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PubMed1979

Central retinal artery spasm.

Central retinal artery spasm, a seldom witnessed ocular sign, has been recognized in one eye of a patient complaining of transient monocular blindness. Removal of an ulcerative atheromatous plaque of the carotid artery on the same side as the eye with central retinal artery spasm resulted in complete disappearance of symptoms. No other signs of ocular pathology were noted in addition to the central retinal artery spasm. Central retinal artery spasm occurring in both eyes simultaneously may be the mechanism explaining the visual loss of amaurosis fugax. Physiologic mechanisms associating brief episodes of monocular blindness and carotid artery obstructive disease with atherosclerosis are discussed. The possibility of central retinal artery spasm initiating occlusion of the same vessel is mentioned.

Arteriosclerosis↗

PubMed1977

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↗

PubMed1979

The mechanism of coronary artery spasm: roles of oxygen, prostaglandins, sex hormones and smoking.

A reduced oxygen supply to the heart causes coronary vasodilatation in the first instance. But if the hypoxia is severe or prolonged, the dilatation passes off and coronary vasospasm develops leading to a vicious circle with a further reduction of myocardial oxygenation. The spasm is associated with increased outflow of prostaglandin (PG)-like material and can be prevented or reversed by inhibitors of PG synthesis such as indomethacin or antagonists of PG action such as chloroquine. The spasm does not appear to be caused by thromboxane (TX) A2 since selective inhibitors of TXA2 synthesis enhance the hypoxic spasm and by themselves can cause spasm even in oxygenated hearts. The mechanism may be related to loss of negative feedback control of the PG pathway by TXA2. Oxygen may enhance TXA2 production and reduce formation of vasoconstrictor PGs, while smoking, because of the formation of carboxyhaemoglobin, may have the opposite effect. Oestradiol and testosterone do not influence the hypoxic spasm but progesterone at physiological concentrations blocks it completely. Progesterone may be the protective female hormone and the increased susceptibility to myocardial infarction in women on oral contraceptives may be related to reduced formation of endogenous progesterone.

Coronary Circulation↗

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↗

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

[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↗

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↗

PubMed1979

Precise characterization and quantification of infantile spasms.

With the use of a time-synchronized video and polygraphic recording system, 5,042 infantile spasms were monitored and analyzed in 24 infants aged 1 to 43 months. Of these, 33.9% were flexor, 22.5% extensor, and 42.0% mixed flexor-extensor. Sometimes the spasms were followed by a period of akinesia and diminished responsiveness lasting up to 90 seconds, and rarely (1.0%) this "arrest" effect constituted the entire seizures. More than one type of seizure occurred in 21 of the 24 infants. In the same number, 78.3% of the seizures occurred in clusters, and the intensity and frequency of the spasms in each cluster often increased to a peak, then progressively decreased until they stopped. Predominantly, the clusters occurred soon after arousal from sleep. The number of seizures occurring at night (55.2%) was similar to the diurnal number (44.8%). The electroencephalographic seizure pattern was variable, but a marked generalized attenuation of electrical activity was a feature of 71.7% of the attacks. Attenuation episodes of similar degree and duration occurred with no evidence of a seizure.

Electroencephalography↗

PubMed1979

Coronary artery spasm: its role in the pathogenesis of myocardial ischemia.

The role of coronary artery spasm in the production of myocardial ischemia has recently become the focus of increased attention. This phenomenon is now well established as a causative mechanism underlying the resting chest pain attacks in Prinzmetal's variant angina. There is also evidence that coronary spasm may play a more significant role in the broad spectrum of ischemic heart disease than can be documented by current techniques. The autonomous nervous system constitutes a major element in the pathophysiology of spasm. Coronary arteriography, in spite of important limitations, remains the only technique for final documentation of this phenomenon, but radionuclide scintigraphy appears to be promising. Nitroglycerin is effective for the relief of the acute attack, while long acting nitrates and the calcium antagonists: nifedipine, perhexiline and verapamil are useful in the prevention of recurrences.

Cardiac Catheterization↗