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PubMed1993

Variations in plasma endothelin concentrations during coronary spasm.

A provocation test using methylergometrine was carried out in patients with a normal coronary angiogram. Patients exhibiting spasm (Group 1, n = 6) were compared with non-spasm patients (Group II, n = 6). The endothelin concentration was determined in all cases at 0800, 1100, 1400, 1600, 1900, 2100, 2300 and 0100 h. The provocation test was carried out at 1700 h and an additional determination was made during spasm if the test was positive. The two groups had similar clinical characteristics and did not differ in terms of risk factors. Apart from the value recorded during spasm, the endothelin plasma level was significantly higher in Group I. A time x measurement interaction was noted in both groups, with a higher endothelin level in the morning. The endothelin level increased significantly during spasm in Group I patients. The plasma concentration of endothelin appeared to be higher in the basal state and during spasm in patients exhibiting spastic angina.

Adult↗
PubMed2000

Sarpogrelate, a selective 5-HT2A serotonergic receptor antagonist, inhibits serotonin-induced coronary artery spasm in a porcine model.

Serotonin is one of the most important vasoactive substances and has been implicated in the pathogenesis of coronary artery spasm and of acute coronary syndrome. We have recently demonstrated that local and long-term treatment with interleukin-1beta(IL-1beta) causes coronary arteriosclerotic changes and hyperconstrictive responses to serotonin in pigs in vivo. However, it remains to be examined which serotonergic (5-HT) receptor subtype mediates coronary spasm and whether alterations in serotonergic receptors are involved in the abnormality. In this study, we examined the inhibitory effect of sarpogrelate, a selective 5-HT2A serotonergic receptor antagonist, on the serotonin-induced coronary spasm as well as the possible alterations of serotonergic receptors in our porcine model. A segment of the porcine coronary artery was carefully dissected and aseptically wrapped with cotton mesh absorbing IL-1beta-bound microbeads from the adventitia. Two weeks after the procedure, angiographic study was performed, followed by binding assay for 5-HT1B and 5-HT2A serotonergic receptors and reverse transcription-polymerase chain reaction (RT-PCR) analysis for mRNA of those receptors. Angiographic study showed coronary vasospastic responses to serotonin at the IL-1beta-treated site. Sarpogrelate dose-dependently inhibited the serotonin-induced coronary spasm, but it did not affect the prostaglandin F2alpha-induced vasoconstriction. Radiolabeled receptor-binding assay showed that receptor affinity or receptor number of the 5-HT1B, or 5-HT2A receptors did not differ significantly between the spastic and the control sites. Furthermore, RT-PCR analysis showed that the expression of neither 5-HT2A nor 5-HT1B receptor mRNA was significantly altered at the spastic site. These results indicate that serotonin-induced coronary spasm is mediated primarily by 5-HT2A receptor in our porcine model, although the 5-HT2A receptor was not up-regulated, suggesting that alteration in the signal-transduction pathway for vascular smooth muscle contraction beyond the 5-HT2A receptor plays a primary role in the pathogenesis of coronary spasm in our porcine model.

Angiography↗
PubMed1975

The incidence and clinical implications of coronary artery spasm.

The total incidence of coronary artery spasm during coronary angiography has been reported to be between 0.26% and 0.93%. The rarity of this phenomenon has been invoked to minimize its clinical significance. Review of a one-year experience in our catheterization laboratory showed that coronary spasm occurred in eight of 274 coronary angiograms (2.93%). In three instances, spasm could not be ascribed to catheter tip irrigation, and was considered to be spontaneous. Since multiple factors during coronary arteriography might inhibit the occurrence of coronary spasm, it is believed that the incidence of spontaneous spasm may be higher than can be documented during angiography. Coronary spasm may have important clinical significance in various chest pain syndromes and greater methodical attention should be directed toward this phenomenon.

Adult↗
PubMed2003

Intravenous immunoglobulin as adjunctive therapy for juvenile spasms.

Intravenous immunoglobulin has been reported to be an effective treatment for infantile spasms. Juvenile spasms are electrically and clinically similar to infantile spasms but occur in a later age group. We retrospectively reviewed the charts of five children (aged 4.5-11.5 years) at our institution. Their primary seizure type was juvenile spasms and they were treated with a single inpatient course of intravenous immunoglobulin (400 mg/kg/day intravenously for 5 consecutive days) on an adjunctive basis. Seizure frequency was determined from parental reports. By 3 months after treatment, improvement (a 50-92% reduction in seizure frequency) was noted in four patients; sustained benefit was seen in three patients for up to 12 months. One patient showed no response at 3 and 6 months and had an increase in seizure frequency at 1 year. We conclude that single-course intravenous immunoglobulin can be effective as adjunctive therapy for juvenile spasms and that benefit can persist for many months. However, larger controlled, prospective clinical trials are needed to validate this unconventional treatment modality for specific seizure types such as juvenile spasms.

Anticonvulsants↗
PubMed1985

Clinical characteristics of coronary artery spasm: electrocardiographic, hemodynamic and arteriographic assessment.

We studied the clinical characteristics of 153 patients with angina pectoris associated with coronary artery spasm (CAS). The study was designed to investigate the relationship of CAS to ST segment deviation and to the site of fixed stenosis, and hemodynamic alteration during a spastic event. Analysis of coronary arteriograms and multilead electrocardiograms obtained simultaneously from 170 events of CAS by the use of radioluscent carbon-fiber electrodes resulted in 58 events with ST elevation which were related to total occlusion of major coronary arteries due to CAS; another 54 events with ST depression, in which the affected coronary arteries demonstrated severe but incomplete occlusion, or total occlusion but were visualized via collateral vessels; and remaining 58 events without ST deviation showing mild occlusion. The results indicate a close correlation between magnitude of CAS and ST segment deviation. CAS occurred at the site of pre-existing fixed stenosis including minor plaque defect in 133 patients and at apparently normal site in 20 patients. In the former group, only four patients had triple vessel disease, while 95 had nonsignificant fixed lesion. In the latter group, 10 patients had minor lesion distant from the site of CAS. Thus, CAS is closely related to fixed stenosis, which may have but a limited role as a cause of CAS. Hemodynamic measurements during spastic events were obtained from 49 patients including 41 events with spasm of the left anterior descending artery (LAD) and 21 events with spasm of the right coronary artery (RCA). The onset of an increase in left ventricular (LV) filling pressure and a reduction in LV dP/dt preceded ST segment deviation in all events. The first hemodynamic variable manifested in the spastic event was the reduction of LV contraction dP/dt in the majority of patients. The increase of LV filling pressure was greater in LAD spasm than RCA spasm (11 +/- 6 mmHg vs 7 +/- 4 mmHg, P less than 0.0125) and in events with ST elevation than with ST depression (11 +/- 5 mmHg vs 6 +/- 5 mmHg, p less than 0.001). Right ventricular functional impairment was mild in most patients during CAS. The study indicates that mechanical impairment precedes electrical impairment during CAS and that LAD spasm with ST elevation represents the most severe LV dysfunction.

Adult↗
PubMed1998

Familial evidence of vasospastic angina and possible involvement of HLA-DR2 in susceptibility to coronary spasm.

An association between genetic factors and susceptibility to coronary spasm has not been proven. Because we encountered 7 patients with familial occurrence of vasospastic angina (VSA) in 3 families, the association of a genetic factor with coronary spasm was assumed. HLA typing as one of the genetic markers was performed in the 3 families, and the affected members in each family were found to share a HLA haplotype, carrying both HLA-DR52 and DQ6. This raised the possibility that one of the susceptibility genes for coronary spasm is located in the HLA region. To assess this possibility, HLA typing was performed and compared in 110 patients with VSA but without a family history of VSA (VSA group) and 55 patients with chest pain syndrome (CPS group) as control subjects. All patients underwent a provocation test for coronary spasm, and spasm was angiographically documented in the VSA group but not in the CPS group. Of all HLA antigens, the frequency of only HLA-DR2 was significantly higher in the VSA group than in the CPS group (39.1% vs 18.2%, p<0.01). The result implied that HLA-DR2 is in linkage disequilibrium with a susceptibility gene of VSA and thus is possibly involved in susceptibility to coronary spasm in some patients with VSA.

Adult↗
PubMed1992

Importance of coronary artery spasm in alcohol-related unexplained syncope.

To examine the role of coronary artery spasm in patients with syncope after alcohol ingestion, we performed an intracoronary ergonovine provocation test in 7 male patients (39 to 73 years old, mean 54 years) with alcohol-related syncope which remained unexplained despite noninvasive cardiovascular and neurological examinations. No patients had structural heart disease or significant coronary artery stenosis. Ergonovine was continuously infused into each coronary artery at a rate of 10 micrograms/min for up to 5 min. Coronary artery spasm with ST-segment elevation was induced in 4 of 7 patients. Chest pain before syncope or history of chest pain were not present in 3 of 4 patients with a positive ergonovine test. Multivessel coronary artery spasm was induced in 3 patients. One patient presented with triple vessel coronary artery spasm progressing to near syncope as a result of profound hypotension and ventricular tachycardia during provocation. Coronary artery spasm was promptly relieved by intracoronary isosorbide dinitrate infusion. All patients with a positive ergonovine test were treated with calcium antagonist and did not experience syncope during follow-up. These results suggest that coronary artery spasm is one of the important causes of syncope after alcohol ingestion.

Adult↗
PubMed1975

Experimental cerebral vasospasm. Part 2: effects of vasoactive drugs and sympathectomy on early and late spasm.

The authors report the effects of vasoactive drugs and sympathectomy on experimental spasm using vertebral angiography. Papaverine and isoxsuprine injections into the vertebral artery released both early and late spasm. The antiserotonin agent, methysergide, adn the alpha adrenergic blocking agent, phentolamine, released early but not late spasm. In sympathathectomized dogs, early spasm was milder than in untreated dogs; however, late spasm was the same as in untreated dogs. The authors discuss an etiological difference between early and late spasm.

Animals↗
PubMed1978

An investigation with serial angiography into the evolution of cerebral arterial spasm following aneurysm surgery.

Serial postoperative angiograms were performed in 28 patients with intracranial aneurysms, 26 of whom had presented with a subarachnoid hemorrhage. The clinical state and intracranial pressure (ICP) were also measured. Angiograms were performed in the ward using a cannula, which was passed into the proximal external carotid artery via the superficial temporal artery. Measurements of the vessel diameters were made, with the preoperative angiogram as a baseline. Patients could be placed into one of five groups depending on the presence or absence of significant arterial spasm, the clinical state of the patient, and the normality or otherwise of the ICP. No patient's condition deteriorated without an elevated ICP and/or significant arterial spasm. The study shows that this spasm is usually associated with a poor clinical state if it reaches a maximum 8 to 12 hours after the operation, although the clinical deterioration is not apparent for a further 6 to 12 hours. Knowledge of the natural history of postoperative arterial spasm may allow earlier treatment of the spasm, which may be more successful than delaying treatment until clinical deterioration has occurred. The worth of the varied drugs proposed for the treatment of spasm may be assessed using this type of protocol.

Adolescent↗
PubMed1999

Evaluation of adjunctive intracoronary administration of acetylcholine following intravenous infusion of ergonovine to provoke coronary artery spasm.

A dilemma arises in patients with chest pain or other symptoms suggestive of coronary artery disease but without significant coronary artery stenosis or spasm even after the spasm provocation test by either ergonovine or acetylcholine. Incremental doses of intracoronary acetylcholine (up to 100 micrograms for left coronary artery and 50 micrograms for right coronary artery) were administered when intravenous infusion of ergonovine 0.4 mg showed negative results. A total of 39 patients were studied. Provocation test was performed because of chest pain suggestive of coronary artery disease (n = 19), atypical chest pain (n = 6), post balloon angioplasty status (n = 6), silent ischemia (n = 4), Adams-Stokes syndrome (n = 3), and dead-on-arrival (n = 1). Characteristics of chest pain indicated variant angina (n = 11), rest angina (n = 4), and effort angina (n = 4). No electrocardiographic evidence of ischemia was detected before this test in any patient. Spasm was induced in 23 patients (59.0%) with complete obstruction in 7 (30.4%), diffuse vasoconstriction (90-99%) in 14 (60.9%), and focal spasm in 2 (8.7%). The patients with chest pain showed the highest positive rate of 78.9%. Further, the patients with atypical chest pain and miscellaneous reasons also revealed positive rates of 33.3% and 42.9%, respectively. One ventricular tachycardia and 2 atrial fibrillations occurred but terminated spontaneously. This test is useful for detecting spasm in a variety of patients in whom intravenous ergonovine infusion fails to induce spasm.

Acetylcholine↗
PubMed1992

Prolonged asymptomatic catheter-induced left and right coronary artery spasm resistant to high dose of intracoronary nitroglycerin.

A 58-year-old woman, referred to our hospital to undergo invasive assessment of mitral valve stenosis, demonstrated prolonged asymptomatic catheter-induced left anterior descending and right coronary artery spasm during coronary arteriography. Coronary spasms were not associated with ECG and arterial blood pressure changes. Intracoronary injection of nitroglycerin (300 and 600 micrograms bolus) did not resolve coronary spasm. Coronary angiography, repeated 24 hours later using the same procedure and materials, did not show any evidence of coronary artery spasm. The present clinical case is interesting for 3 reasons. First, the presence of prolonged proximal double-vessel coronary spasm not associated with symptoms or signs of acute myocardial ischemia; second, the incapacity of high dose of intracoronary nitroglycerin to resolve the coronary spasm; third, the dramatic changes in the sensitivity of coronary artery to mechanical stimulation in different days.

Cardiac Catheterization↗
PubMedDate not supplied

[The angiographic diagnosis of vascular spasm in ruptured cerebral aneurysms].

The authors compared the results of qualitative and quantitative appraisal of arterial spasm according to the angiographic findings in 85 patients with the severity of their condition and neurological symptomatology in the acute period of rupture of a brain aneurysm. The spasm was diagnosed by quantitative appraisal in 80% and by qualitative appraisal in 72.9% of cases. Appraisal of the spasm in various periods after rupture of the aneurysm showed it to be most intense on the 9th-10th day. The vascular spasm (VS) was the main cause of the neurological symptomatology in the acute period of rupture of the aneurysm. Constriction of the arteries to 1.65 in quantitative appraisal of the spasm and its extension to 3-4 segments and more in qualitative appraisal were attended by diffused consciousness and stem and focal hemispheric symptomatology. Simultaneous use of both methods for VS appraisal makes it possible to evaluate its extension and the degree of arterial constriction and distinguish the most severe forms of spasm.

Adolescent↗
PubMed2004

[Intraoperative coronary spasm in non-cardiac surgery].

BACKGROUND: Cardiovascular events are one of the most critical perioperative complications. The purpose of this study is to investigate the clinical characteristics, effective treatments, and clinical outcome of intraoperative coronary spasm through a review of the published literature. METHODS: Reports of intraoperative coronary spasm were identified using the Medline database (1977-2000) or by manually searching the Journal of Anesthesia (1987-2000). The clinical characteristics of intraoperative coronary spasm were analyzed in the 56 patients who had developed coronary spasm during non-cardiac surgery. RESULTS: The mean patient's age was 58 +/- 13 years. The majority of patients were men (75%), Japanese (78%), and had no history of chest pain (75%). Regional anesthesia, vasopressors, alkalosis, hypotension, inadequate depth of anesthesia, and vagal stimulation were noted as major contributing factors. More than half of the patients showed severe hypotension and 30% developed cardiovascular collapse. However, coronary dilators, and nitrates in particular, were very effective for the treatment, and the clinical outcome was relatively good (one death and three cases of myocardial infarction). CONCLUSIONS: Intraoperative coronary spasm may develop in patients with no history of chest pain. Some of the intraoperative conditions themselves are potent vasoconstricting factors. Once coronary spasm occurs, immediate administration of a full dose of coronary dilators is recommended.

Age Factors↗
PubMed2006

[Effects of intra-coronary and intra-graft administration of nicorandil for coronary spasm after coronary artery bypass grafting].

Coronary artery spasm after coronary artery bypass grafting (CABG) is relatively rare, but when it occurs, it is fatal. In cases of circulatory collapse just after surgery, coronary spasm should be suspected, and immediate diagnosis by coronary angiography is necessary. We conducted a study to assess the clinical characteristics of coronary spasm after CABG and the usefulness of intra-coronary and intra-graft administration of nicorandil. Study subjects were 7 patients (6 men and 1 woman, mean age 60.4 years) in whom coronary spasm after CABG was diagnosed angiographically from January 1992 to December 2003. Off-pump CABG (OPCAB) had been performed in 2 patients. Despite continuous administration of nitroglycerin and diltiazem hydrochloride during surgery, sudden circulatory collapse occurred during surgery or within 24 hours after CABG in all 7 patients. All required mechanical circulatory support, and emergency coronary angiography revealed severe graft and native coronary spasms. Intracoronary and/or intra-graft administration of diltiazem hydrochloride or nitroglycerin was not very effective, however, administration of nicorandil was effective for vasodilatation. One patient suffered brain damage and died, but the other 6 patients recovered and were discharged without complication. In conclusion, intra-coronary and/or intra-graft administration of nicorandil appears to be useful for the treatment of coronary spasm after CABG.

Aged↗
PubMed2006

Perioperative coronary artery spasm in off-pump coronary artery bypass grafting and its possible relation with perioperative hypomagnesemia.

PURPOSE: We experienced 3 cases of serious perioperative coronary artery spasm in off-pump coronary artery bypass grafting (OPCAB). In consideration of the causes, we directed our attention to hypomagnesemia, one of the triggers of coronary artery spasm. This study was performed to confirm the tendency to hypomagnesemia in OPCAB. METHODS: First, we report 3 patients having severe coronary artery spasm immediately after OPCAB with consideration of the causes. Second, serial magnesium (Mg) value (xylidyl blue method, normal 1.9-3.1 mg/dl) was measured in 45 consecutive patients with OPCAB between April and October 2002, 1) before starting the operation, and 2) after the patient's entrance into the intensive care unit. RESULTS: Preoperative and postoperative values of Mg (mg/dl) were 2.1+/-0.3, 1.7+/-0.3, respectively (p < 0.01). Postoperative incidence of hypomagnesemia was as high as 89% of the patients (40 out of 45 patients). In this study and thereafter, we corrected hypomagnesemia with magnesium sulfate during and after OPCAB, and no perioperative coronary artery spasm occurred. CONCLUSION: Hypomagnesemia, one of the triggers of coronary artery spasm, is very common in OPCAB. We strongly recommend the correction of hypomagnesemia during and after OPCAB for the prevention of perioperative coronary artery spasm.

Adult↗
PubMed2006

[Brain activities during maximum voluntary clenching with and without soft splint in patients with hemimasticatory spasms by functional magnetic resonance imaging].

OBJECTIVE: Functional magnetic resonance imaging (fMRI) was used to detect the cerebral cortical somatotopy during maximum voluntary clenching with and without soft splint in patients with hemimasticatory spasms (HMS) and the central mechanisms of HMS and the rule of the splint therapy. METHODS: Four HMS patients were selected and the spasms sides were right in two cases and left in the other two cases. FMRI images were obtained on Elscint/GE 2.0 Tesla MR system. Block design was used and the movement pattern was the onset of spasms after maximum voluntary clenching with and without soft splint. The fMRI data were analyzed by SPM99 software. RESULTS: With the onset of spasms after maximum voluntary clenching, the activation of motor cortex in 3 HMS patients was found lateral dominance on the left side, and the other one showed bilateral activation. All the 4 patients were found activation in cingulate area. With the onset of spasms after maximum clenching wearing soft splints, the activation of motor cortex showed no lateral dominance on the left side, and 3 patients were not found activation in cingulate area. CONCLUSIONS: The changes of the activation in motor cortex and cingulate area during the onset of spasms after clenching with and without soft splint might be the central mechanisms of the rule of splint therapy, through which the soft splint might function in alleviating muscle pain.

Brain↗
PubMed2001

Thoracic spine spasms secondary to hemorrhagic intestinal ulcer.

A case of thoracic spine spasms secondary to a bleeding duodenal ulcer is presented. A 41-year-old male with 14-week history of thoracic spine spasm was treated with bed rest, spinal manipulation, physical therapy, medication, and a thoracolumbar brace. Subsequently, a provocative thoracic discogram performed at T9-T10 created periscapular pain and also reproduced the presenting thoracic spasms. Intradiscal electrothermal annuloplasty (IDET) was performed at the T9-T10 level, but without sustained relief. The patient presented to a spine center for evaluation. The diagnosis of thoracic discogenic disease was suspected. A second provocative thoracic discogram was performed and failed to reproduce his thoracic spasms. Three weeks after being referred to a chronic pain management physician, the patient presented to a local emergency room with hema-temesis. An endoscopic evaluation revealed a bleeding duodenal ulcer. Following medical treatment of the duodenal ulcer with a proton pump inhibitor the patient had complete resolution of his thoracic spasms. This represents the first reported case of thoracic spine spasms as an initial presenting symptom of a bleeding peptic ulcer.

Journal Article↗
PubMed1990

[Intraoperative coronary artery spasm--retrospective review of 10 cases].

Ten cases of intraoperative coronary artery spasm were reviewed retrospectively. Four cases were open heart surgeries, one was a surgery for aortic dissecting aneurysm, and the other five were abdominal ones. In the cases of open heart surgery under anesthesia with high dose fentanyl, coronary artery spasm occurred at weaning period from cardio-pulmonary bypass. In the cases of abdominal surgery, all under neuroleptanesthesia with continuous epidural block, coronary artery spasm occurred within one hour after the beginning or before the end of operation. In four of five abdominal surgeries, systolic blood pressure became less than 90 mmHg when coronary artery spasm occurred. Coronary artery spasm brought severe depression of myocardial contractility and life threatening arrhythmias by which weaning from cardiopulmonary bypass became difficult during open heart surgery. There was a case which required several hours before hemodynamics became stable also in abdominal surgery. It was suggested that general anesthesia with continuous epidural block could be a triggering factor of coronary artery spasm when hypotension and insufficient depth of general anesthesia are present simultaneously.

Aged↗