diseases, the intracellular mechanism for the spasm remains to be clarified. We examined the role of myosin light chain (MLC) phosphorylations, a key mechanism for contraction of vascular smooth muscle, in our swine model with interleukin-1beta (IL-1beta). METHODS AND RESULTS: IL-1beta was applied chronically to the porcine coronary arteries from the adventitia to induce an inflammatory/proliferative lesion. Two weeks after the operation, intracoronary serotonin repeatedly induced coronary hyperconstrictions at the IL-1beta-treated site both in vivo and in vitro, which were markedly inhibited by fasudil, an inhibitor of protein kinases, including protein kinase C and MLC kinase. Western blot analysis showed that during serotonin-induced contractions, MLC monophosphorylation was significantly increased and sustained in the spastic segment compared with the control segment, whereas MLC diphosphorylation was noted only in the spastic segment. A significant correlation was noted between the serotonin-induced contractions and MLC phosphorylations. Both types of MLC phosphorylation were markedly inhibited by fasudil. In addition, MLC diphosphorylation was never induced by a simple endothelium removal in the normal coronary artery, whereas enhanced MLC phosphorylations in the spastic segment were noted regardless of the presence or absence of the endothelium. CONCLUSIONS: These results indicate that enhanced MLC phosphorylations in the vascular smooth muscle play a central role in the pathogenesis of coronary spasm in our swine model.

Animals↗

PubMed1994

Involuntary tonic spasms of a limb due to a brain stem lacunar infarction.

BACKGROUND AND PURPOSE: Although repetitive involuntary movements are a well-recognized manifestation of carotid occlusive disease, similar movements have not been reported with a lacunar infarction outside of the basal ganglia or subthalamic nucleus. We describe a man with tonic spasms associated with a lacunar infarction in the right ventral pons. CASE DESCRIPTION: Involuntary tonic spasms of a paretic limb developed acutely in a 69-year-old hypertensive man with a clinical presentation of pure motor hemiparesis. Magnetic resonance imaging demonstrated a lacunar infarction of the ventral pons. There was no evidence for carotid occlusive disease. An electroencephalogram recorded during the movements showed no abnormality. The abnormal movements responded well to treatment with oral diazepam. CONCLUSIONS: A brain stem lacunar infarction may be associated with involuntary tonic limb spasms clinically similar to those reported as paroxysmal symptoms of multiple sclerosis.

Aged↗

PubMed2001

Coronary artery spasm-induced paroxysmal atrial fibrillation--a case report.

Paroxysmal atrial fibrillation is described in a patient that was consistent with the clinical history developed after induction of coronary artery spasm. The mechanism appeared to be sinus node artery spasm inducing sinus node ischemia. Coronary artery spasm can be a cause of paroxysmal atrial fibrillation.

Atrial Fibrillation↗

PubMedDate not supplied

Provocation of microvessel spasm by low-dose acetylcholine in patients with suspected coronary artery disease--two case reports.

Endothelial dysfunction plays an important role in the pathogenesis of cardiac syndrome X, and intracoronary low-dose acetylcholine infusion is a widely used diagnostic modality for studying the coronary artery endothelial function. The authors herein report 2 cases of cardiac syndrome X with coronary artery endothelial dysfunction and microvessel spasm. The findings of non-invasive testing were positive for ischemia. Coronary angiograms appeared entirely normal in both cases. However, the intracoronary infusion of low-dose (1.5-15 microg/minute) acetylcholine demonstrated an impairment of the coronary blood flow response and consequently provoked an ST-segment elevation in an electrocardiogram. The coronary angiograms showed no spasm in the epicardial arteries. These patients are thus suggested to have cardiac syndrome X with microvessel spasms associated with coronary artery endothelial dysfunction.

Acetylcholine↗

PubMed1981

Acute myocardial infarction induced by ergotamine tartrate: possible role of coronary arterial spasm.

A 45-year-old woman with almost normal coronary arteries suffered from acute inferior myocardial infarction after taking 2 tablets (2.0 mg) of ergotamine tartrate for headache. She had had attacks of variant angina and spasm of the right coronary artery had been demonstrated during the attack. After the recovery from myocardial infarction the intravenous injection of ergonovine maleate 0.05 mg induced spasm of the right coronary artery again. We conclude that acute myocardial infarction in this patient was probably caused by coronary arterial spasm induced by ergotamine tartrate.

Angina Pectoris↗

PubMed1994

Alcohol and coronary spasm.

Alcohol is known to sometimes cause coronary spasm, the mechanism of which is still unknown. The authors monitored changes in plasma levels of prostanoids (thromboxane [TX B2], 6-keto prostaglandin F1 alpha [PGF1 alpha]), catecholamines (CA), serotonin (5-HT), cyclic nucleotides (cyclic adenosine monophosphate--cAMP, cyclic guanosine monophosphate--cGMP), and platelet aggregation after alcohol ingestion (Japanese rice wine 400 mL) in 8 patients with alcohol-induced variant angina and 8 healthy men as controls. Coronary spasm was confirmed to have been induced in 4 patients nine hours after alcohol challenge (VA[+]), when their plasma ethanol levels had already returned to a null level. Neither CA nor 5-HT levels showed any change after alcohol ingestion either in patients or controls, though controls showed high levels of CA during alcohol ingestion. TX B2 in VA(+) patients increased gradually after alcohol ingestion to reach up to a statistically significantly high level just before attack, as compared with those of controls and VA(-) patients, who, on the contrary, did not show such changes. The levels of 6-keto PGF1 alpha, however, which were significantly lower in patients than in controls before the test, exhibited a gradual increase in VA(+) patients in parallel with the increase in TX B2. No significant changes in cAMP levels between either controls or patients were present. On the contrary, cGMP levels had a gradual decrease in patients after alcohol ingestion. Especially six hours after alcohol ingestion, cGMP levels in VA(+) patients decreased so much as to make a statistically significant difference, as compared with the level in controls. Platelet aggregability in controls showed a decrease after alcohol ingestion, in spite of no change or even increase in patients. These data suggest that low levels of PGF1 alpha and the decrease of cGMP levels from alcohol ingestion play important roles in the mechanism of coronary spasm induced by alcohol ingestion.

6-Ketoprostaglandin F1 alpha↗

PubMedDate not supplied

Laryngeal spasm: a neurophysiologic redefinition.

Within the limits of standard neurophysiologic techniques, we have attempted to redefine laryngeal spasm as distinct from the glottic closure reflex. This distinction is based upon the observation that laryngeal spasm is solely mediated by the superior laryngeal nerve. Stimulation of other afferent nerves, capable of eliciting the glottic closure reflex, produces little adductor after-discharge activity that is characteristic of laryngeal spasm. In this regard, modification of output function from the adductor motoneuron aggregate by means of temporal and spatial summation of sensory input data has been described, and its characteristics further defined in response to varying ventilatory states and barbiturate levels.

Anesthesia, Intravenous↗

PubMed2006

Intracoronary adenosine triphosphate for refractory coronary artery spasm.

A 62-year-old woman underwent aortic valve replacement for aortic stenosis. Her hemodynamics deteriorated with ST-T depression 6 hours postoperatively. Emergency coronary catheterization showed diffuse right coronary artery spasm. The spasm persisted despite intracoronary infusion of nitrates and calcium antagonists. Intracoronary adenosine triphosphate infusion finally resolved the spasm and stabilized the cardiac function.

Adenosine Triphosphate↗