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At least 631 records · Page 35Linked to original sources
PubMed1976

Prinzmetal's angina with coronary artery spasm. Angiographic, pharmacologic, metabolic and radionuclide perfusion studies.

We studied the effects of coronary artery spasm on perfusion of the microvasculature in a patient with Prinzmetal's angina. Intracoronary injections of 99mTc and 131I-labelled macroaggregated human serum albumin were performed (1) at rest, (2) during spontaneous angina, (3) after the administration of nitroglycerin and (4) during pacing-induced spasm and the resultant scans compared. The resting scan was normal. Pain and spasm were associated with a perfusion defect that was localized to the anterior and inferior walls of the left ventricle. The localization of the perfusion defect corresponded with angiographically demonstrated spasm involving left anterior descending and distal circumflex coronary arteries. A subsequent myocardial infarction was localized by 43K scanning to the same perfusion area. Metabolic and parasympathetic stimulation studies were performed but were inconclusive. The patient's recurrent pains were ultimately controlled with large oral doses of isosorbide dinitrate.

Angina Pectoris↗
PubMed1981

Coronary artery spasm in the denervated transplanted human heart: a clue to underlying mechanisms.

The mechanism of coronary artery spasm has been poorly understood but there has been some suggestion that cardiac autonomic innervation may play an important role. We report coronary artery spasm in a 43 year old man two years after he had received a transplant. Provocative pharmacologic testing suggested functional denervation of the patient's heart. Thus, coronary artery spasm can occur in the transplanted, denervated human heart. Autonomic innervation of the heart is not essential in all cases of coronary spasm, and circulating catecholamines and/or metabolic of hormonal products may play an important role.

Adolescent↗
PubMed1994

Long-term follow-up of coronary narrowing with spasm.

In order to clarify the fate of coronary narrowing with spasm, repeat angiograms of coronary narrowing with and without spasm were compared. The mean interval between the first and second angiograms was 3.6 years (range, 1.1-8.5 years). Improvement of narrowing was more frequent in the vasospastic group (23%) than in the group without spasm (3%, P < 0.005). The cause of this improvement in the vasospastic group may have been the resolution of the spasm in the first angiogram, but the presence of intravascular thrombus or bleeding or edema of the coronary arterial wall may have resolved in the second angiogram.

Angina Pectoris, Variant↗
PubMed1996

The comparison of vascular reactivities of arterial and venous grafts to vasodilators: management of graft spasm.

Graft spasm in the perioperative or postoperative period increases the risk of morbidity and mortality after coronary revascularization and hence necessitates urgent treatment. We have studied the effects of various vasodilators against noradrenaline- and endothelin-1-induced spasms in saphenous vein, internal mammary artery and gastroepiploic artery. In internal mammary and gastroepiploic arteries, the nitrovasodilators, sodium nitroprusside and glyceryl trinitrate, effectively reversed the spasms induced either with noradrenaline (for sodium nitroprusside; internal mammary artery: 101.07% +/- 1.63%; gastroepiploic artery: 94.10% +/- 2.07%) or endothelin-1 (for sodium nitroprusside; internal mammary artery: 97.67% +/- 4.94%; gastroepiploic artery: 90.69% +/- 2.61%). However, in saphenous vein contracted with endothelin-1, the responsiveness to nitrovasodilators was significantly blunted (for sodium nitroprusside: 52.33% +/- 5.19%) than that of rings contracted with noradrenaline (for sodium nitroprusside: 95.04% +/- 1.94%). Both arterial and venous grafts exhibited moderate beta-receptor function in response to isoproterenol. Isoproterenol was less effective in inhibiting the contractions of endothelin-1 in saphenous vein and gastroepiploic artery but not in internal mammary artery. On the other hand, nifedipine and papaverine were fully effective in reversing all the spasms in three of the graft materials. From these results, it can be deduced that saphenous vein is refractory against cyclic guanidine monophosphate (cGMP)-dependent and beta-receptor mediated relaxations when endothelin-1 was used as the spasmogenic agent. Internal mammary artery is the most responsive graft material to the vasodilators regardless of the nature of spasmogenic stimulus. Gastroepiploic artery exhibits functional similarity with internal mammary artery, with the exception of beta-receptor responsiveness.

Adult↗
PubMed1989

Angiographic demonstration of spontaneous diffuse three vessel coronary artery spasm.

The spontaneous occurrence of diffuse three vessel coronary artery spasm was documented during routine coronary angiography in three patients with a history of variant angina. Quantitative angiographic analysis of 18 arterial segments demonstrated that the mean luminal diameter of 1.47 mm during spasm increased to 2.47 mm after the administration of nitroglycerin (p less than 0.0001). The underlying coronary arteries were normal or near normal. Although multivessel spasm has previously been considered to be uncommon and its spontaneous occurrence during angiography only rarely documented, these cases suggest that it may be more common than previously recognized. In addition to important diagnostic considerations, this phenomenon may have important implications regarding the pathophysiologic role of endothelium in coronary artery spasm.

Aged↗
PubMed1993

Myoclonic spasms following intrathecal diamorphine.

The use of intrathecal diamorphine via an implanted portal system is described for pain control in a patient suffering from vertebral metastatic disease. The complication of myoclonic spasms affecting the lower half of the body occurred after 14 days, when increasing the bolus dose to 40 mg. The spasms lasted for 3 hr and then gradually subsided. Diamorphine was subsequently restarted at a lower dose of 15 mg twice daily. On increasing the dose to 20 mg diamorphine 10 days later, severe distressing myoclonic spasms recurred 20 min postinjection. Myoclonus could only be controlled by instituting a local anesthetic intrathecal block. The patient was finally managed with 20 mg diamorphine per day by intrathecal infusion, and the pain was reasonably well controlled for the following 10 weeks without any recurrence of myoclonic spasms.

Anesthesia, Local↗
PubMed2004

Pelvic floor spasms in children: an unknown condition responding well to pelvic floor therapy.

OBJECTIVE: During a study period of 4 years, 21 children are seen for night time pelvic pain. These children typical wake up in the middle of the night with severe lower abdominal or perineal pain. During day some of them suffer urge syndrome. During urodynamic investigation extremely high pelvic floor activity as recorded by high urethral pressure was observed in these children. We therefore started pelvic floor relaxation biofeedback in these children. METHODS: All children diagnosed with pelvic floor spasms underwent biofeedback pelvic floor relaxation therapy in order to learn them to counteract pelvic pain due to these spasms. In those girls in whom detrusor hyperactivity was seen on urodynamics concomitant anticholinergic treatment was given (oxybutynin). RESULTS: Between January 1998 and January 2002 symptomatic pelvic floor spasms were diagnosed in 21 children (19 girls/2 boys). Pelvic floor relaxation biofeedback was successful for treatment of this condition in 17 of 21 children. Mean duration of therapy was 3 months (12 weekly sessions) and on long term follow-up relapse was seen in 3 of 17 successfully treated children. 10 of 17 successfully treated children received anticholinergics. CONCLUSION: Pelvic floor spasms in children (which can be secondary to detrusor overactivity) respond well to pelvic floor relaxation therapy.

Biofeedback, Psychology↗
PubMed2006

Secondary prevention of sudden cardiac death in coronary artery spasm: is implantable cardioverter defibrillator always efficient?

Syncope and/or cardiac arrest in the setting of coronary artery spasm have been associated with atrioventricular block and asystole or ventricular tachyarrhythmias. Ventricular arrhythmias have been predominantly reported in cases of multivessel coronary artery spasm. The present report highlights the case of a young woman who suffered repeated episodes of multivessel coronary artery spasm in association with polymorphic ventricular tachycardia and cardiac arrest. The efficacy of implantable cardioverter defibrillator in secondary prevention of sudden cardiac death due to coronary artery spasm is discussed.

Adult↗
PubMed2006

SPASM: a 3D-ASM for segmentation of sparse and arbitrarily oriented cardiac MRI data.

A new technique (SPASM) based on a 3D-ASM is presented for automatic segmentation of cardiac MRI image data sets consisting of multiple planes with arbitrary orientations, and with large undersampled regions. Model landmark positions are updated in a two-stage iterative process. First, landmark positions close to intersections with images are updated. Second, the update information is propagated to the regions without image information, such that new locations for the whole set of the model landmarks are obtained. Feature point detection is performed by a fuzzy inference system, based on fuzzy C-means clustering. Model parameters were optimized on a computer cluster and the computational load distributed by grid computing. SPASM was applied to image data sets with an increasing sparsity (from 2 to 11 slices) comprising images with different orientations and stemming from different MRI acquisition protocols. Segmentation outcomes and calculated volumes were compared to manual segmentation on a dense short-axis data configuration in a 3D manner. For all data configurations, (sub-)pixel accuracy was achieved. Performance differences between data configurations were significantly different (p<0.05) for SA data sets with less than 6 slices, but not clinically relevant (volume differences<4 ml). Comparison to results from other 3D model-based methods showed that SPASM performs comparable to or better than these other methods, but SPASM uses considerably less image data. Sensitivity to initial model placement proved to be limited within a range of position perturbations of approximately 20 mm in all directions.

Algorithms↗
PubMed2006

ACTH therapy for generalized seizures other than spasms.

PURPOSE: We reviewed our experience with ACTH for the treatment of intractable generalized seizures other than spasms. METHODS: Efficacy and adverse effects of ACTH against intractable generalized seizures other than spasms were retrospectively investigated in 15 patients treated between 1991 and 2003. The median age of the patients at ACTH therapy was 42 months. The targeted type of seizure was brief tonic in 6, atypical absence in 6, atonic in 2, and myoclonic in 1. The dose of ACTH was 0.01-0.015 mg/kg in most patients. The effect of ACTH was determined at the end of ACTH therapy, and 3 months and 1 year after ACTH therapy. RESULTS: Seizure freedom was obtained in 13 of 15 patients. However, 6 of them had a recurrence of seizures within 3 months after ACTH therapy. ACTH was the most effective in patients with atypical absence seizures. Statistical analysis showed that the number of injection and total dose of ACTH were smaller in patients with atypical absence seizures than in those with brief tonic seizures. Adverse effects were frequent but serious one was not observed. CONCLUSION: ACTH therapy was effective in patients with intractable generalized seizures other than spasms. However, its efficacy was often transient. ACTH can be useful for generalized seizures other than spasms but its limitation should be considered.

Adrenocorticotropic Hormone↗
PubMed2000

Myocardial ischemia due to coronary artery spasm during dobutamine stress echocardiography.

Dobutamine stress echocardiography (DSE) is a useful and safe provocation test for myocardial ischemia. Until now, the test has been focused only on the organic lesion in the coronary artery, and positive DSE has indicated the presence of significant fixed coronary artery stenosis. The aim of the present study is to examine whether myocardial ischemia due to coronary spasm is induced by dobutamine. We performed DSE on 51 patients with coronary spastic angina but without significant fixed coronary artery stenosis. All patients had anginal attacks at rest with ST elevation on the electrocardiogram (variant angina). Coronary spasm was induced by intracoronary injection of acetylcholine, and no fixed coronary artery stenosis was documented on angiograms in all patients. DSE was performed with intravenous dobutamine infusion with an incremental doses of 5, 10, 20, 30, and 40 microg/kg/min every 5 minutes. Of the 51 patients, 7 patients showed asynergy with ST elevation. All 7 patients (13.7%) had chest pain during asynergy, and both chest pain and electrocardiographic changes were preceded by asynergy. These findings indicate that dobutamine can provoke coronary spasm in some patients with coronary spastic angina. When DSE is performed to evaluate coronary artery disease, not only fixed coronary stenosis, but also coronary spasm should be considered as a genesis of asynergy.

Adrenergic beta-Agonists↗
PubMed1982

Intraoperative use of nifedipine for hemodynamic collapse due to coronary artery spasm following myocardial revascularization.

Sudden hemodynamic collapse in the perioperative period following myocardial revascularization may be due to coronary artery spasm. Nitroglycerin has been the standard treatment for this; however, it is not always effective, and the resultant morbidity and mortality are high. We present the case of a patient in whom sudden hemodynamic collapse due to coronary artery spasm was refractory to intravenously administered nitroglycerin but was relieved quickly with sublingually administered nifedipine. In certain selected patients in whom coronary artery spasm is responsible for myocardial collapse, the drug nifedipine may be effective in relieving this spasm and allowing for myocardial recovery.

Coronary Vasospasm↗
PubMed1987

Early postoperative spasm in left internal mammary artery bypass grafts.

Two patients with early postoperative spasm of a left internal mammary artery bypass graft are described. To our knowledge, this entity has not been reported previously. Both patients were characterized by vasomotor collapse secondary to intractable spasm responsive only to local application of vasodilator agents. Although the mechanism of graft spasm is not clear, prophylactic nifedipine therapy in appropriate dose may be of some value. The profound hemodynamic effect of internal mammary artery spasm in the immediate postoperative period may allow no time for anything other than emergency reoperation to assess the nature of the problem and treat it appropriately.

Aged↗
PubMed2001

Enhanced platelet aggregation in the coronary circulation after coronary spasm.

A recently developed platelet aggregometer using a laser light scattering method is capable of monitoring the increase in size of small-sized platelet aggregates (diameter 9-25 microm), which cannot be detected with the conventional methods. Whether coronary spasm can cause platelet aggregation in the coronary circulation is unknown. We investigated platelet aggregation, especially small-sized platelet aggregates, simultaneously in the coronary sinus and the aortic root in 18 patients with coronary spastic angina before and after a left coronary artery spasm induced by intracoronary injection of acetylcholine, and in 15 patients with stable exertional angina before and after acute myocardial ischemia induced by rapid right atrial pacing. Platelet aggregation in 12 patients with chest pain syndrome was also examined before and after coronary spasms provoked by acetylcholine. The number of small-sized platelet aggregates increased significantly in the coronary sinus [2.0+/-0.6 x 104 to 4.1+/-1.0 x 104 (V), P<.01] and in the aortic root [1.7+/-0.6 x 104 to 3.2+/-0.6 x 104 (V), P<.05], and the coronary sinus-arterial difference in the number of small-sized platelet aggregates [2.3+/-1.9 x 103 to 1.1+/-0.4 x 104 (V), P<.01] increased significantly after attacks in the coronary spastic angina group, but remained the same in the stable exertional angina group after attacks and in the chest pain syndrome group after the administration of acetylcholine. Therefore, we can conclude that acute myocardial ischemia induced by coronary spasm causes platelet aggregation in the coronary circulation.

Acetylcholine↗
PubMed1985

Smooth muscle contraction bands in the media of coronary arteries: a postmortem marker of antemortem coronary spasm?

To date, no unequivocal morphologic markers have been described that would allow the diagnosis of coronary artery spasm to be made at autopsy. The coronary arteries of 63 adult patients without myocardial infarction were examined at autopsy, and the presence of medial smooth muscle contraction bands in these vessels was correlated with other vascular changes, myocardial pathologic changes and clinical history. These contraction bands have not been reported previously in human coronary arteries, but they were identified in experimental vascular spasm induced with catecholamines. It was found that 47 of the 63 cases were positive for contraction bands. As evidence of an antemortem process, there was a significant correlation between these changes and the presence of nonocclusive microthrombi, found in 25 cases. Contraction bands were also highly correlated with atherosclerotic plaque ruptures and mural plaque hemorrhages, which may be secondary to coronary spasm. In 78.7% of the cases positive for contraction bands, the cause of death was related to a diagnosis possibly associated with high catecholamine levels. On the basis of experimental evidence and the correlations identified in this study, coronary artery medial smooth muscle contraction bands may represent a postmortem marker of antemortem coronary spasm.

Adult↗
PubMed1996

Autonomic changes associated with spontaneous coronary spasm in patients with variant angina.

OBJECTIVES: This study sought to investigate whether changes in nervous autonomic tone may have a role in the mechanisms triggering spontaneous coronary spasm in variant angina. BACKGROUND: Previous studies have suggested that both sympathetic and vagal activation may act as a trigger of epicardial artery spasm in patients with variant angina, but the actual role of autonomic changes in spontaneous coronary spasm remains unknown. METHODS: We analyzed the changes in heart rate variability associated with episodes of ST segment elevation detected on Holter monitoring in 23 patients with variant angina (18 men, 5 women; mean [+/-SD] age 59 +/- 12 years). For study purposes, episodes of transmural ischemia lasting > or = 3 min and without any ST segment changes in the previous 40 min were selected for analysis. Heart rate variability indexes were calculated at 2-min intervals, at 30,15,5 and 1 min before ST elevation and at peak ST segment elevation. Ninety-three of 239 total ischemic episodes (39%) fulfilled the inclusion criteria. RESULTS: The results showed that 1) high frequency (HF) (0.04 to 0.15 Hz), a heart rate variability index specific for vagal activity, decreased in the 2 min preceding ST segment elevation (p < 0.001) and returned to basal levels at peak ST segment elevation; 2) heart rate and low frequency (0.04 to 0.15 Hz), which are partially correlated with sympathetic activity, showed a significant increase at peak ST segment elevation (p < 0.001 for both); 3) the pattern of the HF reduction before ST segment elevation was consistently confirmed in several subgroups of ischemic episodes, including those of patients with or without coronary stenoses, those of patients with anterior or inferior ST segment elevation, those occurring during daily or nightly hours and silent episodes. There were no significant variations in heart rate variability in control periods selected from Holter tapes of patients and before ST segment elevation induced by balloon inflation in 20 patients undergoing coronary angioplasty. CONCLUSIONS: Our data show that changes in autonomic tone are likely to contribute to trigger or predispose to epicardial spasm. In particular, although not excluding an active role for adrenergic mechanisms, our data suggest that a vagal withdrawal may often be a component of the mechanisms leading to spontaneous coronary vasospasm.

Aged↗
PubMed1998

Arrhythmic cardiac arrest due to isolated coronary artery spasm: long-term outcome of seven resuscitated patients.

OBJECTIVES: Our aim was to look at the clinical features and long-term follow-up of seven patients without coronary artery disease, who had a history of life-threatening ventricular arrhythmias due to coronary spasm. BACKGROUND: Arrhythmic cardiac arrest due to isolated coronary spasm is rare, and there is limited information on the patients affected by this entity alone. METHODS: The seven patients were recruited retrospectively from a cohort of survivors of cardiac arrest. None had a history of angina pectoris, structural heart disease or significantly narrowed coronary segments. All had a positive ergonovine provocation test result. RESULTS: The patients' mean age was 44 years; three were male and four female. All were habitual cigarette smokers. No arrhythmias were induced on programmed ventricular stimulation; corrected QT interval (QTc) and corrected JT interval (JTc) dispersion were within normal ranges. After the ergonovine provocation test, treatment with calcium channel blocking agents (diltiazem, verapamil, nifedipine or amlodipine) was initiated at a dose determined by titration until a negative test result was obtained. At a mean follow-up interval of 58 months for the total group, six patients remained free of symptoms, whereas the one patient who did not stop smoking had a new cardiac arrest despite treatment for coronary spasm. CONCLUSIONS: A favorable long-term outcome may be expected in survivors of cardiac arrest due to coronary spasm, in the absence of significant coronary artery disease. Calcium channel blockers are the most appropriate therapy in these patients. These observations provide further evidence for the role of silent ischemia in cardiovascular death.

Adult↗
PubMed1984

[Coronary spasm during repeated anesthesia].

Coronary arterial spasm observed during the course of two repeated anaesthesias in a patient having undergone aorto-femoral bypass grafting is reported by the authors. Such complications are accompanied by serious ventricular arrhythmias, though transient and healing without sequelae. Clinical and electrocardiographic characteristics of peroperative coronary arterial spasm are underlined. In patients prone to developing such spasm, peroperative alkalosis, hypothermia and parasympathetic stimuli should be avoided. Are emphasized the efficiency of preventive treatment with calcium antagonists and that of intravenous nitroglycerin in the treatment of peroperative coronary arterial spasm when it does occur.

Alkalosis↗