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PubMedDate not supplied

Cerebral arterial spasm: A discussion of present and future research.

The author presents a discussion of research on cerebral arterial spasm. Arterial smooth muscle contraction, receptor and relaxation mechanisms are presented in the context of what is known about cerebral arterial spasm and the biochemistry of vascular smooth muscle. Several new experimental approaches are suggested and a theoretical biochemical basis for the idea that damage to the artery alone could cause cerebral arterial spasm is postulated. Methods of determining cerebral arterial spasm and the need for a quantitative, in vivo method are discussed and the question of an irreversible stage of cerebral arterial spasm is considered. Finally, the problems associated with the delivery of a potentially successful treatment to the cerebral arterial smooth muscle cells are examined.

Actins↗

PubMed1977

Cerebral perfusion, vascular spasm, and outcome in patients with ruptured intracranial aneurysms.

In a retrospective study of 44 patients with verified ruptured intracranial aneurysms, the results of radionuclide cerebral perfusion scintigraphy (dynamic brain scanning) and the presence or absence of arteriographic spasm were correlated with the clinical outcome. The data indicated that patients with normal dynamic scans had a better outcome as a group and following intracranial surgery than those in whom perfusion was reduced. Patients with normal perfusion had a higher incidence of preoperative rebleeding from their aneurysms, while patients with reduced perfusion had a higher incidence of infarction, especially after intracranial surgery. There was no correlation between the presence or absence of arteriographic spasm and the results of the dynamic scans, and nor correlation between the presence of absence of spasm and the outcome of the group as a whole. However, in some individual cases with severe spasm, reduced perfusion on the dynamic scan and a poor outcome were noted. It was concluded that the results of the dynamic scan correlated better with eventual patient outcome than the presence or absence of arteriographic spasm. It is therefore suggested that patients in Grades I and II with normal dynamic scans be operated on promptly to prevent rebleeding, and that surgery in patients in Grades I and II with abnormal dynamic scans be delayed until the dynamic scan returns to normal.

Adolescent↗

PubMed1978

Coronary artery spasm and mitral valve prolapse.

Ten patients, representing 1.34 per cent of those patients undergoing selective coronary arteriography, were found to have unequivocal evidence of coronary artery spasm. This involved the proximal right coronary artery in eight patients, the mid-left anterior descending branch in one, and the left main coronary artery in one. Eight of these 10 patients had otherwise normal coronary arteries. Of these 10 patients with coronary artery spasm, nine had evidence of mitral valve prolapse. This involved the posteromedial scallop in six patients; the anterolateral and posteromedial scallops in one; the middle and posteromedial scallops in one; and the anterolateral, middle, and posteromedial scallops in one. These data suggest an association between coronary artery spasm and mitral valve prolapse. Coronary artery spasm may thus be an important factor in the pathogenesis of the chest pain, arrhythmias, electrocardiographic abnormalities, and sudden death, that have already been described in some patients with mitral valve prolapse.

Adult↗

PubMed1978

Infantile spasms and HLA antigens.

21 new cases of infantile spasms were reported in 1976 from paediatric departments in Denmark. The connection between infantile spasms and the Lennox-Gastaut syndrome is mentioned, because of reports of a significantly higher incidence of HLA-B7 in children with Lennox-Gastaut syndrome. The HLA antigen distribution in 19 of the 21 children was compared with that of 1967 healthy adults. No difference in the HLA antigens was demonstrated between children with infantile spasms and controls, whether in the material as a whole, or in the cryptogenic or symptomatic groups. However HLA typing of children with infantile spasms should continue in the search for a potential genetic marker in this grave disease, particularly in view of the reported high incidence of HLA-B7 in children with the Lennox-Gastaut syndrome.

Female↗

PubMed1979

Arteriographic demonstration of spontaneous right coronary artery spasm in a patient with Prinzmetal's angina.

Coronary artery spasm may occur spontaneously during coronary angiography in patients with clinically documented or suspected Prinzmetal's angina. In other patients with Prinzmetal's angina, the spasm can be provoked by the administration of ergonovine. A patient with spontaneous spasm of the right coronary artery during coronary angiography is reported and some considerations for diagnosis and therapy of this entity is offered. Although intraoperative spasm has been reported in the cardiology literature, no such case has been described in the radiology literature.

Angina Pectoris↗

PubMed1979

[Detection of coronary artery spasm by the methylergometrin test. Technic. Results. Indications].

Methylergometrine (Methergin) was given intravenously (0.4 mg) to 118 patients undergoing coronary arteriography. The electrocardiogramme and intraaortic pressure was continuously monitored whilst coronary arteriography was performed, 1,3, and 5 minutes after the injection of the ergot alkaloid. The test was positive if: 1) coronary spasm was observed; 2) if ST segment elevation was recorded with or without pain. Positive tests were obtained in 13 out of 14 patients with Prinzmetal angina. The test was negative in the other patients. However in 3 patients with Prinzmetal angina, the test produced typical coronary spasm without electrocardiographic changes. In Prinzmetal angina the sensitivity of this test was 93 p. 100 with a high specificity: 96-100 p. 100 depending on whether or not electrocardiographical changes associated with spasm are considered. Taking into account current therapeutic methods of treating Prinzmetal angina the indications of this test of coronary spasm are: 1) patients presenting with resting angina whatever the state of their coronary arteries; 2) patients with documented Prinzmetal angina with "angiographically normal" coronary arteries.

Angina Pectoris, Variant↗

PubMed1976

Hemifacial spasm: importance of a complete investigation.

The authors report the experience of the Clinique d'O.R.L. de l'Université de Bordeaux II in the management of hemifacial spasm. The recent diagnostic and therapeutic progress in otoneurology has revealed an organic etiology for many cases of hemifacial spasm. The recent diagnostic and therapeutic progress in otoneurology has revealed an organic etiology for many cases of hemifacial spasm. From their experience, they propose a complete investigation for all cases of hemifacial spasm. The disorder is labelled as being idiopathic only if the complete investigation is negative.

Adult↗

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↗

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↗

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↗

PubMed1992

Pathogenesis of unstable angina with 0- or 1-vessel disease. Important role of coronary artery spasm.

In order to examine the possible role of coronary artery spasm in the pathogenesis of unstable angina, provocative testing for coronary spasm was performed in 43 patients with unstable angina who had 0- or 1-vessel disease. Coronary spasm was induced in 20 (65%) of 31 patients by hyperventilation testing (ST increases in 18, ST decreases in 2). Anginal attacks with either ST-segment elevation or ST-segment depression in patients without a significant organic stenosis were induced in 23 (55%) of 42 patients during treadmill exercise testing. Coronary artery spasm, showing severe (> or = 90%) vasoconstriction with angina and/or ischemic electrocardiographic ST-segment deviation, was also documented angiographically in 42 (98%) of 43 patients following intracoronary injection of acetylcholine. We conclude that dynamic coronary obstruction plays an important role in the genesis of attacks in patients with unstable angina who had 0- or 1-vessel organic coronary artery disease.

Acetylcholine↗

PubMed1979

Coronary artery spasm.

Coronary artery spasm is an important pathogenetic mechanism in some forms of myocardial ischemic disease. Factors that may be important in the genesis of spasm include the autonomic nervous system, prostaglandins, endoperoxides, thromboxanes, and the calcium availability to the contractile apparatus. Spasm results in myocardial ischemia with attendant chest pain and electrocardiographic and hemodynamic changes; it is the primary pathogenetic mechanism in Prinzmetal's variant angina and has been found in association with classic angina pectoris and acute myocardial infarction. Diagnosis of coronary artery spasm is firmly made only by coronary angiography. Treatment includes the use of both short- and long-acting nitrates and the slow-channel blocking agents such as verapamil, nifedipine, and perhexiline.

Angina Pectoris↗

PubMedDate not supplied

[Electroencephalographic reflection of arterial spasm following surgery for saccular cerebral aneurysms].

The purpose of the investigation was to study the electrophysiological manifestations of arterial spasm developing following surgical interventions for cerebral arterial aneurysms. Repeated EEG-recording was undertaken for this purpose in 40 patients with aneurysms of different localization. The EEG data were compared with the results of a neurological examination and angiography performed pre- and postoperatively. It was found that with an uneventful postoperative course no focal changes develop in the bioelectrical activity, and EEG returns to the initial (preoperative) state or to the normal pattern as soon as by the 15th-20th day. In the presence of postoperative arterial spasm, verified clinically and angiographically, the latter is reflected in EEG tracings as peculiar focal changes in the biopotentials. These changes have a nature of a periodically occurring delta-activity recorded predominantly in the zone of ischaemia. Along with a regress of the spasm its EEG manifestations were found to decrease as well. The focal EEG changes observed in postoperative spasm differ from the localization of those EGG changes that are caused by other factors (haematoma, cicatrical processes, etc.).

Adult↗

PubMedDate not supplied

[Prolonged spasm of the arteries of the base of the brain during experimental fibrinolysis in the subarachnoid space].

An ex tempore mixture of fibrinogen (1%--4 ml) and 0.2 ml thrombin solutions forming a compact clot of fibrin in the subarachnoid space was introduced into the cisterna magna of dogs. To dissolve the fibrin clot 2 ml of a fibrinolysin solution with an activity of 400 units were introduced into the same cisterna 10--15 minutes thereafter. A total of 26 experiments were set up, of which 13 were served as controls with separate introduction of the mixture ingredients. Through serial vertebral angiography with a 50 per cent urotrast solution it was found that following introduction of the fibrinogen and thrombin mixture the lumen of the basilar artery and of its branches contracts on the average up to 89.2 +/- 1 per cent. After introduction of fibrinolysis the diameter of the artery initially increases up to 116.3 +/- 2.5 per cent. In 3 hours time a pronounced spasm of the basilar artery and of its branches is seen to develop up to 80.9 +/- 3.6 per cent and after 24 hours -- up to 73.9 +/- 2.1 per cent. The spasm persists for up to 10 days, but its intensity gradually declines. During subsequent 11--18 days the diameter of the brain base arteries returns back to normal. In control experiments no development of protracted spasm was demonstrated. Hence, it is established that the appearance of fibrinolysis products formed in the spinal fluid consequent upon dissolution of a clot of fibrin containing no blood cells is attended by the development of a protracted spasm involving major arteries of the brain.

Animals↗

PubMed1992

[A case of painless myocardial injury probably caused by coronary artery spasm].

A 53-year-old male was admitted to the hospital due to electrocardiographic ST-segment elevation in V1-4 with ST-segment depression in the inferior leads, which suggested acute myocardial infarction. He had a cough and a slight fever without chest pain. Serum creatine kinase and its myocardial band were slightly elevated but creatine kinase value did not exceed twice the normal upper limit. Emergent coronary arteriography (CAG) revealed intact coronary arteries. The CAG in a chronic stage again revealed intact coronary arteries. Intracoronary administration of acetylcholine of 100 micrograms to the left coronary artery and 50 micrograms to the right coronary artery provoked diffuse spasm in the right and left coronary arteries. The electrocardiogram (ECG) during the right coronary artery spasm revealed ST-segment depression in the inferior leads with ST-segment elevation in V2 and V3, which resembled the ECG finding at the time of the patient's admission. With intracoronary isosorbide dinitrate, the spasm and ST-segment elevation were resolved. These findings strongly suggest that coronary spasm can cause myocardial injury indicated by a slight elevation of serum creatine kinase value.

Coronary Angiography↗

PubMed1979

[Muscle spasms in patients with amyotrophic lateral sclerosis (clinico-electromyographnic analysis)].

The diagnostic importance and electromyographic characteristics of the muscular spasms were studied in patients with lateral amyotrophic sclerosis at various stages of the disease. It has been shown that the muscular spasms are a typical symptom of this disease, and may be an early manifestation of the latter. The clinical and electromyographic characteristics of the spasms depend on the depth of the pathological process. Of importance in the origin of the muscular spasms in the lateral amyotrophic sclerosis is involvement of many levels of the cortico-muscular path, however, distrubances of the intraspinal mechanisms are, probably, the leading cause.

Amyotrophic Lateral Sclerosis↗

PubMed1976

Left main coronary artery spasm. A potential cause for angiographic misdiagnosis of severe coronary artery disease.

Two patients had catheter-induced spasm of the left main coronary artery during diagnostic coronary arteriography. One patient had no coronary artery disease, and the other had minimal disease of the right coronary artery. Spasm was relieved by nitrates; however, in one patient several doses were needed over 35 minutes. Catheter-induced spasm must be considered in the diagnosis of left main coronary artery disease, particularly on a patient with isolated left main coronary artery disease.

Angiography↗

PubMed1975

Spasm and operative cholangiography.

Operative cholangiography is a commonly employed adjunct to biliary operation and is useful in identifying unsuspected common duct calculi. Spasm of the sphincter of Oddi from administration of anesthetic agents like fentanyl citrate (Sublimaze) and morphine sulfate and from operative manipulation may lead to misinterpretation of the cholangiograms and unnecessary surgical procedures that increase morbidity and mortality. Six case reports illustrate these hazards, and the influence of medications that exacerbate spasm of the sphincter of Oddi is emphasized. Recognition of the factors that cause spasm of the sphincter of Oddi will prevent unnecessary common duct explorations and reduce morbidity and mortality in biliary tract operations.

Adult↗