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At least 613 records · Page 34Linked to original sources
PubMed1996

[The contribution of "time-of-flight" MRI-angiography in the study of neurovascular interactions (hemifacial spasm and trigeminal neuralgia)].

The purpose of this study was to investigate capabilities of Magnetic Resonance Angiography (MRA) in delineating neurovascular compression which has emerged as the most frequent etiology in cases of Hemi-Facial Spasm and Trigeminal Neuralgia. MR investigations were carried out at 1.5 t unit (Magnetom Vision, Siemens). The examination consisted of 3D time-of-flight MRA (3d TOF) protocol, with a FISP sequence (Fast Imaging Steady Precession) and magnetization transfer. Imaging parameters were; TR 39 ms, TE 7 ms; MX 256-512; FOV 210-210 mm. Time acquisition is 10 mm 30 s. The axially acquired angiographic slices were reformatted with a multiplanar reconstruction program (MPR) along and across the plane of facial and trigeminal nerves. Then millimetric raw data images were postprocessed with a maximum intensity projection (MIP) technique. 58 patients presented either with hemifacial spasm (36 cases, 16 women, 20 men, mean age: 58.5 y) or trigeminal neuralgia (22 cases, 13 women, 8 men, mean age: 51 y) were compared with 17 patients (9 women, 8 men, mean age: 57.5 y) as references. MRA with MIP and MPR techniques reliably demonstrates neurovascular compression at the root entry zone (REZ), and allows recognition of the implicated vascular loop in 34 the cases of hemifacial spasm investigated. Raw data were post-processed in an axially oblique plane parallel to the acoustico-facial bundle and secondarily reconstructed in coronally obliques views. These reconstructed images clearly delineate the cross-compression of the emerging facial nerve. The neurovascular conflict was related to an arterial loop from the postero-inferior cerebellar artery (PICA, 21 cases, 61%) and the antero-inferior cerebellar artery (AICA, 8 cases, 23%). Vertebral artery is implicated in conflicts in 5 cases. In 2 cases MRA exploration was negative. In HFS group distance between Vth nerve emergency and neuro vascular contact was measured and compared with control group; there is a significative difference (p < 0.01). In case of trigeminal neuralgia, MRA demonstrates neurovascular compression at the root entry zone of the Vth nerve of 16 patients. In theses cases, oblique and coronally reconstructed images are crucial in demonstrating neurovascular contacts. The vessel implicated in conflict is always the superior cerebellar artery (SCA). A supero-medial loop of the superior cerebellar artery was depicted in these 16 cases. Although 3 patients had negative MRA and MR studies, a case of compression of the origin of the Vth nerve by a enlarged draining vein in a case of brainstem arterio-venous malformation, a petrous apex meningioma was incidentally discovered and thoroughly investigated with gadolinium T1 weighted sequences and 1 demyelinating plaques located along the intraaxial course of the Vth nerve were noticed. In control group on 34 explanations only there are only 4 contacts between Vth nerve and SCA. MRA with a 3D-TOF FISP sequence allows recognition of neurovascular conflicts in case of hemifacial spasm and trigeminal neuralgia while MIP helps to characterize the implicated vessel. Sources images need to be carefully assessed in order to depict unsuspected pathology.

Adolescent↗
PubMed1978

Hemifacial spasm due to aneurysmal compression of the facial nerve.

Hemifacial spasm developed in a woman as the only symptom of an aneurysm of the posterior inferior cerebellar artery. Using microdissecting techniques, the aneurysm was clipped and moved from its distorting position at the brain stem exit zone of the seventh nerve. After surgery, she experienced immediate relief of her facial spasm of six years' duration. This case supports the finding that hemifacial spasm may be caused by vascular lesions of the seventh nerve at the brain stem junction. Recent surgical experience indicates that the majority of the hemifacial spasm cases may be due to normal but ectatic blood vessels that cross-compress the most proximal portion of the seventh nerve. Relief may be affected without facial paralysis by a retromastoid microvascular decompressive procedure.

Arteries↗
PubMed2005

Feasibility and safety of the transradial approach for the intracoronary spasm provocation test.

An angiography-based spasm provocation test is an accurate diagnostic test of coronary vasospastic angina, but is associated with high patient morbidity, mainly because of the femoral approach and the need for a temporary pacemaker. The purpose of this study was to investigate the safety and feasibility of a transradial ergonovine spasm provocation test. The test was performed prospectively in 174 consecutive patients who were under suspicion of coronary vasospasm at our institution from April 2002 to June 2003. Seventy-eight out of 174 procedures (45%) were performed in an outpatient department. The procedural success rate was 168/174 (96%). All failures were because of access failures, and no major complications were noted. Minor complications were observed in nine patients (severe bradycardia in three, hypotension in two, both in two, and nonsustained ventricular tachycardia in two). The incidence of complications was higher in patients showing prolonged spasm in the right coronary artery. No major local complication was noted other than rebleeding in the puncture site during hemostasis in one patient. The transradial spasm provocation test performed without using a temporary pacemaker may be feasible and safe, with a high success rate and low complication rate as well as low patient morbidity.

Aged↗
PubMed2003

Increased TIMI frame counts in cocaine users: a case for increased microvascular resistance in the absence of epicardial coronary disease or spasm.

BACKGROUND: Cocaine produces adverse cardiovascular effects, some of which cannot be explained by epicardial coronary artery disease (CAD) or spasm. HYPOTHESIS: The hypothesis of this study was that cocaine users would have increased coronary microvascular resistance, even in the absence of recent myocardial infarction (MI), CAD, or spasm. METHODS: Microvascular resistance was assessed by the corrected Thrombolysis in Myocardial Infarction (TIMI) frame count (cTFC) method in a consecutive series of 59 cocaine users without acute or recent MI or angiographically significant epicardial stenosis (> 50%) or spasm. The cTFCs in these patients were compared with 21 normal controls and with published normal cTFC values. RESULTS: The cTFC was significantly elevated (by 26-54%) in cocaine users. The cTFCs in the left anterior descending (LAD), circumflex (LCx), and right coronary (RCA)arteries in cocaine users were 30.0 +/- 10.9,34.1 +/- 11.5, and 28.6 +/- 11.8, respectively, compared with values in normal controls of 21.3 +/- 4.3 (p = 0.001), 24.4 +/- 7.2 (p = 0.001), and 22.7 +/- 5.1 (p = 0.04), respectively, and published normal cTFC values (all p < 0.01). An abnormally high cTFC was present in 61% of patients in the LAD, 69% in the LCx, and 47% in the RCA. CONCLUSIONS: Markedly decreased coronary blood flow velocity, indicating increased microvascular resistance, is present in cocaine users, even in the absence of acute or recent MI, or significant epicardial CAD or spasm. Increased microvascular resistance may explain many important cardiovascular manifestations of cocaine use and has therapeutic implications. Slow coronary filling may also suggest the possibility of cocaine use in patients in whom it was not otherwise suspected.

Adult↗
PubMed1988

Coronary artery spasm and its relationship to exercise in patients without severe coronary obstructive disease.

Coronary artery spasm is reported to occur with exercise. In patients without severe coronary atherosclerosis, the evidence for exercise-induced coronary artery spasm is limited. Three patients with positive exercise tests but no severe coronary atherosclerosis are presented. Coronary artery spasm was provoked and verified by angiography in all three, but coronary angiography during exercise failed to demonstrate spasm. The literature is reviewed and the value of a routine protocol for evaluation is discussed.

Adult↗
PubMed1997

Botulinum toxin A improves muscle spasms and rigidity in stiff-person syndrome.

We studied the effect of botulinum toxin A (BTA) on painful muscular spasms and rigidity in two bedridden patients with clinical, electrophysiologic, and immunologic evidence of stiff-person syndrome. We injected BTA or saline solution into several limb muscles with both the rater and patient blinded to the order of the injections. A physician, unaware of the treatment order, used an objective rating scale for rigidity and spasm frequency scale and independently assessed the treatment results. BTA administration significantly reduced rigidity and stopped the spasms in all limbs. Following BTA injection on one side, the spasm frequency decreased bilaterally possibly because of the spread of hematogenous toxin.

Botulinum Toxins, Type A↗
PubMed1994

Ventricular fibrillation related to coronary spasm in patients without significant coronary or other structural heart disease.

We present three patients without significant coronary or other structural heart disease who were resuscitated after ventricular fibrillation attributed to coronary spasm. Angina pectoris was present in two of the cases and silent myocardial ischemia in the third. All patients were given calcium antagonists at discharge. A defibrillator was also implanted in the patient with silent myocardial ischemia because further episodes of ischemia would probably have occurred without premonitory symptoms. Coronary spasm might be a mechanism of ventricular fibrillation in patients without significant structural heart disease. Diagnostic tests should therefore be performed to confirm or exclude coronary spasm in such cases. The implantation of an automatic defibrillator seems justified in selected patients with documented coronary spasm, silent myocardial ischemia, and associated sustained ventricular tachyarrhythmia, although prospective studies are not yet available.

Adult↗
PubMed1993

Effects of a new calcium antagonist, CD-832, on experimental coronary artery spasm in miniature pigs.

The effects of a new calcium antagonist, CD-832, on experimental coronary artery spasms were studied in Göttingen miniature pigs. Pigs underwent endothelial denudation at the left anterior descending coronary artery using a balloon catheter. Changes in the diameter of the denuded and nondenuded site in response to an intracoronary administration of serotonin (10 micrograms/kg) or histamine (10 micrograms/kg) were assessed quantitatively by selective coronary arteriography 1 week after endothelial denudation. Percent reductions of the coronary artery diameter induced by serotonin or histamine in the denuded site were significantly greater than those in the nondenuded site (p < 0.01). Coronary artery spasm induced by serotonin or histamine in the denuded site was attenuated in a dose-dependent manner by intravenous infusion of CD-832 (10 and 30 micrograms/kg/min) or nifedipine (1 and 3 micrograms/kg/min). The degrees of inhibition of coronary artery spasm by CD-832 were similar to those produced by nifedipine. CD-832 and nifedipine at the high dose caused comparable increases in the basal coronary artery diameter. These results suggest that CD-832 may be a useful drug for the treatment of coronary artery spasm.

Animals↗
PubMed1988

Coronary artery spasm during coronary artery bypass surgery: its diagnosis, treatment and prevention.

Between 1982 and 1983, we experienced four cases of hemodynamic collapse accompanied by an ST-segment depression in the ECG lead II, shortly after the cessation of cardiopulmonary bypass. The bypass graft flows monitored in these patients during the hemodynamic collapse episodes were remarkably low. In three cases, nitroglycerin (0.5-1 mg) was injected directly into the vein graft, which increased the graft flow suddenly, returned the ST-segment to the baseline, and improved the circulatory condition. Since 1984, however, diltiazem has been used in the cardioplegic solution and postoperative drip infusion. Due to the introduction of this drug, coronary artery spasm has not been seen in any of our patients since. These findings show that the monitoring of ST-segment changes and bypass graft flows are useful in the early diagnosis of coronary artery spasm after myocardial revascularization. Direct infusion of nitroglycerin into the vein graft is effective for the treatment of spasm, while diltiazem is useful in the prevention of coronary artery spasm incidental to myocardial revascularization.

Coronary Artery Bypass↗
PubMed2001

Infantile Spasms.

Infantile spasm is a catastrophic form of epilepsy found only in infants and young toddlers. Onset is before one year of age, with a peak incidence occurring between 4 to 7 months of age. The prevalence is difficult to calculate, but previous reviews have estimated between 1 per 2000 to 6000 live births. There are many causes of infantile spasms, including tuberous sclerosis, malformations of cortical development, hypoxic-ischemic injury, congenital infectious diseases, inborn errors of metabolism, genetic syndromes such as Aicardi's syndrome, and chromosomal abnormalities. A small percentage of patients have idiopathic infantile spasms, with no identifiable cause and premorbid normal growth and development. In order to prevent an ongoing epileptic encephalopathy with its concomitant consequences of cognitive impairment and intractable seizures, treatment should be aggressive and immediate. It is not enough to control the clinical infantile spasms. The underlying "interictal" hypsarrhythmia pattern must also be abolished if the prognosis is to be improved. Otherwise, the immature brain appears to remain hyperexcitable.

Journal Article↗
PubMed1979

Exertional angina pectoris caused by coronary arterial spasm: effects of various drugs.

In four patients with exertional angina induced by arm exercise, coronary arteriograms taken before, during and after the attack demonstrated that spasm appeared in the large coronary artery supplying the area of myocardium shown to be ischemic in the electrocardiogram during the attack. The spasm disappeared with subsidence of the attack after administration of nitroglycerin. Anginal attacks induced by treadmill exercise were not suppressed by propranolol, 60 mg orally, in two of the four patients. However, such attacks were suppressed in all patients by oral administration of diltiazem (90 mg, four patients) or nifedipine (20 mg, three patients) or intramuscular injection of phentolamine (0.2 mg/kg body weight, three patients). It is concluded that coronary arterial spasm can be induced by exercise and can cause exertional angina in some patients. Diltiazem and nifedipine, calcium antagonistic drugs, prevent spasm.

Adult↗
PubMed1981

Nifedipine blockade of ergonovine-induced coronary arterial spasm: angiographic documentation.

To determine whether calcium-flux blockade with nifedipine blunts coronary vasospasm, four patients with angiographically demonstrable coronary arterial spasm in the absence of significant fixed coronary arterial stenosis were evaluated with coronary arteriography before and after treatment with nifedipine. After initial coronary arteriography, ergonovine was administered in successive doses of 0.05, 0.1 and (when necessary) 0.2 mg intravenously at 3 minute intervals. Three patients had symptomatic high grade focal coronary arterial spasm with electrocardiographic changes, and the fourth exhibited asymptomatic 60 percent constriction of the left anterior descending coronary artery. A maximal ergonovine challenge was repeated 30 minutes later after each patient had been pretreated with a 20 mg sublingual dose of nifedipine. Under these conditions, no patient had chest pain or electrocardiographic changes. Furthermore, neither focal nor diffuse coronary arterial spasm was demonstrable angiographically after the second challenge. Thus, in each case, a single dose of nifedipine precluded the angiographic expression of ergonovine-provoked coronary arterial spasm.

Angina Pectoris↗
PubMed1982

Postmyocardial infarction angina and coronary spasm.

Coronary spasm can cause chest pain, and may even culminate in a myocardial infarction, but it is not often considered a cause of chest pain in the early postinfarction period. Three patients who had chest pain early (1 day to 3 weeks) after myocardial infarction were shown to have coronary spasm with ergonovine maleate provocation. Two patients had spasm in the coronary artery associated with the acute infarction; the third had spasm in a remote vessel. Two required intracoronary nitroglycerin to establish patency in the affected vessel. It is concluded that coronary vasospasm can result in postinfarction angina.

Adult↗
PubMed1985

Initial coronary air embolus in the differential diagnosis of coronary artery spasm.

Angiographic and electrocardiographic manifestations of initial coronary air embolism were seen in 4 patients and in a dog. All 4 patients had angina pectoris, 2 had ST elevation, 1 patient had ST depression and 1 had no electrocardiographic change after the air embolus. Although the initial diagnosis in these 4 patients was coronary artery spasm, a subsequent ergonovine test response for coronary artery spasm was negative in the 3 patients in whom it was performed. In a dog, initial injection of air in a coronary artery produced ST-segment elevation and delayed clearance of contrast material. The angiographic appearance of initial air embolus was similar in the 4 patients and in the dog. The leading edge of contrast material that followed an air embolus stopped abruptly, appeared hazy and blunt, and pulsated back and forth. The air embolus produced temporary cessation of flow in the main artery and its branches. Initial injection of air during coronary arteriography mimics coronary artery spasm by producing a syndrome characterized by angina, ischemic changes on the electrocardiogram, and delayed flow of contrast material. An initial air embolus may be differentiated from true coronary spasm by several distinctive angiographic features.

Adult↗
PubMed1985

Functional significance of transient collaterals during coronary artery spasm.

Coronary collateral vessels appear transiently during vasospasm. To examine the functional role of such collaterals in acute myocardial ischemia, regional coronary flow was determined in patients who showed isolated total spasm in the proximal left anterior descending coronary artery associated with (n = 7, group I) and without (n = 9, group II) collaterals, which were donated by the nonspastic right coronary artery during ergonovine provocative test. Aortic pressure and heart rate were not significantly different in the 2 groups before and during spasm. During vasospasm, the levels of pulmonary artery end-diastolic pressure were significantly higher in group II (19 +/- 2 mm Hg, mean +/- standard error) than in group I (15 +/- 1 mm Hg, p less than 0.05). Under these conditions, great cardiac vein flow (GCVF) measured by thermodilution was markedly reduced in group II (from 60 +/- 4 ml/min to 37 +/- 4 ml/min, p less than 0.01), whereas GCVF was slightly reduced in group I (from 56 +/- 4 ml/min to 51 +/- 4 ml/min), indicating that residual GCVF was greater in patients with than in those without collaterals (p less than 0.05). The calculated coronary collateral resistance index during vasospasm was significantly lower in group I (2.06 +/- 0.18 mm Hg min/ml) than in group II (2.91 +/- 0.30 mm Hg min/ml, p less than 0.05). Total left anterior descending coronary artery spasm with collaterals was less frequently associated with ST elevation in the precordial electrocardiogram recorded during spasm.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Effect of nicorandil on coronary spasm.

In patients in whom dynamic coronary obstruction plays a predominant role in the pathogenesis of angina pectoris, dilatation of large coronary arteries and relief of coronary spasm account for the main mechanism of action of antianginal drugs. In this study, the acute vasodilating effects of nicorandil, a newly developed antianginal drug, were assessed in 10 patients who had spontaneous and ergonovine-evoked coronary spasms. The prompt, complete relief of both spontaneous and evoked coronary spasms was obtained in all of 10 patients with nicorandil. The coronary spasmolytic effect of nicorandil in the present series is thus considered to be beneficial to the treatment of coronary spasm.

Adult↗
PubMed1989

Coronary artery spasm in the genesis of myocardial ischemia.

Angina pectoris that is mainly caused by coronary artery spasm (coronary spastic angina) has 1 or more of the following characteristics: (1) the attack occurs at rest, (2) the attack is associated with ST-segment elevation on the electrocardiogram (not necessarily so in case of old myocardial infarction), (3) the attack has a variable exercise threshold, and (4) the attack is suppressed by calcium antagonists but not by beta-adrenergic blocking agents. By this criteria, coronary artery spasm is involved in the development of most angina pectoris in patients with 1-vessel disease. The role of coronary artery spasm in the development of acute myocardial infarction is still controversial. However, in this study, injection of nitroglycerin, 0.2 mg, into the totally or subtotally occluded coronary artery either released the occlusion or improved the patency in 13 of the 69 patients (18.8%) with acute transmural myocardial infarction in whom coronary arteriography was performed within 4.0 +/- 1.9 hours of the onset of symptoms. Thus, coronary artery spasm appears to play a role in the production of acute myocardial infarction in these patients.

Circadian Rhythm↗
PubMed1991

Comparative effects of oral molsidomine and nifedipine on methylergometrine-induced coronary artery spasm.

Twelve consecutive patients (10 men and 2 women, mean +/- standard deviation age 49 +/- 9 years) with chest pain, angiographically normal coronary arteries and coronary artery spasm documented by methylergometrine testing received a single oral dose of molsidomine (4 mg) or nifedipine (10 mg) in a randomized, double-blind, crossover fashion at a 24-hour interval. Coronary artery spasm was documented during coronary angiography in 6 patients (left anterior descending artery, 3; right coronary artery, 2; left circumflex, 1). In the remaining 6 patients, coronary artery spasm was documented by a positive methylergometrine test performed at the bedside, which provoked ST-segment elevation in the inferior (n = 3), anterior (n = 1) or lateral (n = 2) leads. Ninety minutes after administration of the study medication, methylergometrine testing was performed at the bedside, using incremental doses of up to 0.4 mg of methylergometrine. After molsidomine, 10 patients (83%) had a negative and 2 had a positive test; after nifedipine, 9 patients (75%) had a negative and 3 a positive test. Only 1 patient had a methylergometrine test that remained positive after either molsidomine or nifedipine. Therefore, molsidomine appears as effective as nifedipine in suppressing methylergometrine-induced coronary artery spasm in patients with variant angina. In addition, patients not responding to 1 of the study medications may respond to the other.

Coronary Angiography↗