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[Coronary spasm during coronary arteriography. Classification and interpretative criteria].

Coronary spasm during selective coronary angiography have multiple explanation. In some instances there is no true pathological implication (catether induced spasm), in other instances, instead, a clear relationship with "functional" angina and myocardial infarction exists. Moreover, in few occasions may only be a false positive radiologic image (apparent spasm). The angiographic features of coronary spasm, however, are always the same, indipendently from its clinical significance and pathophysiologic mechanism. In this paper the Authors are not limiting their experience to the morphologic description of this event, rather describe the clinical criteria which, together with angiographic picture, may be useful in the interpretation of the physiopathology of the coronary artery spasm.

Angiography↗

Hemifacial spasm: an electrophysiological evidence of facial motorneurons hyperexcitability.

Twenty patients with primary hemifacial spasm and ten patients with Parkinson's disease were studied by means of paired stimuli blink reflex. The second stimuli were delivered at a varying time interval between 50-900 ms. The R2 response's absolute refractory periods were compared between patients and twenty one age-matched normal controls as well as between hemifacial spasm and Parkinson's disease. In normal subjects, the mean absolute refractory period was found to be 271.42 +/- 64.36 ms, in hemifacial spasm 160.00 +/- 50.62 ms and in Parkinson's disease 157.14 +/- 53.45 ms. The absolute refractory periods obtained from patients were significantly shorter than in normal controls (p < 0.05). However the values between patients with hemifacial spasm and Parkinson's disease were not (p > 0.05). This result strongly supports bilateral facial motoneurons hyperexcitability as the underlying mechanism of hemifacial spasm.

Adult↗

[Neurophysiological study of hemifacial spasm--F wave of the facial muscles].

We studied the F wave of the facial muscles on both the normal side and the spastic side in 14 patients with hemifacial spasm. The purpose of this study was to determine if the mechanism of hemifacials spasm originates in ephaptic transmission in the facial nerve at the site of vascular compression or in a hyperexcited facial motor nucleus. Larger amplitude, longer duration and shorter latency F waves in the peripheral nerves than in normals indicate anterior horn cell hyperexcitability. We found abnormal potentials exhibiting synkinesis (lateral spread), a typical electrophysiological finding in hemifacial spasm, in the facial nerve evoked electromyograms of the 14 patients, none of whom had experienced facial palsy or facial nerve block. Electrical stimulation was delivered transcutaneously to the most distal portion of the marginal mandibular branch of the facial nerve. Using surface electrodes the F waves were obtained over the mentalis muscle as the second response after the M wave. While the F waves were normal on the patients' normal side, on the spastic side, their duration was longer (mean duration about 1.9 times that of the normal side), their onset latency was slightly shorter, and their F/M amplitude latency was greater than on the normal side. After microvascular decompression, the facial spasm and abnormal F-wave findings resolved. Onset latency was not increased, and on the spastic side some patients displayed facial spasm clinically and electrophysiologically for one year after MVD. In other words, there was hardly any focal demyelination of the facial nerve, so it is possible that ephaptic transmission and ectopic excitation are the mechanism of HFS.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

[Lennox-Gastaut syndrome with series of spasms intermixed with tonic seizures].

A patient with Lennox-Gastaut syndrome developed an unusual feature of periodic spasms (PS), intermixed with tonic seizures. At age 14, she began to have unilateral seizures on awaking, followed by series of spasms Each spasm consisted of rotation of the head to the left and global muscle contraction of the whole body lasting for 0.5-1 second. Ictal EEGs revealed diffuse high voltage slow waves (HVSW), sometimes superimposed upon by diffuse low voltage fast activity, which was related to the increase of muscle activity following the spasms. When the duration of the fast activity on EEG became longer than 2 seconds, the peculiar seizures consisting of combination of asymmetrical spasms and tonic seizures occurred. It is speculated that the fast activity superimposed on HVSW seen in PS represents a transition from PS to tonic seizures.

Adolescent↗

[A case of progressive continuous muscular rigidity and painless and rhythmic muscle spasm associated with autoantibody against glutamic acid decarboxylase].

We described a 60-year-old man with 5-year history of insulin dependent diabetes mellitus who developed continuous rigidity of truncal muscle and painless, rhythmic muscular spasm of trunk and proximal lower and upper extremities. The rigidity continued even in sleep. The painless muscle spasm was often precipitated by volitional movement and emotional stimuli. Intravenous administration of diazepam strongly attenuated the muscle spasm as well as truncal rigidity. Surface electromyography showed the continuous contraction of abdominal and paraspinal muscles. The rhythmic, clonic spasm of shoulder, triceps brachii, intercostal, abdominal, paraspinal and quadriceps femoris muscle induced by voluntary neck flexion was not compatible with typical stiff-man syndrome. Antibody against glutamic acid decarboxylase (GAD) was detected in the serum and cerebrospinal fluid of this patient. His condition was getting well with oral intake of sodium valproate. While painless, rhythmic spasm and persistent rigidity during sleep ruled out the patient from typical stiff-man syndrome, he was supposed to have the same pathophysiological mechanism as the anti-GAD autoantibody positive stiff-man syndrome.

Analgesia↗

[Neuro-vascular decompression in hemifacial spasm: anatomical, electrophysiological and therapeutic results apropos of 100 cases].

Hemifacial spasm is a neurological disorder due to abnormal hyperactivity of the facial nerve. The most common cause of hemifacial spasm is a neuro-vascular conflict in the cerebellopontine angle between a vascular loop and the root of the facial nerve (96% of cases). Tumors are the cause of hemifacial spasm in only 1% of cases). The authors present their results in 100 patients who underwent microvascular decompression for essential hemifacial spasm between 1990 and 1995. They used microsurgical and endoscopic procedures by a minimal retrosigmoid approach in all cases. The most common offending vessels were the posterior inferior cerebellar artery (70%), the vertebral artery (41%) and the anterior inferior cerebellar artery (28%). An aberrant vein was found in 2 cases. There were 38% of multiple artery-nerve conflicts. Physiopathology of hemifacial spasm is explained by two principal theories: in the ephaptic theory, hyperactivity and an abnormal nervous impulse pathway are due to a short demyelinated area on the nerve trunk caused by the offending vessel, inducing short circuiting between adjacent nerve fibers. In the nuclear theory, hyperactivity of the facial nerve is due to an abnormal and automatic activity of the facial nerve nucleus itself, induced by the vessel. The authors used pre and postoperative electromyographic tests and intraoperative electromyographic tests. Their results tend to prove the nuclear theory. Ninety per cent of the patients had a good result, with a mean follow-up time of 30 months in 60 cases. In 82% of the cases, there was a total recovery after a single procedure. There was no mortality and no facial palsy. Hearing loss occurred in less than 5%.

Electromyography↗

Stenting for coronary artery spasm.

We evaluated coronary stenting in nine patients with clinically severe, angiographically documented spasm refractory to aggressive pharmacologic management. No patient subsequently developed unstable ischemia requiring hospitalization as a consequence of recurrent spasm within the stent. Mechanisms of therapeutic failure included both persistent spasm and spasm in a different artery in one patient. Restenosis occurred in three patients who subsequently underwent repeat revascularization. In the rare, carefully selected patient, stents may represent an adjunct in the management of focal coronary artery spasm, although currently medical therapy remains the standard initial approach.

Adult↗

Coronary spasm in patients with coronary ectasia.

The incidence of coronary ectasia (CE) and the relationship between CE and coronary spasm that was said not to be apt to occur in patients with CE were studied. The study consisted of 1,373 patients (including 1,008 patients with ischemic heart disease) who underwent cardiac catheterization. In 74 patients with CE, coronary spasm was tested in 33 patients subjected to acetylcholine (ACh) provocation and in 17 patients subjected to ergonovine (Ergo) provocation. CE was found in 74 patients (5.4%), and its incidence was significantly higher (6.7%) in patients with ischemic heart disease. In addition, ACh and Ergo provocation tests gave positive results in 12 (36%) and 4 patients (24%), respectively. Spasm was not provoked as frequently in the ectatic portion as elsewhere. In addition, spasm was often found at the borders of the ectatic portion in both provocation tests. The incidence of coronary ectasia was higher than that described in previous reports, and coronary spasm was more often observed at the borders between ectatic and normal portions than elsewhere.

Acetylcholine↗

The use of intrathecal phenol for muscle spasms in multiple sclerosis. A description of two cases.

Two cases of multiple sclerosis are described, in both of whom the disease started in yound adult life. This disability gradually progressed to the stage of paraplegia-in-flexion in which the lower limbs were fixed in adduction-and-flexion. Both patients developed painful muscle spasms which made life intolerable. These patients were treated by intrathecal phenol in glycerine in an effort to convert this spastic paralysis into a flaccid paralysis. The three advantages sought were: 1. To relieve the muscle spasms so that the patient could sit in a wheelchair and propel herself. 2. To relieve the pain of the spasms. 3. To allow access to the perineum for proper hygienic care of bladder and bowel function. The first patient obtained an excellent result (Figures 1, 2, 3) but blocks had to be repeated after approximately five months. The second patient after the block developed a good result in the right leg, but still had mild, but painless spasms in the muscles of the left leg (Figures 4 and 5). However, she was able to use a wheelchair and was discharged to a chronic hospital where she died of bulbar paralysis six months later. Intrathecal phenol thus appears to be a useful method for relieving muscle spasms and pain in the lower extremities in advanced cases of multiple sclerosis.

Adult↗

Coronary artery and graft spasm after off-pump coronary artery bypass grafting.

We report a case of a 52-year-old man with severe coronary artery and graft spasm after triple-vessel off-pump coronary artery bypass grafting. Emergent coronary angiography was performed to identify the location and severity of the spasm. Intracoronary injections of several vasodilators failed to relieve the spasm. Observational treatments including intra-aortic balloon pump and inotropic drugs to increase coronary flow were performed until the spasm resolved. The patient recovered and was discharged. A follow-up coronary angiography revealed patent native coronary artery and bypass grafts without evidence of residual spasm.

Coronary Artery Bypass, Off-Pump↗

Blepharospasm and Hemifacial Spasm.

The main objective in the treatment of blepharospasm is to decrease or cease the unwanted, repeated forced closure of the eyelids. This is best achieved by the use of botulinum toxin. In a minority of patients, botulinum toxin is either ineffective or poorly tolerated. In this group of patients, a trial with oral medication in the following order is warranted: trihexyphenidyl, baclofen, clonazepam, and tetrabenazine. Before going to the next medication, each of these drugs should be administered at the highest tolerated dosage for a period of 1 or 2 months. If, as often happens, all pharmacologic treatment attempts fail, and the patient is too disabled to remain untreated, he or she can be referred to an experienced plastic surgeon for a myectomy of the eyelid protractors. For treatment of apraxia of eyelid opening, botulinum toxin should be administered as the first treatment. If this fails, and vision is significantly impaired, the patient may be referred to a plastic surgeon for a frontalis suspension of the eyelid. Treatments of hemifacial spasm are aimed at decreasing or ending the annoying twitches of one side of the face. In this disorder, interference with vision is not a problem unless the contralateral eye is amblyopic. Despite isolated reports of spasm relief by drugs such as carbamazepine, oral medication is unlikely to be helpful. Botulinum toxin is the preferred treatment in hemifacial spasm patients. In some patients, relief from spasms can only be obtained at the cost of an ipsilateral upper lip droop of varying severity. Patients who are dissatisfied with the results of treatment with botulinum toxin, and are not willing to tolerate their condition, can be referred to an experienced neurosurgeon for microvascular decompression of the facial nerve. Pending success of ongoing attempts to reduce adverse effects, we believe that doxorubicin chemomyectomy, a recent treatment that has been used for both facial spasm and blepharospasm, is best administered in a research setting.

Journal Article↗

Statistical analysis of clinical risk factors for coronary artery spasm: identification of the most important determinant.

Coronary artery spasm plays an important role in acute ischemic events, and it has a close relationship with coronary atherosclerosis. Thus we attempted to determine the most significant risk factor for coronary artery spasm. Among 3000 consecutive patients who underwent coronary cineangiography with ergonovine maleate testing, 330 with typical angina pectoris (group 1) and 294 with old myocardial infarction (group 2) were studied. We divided each group into three or four subgroups according to the presence of fixed organic stenosis (FOS+) or a positive reaction to ergonovine maleate (coronary artery spasm [CAS]+). We examined the relationship between coronary artery spasm and eight coronary risk factors: age, sex, hypertension, diabetes mellitus, smoking, and serum cholesterol, uric acid, and high-density lipoprotein cholesterol levels. The proportion of smokers in the subgroups with CAS(+) was significantly higher than in the subgroups with CAS(-)(p less than 0.01). There was no correlation between smoking and fixed organic stenosis. According to the results of multiple regression analysis, there was a positive correlation between smoking and CAS(+) and between serum high-density lipoprotein cholesterol levels and CAS(+)(p less than 0.01). Thus we concluded that smoking is the most significant risk factor in discriminating between patients with and without coronary artery spasm.

Cholesterol, HDL↗

Spectrum of coronary arterial spasm. Clinical, angiographic and myocardial metabolic experience in 29 cases.

A relationship of coronary arterial spasm to variant angina pectoris, subendocardial ischemia, major ventricular arrhythmias and myocardial infarction has been demonstrated. In 29 patients, spasm was angiographically observed in normal-appearing coronary arteries (7 patients) as well as superimposed on various degrees of coronary atherosclerotic obstruction (22 patients). All patients experienced an atypical anginal syndrome;16 patients also experienced typical exertional angina. Coronary spasm appeared to be a major contributory factor in eight occurrences of myocardial infarction and in 11 incidents of ventricular tachycardia, ventricular fibrillation and heart block. Coronary spasm in the 29 cases was distributed in the following fashion: left main trunk, 6 cases; right main trunk, 12 cases; proximal left anterior descending artery, 13 cases; proximal circumflex artery, 1 case; distal left anterior descending artery, 1 case; and distal circumflex artery, 2 cases. In 5 cases coronary spasm was noted at multiple sites.

Adult↗

Provocation of coronary spasm with ergonovine maleate. New test with results in 57 patients undergoing coronary arteriography.

Ergonovine maleate (Ergotrate) was given to 57 patients undergoing coronary arteriography for investigation of angina occurring at rest or without provocation when routine study showed normal arteries or insufficient occlusive disease to explain their symptoms. This provocative test induced coronary arterial spasm in 13 patients, 10 of whom had definite Prinzmetal's angina. The spasm was easily reversed with sublingually administered nitroglycerin. The spasm was occlusive or nearly occlusive in nine patients, and there was associated reproduction of the chest pain and S-T elevation similar to the spontaneous episodes. One patient with Prinzmetal's angina had S-T depression rather than elevation in association with the chest pain. The other three patients without Prinzmetal's angina had focal narrowing without coronary occlusion, reproduction of the chest pain or electrocardiographic changes. Of the 44 patients who did not demonstrate coronary spasm in response to ergonovine, 29 had normal coronary arteries and 15 had various degrees of atherosclerotic occlusive disease. We conclude that cautious administration of ergonovine maleate during coronary arteriography can be safely used to elicit coronary spasm in some patients who have insufficient fixed occlusive disease to explain their symptoms.

Adult↗

Simultaneous multivessel coronary artery spasm demonstrated by quantitative analysis of thallium-201 single photon emission computed tomography.

Thallium-201 myocardial scintigraphy with quantitative analysis of emission computed tomography was performed during episodes of angina in 19 patients with variant angina and nearly normal coronary arteriographic findings. Eleven patients (group I) were shown by arteriography to have spasm in 2 or more large coronary arteries. Eight patients (group II) had spasm in only 1 coronary artery. In 7 patients in group I, significant diffuse perfusion defects simultaneously appeared in multiple coronary artery regions on the scintigram (group IA). The extent and severity of the perfusion defect as measured by thallium-201 tomography were significantly greater in group IA than in group II (p less than 0.001 and p less than 0.01, respectively). The duration of transient ST-segment elevation during the attack in group IA was significantly longer than in group II (p less than 0.001). The incidence of ventricular arrhythmias, including ventricular tachycardia, or complete atrioventricular block during the anginal attack was significantly higher (p less than 0.05) in group IA than in group II. In all study patients, neither attack nor scintigraphic perfusion defect appeared on the repeat test after oral administration of nifedipine. In conclusion, multivessel coronary artery spasm simultaneously appears and causes the attack in many patients with variant angina and nearly normal coronary arteriographic findings, and myocardial ischemia due to simultaneous multivessel coronary spasm is likely to be more extensive and severe, persist longer and have a higher frequency of potentially dangerous arrhythmias than that due to spasm of only 1 coronary artery.

Angina Pectoris, Variant↗

Possible role of coronary artery spasm in unexplained syncope.

Coronary spasm provocation by intracoronary methylergonovine was performed in 14 patients (8 men and 6 women, mean age 56 +/- 6 years) with syncope that remained unexplained despite neurologic and noninvasive cardiac evaluations. Electrophysiologic testing was also performed in 6 of 14 patients. No patient had structural heart disease or significant fixed stenosis of greater than or equal to 75% in the coronary arteries. Six patients had no history of chest pain even when they developed syncope. Serious arrhythmia was documented in 2 patients, cardiac standstill in 1 and complete atrioventricular block in the other. Coronary spasm was induced in 9 patients using the methylergonovine provocation test. Multivessel spasms were found in 3 patients. Coronary spasm was induced in the artery supplying the inferior wall in 7 of 9 patients with positive results. In 4 of 9 patients who had a positive result, there was no prior history of chest pain. In 1 patient, whose electrocardiogram was recorded during syncope, cardiac standstill was documented and cardiac standstill and syncope also occurred during the provocation test. Monomorphic ventricular tachycardia was not induced by the electrophysiologic study. These results suggest that coronary spasm is involved in unexplained syncope.

Cardiac Pacing, Artificial↗

Increased plasma level of endothelin-1-like immunoreactivity during coronary spasm in patients with coronary spastic angina.

To examine the role of endothelin in coronary spasm, the plasma endothelin-1-like immunoreactivity in the coronary sinus and the aortic root was measured before and during spasm of the left coronary artery induced by injection of acetylcholine (20 to 100 micrograms) into the left coronary artery in 26 patients with coronary spastic angina. The plasma level of endothelin-1-like immunoreactivity was measured by the radioimmunoassay with a monoclonal antibody against endothelin-1. Plasma lactate levels in the coronary sinus and the aortic root were also measured to evaluate myocardial lactate metabolism during spasm. In 13 patients who had myocardial lactate production during spasm, the plasma level of endothelin-1-like immunoreactivity in the coronary sinus increased from 19.8 +/- 3.0 to 25.7 +/- 6.4 pg/ml (p less than 0.01), while that in the aortic root remained unchanged (from 20.2 +/- 5.9 to 21.3 +/- 5.8 pg/ml). No significant changes in the plasma levels of endothelin-1-like immunoreactivity in the coronary sinus (from 21.1 +/- 7.3 to 19.7 +/- 5.2 pg/ml) and the aortic root (from 21.1 +/- 5.7 to 19.7 +/- 5.6 pg/ml) were observed in 13 patients who did not show myocardial lactate production during spasm. On the other hand, 16 patients without ischemic heart disease showed no significant changes in the plasma levels of endothelin-1-like immunoreactivity in the coronary sinus (from 24.4 +/- 9.7 to 25.8 +/- 6.9 pg/ml) and the aortic root (from 23.0 +/- 7.1 to 23.4 +/- 5.8 pg/ml) by acetylcholine injection (100 micrograms).(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗

Angioscopy in variant angina: coronary artery spasm and intimal injury.

Studies in pigs and dogs show that intimal injury is related to coronary artery spasm; it is not known whether intimal injury is related to coronary artery spasm in human beings. We examined intima at the site of coronary artery spasm by percutaneous transluminal coronary angioscopy in 10 of 13 consecutive patients with variant angina. Coronary artery spasms occurred spontaneously or were induced by intracoronary acetylcholine (10-100 micrograms). Angioscopy showed intimal injuries (haemorrhage, flap, thrombus, or ulcer) in 4 of the 10. We suggest that intimal injury is related to coronary artery spasm in human beings.

Acetylcholine↗