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At least 1,099 records · Page 61Linked to original sources
PubMed1978

Cerebral aterial spasm. I. Adrenergic mechanism in experimental cerebral vasospasm.

This study demonstrates that an adrenergic mechanism plays an important role in producing the delayed cerebral vasospasm which follows subarachnoid hemorrhage. Results were as follows: 1. Experimental subarachnoid hemorrhage (SAH) was produced by injection of fresh arterial blood into the cisterna magna in cats. The cerebral vasospasm was shown angiographically to be biphasic in nature: immediate constriction lasting 1 h and marked prolonged spasm occurring between the 3rd and 5th day after SAH. The amount of noradrenaline (NA) and dopamine-beta-hydroxylase (DBH) activity decreased over a period of 24 h both within the wall of the basilar artery and in the locus ceruleus and then gradually increased, reaching a maximum on the 3rd day after SAH. 2. Topical application of spasmogenic substances (NA and blood) produced a marked constriction of the hypersensitive basilar artery on the 3rd day after SAH. 3. 6-Hydroxydopamine (6-OHDA) injection into the cisterna magna produced prolonged vasocilatation. The dilated vessel responded with mild transient constriction after the topical application of NA or fresh blood. DBH activity and NA concentration in the vessels, locus ceruleus and medial hypothalamus decreased markedly on the 3rd day after the cisternal injection of 6-OHDA. 4. Various spasmogenic substances (i.e. serotonin, NA, prostaglandins and methemoglobin) were measured in a mixture of equal volume of CSF and blood in cats. ONly the serotonin in the mixed fluid produced vasoconstriction. Spasmogenic substances decreased markedly in the mixed fluid incubated for 3 days at 37 degrees C, and none of these substances apart from methemoglobin was present in a concentration sufficient to produce constriction of vessels. 5. These results suggest that early spasm is induced by serotonin around the arteries of the cranial base, and delayed spasm might be caused by hyperreaction of cerebral vessels to spasmogenic substances such as methemoglobin, during the accumulation of excess NA in the cerebral vessel wall.

Animals↗
PubMed1992

[A case of acute myocardial infarction following intracoronary thrombi caused by coronary artery spasm].

A 65-year-old man underwent coronary angiography (CAG) after 10 hours from the onset of myocardial infarction. We observed large Thrombi at the filling defect in the proximal site and mid-portion of the right coronary artery. CAG showed that they had disappeared completely without residual stenosis on the 4th day. In addition to this segmental spasms developed spontaneously at the proximal site of a thrombus accompanied by ST elevation, but these spasms recovered after intracoronary infusion of isosorbide dinitrate on the 26th day CAG. Thus, our case indicates that acute myocardial infarction may be caused by secondary coronary artery thrombosis and accompanying coronary artery spasm.

Aged↗
PubMed1985

Aortocoronary vein graft spasm: case report with brief review.

Some reports of coronary bypass spasm recently published in the literature aroused skepticism and discussions. Our own doubts were shared by many who have been doing coronary bypass angiography without ever finding such spasms. However, we report a case of a 45-year-old woman with spasm of a vein graft inadvertently induced by catheter manipulation.

Journal Article↗
PubMed1984

Acute spasm of vein bypass graft and recipient artery in the immediate postoperative period.

This is a report of an unusual condition in a patient with simultaneous spasms of a vein graft and recipient artery, resulting in acute left ventricular failure in the immediate postoperative period. It is known that coronary artery spasm can complicate perioperative management of the cardiac surgical patient, and spasm of vein bypass grafts themselves can also occur in rare instances. Possible causes of the complication and successful management of this patient are discussed.

Journal Article↗
PubMed1988

Arteriographic demonstration of coronary artery spasm during thrombolysis.

A 60-year-old man with an acute inferior-wall myocardial infarction was noted, on arteriography, to have an occluded distal right coronary artery. The vessel was reopened with intravenous tissue plasminogen activator; during resolution of the clot, spasm was observed arteriographically but was successfully treated with intracoronary nitroglycerin. Follow-up arteriography showed a normal right coronary artery. The significance of this case lies in the fact that we were able to document the occurrence of spasm during coronary thrombolysis; such documentation supports the hypothesis that spasm may be a factor in the initiation of coronary thrombosis.

Journal Article↗
PubMed1992

[A case of posttraumatic delayed cerebral arterial spasm; case report and review of the literature on the pathogenesis].

A case of posttraumatic delayed cerebral arterial spasm is presented. A 71-year-old man was admitted to our hospital with head injury. Neurological examination on admission only revealed consciousness disturbance (Japan Coma Scale 30). CT scan 19 hours after the injury demonstrated a contusional hematoma in the right frontal lobe, faint subarachnoid hemorrhage in the left sylvian fissure and subdural hematoma in the interhemispheric fissure. His consciousness was disturbed on the 14th day. CT scan demonstrated a left subdural effusion, which was surgically evacuated. However, from the next day the patient developed left hemiparesis. Right carotid angiogram on the 17th day after the injury revealed multiple segmental arterial narrowing in the right anterior cerebral artery (ACA) and middle cerebral artery (MCA). We diagnosed a posttraumatic delayed cerebral arterial spasm. CT scan revealed low density areas in the right ACA and MCA territory. The pathogenesis of posttraumatic delayed arterial spasm is not yet well known. Now, four theories have been suggested as follows: (1) Subarachnoid hemorrhage, (2) Direct mechanical injury to the arterial wall, (3) Hypothalamus dysfunction, and (4) Disturbed autoregulation. In our case, three important factors are suggested. The first is direct injury to the artery, the second is cerebral contusion, and the third is subdural effusion.

Aged↗
PubMed1992

Syncope: a symptom of coronary artery spasm after cardiac transplantation.

Two cases of coronary spasm in cardiac transplant recipients in which the presenting symptom was syncope without chest pain are reported. Diagnosing coronary spasm in transplant patients appears to be important because, based upon the few cases in the literature, prognosis is very poor. Coronary spasm may be related to accelerated atherosclerosis occurring in the transplanted heart.

Coronary Artery Disease↗
PubMed2005

[A case of severe coronary artery spasm associated with anaphylactic reaction caused by protamine administration].

A 65-year-old man with mitral regurgitation and atrial fibrillation underwent mitral valve plasty and Maze's operation. Cardiopulmonary bypass (CPB) was finished uneventfully. But after protamine administration, severe systemic hypotension occurred suddenly with electrocardiographic ST-segment elevation and wide QRS intervals. We thought that this reaction had been caused by coronary spasm and not by anaphylactic reaction because he was without typical anaphylactic manifestations such as general rash and bronchospasm. We administered epinephrine, methylprednisolone, heparin for restarting CPB, and used IABP support to assist systemic circulation. We again tried to administer protamine to neutralize the anticoagulative effect of heparin when his vital sign had recovered, but the same reaction occurred immediately with small amounts of protamine. The second CPB was necessary for some time. This case suggests that coronary artery spasm associated with anaphylactic reaction was induced by administration of protamine. It is known that intravenous protamine administration sometimes causes adverse events. As in this case, we should consider the possibility of severe coronary spasm associated with anaphylactoid reaction even if other symptoms of anaphylactic reactions such as cutaneous manifestation and bronchospasm are not present.

Aged↗
PubMed1991

Histamine-induced coronary artery spasm: the concept of allergic angina.

Histamine, the main amine released during allergic reactions, can provoke coronary arterial spasm manifested as angina pectoris. This has been shown during clinical and laboratory studies. The effects of histamine on cardiac function are mediated via H1- and H2- receptors situated on the four cardiac chambers and coronary arteries. Coronary arteries of cardiac patients are hyperactive and contain stores of histamine which can initiate coronary artery spasm. Clinical observations indicate that angina pectoris or acute myocardial infarction can be provoked by acute allergic reaction. The coincidental occurrence of chest pain and allergic reaction accompanied by clinical and laboratory findings of classical angina pectoris seems to constitute the syndrome of allergic angina. The clinical symptoms of allergic angina include chest discomfort, dyspnoea, faintness, nausea, pruritus and urticaria. They are accompanied by signs such as hypotension, diaphoresis, pallor and bradycardia. There are also electrocardiographic findings indicating myocardial ischaemia, arrhythmias and conduction defects. Thus, in patients undergoing acute allergic reaction, the development of chest pain could be explained by the mechanism of coronary arterial spasm provoked by the release of histamine, which constitutes the syndrome of allergic angina.

Angina Pectoris↗
PubMed1991

[Coronary spasm and diffuse coronary vasoconstriction responsible for transient left ventricular insufficiency].

A 52 year old patient presenting with spontaneous anginal chest pain for 4 days was admitted to hospital for a more intense and prolonged chest pain associated with signs of left ventricular failure (gallop, pulmonary crepitations, hypoxemia). Coronary angiography showed marked septal hypokinesia and spontaneous localised spasm of the left anterior descending and marginal arteries with a variable degree of luminal narrowing of the other segments of these two arteries and of the right coronary artery. These changes regressed after intracoronary injection of molsidomine. The signs of left ventricular failure disappeared in 48 hours. The wall motion abnormality, monitored by 2D echocardiography, regressed slowly over 3 days. On the other hand, the electrocardiogram, which showed anterior wall subendocardial ischaemia with prolongation of the QTc interval during the spasm, remained abnormal for a long time. Therefore, in the absence of organic heart disease, coronary spasms associated with vasoconstriction can induce a sufficiently severe and durable alteration of left ventricular function to create clinical signs of cardiac failure and profound and prolonged ST-T wave changes on the electrocardiogram.

Coronary Angiography↗
PubMed1991

[A case of bilateral internal thoracic artery bypass grafting in sudden death survivor with multivessel coronary spasms].

We report a 58-year-old male with a history of cardiac arrest due to coronary artery spasm, preoperative coronary arteriograms showed multivessel coronary spasm after the administration of ergonovine maleate associated with triple vessel fixed stenotic lesions. Under the use of cold diltiazem potassium-blood cardioplegic solution to prevent perioperative coronary spasm, coronary artery bypass grafting was performed. The right internal thoracic artery (ITA) was anastomosed to the left anterior descending artery and the left ITA to the circumflex artery. A saphenous vein graft was anastomosed to the right coronary artery. The postoperative course was uneventful. In postoperative coronary angiography with ergonovine stimulation, neither ITA grafts showed spastic changes, and the coronary artery distal to the anastomotic sites were well perfused through the ITA grafts. The patient has been free of angina without administration of calcium antagonist and been doing well for 2 years and 5 months since the operation.

Coronary Artery Bypass↗
PubMed1978

Cerebral arterial spasm. II. Etiology and treatment of experimental cerebral vasospasm.

Delayed cerebral vasospams is caused by excessive accumulation of dopamine-beta-hydroxylase (DBH) and noradrenaline in cerebral vessel walls. This study demonstrates the mechanisms of delayed spasm, particularly the role of red blood cell components, and the successful relief of delayed cerebral vasospasm. Spasmogenic substances which contained a heme component, such as methemoglobin, methemalbumin and catalase enhanced DBH activity in human serum as measured by a one step chemical spectrophotometric assay. The concentration which gave the highest DBH activity caused the maximum constriction of the basilar artery, when the substances were applied topically. Among components of red cells, methemoglobin, methemalbumin, catalase and nicotinamid adenin dinucleotide (NADH) caused constriction of basilar artery in cats, when applied topically, whereas hematin, hemin and bilirubin caused no significant spasm. An oxyhemoglobin solution obtained by mixture with methemoglobin and ascorbic acid produced no significant vascular spasm either. Relief of delayed cerebral vasospasm was obtained with topical application of specific alpha adrenergic blocking drug such as phenoxybenzamine, specific inhibitors of DBH such as fusaric acid, o-phenanthroline and alphaalpha' dipyridyl beta2 adrenergic stimulants such as salbutamol, and a phosphodiesterase inhibitor, ascorbic acid.

Albuterol↗
PubMed1990

[Long-term prognosis of coronary artery spasm].

This study analyses the long-term prognosis of 210 patients with coronary spasm documented at coronary angiography. All patients with a previous history of myocardial infarction or who had undergone coronary angioplasty were excluded. The average follow-up was 55 months and only 11 patients were lost to follow-up. The actuarial survival figures showed the 1 year, 2 year and 5 year survival rates to be 95, 92 and 89 per cent respectively. Extracardiac mortality was mainly related to smoking (lung cancer, laryngeal cancer, etc.) and was higher than cardiac mortality. More than half of the cardiovascular events (sudden death, myocardial infarcts) occurred during the first year of follow-up. Ten patients (4.7%) died suddenly. The predictive factors of this event were: previous syncopal episodes or syncopal angina due to coronary spasm, percritical arrhythmias and the documentation of multiple spasms at coronary angiography. Myocardial infarction was observed in 10.6 per cent of patients. Only those with significant coronary arterial lesions developed this complication. At the end of the follow-up period, 75 per cent of patients were asymptomatic or had only atypical chest pain. No significant differences were observed between the two groups treated medically, by aortocoronary bypass or by the association of coronary bypass and plexectomy with the exception of non-lethal myocardial infarcts being significantly less common in patients treated medically. Therefore, the long-term prognosis of patients with coronary spams is relatively satisfactory.

Actuarial Analysis↗
PubMed1990

[Coronary spasm during laryngoplasty].

A 63-yr-old man weighing 56kg was scheduled for pharyngoplasty under general anesthesia. The patient had no history of ischemic heart disease. Preoperative ECG showed incomplete right branch block. We administered thiopental and succinylcholine for intubation. Anesthesia was maintained with enflurane, nitrous oxide, oxygen and pancuronium bromide. Thirty minutes after the start of incision, the patient developed a severe hypotension and ECG revealed ST elevation and complete AV block. We administered ephedrine hydrochloride, phenylephrine hydrochloride and atropine sulfate. The ECG returned to sinus rhythm but ST segment was depressed this time. We considered it due to coronary spasm, so we started continuous intravenous administration of nitroglycerin (0.5 microgram. kg-1. min-1). One hour later, ST segment returned to normal. ECG showed no remarkable changes and no symptoms were seen after the operation. We found it important to suspect coronary spasm when ECG showed PVC-like abnormal waves with ST elevation. We consider that continuous administration of nitroglycerin at a rate of 0.5 microgram. kg-1. min-1 was effective for the treatment of coronary spasm in this case.

Coronary Vasospasm↗
PubMed1989

Coronary artery spasm and acute myocardial infarction.

From the studies and observations reviewed in this chapter, it can be appreciated that there is considerable direct and circumstantial evidence to implicate coronary artery spasm as a primary phenomenon in some patients with myocardial infarction. Although currently available data indicate that the number of acute myocardial infarctions due primarily to "pure" coronary artery spasm is relatively small, it should be emphasized that essentially very little if any data exist at "time zero" or at the actual onset of infarction. Most myocardial infarctions are probably multifactorial in etiology. To what extent coronary artery spasm, atherosclerosis, platelets, in situ thrombosis, endothelial mediators, and passive influences on vascular caliber interact in the pathogenesis of acute myocardial infarction remains incompletely understood.

Aged↗
PubMed1989

[Cardiotoxicity of 5-fluorouracil: coronary spasm? Apropos of 2 cases with normal coronarography].

Five fluoro-uracil (5-FU) is a cytotoxic drug which has been extensively used for chemotherapy since 1957. Ischaemic heart disease resulting from its administration is rare. Spontaneous angina during infusions of 5-FU was observed in two patients with electrocardiographic changes suggesting coronary spasm. After treatment, clinical examination, electrocardiogram, echocardiogram, stress test, coronary angiography with left ventriculography were all normal. An Ergonovine test was performed in one patient but failed to elicit coronary spasm. In the other patient, intravenous trinitrin and diltiazem were ineffective in preventing the ischaemic changes. A review of the literature is presented (51 cases). The pathophysiology of 5-FU-induced ischaemic heart disease is not fully understood. In 9 cases, coronary angiography was normal and coronary spasm was suggested as a possible cause. However, antispastic drugs are usually ineffective. It has been shown experimentally that 5-FU has a direct toxic effect on the myocardium.

Adult↗
PubMed1989

Effect of intracoronary nicardipine on methylergonovine-induced coronary artery spasm in patients with variant angina.

In a double-blind, randomized placebo controlled study, the effect of intracoronary (IC) nicardipine (0.4 mg) on methylergonovine (0.4 mg) induced coronary artery spasm was assessed in 16 patients with a history of variant angina. Reversal of the methylergonovine-induced coronary artery spasm was observed in 100% of patients treated with IC nicardipine and 25% of patients treated with placebo (p less than 0.01). There were no significant differences between the nicardipine and placebo treatment groups with respect to heart rate, blood pressure, proportion of patients experiencing chest pain or ST segment changes. These findings demonstrate that IC nicardipine is safe and could be effective in the reversal of coronary artery spasm in patients with variant angina.

Angina Pectoris, Variant↗
PubMed1987

Patient with coronary artery spasm and role of the critical care nurse.

Review of the literature reveals that coronary artery spasm exhibits a wide variation in clinical presentation. This variation makes accurate diagnosis and management difficult; however, precise diagnosis is essential so that appropriate therapy can be given. Critical care nurses are in an excellent position to assess patient findings that may help suggest or exclude the presence of coronary artery spasm as the cause of the myocardial ischemia. Critical care nurses also can play an important part in suggesting and carrying out appropriate management of coronary artery spasm.

Aged↗