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PubMed2002

Warm water irrigation for dealing with spasm during colonoscopy: simple, inexpensive, and effective.

BACKGROUND: Colonic spasm can interfere with colonoscopy by hindering insertion of the colonoscope and by making polypectomy difficult, painful, and dangerous. Methods for dealing with colonic spasm include waiting for it to subside and administration of antispasmodic agents such as glucagon or hyoscyamine. Glucagon is expensive and hyoscyamine has side effects. This study evaluated an inexpensive technique, warm water irrigation, for overcoming colonic spasm during colonoscopy. METHODS: A prospective, randomized, controlled trial in a consecutive series of patients was conducted to compare warm water irrigation for relaxation of spasm with standard examination techniques. Patients in whom the sigmoid colon had been resected were excluded. In the test group, water from the hot water tap at approximately body temperature was instilled into the colon by means of the accessory channel of the colonoscope with a 30 mL syringe. Any irrigation, either for removal of stool or control of spasm, was performed with warm water in the test group and water at room temperature in the control group. After each colonoscopy, the level of pain experienced by the patient was recorded with a linear analog scale. RESULTS: Sixty-nine patients were randomized. The groups were similar with respect to gender distribution, age, and degree of spasm. There was no difference between groups for insertion time, total duration of colonoscopy, dose of midazolam administered, or frequency of severe spasm. Patients who had warm water irrigation had significantly less discomfort than control patients (median 2.0, interquartile range: 1-4 on a 10 point linear analog scale, vs. 4.0, interquartile range: 2-5). CONCLUSIONS: Although glucagon and hyoscyamine remain options for treatment of colonic spasm, the results of this study suggest that warm water is also effective. It has no side effects and costs practically nothing.

Aged↗
PubMed2000

Do cerebral potentials to magnetic stimulation of paraspinal muscles reflect changes in palpable muscle spasm, low back pain, and activity scores?

OBJECTIVE: Previous studies have shown that cortical-evoked potentials on magnetic stimulation of muscles are influenced by muscle contraction, vibration, and muscle spasm. This study was carried out to determine whether these potentials correlate with palpatory muscle spasm, patient symptoms, and disability in patients with low back pain. METHODS: A prospective observational study was performed on 13 subjects with a history of low back pain visiting an orthopedic hospital-based clinic. Patients were screened for serious pathologic conditions by an orthopedic surgeon. The patients were then evaluated for the presence of muscle spasm by one of the investigators who was blinded to the results of the evoked potential studies. Patients were asked to complete a low back pain visual analogue scale (VAS) and a Roland-Morris Activity Scale (RMAS). Cortical-evoked potentials were recorded with a magnetic stimulator placed over the lumbar paraspinal muscles with the patient in the prone position. The palpatory examination, VAS, RMAS, and the cortical potentials were repeated after 2 weeks of therapy commonly used to reduce muscle spasm. RESULTS: The patients demonstrated a significant decrease in low back pain VAS and RMAS scores after treatment compared with before treatment. There was a reduction in the amount of palpatory muscle spasm in 11 of 13 cases. The cortical potentials before treatment were attenuated compared with previously reported controls and showed a significant increase before and after treatment in the amplitude of these potentials with multivariate analysis of variance. There was significant correlation between the changes in cortical potentials after treatment and the changes noted in paraspinal muscle spasm and VAS and RMAS scores. CONCLUSIONS: This study confirms the previous report that the amplitude of cerebral-evoked potentials on magnetic stimulation of paraspinal muscles is depressed in the presence of palpable muscle spasm. The close correlation among these potentials, paraspinal muscle spasm, and clinical symptoms suggests that the measurement of muscle activity may be more important in the assessment of low back pain than is commonly accepted.

Adult↗
PubMed1997

Excitatory amino acid levels in cerebrospinal fluid of patients with infantile spasms.

Infantile spasm is an age-specific epileptic encephalopathy. Long-term intellectual outcome of affected infants remains poor. The pathogenesis of infantile spasms, as well as the development of mental retardation, remains unclear. Increased excitatory amino acid neurotransmission may play a role in neuronal dysfunction and epilepsy. To study the significance of cerebrospinal fluid excitatory amino acids in infantile spasms, we determined glutamate and aspartate concentrations in cerebrospinal fluid of 13 patients with infantile spasms and 13 controls. The aspartate level in cerebrospinal fluid of the patients with infantile spasms (968 +/- 416 nmol/l) was higher than the control group (426 +/- 272 nmol/l). No difference in the mean glutamate levels was found between the patients (966 +/- 395 nmol/l) and the controls (1135 +/- 594 nmol/l). The elevated aspartate levels in cerebrospinal fluid of the patients with infantile spasms might be secondary to change in metabolism of aspartate. Aspartate is an excitatory and neurotoxic neurotransmitter, which might have a role in triggering the spasms and the development of neuronal dysfunctions in the patients with infantile spasms.

Aspartic Acid↗
PubMed2004

Smooth muscle cell-extrinsic vascular spasm arises from cardiomyocyte degeneration in sarcoglycan-deficient cardiomyopathy.

Vascular spasm is a poorly understood but critical biomedical process because it can acutely reduce blood supply and tissue oxygenation. Cardiomyopathy in mice lacking gamma-sarcoglycan or delta-sarcoglycan is characterized by focal damage. In the heart, sarcoglycan gene mutations produce regional defects in membrane permeability and focal degeneration, and it was hypothesized that vascular spasm was responsible for this focal necrosis. Supporting this notion, vascular spasm was noted in coronary arteries, and disruption of the sarcoglycan complex was observed in vascular smooth muscle providing a molecular mechanism for spasm. Using a transgene rescue strategy in the background of sarcoglycan-null mice, we replaced cardiomyocyte sarcoglycan expression. Cardiomyocyte-specific sarcoglycan expression was sufficient to correct cardiac focal degeneration. Intriguingly, successful restoration of the cardiomyocyte sarcoglycan complex also eliminated coronary artery vascular spasm, while restoration of smooth muscle sarcoglycan in the background of sarcoglycan-null alleles did not. This mechanism, whereby tissue damage leads to vascular spasm, can be partially corrected by NO synthase inhibitors. Therefore, we propose that cytokine release from damaged cardiomyocytes can feed back to produce vascular spasm. Moreover, vascular spasm feeds forward to produce additional cardiac damage.

Alleles↗
PubMed2003

Prospective preliminary analysis of the development of autism and epilepsy in children with infantile spasms.

The objective of this study was to compare the efficacy of corticotropin (ACTH) versus vigabatrin in treating infantile spasms and to determine which medication has a more favorable long-term outcome in terms of cognitive function, evolution of epilepsy, and incidence of autism. Patients with infantile spasms were included in the study if they were 3 to 16 months old, had hypsarrhythmia, and had no previous treatment with vigabatrin or corticosteroids. Patient evaluation included electroencephalographic and psychometric measures before and after treatment. Patients were stratified based on etiology (idiopathic or symptomatic) and sex and then randomized between the ACTH and vigabatrin treatment groups. Each of the treatment groups received either ACTH or vigabatrin for 2 weeks. At the end of 2 weeks of treatment, patients were considered responders if spasms and hypsarrhythmia resolved. Nonresponders were crossed over and treated with the alternate drug. Nine patients were included in the study. Three patients received ACTH, one of whom was a responder. Six patients received vigabatrin, three of whom were responders. The five nonresponders received both therapies. All patients had some degree of developmental plateau or regression before the initiation of treatment. Four patients with idiopathic infantile spasms showed improved cognitive function following treatment. The remaining five patients remained significantly delayed. Five patients with symptomatic infantile spasms had epilepsy following treatment; three of them were in the autistic spectrum. The small number of infants in this pilot study is insufficient to determine which of the two drugs is more effective. However, the following trends were identified: vigabatrin may be more effective for patients with symptomatic infantile spasms; patients with idiopathic infantile spasms tend to have a better cognitive outcome; and patients with symptomatic infantile spasms tend to develop both epilepsy and autism.

Adrenocorticotropic Hormone↗
PubMed1991

The epidemiology and natural history of infantile spasms.

Few population-based studies of infantile spasms have been done, and most reports have not included comparison groups. In spite of these limitations, this review attempts to summarize what is known about the distribution, etiology, and natural history of infantile spasms in populations; discusses the limitations of current data; and includes suggestions for further population-based research. Most estimates of the incidence of infantile spasms are between 0.25 and 0.42 per 1000 live births per year. Among children less than 10 years of age, the annual prevalence of infantile spasms is 0.14 to 0.19 per 1000. The peak age at onset of spasms is 4 to 6 months, and there appears to be a slight excess of male cases. The etiology of infantile spasms is unknown for 40% to 50% of affected children. Selected syndromes (eg, Aicardi syndrome, Down syndrome, etc) and inherited disorders (eg, tuberous sclerosis) may account for as many as one third of cases. Other factors, such as intrauterine infection, "birth injury," and head trauma have not been systematically evaluated, and thus, their contribution to the etiology of infantile spasms is uncertain. Areas for future etiologic research include controlled studies of immunologic factors and in utero and postnatal infections and further exploration of the interrelationship between infantile spasms and Lennox-Gastaut syndrome.

Cross-Cultural Comparison↗
PubMed2004

Practice parameter: medical treatment of infantile spasms: report of the American Academy of Neurology and the Child Neurology Society.

OBJECTIVE: To determine the current best practice for treatment of infantile spasms in children. METHODS: Database searches of MEDLINE from 1966 and EMBASE from 1980 and searches of reference lists of retrieved articles were performed. Inclusion criteria were the documented presence of infantile spasms and hypsarrhythmia. Outcome measures included complete cessation of spasms, resolution of hypsarrhythmia, relapse rate, developmental outcome, and presence or absence of epilepsy or an epileptiform EEG. One hundred fifty-nine articles were selected for detailed review. Recommendations were based on a four-tiered classification scheme. RESULTS: Adrenocorticotropic hormone (ACTH) is probably effective for the short-term treatment of infantile spasms, but there is insufficient evidence to recommend the optimum dosage and duration of treatment. There is insufficient evidence to determine whether oral corticosteroids are effective. Vigabatrin is possibly effective for the short-term treatment of infantile spasm and is possibly also effective for children with tuberous sclerosis. Concerns about retinal toxicity suggest that serial ophthalmologic screening is required in patients on vigabatrin; however, the data are insufficient to make recommendations regarding the frequency or type of screening. There is insufficient evidence to recommend any other treatment of infantile spasms. There is insufficient evidence to conclude that successful treatment of infantile spasms improves the long-term prognosis. CONCLUSIONS: ACTH is probably an effective agent in the short-term treatment of infantile spasms. Vigabatrin is possibly effective.

Administration, Oral↗
PubMedDate not supplied

[Costs and efficacy of type A botulinum toxin for the treatment of essential blepharospasm and hemifacial spasm].

PURPOSE: To evaluate the costs and efficacy of type A botulinum toxin in the treatment of essential blepharospasm and hemifacial spasm. METHODS: Pacients with essential blepharospasm and hemifacial spasm had their files analyzed. All patients were treated with type A botulinum toxin (Dysport) between April 2002 and May 2004 at the Oculoplastic Clinics of "Santa Casa de São Paulo". Twenty-seven patients presented essential blepharospasm and 23 presented hemifacial spasm. Information about the patient's degree of satisfaction after treatment, complaints and personal costs were recorded by a questionnaire, and information about the costs of Dysport treatment were obtained at the administration department of "Santa Casa de São Paulo". Wilcoxon and Mann-Whitney tests were used for statistical analysis. RESULTS: 1- The annual treatment costs were R Dollars 1,239.32 for essential blepharospasm and R Dollars 661.72 for hemifacial spasm. 2- The patient's annual costs were R Dollars 145.48 for essential blepharospasm and R Dollars 6.07 for hemifacial spasm. 3- The hospital's annual costs for the treatment were R Dollars 1,095.84 for essential blepharospasm and R Dollars 535.65 for hemifacial spasm. 4- Dysport treatment is successful in both essential blepharospasm and hemifacial spasm. CONCLUSIONS: The costs of essential blepharospasm and hemifacial spasm treatment with Dysport are high, mainly because of the toxin price. On economic analysis of health, we can conclude that this procedure has an excellent cost-benefit ratio.

Aged↗
PubMed2001

A risk-benefit assessment of treatments for infantile spasms.

Infantile spasms are a devastating epileptic encephalopathy of the young child. The continuing spasms and hypsarrhythmia have a deleterious effect on brain maturation and further cognitive development. Corticotropin (adrenocorticotropic hormone) or corticosteroids have been the gold standard treatment for the last 40 years, but there is little agreement on the best agent to use, or the dosage and duration of the treatment. Despite this empirical approach, corticotropin or corticosteroids are effective in controlling spasms and normalising electroencephalograms in about 60% of cases. The major concern with this treatment is the occurrence of frequent and severe adverse effects. The introduction of vigabatrin in the 1990s improved the outcome of infantile spasms. Vigabatrin shows an efficacy at least equal to that of corticosteroids, and even higher in specific groups such as those with tuberous sclerosis. The major advantages of vigabatrin are the ability to initiate treatment at the full dosage. rapid efficacy, suitability for outpatient treatment and particularly good tolerability with only minor adverse effects. Recently, however, the safety of vigabatrin has caused concern since a specific visual field loss has been reported in treated adults. The current problem is determining the risk-benefit ratio of vigabatrin and corticosteroids/corticotropin in children with infantile spasms, and to specify the groups where their use could be optimal. Visual field loss is usually asymptomatic and can be detected only by perimetric visual field studies. In children, especially in the young or disabled, it is difficult if not impossible to detect the visual field loss and it is not yet known if children are at higher or lower risk for this adverse effect. Until a clear answer about the occurrence of this adverse effect in children has been established through randomised study, vigabatrin may still be considered first-line therapy in infantile spasms. Children who do not achieve a good response to vigabatrin should be switched to corticotropin/corticosteroid therapy. Despite the efficacy of corticosteroids and vigabatrin, the use of the conventional antiepileptic drugs, the newly developed antiepileptic drugs and some promising results with ketogenic diet, 25 to 30% of patients with infantile spasms continue to have spasms and experience psychomotor regression. These drug-resistant patients could be candidates for surgery.

Adrenocorticotropic Hormone↗
PubMed2005

[Radial artery spasm in transradial cardiac catheterization. Assessment of factors related to its occurrence, and of its consequences during follow-up].

INTRODUCTION AND OBJECTIVES: Radial artery spasm is the most frequent complication of transradial cardiac catheterization. It causes patient discomfort and reduces the procedure's success rate. The aims of this study were to identify variables associated with this complication, such as clinical parameters, angiographic characteristics of the radial artery and factors related to the procedure, and to analyze the clinical consequences of spasm, both generally and for radial artery patency, during follow-up. PATIENTS AND METHOD: The study included 637 patients who were undergoing transradial cardiac catheterization. Radial artery spasm was recorded using a scale that reflected the presence of pain and the technical difficulty of the procedure. RESULTS: Radial artery spasm was reported in 127 patients (20.2%). Multivariate analysis showed that the variables associated with radial artery spasm were radial artery anatomical anomalies (odds ratio [OR]=5.1; 95% confidence interval [95% CI]: 2.1-11.4), use of >size-3 catheters (OR=3.0; 95% CI: 1.9-4.7), moderate-to-severe pain during radial artery cannulation (OR=2.6; 95% CI: 1.4-4.9), the use of phentolamine as a spasmolytic (OR=1.8; 95% CI: 1.1-2.9), and postvasodilation radial artery diameter (OR=0.98; 95% CI: 0.98-0.99). At follow-up [20 (18) days], severe pain in the forearm was more frequent in patients who presented with radial artery spasm (12.4% vs 5.3%), but there was no significant difference in the radial artery occlusion rate (4.5% vs 2.2%). CONCLUSION: Radial artery spasm during transradial catheterization mainly depends on radial artery characteristics and procedural variables. At follow-up, radial artery spasm was associated with more frequent severe pain in the forearm, but the radial artery occlusion rate was not increased.

Cardiac Catheterization↗
PubMed1991

[Clinical aspects, diagnosis and treatment of esophageal spasm].

Esophageal spasm Teschendorf 's syndrome) is rarely distinguished among neuromuscular diseases of the esophagus, which leads to improper treatment. Primary esophageal spasm and secondary esophageal spasm should be distinguished, the latter developing in cardiospasm or achylia of the cardia. Retrosternal pain and dysphagia prevail in the clinical picture of ++esophageal spasm . X-ray and esophagomanometry are the most informative among the objective methods of examination. In a group of 106 patients 49 had primary and 57 had secondary esophageal spasm . A complex of measures should be applied in the management of esophageal spasm+. Primary esophageal spasm is treated only by nonoperative measures (spasmolytics, tranquilizers, vitamins, acupuncture reflex therapy and psychotherapy according to a suggested scheme), a course of pneumocardiodilatation (no more than 5 sessions) is included in the management of secondary esophageal spasm+. Such treatment produced good and satisfactory results in 100% of patients with primary and in 72% of patients with secondary esophagitis. The management of secondary esophagitis is a more difficult problem which calls for further study.

Adult↗
PubMed1989

Lower esophageal sphincter dysfunction in diffuse esophageal spasm.

Although lower esophageal sphincter (LES) dysfunction has been reported in patients with diffuse esophageal spasm, recent changes in manometric criteria for spasm and for LES relaxation suggested a need for reassessment. Moreover, LES relaxation in reflux-associated spasm has not been reported previously. On clinical criteria and independent of manometric findings, 22 patients with spasm were assigned to either idiopathic (I-DES, N = 9) or reflux-associated spasm (R-DES, N = 13) groups. Patients who underwent manometry for chest pain (C-NL, N = 10) or reflux (R-NL, N = 10) and had normal peristalsis served as control groups. Percent LES relaxation was significantly reduced in both spasm groups, and R-DES had significantly lower percent relaxation than I-DES. Post-deglutitive nadir sphincter pressure was significantly greater in R-DES than in I-DES. Duration of relaxation was normal in I-DES, but was significantly decreased in R-DES. This study indicates that 1) LES relaxation may be impaired in I-DES patients meeting current criteria for spasm, 2) the impairment in I-DES is primarily in "amplitude" of relaxation, i.e., percent relaxation and nadir pressure, but not duration, 3) LES relaxation may also be impaired in R-DES, and 4) the impairment in R-DES is to a greater degree than in I-DES patients and may be seen in both "amplitude" and duration of relaxation. This study shows that there is a spectrum of sphincter dysfunction in patients with esophageal spasm. It also suggests that there may be separate mechanisms for LES relaxation in R-DES patients, one with impaired relaxation and the other with near complete relaxation, "transient" or otherwise, to allow for reflux.

Adult↗
PubMed1977

[Coronary artery spasms].

In a series of 2000 coronary arteriographies, spasm of the coronary artery was found in 52 cases, which were divided into three groups: 41 cases of "iatrogenic" spasm caused by stimulating the ostium of the coronary artery (usually the right) with the tip of the catheter; 8 cases of spasm on top of an organic fixed lesion; 4 cases of coronary spasm on a coronary artery which was reported as "radiologically normal". The study includes a review of the circumstances which favour or impede discovery of coronary spasm, as well as a provocation test using methyl ergometrine. This test seems to be specific in that it only produced coronary spasm in patients with Prinzmetal's syndrome, and excluded the cases of angina with normal coronary arteriography. The patients with spasm on top of a fixed organic lesion underwent a successful aorto-coronary bypass graft together with resection of the pre- and sub-aortic nerve plexus. Patients with a spasm in an artery which was "arteriographically normal" were treated medically by nitrate compounds and vaso-dilators. Three of these patients had an excellent result with medical treatment. Treatment failed in the fourth patient, who then obtained benefit from straight-forward resection of the pre- and sub-aortic nerve plexus with an excellent result which has been maintained for over six months.

Adult↗
PubMed2001

Clinical characteristics of perioperative coronary spasm: reviews of 115 case reports in Japan.

PURPOSE: Factors affecting perioperative development of coronary spasm have not been elucidated. A number of case reports describing perioperative coronary spasm have appeared in Japanese anesthesia journals, mostly published in Japanese. The purpose of this study was to investigate the contributing factors affecting perioperative coronary artery spasm by reviewing the published articles. METHODS: Reports were identified by using Medline database (1968-1998) or by manually searching nonindexed Japanese journals. The clinical characteristics of perioperative coronary spasm were analyzed in 115 patients who developed coronary artery spasm during the perioperative period. RESULTS: The mean age of the patients was 64 +/- 9 years (range, 36 to 87 years). There were 97 men (84%) and 18 women (16%). Preoperative risk factors included hypertension (27%), angina pectoris (27%), cigarette smoking (13%), and diabetes mellitus (11%). The attack was related to inadequate depth of general anesthesia (23%), use of vasopressors (22%), vagal reflex (19%), administration of drugs other than vasopressors (17%), and epidural block (15%). About 85% of patients showed no ischemic abnormality on the preoperative electrocardiogram, whereas 56% had significant coronary stenosis on postoperative coronary arteriography. Coronary spasm tended to occur in patients under inhalation anesthesia combined with epidural block. Nitrates alleviated the episode in the majority of cases, whereas defibrillation and cardiac massage were required in 19% of patients. No deaths were reported. CONCLUSION: Perioperative coronary spasm is prevalent in elderly male patients with coronary risk factors who undergo abdominal or thoracic surgery under inhalational anesthesia combined with epidural anesthesia. Instability of the autonomic nervous system and/or vascular hyperreactivity may be the underlying pathogenic mechanisms of perioperative coronary spasm.

Journal Article↗
PubMed1982

Coronary artery spasm: prevalence, clinical significance, and provocative testing.

Recent clinical and laboratory observations indicate that coronary artery spasm may play a role in the pathophysiology of ischemic heart disease. The majority of patients with ischemic heart disease have coronary atherosclerosis. The prevalence of coronary artery spasm in these patients is unknown. However, current evidence suggests that patients with rest angina have a higher incidence of coronary artery spasm than do patients with reproducible effort angina. Coronary artery spasm may initiate or contribute to acute myocardial infarction, but recent evidence obtained in patients undergoing thrombolytic therapy during the early phases of myocardial infarction suggests that it is not a common occurrence. Although numerous examples of ventricular tachycardia and ventricular fibrillation occur during episodes of coronary artery spasm, the incidence of coronary artery spasm in association with sudden death is unknown. Provocative testing with ergonovine maleate reveals that the highest incidence of provocable coronary artery spasm is found in patients with rest angina. In patients with the syndrome of variant angina, coronary artery spasm is nearly always provocable.

Angina Pectoris↗
PubMed1989

Vascular spasm complicates continuous wave but not pulsed laser irradiation.

Preliminary clinical experience with laser angioplasty has suggested that arterial spasm may complicate attempts to employ laser light to accomplish vascular recanalization. The present study was designed to investigate the role of energy profile on the development of arterial spasm during laser angioplasty. Laser irradiation was delivered percutaneously in vivo to New Zealand white rabbits and to Yucatan microswine with or without atherosclerotic lesions induced by a combination of balloon endothelial denudation and atherogenic diet. Continuous wave (CW) laser irradiation from an argon ion gas laser (wavelength 488 to 514 nm) was applied to 23 arteries, while 16 arteries were irradiated using a pulsed xenon chloride (308 nm) or xenon fluoride (351 nm) excimer laser. Arterial spasm, defined as greater than 50% reduction in luminal diameter narrowing, complicated delivery of laser light to 17 (74%) of the 23 arteries irradiated with the CW argon laser. Spasm was consistently observed at powers greater than 2 W, at cumulative exposures greater than 200 seconds, and at total energy greater than 200 joules. Spasm was typically diffuse (including the length of the vessel) and protracted (lasting up to 120 minutes). Intra-arterial nitroglycerin (up to 300 micrograms) produced only temporary and incomplete resolution of laser-induced spasm. In contrast, spasm was never observed in any of the 16 arteries in which laser angioplasty was performed using a pulsed laser (0.95 to 6.37 joules/cm2, 10 to 50 Hz, 48 to 370 seconds). Thus CW but not pulsed laser angioplasty may be complicated by arterial spasm.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiography↗
PubMed1992

Induction of coronary artery spasm by intracoronary acetylcholine: comparison with intracoronary ergonovine.

To investigate the mechanism of coronary spasm, we compared the action of acetylcholine with that of ergonovine in 11 patients with vasospastic angina (group 1) and in 15 patients with chest pain (group 2). Coronary arteriography was performed immediately after the patients received intracoronary injections of titrated increments of each agent. In the patients in group 1 occlusive or near-occlusive (99% luminal narrowing) coronary spasm associated with angina and ischemic electrocardiographic ST changes was noted in nine of 11 patients receiving acetylcholine and in all 11 patients receiving ergonovine. The region and the degree of the most severe coronary spasm on coronary arteriograms evoked by the two agents were the same in nine of the 11 patients in group 1. In the other two patients in group 1, spontaneous focal coronary spastic stenosis in the baseline coronary arteriogram was relieved by the intracoronary injection of acetylcholine, and a focal coronary occlusive spasm in the same region was induced repeatedly by the subsequent intracoronary injection of ergonovine (paradoxic phenomenon). In contrast, occlusive or near-occlusive coronary spasm was not induced by either agent in any patient in group 2. These results suggest that the two provocative tests for coronary spasm that involve acetylcholine and ergonovine are clinically useful in the diagnosis of vasospastic angina, but testing with intracoronary ergonovine is needed when a spontaneous focal coronary spasm is relieved by the intracoronary injection of acetylcholine. The results also indicate that in many patients with vasospastic angina, nonspecific hypersensitivity to acetylcholine or ergonovine in a definite region of the coronary arteries generally plays an important role in the induction of coronary spasm.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1992

The sensitivity of intracoronary injection of acetylcholine in inducing coronary spasm differs in patients with stable and unstable angina.

In an attempt to clarify the role of coronary artery spasm in the pathogenesis of unstable angina, acetylcholine (20 and 50 micrograms) was injected directly into the coronary arteries of 19 patients with unstable effort angina (group 1), 30 patients with unstable spontaneous angina (group 2), and 15 patients with stable effort angina due to coronary artery organic stenosis (greater than or equal to 75%) (group 3). Coronary spasm was defined as severe vasoconstriction (greater than or equal to 90% of luminal diameter) with chest pain and/or ischemic ST-segment changes. Intracoronary injection of acetylcholine induced spasm of at least one coronary artery in 19 patients (100%) of group 1 and 28 (93%) of group 2 but only 3 (20%) of group 3 (p less than 0.01). When acetylcholine was injected into the left and right coronary arteries separately, multivessel spasm (spasm of both coronary arteries) was induced in 5 of 12 (42%) patients of group 1 and in 9 of 23 (39%) patients of group 2. In contrast, intracoronary acetylcholine did not cause multivessel coronary spasm in any of 15 patients of group 3 (0%). These results suggest that coronary arteries in patients with unstable effort angina as well as spontaneous angina are susceptible to spasm and that coronary artery spasm may be responsible at least in part for the genesis of attacks in these patients.

Acetylcholine↗