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At least 991 records · Page 55Linked to original sources
PubMed1987

Platelets in the subarachnoid space. A cause of acute and delayed arterial spasm, intimal damage and cerebral infarction.

In nine baboons following intracisternal injection of a suspension of their own washed platelets, biphasic spasm was demonstrated by vertebral angiography. Constriction of the intra-arachnoid portion of the vertebral artery and the basilar artery was severe 10 minutes after the platelet injection, had begun to relax after one hour, but had returned on day 2 or 3. It persisted for about 8 days. The animals showed clinical evidence of neurological damage. At autopsy the vertebral and basilar arteries showed stripping of the endothelium, with adherent platelets, protein and other cells. There was blockage of some small branches. The brains showed ischaemic changes. The clinical phenomenon of spasm after subarachnoid haemorrhage was thus fairly closely modelled by the injection of platelets alone. There was some evidence that 5HT was probably not responsible for the delayed phase of spasm. Some suggestions are made about the mechanism.

Animals↗
PubMed1996

A rare indication for stenting: persistent coronary artery spasm.

A 34-year-old man presenting with angina both at rest and on exertion was investigated. He developed severe ST segment elevation and a brief period of ventricular tachycardia during an exercise tolerance test. On coronary angiography, 60% fixed luminal narrowing was observed in the proximal left anterior descending coronary artery and a severe spasm developed at this site, leading to temporary total occlusion of the vessel. Successful coronary angioplasty (PTCA) was performed on this lesion, with a residual 15% narrowing. However, the patient had a recurrence of angina 3 weeks later, despite being administered high doses of nitrate and calcium antagonist. During control angiography, the lesion severity was unchanged, but spasm developed again following contrast injection. At this time, a Palmaz-Schatz stent was implanted. Calcium antagonist, nitrate, Ticlopidine and low molecular weight heparin therapy was started. There was no recurrence of symptoms during a 3-month follow-up. The exercise tolerance test, and myocardial perfusion scintigraphy findings were normal and the stent was patent without restenosis at the end of the 3-month follow-up. Intracoronary stent implantation for persistent coronary spasm refractory to conventional medical therapy can be considered a feasible and attractive treatment modality for the control of symptoms.

Adult↗
PubMed2006

Coronary artery spasm of the native right coronary artery during off-pump coronary surgery of the left coronary artery system.

Native coronary artery spasm is a very rare complication during off-pump coronary artery bypass grafting. We report the case of a 74-year-old man who experienced angiographically documentated right coronary artery spasm while undergoing off-pump coronary artery bypass grafting on the diseased left coronary system. Despite two episodes of ventricular fibrillation and persistent ST segment elevation of the posterior wall, the off-pump procedure was successfully completed by grafting the left internal thoracic artery to the left anterior descending artery and a saphenous vein graft to the Ramus intermedius. The immediate postoperatively performed coronary angiography demonstrated patent anastomoses and two areas of significant spasticity within the course of the right coronary artery. Intracoronary nitroglycerin infusion into the ostium of the right coronary artery resolved the spasms of this nondiseased vessel as well as the associated ST segment elevations.

Aged↗
PubMed2000

Coronary Artery Spasm.

Attacks of variant angina usually respond promptly to sublingual administration of short-acting nitrates (nitroglycerin, 0.3 to 0.4 mg, or isosorbide dinitrate, 5 to 10 mg), which may be repeated after 3 to 5 minutes if pain persists. In the rare cases resistant to sublingual nitrates, sublingual nifedipine (5 to 10 mg) or, when readily available, intravenous nitrates (nitroglycerin or isosorbide dinitrate, 2 to 10 mg) or calcium antagonists (verapamil, 5 to 10 mg, or diltiazem, 0.15 mg/kg) can be given. All attempts to prevent ischemic attacks by means of specific receptor blockade in patients with vasospastic angina have been unsatisfactory. This may be either because the doses of the blockers used were insufficient or, more likely, because the blockade of a single receptor-agonist interaction leaves receptors for other vasoconstrictor stimuli unopposed and therefore capable of eliciting spasm. Thus, for instance, alpha-adrenergic, serotoninergic, and thromboxane A(2) antagonists all failed to reduce significantly the number of anginal attacks, although they appeared to be effective in some patients. Until the actual causes of the coronary smooth muscle hyperreactivity to constrictor stimuli are known, treatment of vasospastic angina is based on the use of nonspecific vasodilators. Indeed, the mainstay of pharmacologic treatment of coronary artery spasm is calcium channel blocking agents together with nitrates to cover the periods in which spasm is most likely to occur. These powerful vasodilating agents, at their usual doses, are able immediately and completely to control the recurrences of ischemic attacks in as many as 80% of patients. Moreover, some studies have shown that use of calcium antagonists significantly improves clinical outcome in patients with variant angina.

Journal Article↗
PubMed2006

Treatment of infantile spasms.

Infantile spasms are associated with a diverse range of conditions, and treatment options are available. However, outcomes remain generally poor, particularly for those with symptomatic etiologies. First-line therapy is considered to be hormonal (adrenocorticotropic hormone; ACTH), which some evidence suggests is more effective when started early. However, side effects may place limits on its use acutely and long-term. There is additional evidence for vigabatrin, specifically for infantile spasms secondary to tuberous sclerosis complex. In refractory cases, candidacy for surgical management should be explored, along with new-generation anticonvulsants (eg, topiramate, zonisamide) and the ketogenic diet. There is urgent need for further treatment trials comparing anticonvulsants with ACTH and a satisfactory animal model for the study of spasms.

Journal Article↗
PubMed1983

Electrocardiographic changes with coronary artery spasm.

The presence or absence of important ECG changes (e.g., ST elevation or depression greater than or equal to 1 mm) was evaluated in 79 consecutive patients with coronary artery spasm. In eight of these patients ECG changes usually did not accompany episodes of rest angina. Evaluation before, during, and after cardiac catheterization included multiple ECGs and ambulatory monitoring during angina. Our observations suggest that the ECG may not always be a sensitive indicator of coronary spasm. Thus the diagnosis of transient myocardial ischemia secondary to coronary spasm should not necessarily be excluded because of a lack of ECG changes during rest angina.

Aged↗
PubMed1987

Comparison of electrocardiography and thallium-201 myocardial scintigraphy for the detection of ergonovine-induced coronary artery spasm: angiographic correlation.

This study was performed to determine the sensitivity of thallium imaging vs ECG monitoring for detecting coronary artery spasm noninvasively following intravenous ergonovine administration as compared to simultaneous coronary angiography. Thirty-two patients with insignificant coronary artery disease and chest pain underwent 12-lead ECG monitoring, thallium imaging, and coronary arteriography following the administration of 0.05, 0.1, 0.2, and 0.3 mg of ergonovine given 5 minutes apart or until chest pain occurred. One minute following the last dose of ergonovine, 2.5 mCi of thallium-201 was injected intravenously, and a final ECG was recorded and repeat coronary arteriography performed. Within 10 minutes following the injection of thallium, imaging was performed in the 40-degree and 70-degree left anterior oblique and anterior projections. The ECG, thallium study, and coronary arteriogram were read blindly and results were compared. The ECG, angiogram, and thallium study were read as positive if the following occurred, respectively: greater than or equal to 1 mm ST segment elevation, depression, or T wave reversal; greater than 50% vessel narrowing,; and reversible perfusion defect. Five patients were excluded from analysis because of either catheter-induced spasm, suboptimal thallium studies, or protocol violations. Of the 27 patients included for analysis, six had chest pain, five had a positive angiogram, five had a positive thallium study, and one had a positive ECG. The sensitivity of thallium vs ECG monitoring was 80% vs 25%, and the accuracy was 92% vs 80%. We conclude that thallium imaging greatly increases the noninvasive detection of ergonovine-induced coronary spasm as compared with the ECG with no loss of accuracy.

Adult↗
PubMed1992

Various 12-lead electrocardiographic findings of diffuse three-vessel coronary artery spasm.

Electrocardiographic signs of diffuse three-vessel coronary artery spasm may show various findings including no ST segment changes, according to whether or not a difference of an electrical gradient develops between the anterior and inferior regions because of global ischemia. This study suggests that diffuse three-vessel coronary artery spasm must be considered when the 12-lead electrocardiogram (ECG) shows no important ST segment changes with episodes of angina and diffuse coronary artery spasm during an ergonovine provocation test in patients with strongly suspected variant angina.

Adult↗
PubMed1994

Comparison of the distribution of myocardial blood flow between exercise-induced and hyperventilation-induced attacks of coronary spasm: a study with thallium-201 myocardial scintigraphy.

Exercise and hyperventilation tests are often used as the provocative tests for coronary artery spasm. To examine the distribution of myocardial blood flow during exercise-induced and hyperventilation-induced attacks of coronary spasm, thallium-201 myocardial scintigraphy was performed in 47 patients with variant angina. The extent and severity scores and severity index (severity score/extent score) of scintigraphic perfusion defect were calculated. In 32 patients, anginal attack associated with ST elevation on the electrocardiogram was induced by exercise; in 23 patients, the attack was induced by hyperventilation. In patients with either anterior or inferior wall ischemia, both the extent and severity scores and severity index in the scintigram were significantly greater in exercise-induced anginal attack than those in hyperventilation-induced attack. In patients with simultaneous anterior and inferior wall ischemia, they tended to be greater in exercise-induced attack. In eight patients in whom anginal attack was induced by both exercise and hyperventilation, these scores and index were significantly greater in exercise-induced attack than those in hyperventilation-induced attack. These data suggest that myocardial ischemia during exercise-induced attack is enhanced as compared with that during hyperventilation-induced attack. Thallium-201 scintigraphy combined with exercise testing seems to be more sensitive for detecting myocardial ischemia induced by coronary spasm.

Aged↗
PubMed1980

Efficacy of diltiazem for control of symptoms of coronary arterial spasm.

To evaluate the efficacy of the calcium antagonist diltiazem for therapy of active coronary arterial spasm, 13 patients with clinical variant angina attributed to documented coronary arterial spasm completed a prospective randomized double-blind crossover trial of diltiazem (120 and 240 mg/day) versus placebo. Response was assessed with the diary technique measuring frequency of angina, consumption of nitroglycerin and percent of pain-free days. When 120 mg of diltiazem/day was compared with the paired placebo period there was a significant increase in percent of pain-free days (from 43 to 71 percent [p = 0.03]), but no significant decrease in frequency of angina (p = 0.06) or consumption of nitroglycerin (p = 0.32). When 240 mg of diltiazem/day was compared with the paired placebo period there was a significant increase in percent of pain-free days (from 50 to 79 percent [p = 0.03]) and a significant decrease in both frequency of angina (from 1.6 to 0.4 episodes/day [p = 0.03]) and consumption of nitroglycerin (from 1.3 to 0.4/day [p = 0.01]). Diltiazem was found to be a highly effective drug for control of symptoms of active coronary arterial spasm, without side effects and with excellent patient tolerance.

Aged↗
PubMed1981

Complete denervation of the heart (autotransplantation) for treatment of severe, refractory coronary spasm.

A 49 year old man had severe refractory Prinzmetal's variant angina and angiographically documented coronary arterial spasm of a dominant circumflex artery. The spasm was provoked by methergine (an ergot alkaloid) and seemed resistant to various forms of medical therapy including administration of nitrates, nifedipine, verapamil, diltiazem and amiodarone. The attacks of angina at rest persisted at the rate of 7 to 15/day and were frequently associated with atrioventricular (A-V) block. After unsuccessful plexectomy performed in another institution, the patient underwent complete cardiac denervation (produced by autotransplantation). The follow-up data have interesting implications in relation to treatment of refractory variant angina, as well as possible mechanisms of coronary arterial spasm.

Angina Pectoris↗
PubMed1982

Sudden death in Prinzmetal's angina with coronary spasm documented by angiography. Analysis of three necropsy patients.

Clinical and necropsy findings are described in three patients who had angina pectoris at rest, S-T segment elevation on electrocardiography during chest pain, coronary arterial spasm on angiography and sudden death. Although significant "fixed" coronary narrowing (that is, narrowing due to atherosclerotic plaques) was appreciated by angiography in only one of the three patients, necropsy disclosed in all three patients severe fixed coronary narrowings involving particularly the artery in which spasm had been demonstrated during life. Additionally, examination of each 5-mm long segment of the coronary artery that had been spastic during life (two patients) disclosed several focally spastic segments at necropsy, indicating that spasm persisted after death. Although most previously described necropsy patients with Prinzmetal's angina had some fixed coronary narrowing, underlying fixed narrowing may be difficult to identify angiographically as demonstrated by the three patients in this study.

Adult↗
PubMed1983

Detrimental effect of propranolol in patients with coronary arterial spasm countered by combination with diltiazem.

This study determines, with quantitative variables, if propranolol is detrimental in patients with documented coronary arterial spasm and if this drug can be used in combination with calcium antagonists. Eleven patients with documented coronary spasm were entered prospectively in a study with 4 phases of 2 days each: (1) control, (2) diltiazem or propranolol (mean 225 +/- 75 mg/day), (3) propranolol or diltiazem (360 mg/day), (4) propranolol and diltiazem. The effects of the drugs were assessed by the detection of ischemic electrocardiographic episodes (24-hour electrocardiographic monitoring) and provocative tests with ergonovine. During the period of treatment with propranolol, the number and the duration of attacks increased and provocative tests had positive results in all patients. Diltiazem completely abolished spontaneous episodes, but 6 of 11 patients remained sensitive to the administration of ergonovine. The association of the 2 drugs led to a disappearance of ischemic episodes. In conclusion, propranolol is ineffective in patients with coronary artery spasm. It can be used in combination with diltiazem, but without any advantage over diltiazem alone.

Adult↗
PubMed1985

Role of calcium antagonists in cerebral arterial spasm.

Spasm of the large cerebral arteries at the base of the brain causes delayed ischemic neurologic deficits in approximately 30% of patients after a subarachnoid hemorrhage from an intracranial aneurysm. In vitro chamber studies have shown that both dog and human large cerebral artery segments contract to a variety of vasoactive agents, and the dog and human segments are remarkedly similar in their responses. The source of calcium necessary to initiate contraction was found to be extracellular for large cerebral arteries. In contrast, systemic arteries such as the femoral artery use a bound intracellular pool of calcium for contraction. The calcium antagonists nifedipine and nimodipine were found to selectively inhibit the contractions of large cerebral arteries but not the femoral artery. In vivo experiments demonstrated that both nifedipine and nimodipine, given sublingually, would prevent and reverse cerebral arterial spasm in the dog after a subarachnoid hemorrhage. Nimodipine was found to be more potent, both in the chamber and in the live dog experiments. Nimodipine significantly decreased the occurrence of severe neurologic deficits from spasm alone in a multi-institutional, prospective, double-blind, randomized, placebo-controlled trial.

Animals↗
PubMed1985

Microvascular spasm as a cause of cardiomyopathies and the calcium-blocking agent verapamil as potential primary therapy.

The origin of cardiomyopathies, a major cause of cardiac disability and death, has been largely unexplained. Pathologic features, common to all cardiomyopathies independent of origin, include ventricular hypertrophy and diffuse scarring with variable amounts of ventricular dilatation. This problem was studied experimentally in 2 models of congestive cardiomyopathy: the hereditary cardiomyopathic Syrian hamster and the hypertensive-diabetic rat. In both the genetic and the acquired disease models, there is focal myocytolytic necrosis followed by healing with focal scars, ventricular wall hypertrophy, ventricular dilatation with congestive heart failure and, ultimately, death. In view of the heterogeneous pathologic features of both diseases, silicone rubber perfusions have been used to study the microcirculation of the heart in these animals; microvascular spasm has been demonstrated early in the disease associated with small areas of myocytolytic necrosis that undergo subsequent fibrosis. Reactive hypertrophy then ensues as a compensatory response to this myocellular necrosis; it is the combination of cell loss and slowly decreasing contractility resulting from the reactive hypertrophy, which culminates in a cardiomyopathy. Administration of verapamil or prazosin to the cardiomyopathic Syrian hamster prevents microvascular spasm and development of cardiomyopathic changes in the myocardium. In view of these and other findings related to the anatomy and hyperreactivity of microcirculation, it is concluded that hypertrophic congestive cardiomyopathies may be caused by focal cell loss due to microvascular spasm and reperfusion injury, with the subsequent development of focal fibrosis and reactive hypertrophy in response to the myocardial necrosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Usefulness of radionuclide ventriculography in assessment of coronary artery spasm.

Provocative tests that permit detection of coronary artery spasm are widely used in patients with ischemic syndromes. To assess the usefulness of radionuclide ventriculography combined with provocative tests for diagnosis of coronary spasm, the left ventricular (LV) response to exercise, hyperventilation and a cold pressor test was determined in 3 groups. Group I included 10 normal subjects; group II, 49 patients with typical effort angina and fixed obstructive coronary artery disease at catheterization; and group III, 19 patients suspected of having vasospastic angina based on clinical and electrocardiographic findings, each of whom had normal coronary angiographic findings. In group I, LV ejection fraction (EF) increased during hyperventilation and exercise testing in 9 of 10 subjects (90%) and failed to decrease 5% in 9 of 10 subjects (90%) during cold testing. In contrast, while 18 of 49 patients (37%) of group II showed LV dysfunction with cold testing and 8% with hyperventilation, all showed abnormal LV function during exercise. Finally, in group III, LVEF increased during exercise, mimicking the response in normal group, while dysfunction was present in 14 of 19 (74%) during hyperventilation and in 17 of 19 (89%) during cold testing. When results of hyperventilation and cold testing were combined, abnormal responses were present in all patients. Thus, radionuclide ventriculography, when performed in association with 3 forms of stress--exercise, hyperventilation and cold testing--allows accurate identification of patients likely to have coronary spasm.

Adult↗
PubMed1989

Enhanced responsiveness of smooth muscle, impaired endothelium-dependent relaxation and the genesis of coronary spasm.

Pathophysiology and genesis of coronary artery spasm were examined in vivo and in vitro in Göttingen miniature pigs. Five of 36 consecutive pigs before endothelial denudation showed evidence of regional hyperconstriction after intracoronary administration of histamine (group 1). Histologic examination revealed intimal thickening along the spastic site. Because 5 pigs died during endothelial denudation, cholesterol feeding was randomly assigned to 13 of the remaining 26 pigs (group 2) and others were fed a regular low cholesterol diet (group 3) for 3 months. Regional coronary hyperconstriction was also evident after intracoronary administration of histamine at the site of denudation, and the degree of constriction was 78 +/- 3 and 74 +/- 4% in groups 2 and 3, respectively. Because the intimal thickening was confirmed at the site of spasm in groups 2 and 3, spontaneous as well as denudation-induced intimal thickening accompanied the enhanced responsiveness to histamine, irrespective of the level of serum cholesterol. However, the role of geometry on histamine-induced luminal narrowing was only 6% and was not physiologically significant. Augmented responses of the coronary artery to histamine, but not to phenylephrine or potassium chloride were reproduced in the nonbeating isolated heart preparations perfused at 90 mm Hg with oxygenated Krebs-Henseleit solution, and the degree and location of in vitro hyperconstriction were similar to that in vivo and were not attenuated after pretreatment with the nerve transmitter blockers, guanethidine (3 X 10(-6) M), atropine (10(-6) M) and tetrodotoxin (3 X 10(-7) M). Accordingly, spasm can be provoked without the influence of blood constituents and neural factors.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Microvascular spasm is mediated by vasopressin fibers in the rat hippocampal slice.

Microvessels in the rat hippocampal slice can be used as an in vitro model for the study of cerebral vasospasm. Serum from coagulated blood causes prompt and long-lasting microvascular constriction that is neurogenic in nature. Here we show that a candidate spasmogen, thromboxane B2, has excitatory action on neural elements in the slice. However, spasmogenic serum lacks this excitatory effect. Instead, it is inhibitory for a major population of slice neurons. Thus, neurogenic microvascular spasm is produced by a subpopulation of slice neurons or projection fibers, not all neurons acting in concert. Arginine vasopressin (AVP) is contained in fibers that project to the hippocampus, and hippocampal microvessels contain pressor (V1) receptors for the peptide. AVP causes vasoconstriction in the slice, and a specific V1 antagonist for the peptide blocks the microvascular spasm induced by blood serum. The results are interpreted to mean that neurogenic microvascular spasm is mediated by locally released AVP.

Animals↗