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At least 55 records · Page 3Linked to original sources
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↗
PubMed1995

Cellular localization of the inhibitory action of relaxin against uterine spasm.

1. The aim of this study was to determine whether the site of action of relaxin as a relaxant of rat myometrium is at the cell membrane or at an intracellular-site. Therefore, the potency of relaxin was determined against spasms reliant predominantly upon either extracellular Ca2+ or intracellular Ca2+. Uterine spasms dependent upon extracellular Ca2+ were elicited by (i) oxytocin (0.2 nM) (ii) Bay K 8644 (1 microM) in 10 mM K(+)-rich PSS and (iii) KCl (80 mM). Uterine spasm dependent upon intracellular Ca2+ was elicited by oxytocin (20 nM) in the presence of nifedipine (500 nM). The effects of relaxin against these spasmogens were compared with those of levcromakalim, nifedipine and salbutamol. 2. Relaxin (0.2-6.3 nM), levcromakalim (25-800 nM), salbutamol (1-63 nM) and nifedipine (1-250 nM) caused concentration-dependent inhibition of the spasm evoked by oxytocin (0.2 nM) and relaxin was the most potent relaxant. 3. Relaxin and nifedipine were slightly less potent against the spasm induced by Bay K 8644 (1 microM) than against spasm induced by oxytocin (0.2 nM) (15 fold and 13 fold respectively). Levcromakalim and salbutamol were equipotent against the spasm evoked by Bay K 8644 (1 microM) and that evoked by oxytocin (0.2 nM). 4. Relaxin induced only 47 +/- 7% inhibition of the KCl (80 mM)-evoked spasm at a concentration of 0.8 microM. Levcromakalim was much less potent (427 fold) against the spasm evoked by KCl (80 mM) than against the spasm evoked by oxytocin (0.2 nM). The potency of salbutamol against the spasm evoked by KCl (80 mM) was modestly reduced (14 fold) compared to that against the spasm evoked by oxytocin (0.2 nM). The potency of nifedipine against the KCl (80 mM)-evoked spasm was not different from that against the oxytocin (0.2 nM)-evoked spasm. 5. The potencies of relaxin and levcromakalim against the spasm evoked by oxytocin (20 nM) + nifedipine (500 nM) were greatly reduced (74 fold and 234 fold respectively) compared to their potencies against the spasm evoked by oxytocin (0.2 nM). The potency of salbutamol against these two spasmogens was not different. 6. Relaxin was much less potent against the spasm dependent upon intracellular Ca2+ (that induced by oxytocin (20 nM) + nifedipine (500 nM)) than against the spasms dependent upon extracellular Ca2+, those induced by oxytocin (0.2 nM) and Bay K 8644 (1 microM). In this regard, relaxin resembled levcromakalim and nifedipine rather than salbutamol. Therefore, the major site of action of relaxin appears to be located at the plasma membrane rather than at an intracellular level. The observation that relaxin was less effective against the KCl (80 mM)-induced spasm than against the oxytocin (0.2 nM)-evoked spasm may indicate that relaxin has a minor action involving K(+)-channel opening. 7. High concentrations of relaxin (up to 1 microM) induced significant inhibition of the spasm dependent upon intracellular Ca2+. Thus at high concentrations relaxin also appears to have an additional intracellular action.

Adrenergic beta-Agonists↗
PubMed2006

[Clinical features of patients with atypical coronary artery spasm].

OBJECTIVE: This study is aimed to compare the clinical characteristics of patients with typical and atypical coronary artery spasm. METHODS: Out of 64 patients with chest pain at rest and without significant coronary artery stenosis, coronary artery spasm was provoked by intracoronary injection of acetylcholine in 46 patients, including 12 with ST segment elevation (typical coronary artery spasm group) and 34 without ST segment elevation (atypical coronary artery spasm group). The demographic data, coronary angiographic findings, treadmill electrocardiogram, dipyridamole and rest thallium-201 myocardial perfusion computed tomography, and the follow-up clinical data of the two groups were compared. RESULTS: The patients with typical coronary artery spasm were younger (47 +/- 6 vs. 58 +/- 12, P < 0.05) than patients with atypical coronary artery spasm group. Hyperlipidemia were more common in atypical coronary artery spasm group (74% vs. 33%, P < 0.05) and myocardial bridging was more common in patients with typical coronary artery spasm group (67% vs. 32%, P < 0.01). Focal coronary spasm during acetylcholine provocation was seen in 92% patients with typical coronary spasm and in 32% patients with a atypical coronary artery spasm (P < 0.01) while diffuse coronary spasm was seen in 8% patients with typical coronary spasm and in 68% patients with a atypical coronary artery spasm (P < 0.01). All patients with coronary artery spasm were treated with aspirin, calcium channel blockers, long-acting nitroglycerine, with or without lipid-lowering drugs, 2 patients with typical coronary spasm and 4 patients with atypical coronary spasm were rehospitalized due to chest pain and rest of the patients remained free of chest pain during the median follow-up period of 18 +/- 14 months. CONCLUSION: Atypical coronary artery spasm is common in patients with rest angina and diffuse coronary microvascular spasm might be the cause of chest pain in these patients.

Acetylcholine↗
PubMed2005

Origin and propagation of epileptic spasms delineated on electrocorticography.

PURPOSE: Ictal electrographic changes were analyzed on intracranial electrocorticography (ECoG) in children with medically refractory epileptic spasms to assess the dynamic changes of ictal discharges associated with spasms and their relation to interictal epileptiform activity and neuroimaging findings. METHODS: We studied a consecutive series of 15 children (age 0.4 to 13 years; nine girls) with clusters of epileptic spasms recorded on prolonged intracranial subdural ECoG recordings, which were being performed for subsequent cortical resection, and in total, 62 spasms were analyzed by using quantitative methods. RESULTS: Spasms were associated with either a "leading" spike followed by fast-wave bursts (type I: 42 events analyzed quantitatively) or fast-wave bursts without a "leading" spike (type II: 20 events analyzed quantitatively). Twenty-three of the 42 type I spasms but none of the 20 type II spasms were preceded by a focal seizure. A "leading" spike had a focal origin in all 42 type I spasms and involved the pre- or postcentral gyrus within 0.1 s in 37 of these spasms. A leading spike was associated with interictal spike activity >1/min in 40 of 42 type I spasms and originated within 2 cm from a positron emission tomography glucose hypometabolic region in all but two type I spasms. Failure to resect the cortex showing a leading spike was associated with poor surgical outcome (p = 0.01; Fisher's exact probability test). Fast-wave bursts associated with spasms involved neocortical regions extensively at least in two lobes within 1.28 s in all 62 spasms and involved the pre- or postcentral gyrus in 53 of 62 spasms. CONCLUSIONS: Epileptic spasms may be triggered by a focal neocortical impulse in a subset of patients, and a leading spike, if present, might be used as a marker of the trigger zone for epileptic spasms. Rapidly emerging widespread fast-wave bursts might explain the clinical semiology of epileptic spasms.

Brain Mapping↗
PubMed1999

Prognostic significance of the pattern of multivessel spasm in patients with variant angina.

Multivessel spasm in variant angina is believed to be a major prognostic factor. Three patterns of multivessel spasm have been detected: (1) spasm at different sites on different occasions (migratory spasm); (2) spasm sequentially affecting 2 different sites (sequential spasm); and (3) simultaneous spasm at more than 1 site (simultaneous spasm). The present study investigated the prognosis based on this factor for variant angina without fixed coronary stenosis and examined the influence of multivessel spasm on cardiac events. Twenty-six patients were diagnosed as having variant angina without fixed coronary stenosis using 12-lead 24-h ECG recording system and coronary cineangiography. These patients were followed up prospectively for 57.1+/-7.6 months. Of the 26 patients 13 had single-vessel spasm, 6 had migratory multivessel spasm angina, and 7 showed sequential and/or simultaneous multivessel spasm angina. The survival free of serious cardiac events and of all cardiac events was significantly lower for patients with sequential and/or simultaneous multivessel spasm than for those with migratory multivessel spasm (p<0.05, p<0.05), whereas for patients with migratory multivessel spasm the difference comparison with single-vessel spasm did not attain statistical significance (p = ns, p = ns). The results of this study suggest that there seems to be a high-risk subgroup (i.e., sequential and/or simultaneous multivessel spasm) among patients with variant angina.

Aged↗
PubMed2000

New combined spasm provocation test in patients with rest angina: intracoronary injection of acetylcholine after intracoronary administration of ergonovine.

The incidence of provoked coronary spasm with the standard single spasm provocation test has been relatively low in patients with rest angina. The present study examined the clinical usefulness of a newly designed spasm provocation test, an intracoronary injection of acetylcholine (ACh) following an ergonovine (ER) test, in patients with rest angina who demonstrated low disease activity and atypical chest pain. Triple sequential spasm provocation tests were performed in 24 patients with atypical chest pain who had no ischemia and in 40 patients with rest angina who had distinct ischemia. Initially, an ACh test (20-100 microg) and then an ER test (40-64 microg) were performed and then, if no spasm was provoked, an intracoronary injection of ACh was given after the ER test to evaluate coronary spasm. Coronary spasm was defined as total or subtotal occlusion. In the 24 patients with atypical chest pain, no spasm was provoked by intracoronary injection of either ACh or ER, but coronary spasms were induced in 2 patients using the new method, with the remaining 22 not experiencing spasm (specificity of new method, 92%). In the 40 patients with rest angina, intracoronary injection of ACh induced coronary spasm in 22 patients (group I) and 6 (group II) demonstrated spasm with intracoronary injection of ER. Coronary spasm was not induced by either the ACh test or the ER test in 12 patients (group III). The intracoronary administration of ACh after the ER test provoked spasm in 11 of 12 patients. Diffuse spasms were provoked in 10 of 11 patients. In patients with rest angina, the frequency of chest pain attacks in 1 month experienced by patients in group III (0.8+/-0.8) was significantly lower than that of patients in group I (7.0+/-5.3, p<0.01) or II (3.5+/-2.3, p<0.05). No serious or irreversible complications related to this new combined method were observed. In conclusion, this method was safe and reliable for the induction of coronary spasm in patients with rest angina who may have low disease activity.

Acetylcholine↗