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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↗
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↗
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↗
PubMed1976

Cerebral arterial spasm. Part 8: The treatment of delayed cerebral arterial spasm in human beings.

Three patients who had neurological deficits from delayed cerebral arterial spasm following rupture of posterior communicating artery aneurysms were treated with continuous, simultaneous, intravenous injections of phenylephrine and nitroprusside. The results were determined by cerebral angiography before and after treatment. A dramatic increase in the cross-sectional area of the large cerebral arteries was found after treatment. The clinical implications of this treatment are discussed.

Adolescent↗
PubMed1976

Is angiographic spasm real spasm?

Systematic morphological study of the cerebral arteries was made in six autopsy cases of ruptured aneurysms. The time course of the arterial luminal narrowing was observed by repeated angiograms, and segments of the narrowed arteries were studied histologically. Various histological changes were found consistent with the angiographic findings. We have devided these into three stages according to the duration of the disease. In the acute stage (less than one day) the contraction of the medial smooth muscle cells may be the main cause of the luminal narrowing. In the subacute stage, arteries showed a reduction in lumen size with medial thickening, marked corrugation of the internal elastic lamina, and thrombus formation attached to the endothelial surface. If vasoconstriction remained localized to the same segment for several days, the intimal or medial thickening and thrombus might produce the luminal narrowing consistent with the angiographic narrowing. In the chronic stage (more than two weeks), most cases showed dilatation of the arterial lumen on angiography. These arteries showed frank necrosis of the smooth muscle cells histologically. In a case which demonstrated progressive luminal narrowing on angiograms over 2 weeks, the arterial wall showed luminal narrowing with cellulofibrous thickening of the intima and organization of the thrombus. The presence of these structural changes in the narrowed arteries seen at angiography seems to be very important for proper understanding and treatment of vasospasm.

Acute Disease↗
PubMed2026

Late-onset epileptic spasms: presentation, aetiology and outcome.

Late-onset epileptic spasms (LOES) are epileptic spasms (ES) commencing after age 12 months, often misdiagnosed and having uncertain relationship to infantile spasms. Previous studies of mostly small LOES cohorts frequently reported 'cryptogenic' aetiologies. We studied the presentations, aetiologies, treatment responses and outcomes in a large LOES cohort, evaluated with modern neuroimaging and genomic testing. In this retrospective cohort study, 62 children with video-confirmed epileptic spasms, diagnosed between 2011 and 2021, were included. All had epileptiform activity on EEG, but none had hypsarrhythmia. Median age at epileptic spasms onset was 23 months (range 1-15 years) and median delay to diagnosis was 8 months (interquartile range: 3-15). Only 24% children were correctly diagnosed at presentation, common misdiagnoses being myoclonic epilepsies and non-epileptic phenomenon. Aetiology was identified in 95%. Structural-malformative aetiologies were present in 63% (most commonly focal cortical dysplasia and mild malformation of cortical development with oligodendroglial hyperplasia in epilepsy). Other aetiologies were structural-acquired in 13% (mostly postnatal stroke and CNS infections), genetic in 13% (mostly intragenic variants and chromosomopathies) and oncological in 6% (history of leukaemia, two with CNS involvement). Children with structural aetiologies often had normal development prior to onset of epileptic spasms, a later median age of epileptic spasms onset and were more likely to have asymmetric or subtle epileptic spasms and additional seizures prior to epileptic spasms. Epileptic spasms ceased in 29% children treated with prednisolone, most having genetic aetiologies and in 35% treated with vigabatrin, all having structural-malformative aetiologies. Apart from clobazam, which was effective in 17% of children, all other antiseizure medications, vagus nerve stimulation and ketogenic diet therapy were ineffective. Epileptic spasms ceased in 86% (18/21) of children who underwent epilepsy surgery. At median follow-up of 10.3 years, 53% children were free of all seizures and 76% were free of epileptic spasms. More children with unilateral structural-malformative aetiologies achieved seizure freedom than other aetiologies, most commonly following surgery but occasionally following treatment with vigabatrin or clobazam. Impairment of cognitive function or adaptive behaviour (formally assessed in 90%) was significantly more common in children with genetic than structural aetiologies, and in children with ongoing seizures than seizure freedom. Among children who underwent epilepsy surgery, 62% achieved average or low-average adaptive functioning or normal intellectual capacity. This study highlights the importance of prompt recognition of epileptic spasms in older children for improved seizure and developmental outcomes. Brain malformations and insults are the predominant causes of LOES, and when unilateral, respond best to epilepsy surgery.

cognitive outcome↗
PubMed1978

[A regional cerebral blood flow in patients with acute subarachnoid hemorrhage--with special references to spasm (author's transl)].

Measurements of the regional cerebral blood flow (rCBF) were performed 44 times on patients with subarachnoid hemorrhage, using the 133-Xe clearance method with aid of the 8 channel detector unit. The patients consisted of 31 preoperative cases within 3 weeks of the last subarachnoid hemorrhage. The sites of the ruptured aneurysms included 11 anterior communicating arteries, 8 middle cerebral arteries, 7 internal carotid arteries and 3 anterior cerebral arteries. In 2 cases, the aneurysms were not identified with the cerebral angiograms. The purpose of this study was to investigate the effect of spasm on the rCBF. The subjects were divided into two groups: those with and without spasm. Furthermore, the group with spasm was divided into three subgroups according to the degree of spasm. The findings obtained were as follows; The group with spasm showed a statistically significant decrease in the mean of the rCBF. The MrCBF was not influenced by the distribution of spasm, however. In the group without spasm, the MrCBF had a good correlation with the cerebrospinal fluid pressure (CSF-P) or the level of consciousness. In the group with spasm, there was no correlation between the MrCBF and the CSF-P or the level of consciousness. For example that marked reduction of the MrCBF were seen in some cases with low CSF-P or only slight disturbance of consciousness. The rCBF was measured 2 or 3 times in 5 cases with spasm. The decrease in MrCBF occured about one week after the incidence of the subarachnoid hemorrhage but MrCBF recovered with the disappearance of spasm 2 or 3 weeks after the attack. There was a poor correlation between spasm and relative flow patterns. The good correlation, however, was found in only one case with the severe spasm at the middle cerebral artery.

Acute Disease↗
PubMed1992

Treatment of infantile spasms: medical or surgical?

Although infantile spasms were initially described in 1841, remarkably little progress has been made in understanding the pathophysiology of this "peculiar form of infantile convulsions." Consequently, our ability to treat infantile spasms is limited. Infantile spasms are classified as a "generalized" seizure disorder in the international classification system, which suggests that the underlying brain abnormality causing the seizures also must be diffuse or generalized. As the classification suggests, there are many diffuse, or multifocal, brain disorders related to infantile spasms, e.g., inborn errors of metabolism, hypoxic-ischemic brain injury, and developmental brain defects such as tuberous sclerosis or Aicardi's syndrome. On the other hand, infantile spasms have been reported in which a localized brain abnormality was present, e.g., tumor, stroke, and trauma. On rare occasions, removal of a tumor has resulted in cessation of the generalized infantile spasms. This finding suggests that focal cortical abnormalities can cause infantile spasms and that removing the abnormality can stop the seizures. At University of California, Los Angeles, the Pediatric Epilepsy Surgery Program has developed new approaches to the treatment of infantile spasms. The principal underlying concepts are (a) children with medically refractory infantile spasms may have an area of cortical defect (called the zone of cortical abnormality) that causes the seizures and (b) infantile spasms are usually generalized seizures. Thus, the goal of the surgical assessment is not the identification of the focus of seizure onset but rather the identification of the zone of cortical abnormality.

Adrenocorticotropic Hormone↗
PubMed1992

Purinoceptors mediating relaxation and spasm in the rat gastric fundus.

1. The relaxant and spasmogenic effects of purines and analogues were studied in longitudinal strips of rat gastric fundus to characterize the purinoceptors involved. Classification was studied by use of agonist potency orders and of antagonists in circumstances where the influence of confounding factors was reduced. In general tone was raised by carbachol (0.1 microM). 2. Adenosine produced relaxation and was potentiated by nitrobenzylthioinosine (NBTI, 0.3 and 30 microM), an adenosine-uptake inhibitor. 8-Sulphophenyl-theophylline (8-SPT, 30 microM), a selective P1-purinoceptor antagonist, antagonized adenosine and 5'-N-ethylcarboxamidoadenosine (NECA), a selective agonist at P1-purinoceptors. 3. At resting tone, adenosine 5'-triphosphate (ATP) induced a small, phasic relaxation followed by a maintained spasm. When tone was raised by carbachol, ATP induced a larger relaxation followed by a smaller spasm. NBTI did not potentiate ATP, nor did 8-SPT antagonize ATP, suggesting that ATP does not act directly or indirectly at P1-purinoceptors. 4. With raised tone, and in the presence of indomethacin (10 microM) and 8-SPT (30 microM), 2-methylthio ATP (2-MeSATP) and ATP produced relaxations followed by spasms while alpha,beta-methylene ATP (alpha,beta-MeATP) induced only relaxation; all responses were concentration-dependent. The compounds had similar slopes and maxima for relaxation and spasm. The rank orders of potency were 2-MeSATP much greater than alpha,beta-MeATP greater than ATP for relaxation and 2-MeSATP much greater than ATP for spasm.5. With raised tone, and in the presence of indomethacin and alpha 8-SPT, desensitization to alpha,beta-MeATP (100microM) completely and only slightly suppressed responses to ATP and 2-MeSATP, respectively, as relaxants but had no effect on relaxant responses to adenosine. The magnitude of the spasms to ATP and 2-MeSATP was considerably increased by desensitization with alpha,beta-MeATP but the spasm to KCl was not affected.6. With raised tone, and in the presence of indomethacin and 8-SPT, reactive blue 2 (10 AM) nonselectively antagonized ATP, 2-MeATP, a,P-MeATP, adenosine and isoprenaline as relaxants. Reactive blue 2 prevented the spasms to ATP and 2-MeSATP but not spasm to KC1.7. With raised tone, and in the presence of indomethacin, suramin (100 microM) antagonized ATP, but not adenosine, as relaxants and antagonized ATP, but not KC1, as spasmogens.8. It is proposed that adenosine is susceptible to nucleoside-specific uptake and acts predominantly via a P,-purinoceptor and also by a non-PI-purinoceptor mechanism. ATP- and alpha,beta-MeATP-induced relaxations probably occur via a P2x-purinoceptor. The anomalous nature of the 2-MeSATP-induced relaxation suggests it acts both via a P2x-purinoceptor and an additional mechanism. A P2y-purinoceptor is most likely to be involved in the spasms to ATP and 2-MeSATP. Therefore, the functional nature of the responses mediated by P2X- and P2y-purinoceptors, relaxation and spasm respectively, are opposite to those seen in most smooth muscles.

Adenosine Triphosphate↗
PubMed1977

Coronary artery spasm. medical management, surgical denervation, and autotransplantation.

Coronary artery spasm was induced by intravascular administration of ergonovine maleate (Ergotrate) during cardiac catheterization. In 78 patients suspected to have Prinzmetal's angina, no morbidity or death has resulted despite complete occlusive spasm in two and three coronary arteries. Typical EKG changes and akinesia of the myocardium in the distribution of the occluded vessels documented functional myocardial ischemia during spasm. The occlusive spasm is readily reversed by sublingual or intravascular nitroglycerin, and ventricular contractility returns to normal following relief of spasm. Occlusive spasm has been demonstrated in 15 patients with clinical evidence of Prinzmetal's angina. Symptoms have been effectively relieved by coronary vasodilators in 10 patients. Of the 5 patients in whom medical therapy failed, 4 were treated surgically. These 4 patients were in the intensive care unit with protracted, prolonged pain, subendocardial infarctions, and persistent failure of coronary vasodilators. Aorta-coronary bypass grafts have been combined with total cardiac denervation by autotransplantation (one patient) and total cardiac denervation by stripping of the great vessels (3 patients). Two of the patients treated by cardiac denervation died in the early postoperative period. The patient treated by autotransplantation has total relief of symptoms but persistent spasm on angiography. The angiographic demonstration of occlusive coronary spasm remains a valuable diagnostic tool to document definitively the presence of spasm. The surgical results question the value of surgical intervention in this disease.

Adult↗
PubMed1975

[Experimental Subarachnoid hemmorrhage in dogs--effect of various drugs and sympathectomy on cerebral arterial spasm (author's transl)].

Adult mongrel dogs were used. The posterior communicating artery was punctured with a fine needle and subarachnoid hemorrhage was produced, which simulated aneurysmal rupture in human. The cerebral basal arteries were constricted remarkably after the puncture. However this vasospasm disappeared in about 60-120 minutes. After this restoration, the vessels began to be constricted again and reduced their diameter in greater degree with lapse of time. Effect of various drugs and sympathectomy on the experimental spasm induced by this method were studied utilizing the magnified vertebral angiography. The drugs used were papverine, isoxuprine, methysergide, phentolamine and propranolol. One of these drugs was given to each dog into the vertebral artery 15 minutes after the puncture of the artery for study of the early spasm, and the same procedure was carried out 24 hours after the late spasm. Vertebral arteriograms were taken immediately after and at 5, 10 and 30 minutes after injection of the drug. Diameter changes of the cerebral basal arteries were measured on the film. Smooth muscle relaxtants, papaverine and isoxsuprine, were effective on relieving the early and the late spasm. An antiserotonin agent, methysergide, relieved slightly the early spasm, but it had no effect on the late spasm. Phentolamine, that is an adrenergic blocking agent, relieved the early spam remarkably, but it was less effective on the late spam. A beta adrenergic blocking agent, propranolol, was effective on relieving neither the early nor the late spasm. Two weeks after the removal of the bilateral upper cervical ganglia, subarachnoid hemorrhage was produced by the smae method as mentioned above in four dogs. Arteriograms taken 24 hours after puncture of the posterior communicating artery in these dogs showed vasoconstriction as same as in the non-sympathectomized dogs. From these experimental results, it was suggested that an etiological difference in the early and the late spasm may exist, and that the occurence of the late spasm may not be influenced by the sympathetic system.

Animals↗
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↗
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↗
PubMed1992

A study on coronary hemodynamics during acetylcholine-induced coronary spasm in patients with variant angina: endothelium-dependent dilation in the resistance vessels.

The epicardial coronary artery of patients with variant angina is hyperreactive to the constrictive effect of acetylcholine, but it is not known whether the coronary microvasculature also constricts in response to acetylcholine. Incremental doses of acetylcholine were injected into the left coronary artery of 57 patients with variant angina and with spasm in this artery. By measuring coronary sinus blood flow, coronary hemodynamic status just before angiographic documentation of spasm was examined. Acetylcholine induced spasm in the left coronary artery in all patients. It also decreased the diameter of the nonspasm artery by 36 +/- 19% from baseline. For all patients, coronary sinus blood flow was 89 +/- 38 ml/min at baseline and increased to 104 +/- 61 ml/min during an acetylcholine-induced anginal attack (p less than 0.01). In 10 patients with spasm in both the left anterior descending and left circumflex arteries (that is, multivessel spasm), coronary sinus blood flow decreased from 84 +/- 21 to 52 +/- 26 ml/min (p less than 0.01). In the other 47 patients with spasm in only one of these two arteries (that is, single-vessel spasm), coronary sinus blood flow increased from 90 +/- 41 to 115 +/- 61 ml/min (p less than 0.01) without change in the rate-pressure product. It is concluded that in patients with variant angina, acetylcholine induces spasm and constriction in the epicardial coronary artery, whereas it dilates the resistance vessels presumably through the release of the endothelium-dependent relaxing factor.

Acetylcholine↗