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At least 19 recordsLinked to original sources

PubMed1979

Coronary spasm: Prinzmetal's variant angina vs. catheter-induced spasm; refractory spasm vs. fixed stenosis.

An analysis of 2,394 selective coronary angiograms yielded 23 examples of coronary artery spasm. Of these, nine occurred in patients with Prinzmetal's variant angina and 14 were instances of catheter-induced spasm. Angiographic criteria can distinguish between the spasm of variant angina and catheter-induced spasm. The latter is usually asymptomatic, almost invariably in the right coronary artery, at the catheter tip, smooth, concentric, and less than 2 mm long. The former can occur in any coronary artery at a distance of 1--4 cm from the catheter tip, is usually irregular and eccentric, and is associated with angina, ST segment elevation, hypotension, and dysrhythmia. Response to nitroglycerin is often, but not always, complete in both. Stenoses that seem to be fixed in patients with Prinzmetal's angina should be suspected to be spasm even if unresponsive to nitroglycerin, especially when the rest of the vessel is normal. Additional pharmacologic manipulation and even recatheterization may be necessary to prove the dynamic nature of the lesion and avoid unnecessary surgery.

Adult↗

PubMed2002

Treatment of infantile spasms.

BACKGROUND: Infantile spasms (West's Syndrome) is a syndrome which includes a peculiar type of epileptic seizure, usually hypsarrhythmia and in the majority of patients, psychomotor retardation. It remains poorly understood and despite modern imaging techniques an underlying cause is often not found. Little is known about their pathophysiological basis and treatment remains problematic. OBJECTIVES: To compare the effects of single drugs used to treat infantile spasms upon long-term psychomotor development, subsequent epilepsy, control of the spasms and side effects. SEARCH STRATEGY: Our search included the Cochrane Epilepsy Group trials register, MEDLINE (1960 to 2001), EMBASE (1981 to 2001), contacting pharmaceutical companies and appeals at international conferences. SELECTION CRITERIA: Randomized controlled trials (RCTs) of the administration of drugs to people with infantile spasms. DATA COLLECTION AND ANALYSIS: Three reviewers independently selected trials for inclusion and extracted data. Study quality and potential sources of heterogeneity were assessed. Outcomes included cessation of spasms, time to cessation of spasms, participants with cessation of spasms remaining spasm free, reduction in spasms, resolution of hypsarrhythmia, subsequent epilepsy rates and side effects. MAIN RESULTS: Ten small RCTs were included. In total these studies recruited just 335 participants and tested eight different drugs. Overall, studies were of poor methodological quality. No study assessed long-term psychomotor development or the development of other seizure types. One small study found vigabatrin to be more efficacious than hydrocortisone in stopping infantile spasms in a group of people with tuberous sclerosis. One underpowered study showed a trend for vigabatrin to be more efficacious than placebo in stopping infantile spasms, two small studies when combined showed ACTH to be more efficacious than low-dose prednisone (2mg/kg). It was not possible to compare reduction in the number of spasms between the different treatments because of differences in methods of analysis. Overall, only nine participants were reported to have been withdrawn from the trial treatments due to side effects and two deaths were reported. REVIEWER'S CONCLUSIONS: We found no reliable evidence that any of the treatments assessed were more efficacious than any other. Few studies considered psychomotor development or subsequent seizure rates as outcomes and none had long term follow-up. Further trials with larger numbers of participants, and longer follow-up are required.

Anticonvulsants↗

PubMed1996

Comparison of clinical and laboratory findings between patients with diffuse three-vessel coronary artery spasm and other types of coronary artery spasm.

Our purpose was to compare patients with diffuse three-vessel coronary artery spasm and other types of coronary artery spasm without significant organic stenosis, and to elucidate clinical characteristics and risk factors. Patients were divided into two groups: group I consisted of 26 patients showing other types of coronary artery spasm; group II consisted of 5 patients with diffuse three-vessel coronary artery spasm. The mean age of patients in groups I and II was 52 and 50 years, respectively. The incidence of variant angina was higher in men than in women. The incidence of smoking was high in each group, but not significantly different. Exercise tests showed no significant differences between groups. All mean values of laboratory data, including lipoprotein (a) and low-density lipoprotein cholesterol in the two groups, were within normal ranges. There was no significant difference between groups. The incidence of spontaneous spam was much higher in patients with diffuse three-vessel coronary artery spasm (P < 0.01). Electrocardiographic (ECG) findings before the spasm were almost normal. All 5 patients with diffuse three-vessel coronary artery spasm demonstrated no important ST segment changes with episodes of angina during a coronary angiography on 12-lead ECG, compared to patients with other types of coronary artery spasm (P < 0.01). First, we conclude, diffuse three-vessel coronary artery spasm mostly occurs spontaneously. Second, we emphasize that diffuse three-vessel coronary artery spasm must be considered when 12-lead ECG shows no important ST segment changes with episodes of angina. Third, it is not easy to distinguish diffuse three-vessel coronary artery spasm from other types of coronary artery spasm on the basis of history, laboratory data, or electrocardiographic findings, including exercise tests.

Angina Pectoris, Variant↗

PubMed1998

[Absence of induced spasm by intracoronary injection of 50 micrograms acetylcholine in the right coronary artery: usefulness of 80 micrograms of acetylcholine as a spasm provocation test].

This study investigated whether the maximal dose of 50 micrograms acetylcholine for the induction of coronary spasm in the right coronary artery is adequate. The acetylcholine test was performed in 388 consecutive patients to evaluate spasm from January 1994 to December 1997. Coronary spasm in the right coronary artery was induced in 43 patients, 37 men and 6 women with a mean age of 63 +/- 8 years by intracoronary injection of 80 micrograms of acetylcholine rather than 50 micrograms. These included 15 patients (35%) with rest angina, 23 patients with ischemic heart disease other than rest angina and 5 patients (12%) with non-ischemic heart disease. Acetylcholine was injected in incremental doses of 20, 50 and 80 micrograms into the right coronary artery. Positive spasm was defined as induction of more than 90% reversible narrowing associated with either usual chest pain or ischemic electrocardiographic changes. Clinical and angiographical characteristics was studied in these patients. Fifteen (35%) patients had rest angina and 4 patients had variant angina with ST elevation in the inferior leads. Two thirds of the patients had coronary spasm in the distal portion of the right coronary artery and one third of those disclosed spasm focally. Coronary spasm was induced in 38 (15%) of 246 patients with ischemic heart disease and in 5 (4%) of 142 patients with non-ischemic heart disease. The prevalence of positive spasm in patients with ischemic heart disease was significantly higher (p < 0.01) than in patients with non-ischemic heart disease. A dose of 80 micrograms of acetylcholine, more than the maximal standard dose, might be clinically useful for the induction of spasm in the right coronary artery if coronary spasm of this artery is strongly suspected.

Acetylcholine↗

PubMed1976

The long-term prognosis infantile spasms--the present condition of cases of infantile spasms followed in school age.

A follow-up study has been made of 25 cases with infantile spasms, all of whom were six years old or more at review. Only four (16%) out of 25 cases made a full recovery and attended normal school. Spasms ceased in 96% of all cases, but fits other than spasms (grand mal, tonic seizure, atonic seizure, myoclonic seizure, atypical absence and psychomotor seizure) occurred subsequently in 11 cases (44%). The EEG became normal in two cases (8%), but still showed modified hypsarhythmia in three cases (12%), "epileptic non-hypsarhythmic" discharges in 17 cases (68%) and non-specific abnormalities in three cases (12%). The important factors associated with good prognosis were normal development before the onset of spasms, late onset (seven months old or over) and short duration of spasms, the absence of other types of fit following spasms and lack of neurological abnormality. A bad prognosis was associated with abnormal development prior to the onset of spasms, early onset and long duration of spasms, the presence of other types of fit following spasms and evidence of any neyrological abnormality This follow-up may confirm that the therapy with ACTH-A has no significant effect on final mental state.

Adolescent↗

PubMed1993

Role of coronary artery spasm in progression of organic coronary stenosis and acute myocardial infarction in a swine model. Importance of mode of onset and duration of coronary artery spasm.

BACKGROUND: Coronary spasm may play an important role in progression of organic coronary stenosis and myocardial infarction, but the mechanisms responsible for these complications are not known. This study aimed to examine whether the mode of onset and the duration of coronary spasm influenced progression of organic coronary stenosis and acute myocardial infarction in a swine model of coronary spasm. METHODS AND RESULTS: Göttingen miniature pigs were subjected to cholesterol feeding, balloon-induced coronary arterial denudation, and x-ray irradiation. Five months later, coronary spasm was induced by intracoronary injection of serotonin. In 10 pigs, coronary spasm was provoked abruptly and maintained for 25 minutes by five repeated intracoronary injections of serotonin (10 micrograms/kg) every 5 minutes (group A, abrupt onset and short duration). In group B, coronary spasm was provoked gradually by intracoronary injections of serotonin at graded doses of 0.1, 0.3, and 0.6 microgram/kg every 5 minutes and was then maintained for 25 minutes in four pigs (group B1, gradual onset and short duration) and for 120 minutes in six pigs (group B2, gradual onset and long duration) by repeated intracoronary injections of serotonin (10 micrograms/kg) every 5 minutes. Intramural hemorrhage was noted histologically at the spastic site more frequently in group A with abrupt onset (nine of 10 pigs) than in group B with gradual onset (two of 10 pigs) (p < 0.01). Progression of organic coronary stenosis due to intramural hemorrhage was noted in seven pigs (six pigs in group A and one pig in group B), including three cases of total coronary occlusion. Evidence for the evolution of acute myocardial infarction (serial ECG findings, left ventriculograms, and histological findings) was noted in one pig (7%) of group A or B1 with short duration and in five of six pigs (83%) in group B2 with long duration (p < 0.01 versus group A and B1). CONCLUSIONS: These results indicate that: 1) intramural hemorrhage was frequently induced by coronary spasm of abrupt but not of gradual onset, 2) intramural hemorrhage resulted in acute progression of coronary stenosis and sometimes resulted in persistent total coronary occlusion leading to acute myocardial infarction, and 3) prolonged coronary spasm resulted in acute myocardial infarction without progression of organic coronary stenosis.

Animals↗

PubMed1985

Histamine-induced spasm not significantly modulated by prostanoids in a swine model of coronary artery spasm.

The role of prostanoids in a swine model of coronary artery spasm was examined. Eighteen miniature pigs underwent endothelial denudation of the left coronary artery (left circumflex branch in 14 pigs and left anterior descending branch in 4 pigs) followed by high cholesterol feeding. Three months after the denudation, when coronary artery spasm was repeatedly provoked along the denuded portion of the coronary artery by histamine, the vasoconstrictive effect of thromboxane A2 and the preventive effects of indomethacin and prostacyclin against histamine-induced coronary artery spasm were examined. Intracoronary administration of thiothromboxane A2, 200 micrograms, a stable thromboxane A2 analog, failed to provoke coronary artery spasm (seven of seven cases) but nonselectively constricted the coronary artery by 33%. Intravenous administration of indomethacin, 2 mg/kg, or continuous intravenous infusion of prostacyclin, 50 ng/kg per min, failed to prevent histamine-induced coronary artery spasm (four of four and eight of eight cases, respectively), yet the spasm was all but prevented by intravenous pretreatment with diphenhydramine at a dose of 1 mg/kg. Thus, in this swine model, prostanoids may not play a primary role in the occurrence of coronary artery spasm.

Animals↗

PubMed1987

Tetraethylammonium induced coronary spasm in isolated perfused rabbit heart: a hypothesis for the mechanism of coronary spasm.

The vasoactive effect of tetraethylammonium, which is known to reduce potassium conductance of the membrane of arterial smooth muscle cells, was tested on large epicardial coronary arteries in isolated perfused rabbit hearts. These hearts were perfused selectively through the right and left coronary arteries. Left coronary angiography was performed using Krebs-Henseleit solution containing phenolsulfonphthalein under constant pressure, and the epicardial electrogram was recorded. In 59 of 114 hearts 30 mmol.litre-1 tetraethylammonium induced severe constriction of the left epicardial coronary artery, which was associated with electrocardiographic ST segment elevation in some cases. The induced spasm was prevented by diltiazem (200 nmol.litre-1), glyceryl trinitrate (2 mumol.litre-1), or nicorandil (10 mumol.litre-1), but not by phentolamine (1 mumol.litre-1) or atropine (1 mumol.litre-1). In hearts in which tetraethylammonium did not induce spasm, subsequent addition of ergonovine (100 nmol.litre-1) or alkalinisation of the perfusate (pH 7.65-7.70) provoked spasm. The tetraethylammonium induced spasm resembled the coronary spasm seen in patients with variant angina and was a reproducible in vitro model of coronary spasm. These observations support the hypothesis that the primary defect in patients with coronary spasm is decreased potassium permeability of the membrane of coronary arterial smooth muscle cells.

Animals↗

PubMed1986

Oesophageal spasm in patients with coronary artery spasm.

Oesophageal manometry was performed in 20 patients with chest pain, of whom 10 showed coronary artery spasm (group I) and 10 did not (group II). In the basal state oesophageal spasms were recorded in 6 patients from group I but in none from group II (p less than 0.05). In group I the duration of oesophageal contractions was 4.50 +/- 0.65 s compared with 2.86 +/- 0.36 s in group II (p less than 0.05). Prolonged hyperventilation was performed during manometry by 7 patients from each group. In group I this caused chest pain in all 7, with electrocardiographic changes in 6; at the same time oesophageal spasms were intensified in 5 patients and began anew in 1. In group II no electrocardiographic changes were seen with hyperventilation, and 1 patient showed oesophageal spasm. These observations suggest a relation between spasm of the coronary arteries and spasm of the oesophagus.

Adult↗

PubMed1982

The injury-spasm (ischemia-induced hemostatic vasoconstrictive) and vascular autoregulatory hypothesis of ischemic disease. Resistance vessel-spasm hypothesis of ischemic disease.

THe injury-spasm concept assumes that severe myocardial ischemia secondary to stenotic coronary artery disease causes spasm of resistance vessels through ischemic tissue injury. In this communication the concept is developed further and is now extended to include other diseases. It is suggested that relative arterial insufficiency, as traditionally understood, is an invalid concept and that disorders usually attributed to it, including congestive heart failure and peripheral vascular disease, should be attributed to injury-spasm. Because a basic reaction to injury is to prevent bleeding, injury-spasm is identified as an exaggerated form of hemostatic vasoconstriction, and spasm is related to distorted vascular autoregulatory activities of resistance vessels. It is asserted that blood platelets probably are not involved int he initiation of ischemic attacks, and instead of a platelet thromboxane/vessel prostacyclin vasomotor balance of epicardial coronary arteries, the vasoconstrictive/vasodilative balance is centered in resistance vessels and is based on autoregulatory processes such as the hemostatic injury-spasm reaction and reactive hyperemia.

Animals↗

PubMed2000

Difference in fibrinolytic activity between multivessel coronary spasm and one-vessel coronary spasm.

Plasminogen activator inhibitor activity was higher in 18 patients with multivessel spasm than in 20 patients with 1-vessel spasm and in 22 control patients. Tissue plasminogen activator antigen was also higher in patients with multivessel spasm than in those with 1-vessel spasm and control patients. The increased plasminogen activator inhibitor activity in patients with multivessel spasm indicates that the fibrinolytic system is more impaired in such patients than in those with 1-vessel coronary spasm; this may be related to the higher incidence of refractory angina during hospitalization and cardiac events during the follow-up period.

Angina Pectoris↗

PubMed1986

Induction of coronary artery spasm by acetylcholine in patients with variant angina: possible role of the parasympathetic nervous system in the pathogenesis of coronary artery spasm.

We injected acetylcholine (ACh), the neurotransmitter of the parasympathetic nervous system, into the coronary arteries of 28 patients with variant angina. Injection of 10 to 80 micrograms ACh into the coronary artery responsible for the attack induced spasm together with chest pain and ST segment elevation or depression on the electrocardiogram in 30 of the 32 arteries of the 25 of the 27 patients. The injection of 20 to 100 micrograms ACh into the coronary artery not responsible for the attack in 18 patients resulted in various degrees of constriction in most of them, but no spasm in any of them. After intravenous injection of 1.0 to 1.5 mg atropine sulfate, the injection of ACh into the coronary artery responsible for the attack did not induce spasm or attack in any of the nine coronary arteries injected in eight patients. We conclude that the intracoronary injection of ACh induces coronary spasm and attack in patients with variant angina and that the activity of the parasympathetic nervous system may play a role in the pathogenesis of coronary spasm. We also conclude that the intracoronary injection of ACh is a useful test for provocation of coronary spasm.

Acetylcholine↗

PubMedDate not supplied

Methylergonovine-induced diffuse coronary spasm in a patient with exercise-induced coronary spasm after heart transplantation.

Coronary artery spasm is a rarely reported condition after heart transplantation. We report a case of exercise-induced coronary artery spasm in a patient 1-year after orthotopic heart transplantation. Serial quantitative coronary angiography showed significant diffuse loss of luminal diameter. Provocative testing with intracoronary acetylcholine and intravenous methylergonovine maleate was performed in an effort to document efficacy of the antispasm regimen. Infusion of acetylcholine into the left anterior descending coronary artery resulted in transient closure of the vessel. Diffuse spasm resulting in hypotension and ventricular fibrillation occurred with intravenous methylergonovine maleate administration. Because of the risk of provoking diffuse spasm, intravenous administration of methylergonovine maleate should be avoided in the posttransplantation setting. Review of the literature suggests that coronary artery spasm after transplantation is often associated with severe transplant coronary artery disease and may be associated with a poor prognosis. Coronary artery spasm may be a more common cause of syncope and death after transplantation than it is currently thought to be.

Acetylcholine↗

PubMed1981

Coronary arterial spasm versus esophageal spasm. Response to ergonovine.

In this report we show that coronary arterial and esophageal spasm are sometimes clinically indistinguishable. Pain patterns can be identical, nitroglycerin can bring relief, interval electrocardiograms and exercise electrocardiograms generally disclose no abnormalities, coronary arteriograms may be within normal limits or nearly so, and, importantly, an ergonovine provocative test can provoke esophageal spasm accompanied by pain mistaken for Prinzmetal's angina. Accordingly, chest pain in response to the administration of ergonovine is not evidence of coronary arterial spasm without simultaneous arteriographic proof together with changes in the monitoring electrocardiogram. Conversely, gastroenterologists should not expose patients to the risk of ergonovine without prior assurance that the coronary arterial response is normal. Our observations illustrate these points and identify a patient with symptomatic esophageal spasm previously diagnosed as Prinzmetal's angina.

Angina Pectoris↗

PubMed2003

Diffuse esophageal spasm: not diffuse but distal esophageal spasm (DES).

Diffuse esophageal spasm is an uncommon motility disorder that is found in less than 5% of patients undergoing esophageal motility testing for dysphagia. It is defined manometrically by the presence of 20% or more simultaneous contractions in the distal esophageal body with normal peristalsis. This motility abnormality has been traditionally identified as occurring primarily in the smooth muscle portion of the distal esophagus yet, the term "diffuse" persists in the medical literature to identify DES. The aim of our study was to assess the diffuse or limited nature of this entity by evaluating the prevalence of simultaneous contractions in both proximal and distal esophagus in patients with DES. We reviewed esophageal motility tracings of 53 consecutive patients (32 F, 21 M) with DES and compared them with 53 age-matched patients with manometric normal studies. In the distal esophagus we found 195 simultaneous contractions (37% of swallows) with a median of 3 and range of 2-7 per patient. Of the 53 patients with DES a total of 13 simultaneous contractions (2% of swallows) occurred in the proximal esophagus with only 3 (5.6%) of the 53 patients having 2 or more simultaneous contractions in 10 swallows. None of the patients with normal manometry showed more than one simultaneous contraction in either proximal or distal esophagus. In conclusion, these findings suggest that the term diffuse esophageal spasm is a misnomer and the DES is more appropriately described as "distal" esophageal spasm.

Adult↗

PubMed1999

Treatment of infantile spasms: results of a population-based study with vigabatrin as the first drug for spasms.

PURPOSE: The efficacy of a protocol consisting of vigabatrin (VGB) as the first and adrenocorticotropic hormone (ACTH) or valproate (VPA) as the second drug was studied in the treatment of newly diagnosed infantile spasms (IS) during 1994 to 1997 in a population-based design. METHODS: Only total disappearance of the spasms with a minimal duration of 1 month was accepted as a response. The treatment response was confirmed by video-EEG study. All infants were studied by magnetic resonance imaging (MRI) or computed tomography (CT) for etiology. RESULTS: Altogether 42 infants, 10 with cryptogenic and 32 with symptomatic etiology, were treated. Eleven (26%) responded to VGB, five (50%) with cryptogenic, and six (19%) with symptomatic etiology; 91% of infants responded to a dose of 50-100 mg/kg/day, and 82% of them within 1 week. ACTH was offered in combination with VGB to 22 and VPA to four infants for whom VGB failed. Eleven responded to ACTH and one to VPA. In total, 26 (62%) infants responded to the treatment protocol; all (100%) with cryptogenic etiology and 16 (50%) with symptomatic etiology. ACTH treatment was associated with more severe side effects than VGB or VPA. Only one infant relapsed after a spasm-free period with VGB of >4 months, but none after ACTH was combined with VGB. CONCLUSIONS: We suggest VGB as a first drug to all infants with IS. After a treatment trial of 10-14 days with increasing dose from 50 to 150 mg/kg, ACTH should be considered.

4-Aminobutyrate Transaminase↗

PubMed1992

[The multiple coronary spasm as the cause of acute ischemic events. A case report of a simultaneous spasm of the anterior descending and the circumflex during coronary angiography].

A case of simultaneous coronary artery spasm during coronary arteriography is reported. The patient, a 48-year-old male smoker, with an important family history of sudden death, underwent coronary angiography 5 months after anterior myocardial infarction. There were no lesions in the coronary arteries at the angiographic study. At the end of the procedure there was a sudden contemporary spasm of the anterior descending and circumflex coronary arteries. This severe condition was resolved with intra-arterial nitroglycerin. The relevance of multicoronary spasm as a cause of acute ischemic events and the possible influence of family history are discussed.

Acute Disease↗

PubMed1979

Cerebral arterial spasm: part 10. Reversal of acute and chronic spasm in dogs with orally administered nifedipine.

In vivo experiments in dogs demonstrated angiographically that the subarachnoid injection of blood produced cerebral arterial apasm both immediately after the injection of blood and 2 days later. The sublingual adminstration of nifedipine reversed both the acute and the delayed cerebral arterial spasm. In addition, sublingual administration of nifedipine 20 minutes before the subarachnoid injection of blood prevented the acute spasm.

Acute Disease↗