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PubMed1985

Embolization from angiographic catheter during angiography simulating vascular spasm. Report of a case with postmortem verification.

The initiating event in the pathogenesis of acute coronary thrombosis, especially the role played by vasospasm, remains controversial. Recently an angiographic sequence of events has been reported which should conclusively prove that spasm of a normal coronary artery might lead to occlusive thrombosis. The patient survived, and thus this conclusion was reached without morphological verification. The present report describes an almost identical angiographic sequence of events in a cerebral artery initially interpreted in the same way: spasm leading to thrombosis. The patient died, and an embolus derived from the angiographic catheter was found at postmortem examination exactly where angiography had shown "spasm". A "catheter embolus" simulating vascular spasm could as well explain the basic angiographic findings in the previously reported case. Thus, it still remains to be proved that spasm of a normal artery may lead to occlusive thrombosis.

Aged↗
PubMed1995

Spinal anesthesia attenuates myocardial ischemia during coronary artery spasm induced by intraaortic methacholine in rats.

Coronary artery spasm is not rare in patients with coronary artery disease, but the influence of regional anesthesia on spasm-induced myocardial ischemia is not known. We investigated the effects of spinal anesthesia on myocardial ischemia during coronary artery spasm in rats, and compared these with the effects of an alpha- and beta-adrenergic antagonist, and an alpha-adrenergic agonist. An intraaortic catheter was inserted via the right internal carotid artery so that the tip of the catheter was placed near the coronary ostium. An intrathecal catheter was placed at lumbar level. Coronary spasm was induced by the intraaortic injection of methacholine, and we identified the thresholds of myocardial ischemia, defined as the dose of methacholine that induced ST-segment elevation. Subsequently, the thresholds were determined after spinal anesthesia, and after the intraaortic injection of phentolamine and propranolol. The thresholds of myocardial ischemia increased significantly after intrathecal bupivacaine. In contrast, the threshold did not change after the injection of phentolamine. The thresholds increased significantly after the injection of propranolol. Methoxamine significantly decreased the threshold of ischemia. These results demonstrated that spinal anesthesia attenuated myocardial ischemia during methacholine-induced coronary spasm. This effect was equivalent to that of propranolol.

Adrenergic alpha-Agonists↗
PubMed1987

Coronary artery spasm.

Coronary artery spasm is a transient reduction in lumen diameter of an epicardial coronary artery of sufficient degree to produce objective evidence of myocardial ischemia in the absence of any significant increase in heart rate or blood pressure. In this article are summarized pathophysiological observations, the coronary angiographic anatomy of patients with coronary spasm, etiologic considerations, methods to provoke coronary artery artery spasm and their clinical usefulness, the role of coronary artery spasm in patients with clinical angina pectoris and myocardial infarction, and finally, the role of coronary artery spasm in patients undergoing coronary artery surgery.

Coronary Vasospasm↗
PubMed1987

Percutaneous transluminal coronary angioplasty in patients with spasm superimposed on atherosclerotic narrowing.

Of 552 patients undergoing percutaneous transluminal coronary angioplasty 102 had coronary artery spasm superimposed on atherosclerotic narrowing. Coronary angioplasty was successful in 97 (95%). The patients were discharged on a regimen of nifedipine (40-60 mg/day). Seventy six patients were symptom free 6-8 months after the procedure. Restenosis was detected in 35% of patients. Coronary artery spasm was provoked in 38 (44%) of the 87 patients who underwent an ergometrine maleate test. Twenty seven of the 34 patients with restenosis had a provocation test and coronary artery spasm was superimposed on restenosis in 22 (81.5%). Coronary angioplasty is feasible in patients with coronary artery spasm superimposed on atherosclerotic narrowing but the rate of restenosis is high and coronary artery spasm could have a role in the pathogenesis of restenosis.

Angioplasty, Balloon↗
PubMed1976

Arterial spasm and recovery from subarachnoid haemorrhage.

In a series of 120 cases of subarachnoid haemorrhage due to ruptured intracranial aneurysm the occurrence of preoperative arterial spasm was found to have no effect upon the clinical outcome. After surgery, generalised arterial spasm was found to lead to an increased probability of fatality, and to an increased probability of psychological impariment among the survivors. The occurrence of spasm only in the vessels immediately adjacent to the haemorrhage did not constitute a risk to survival. However, the presence of generalised or localised spasm led to an increased risk of neurological impairment. It is suggested that the mechanisms by which postoperative arterial spasm is responsible for fatalities and for neurological impairment are distinct.

Cerebral Arterial Diseases↗
PubMed2002

High-dose intravascular beta-radiation after de novo stent implantation induces coronary artery spasm.

BACKGROUND: Intracoronary brachytherapy is effective in preventing restenosis after coronary interventions. However, in vitro and animal studies have shown that irradiation produces immediate and sustained endothelial dysfunction. This study assesses the clinical relevance of impaired vasomotoric function induced by brachytherapy. METHODS AND RESULTS: We analyzed the occurrence of postradiation coronary artery spasms in 1 animal study and 2 clinical trials investigating the effects of high-dose intracoronary beta-radiation after de novo coronary artery stenting. Irradiated segments (IRSs) proximal and distal to the stent were studied by quantitative coronary angiography after stenting, after radiation, and at the end of the procedure. There was an 67% overall incidence of coronary artery spasm in the IRSs immediately after beta-radiation compared with 9% after sham treatment (P<0.001). Whereas in most cases this phenomenon was only minor or moderate, in 12 cases, 4 (22%) animals and 8 (28%) patients, severe coronary spasm (>90% diameter stenosis) with significant ECG-changes or hemodynamic instability was observed. Relief of spasms was protracted (mean time until complete relief of spasm 423+/-122 seconds) and required repetitive intracoronary administration of nitroglycerin (mean dose: 1.2+/-0.6 mg). CONCLUSIONS: Vasoconstriction is a frequent reaction of coronary arteries after high-dose intracoronary beta-radiation, necessitating repetitive administration of vasodilators.

Animals↗
PubMed1982

Action of intracoronary nitroglycerin in refractory coronary artery spasm.

Coronary artery spasm usually responds to sublingual nitroglycerin. This report describes four patients with variant angina and one patient with rest angina who had coronary spasm that was refractory to sublingual or i.v. nitroglycerin. In four patients, spasm occurred spontaneous and in one patient after 0.05 mg of ergonovine. In each case, 25-100 micrograms of intracoronary nitroglycerin promptly (30-45 seconds) resulted in reopacification of the vessel involved in spasm and resolution of evidence for ischemia. Thus, intracoronary nitroglycerin can reverse coronary artery spasm that does not respond to systemic nitroglycerin administration.

Adult↗
PubMed1995

Soluble P-selectin is released into the coronary circulation after coronary spasm.

BACKGROUND: The glycoprotein P-selectin is an adhesion molecule involved in the property change of leukocytes at the initiation of the inflammatory process. The purpose of the present study was to determine whether acute myocardial ischemia induced by coronary spasm causes an acute inflammatory response in the coronary circulation. METHODS AND RESULTS: We examined plasma soluble P-selectin levels in the coronary sinus and the aortic root simultaneously in 16 patients with coronary spastic angina before and after left coronary artery spasm induced by intracoronary injection of acetylcholine and in 15 patients with stable exertional angina before and after acute myocardial ischemia induced by rapid atrial pacing. Ten control patients with chest pain but normal coronary arteries and no coronary spasm also received intracoronary acetylcholine. Plasma soluble P-selectin levels were increased significantly in the coronary sinus (32.8 +/- 3.6 to 52.8 +/- 5.9 ng/mL, P < .001) and in the aortic root (34.6 +/- 3.7 to 41.9 +/- 4.4 ng/mL, P < .05) after the attacks in the coronary spastic angina group but remained unchanged in the stable exertional angina group after the attacks and in the control group after the administration of acetylcholine. Furthermore, the coronary sinus-arterial difference of soluble P-selectin increased significantly after the attacks in the coronary spastic angina group (-1.8 +/- 2.2 to 10.9 +/- 2.7 ng/mL, P < .001). CONCLUSIONS: Our data indicate that soluble P-selectin is released into the coronary circulation after coronary artery spasm. We conclude that coronary artery spasm may induce the leukocyte adhesion in the coronary circulation and may lead to myocardial damage.

Acetylcholine↗
PubMed1989

Intramural hemorrhage and endothelial changes in atherosclerotic coronary artery after repetitive episodes of spasm in x-ray-irradiated hypercholesterolemic pigs.

To assess whether coronary spasm affects the progression of atherosclerosis and results in evolution of myocardial infarction, the role of coronary spasm on the fine structure of conduit coronary arteries was studied morphologically. Göttingen miniature pigs were fed a semisynthetic diet containing 2% cholesterol and 1.1% sodium cholate. One month after being on this diet, the pigs were anesthetized and the endothelium of a branch of the left coronary artery was denuded using a balloon catheter. X-ray irradiation in a dose of 1,500 rad was given twice selectively to the area denuded, after 4 and 5 months of cholesterol feeding. Five months after endothelial denudation, transient (group A) and repetitive episodes (group B) of coronary spasm were provoked by single and periodic (five times every 5 minutes) intracoronary injections of serotonin (10 micrograms/kg/injection), respectively. The extent of spasm by serotonin at the previously denuded site was 84 +/- 4% (n = 4) and 90 +/- 5% (n = 6) narrowing in groups A and B (p = NS between groups), respectively. Forty minutes after the final administration of serotonin, the left coronary artery was relaxed by nitroglycerin, and the heart was isolated and perfuse-fixed under physiological pressure. Intramural hemorrhage was noted at the spastic site in six pigs of group B but not in group A. The average percent luminal narrowing, on cross sections at the spastic site in group B, was significantly greater than in group A (56 +/- 7% vs. 23 +/- 5%, p less than 0.01). Scanning electron micrographs revealed that the endothelial lining was intact at the nonspastic site in both groups. In addition to the appearance of intercellular bridges at the spastic site in both groups, squeezing of endothelial cells and adhesion of white blood cells were present at the spastic site exclusively in group B. These findings are consistent with the hypothesis that repetitive spasm may have an important role in the progression of atherosclerosis and/or myocardial infarction.

Angiography↗
PubMedDate not supplied

Severe coronary artery spasm with anaphylactoid shock caused by contrast medium--case reports.

This study reports 2 cases of severe coronary artery spasm with anaphylactoid shock caused by contrast medium. The first patient had anaphylactoid shock in response to contrast medium and severe coronary spasms of both the left anterior descending coronary artery and the left circumflex coronary artery. The patient developed ventricular arrhythmia and complete atrioventricular block following the severe coronary spasm. The second patient had a totally occluded right coronary artery, owing to a spasm after anaphylactoid shock. Anaphylactoid shock should always be considered when persistent shock is noted after the coronary artery spasm has been relieved.

Adrenergic alpha-Agonists↗
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↗
PubMed2006

Coronary artery spasm and the polymorphisms of the endothelial nitric oxide synthase gene.

BACKGROUND: Coronary artery spasm plays an important role in the pathogenesis of vasospastic angina, and contributes to the development of several acute coronary syndromes. Endothelial nitric oxide synthase (ecNOS) catalyzes the synthesis of nitric oxide, which regulates vascular tone, and may be related to coronary vasospasm. The present study investigated whether coronary spasm is related to particular polymorphisms of the ecNOS gene. METHODS AND RESULTS: Spasm provocation by serial infusions of acetylcholine was performed on 165 patients who were clinically suspected of having angina. In both study patients and healthy controls (n=400), genomic polymorphisms of the ecNOS gene were determined by using polymerase chain reaction. Quantitative luminal diameter measurements of the 3 major coronary arteries were initially obtained before and after acetylcholine injection, and then after isosorbide dinitrate injection, by using a computer-assisted analysis system. Logistic multiple regression analysis identified the a/a or a/b genotype in intron 4 of ecNOS (NOS4a: p=0.0431, odds ratio (OR) 2.43) and diabetes mellitus (p=0.0060, OR 4.88) as significant predictors of coronary spasm. In the patients with NOS4a, both the induced and spontaneous contractions were augmented. CONCLUSION: The present study results indicated that NOS4a could be a good marker for coronary artery spasm.

Acetylcholine↗
PubMed1985

Animal models of coronary spasm and the pathophysiological events in regional vascular hypercontraction.

An animal model of coronary spasm was designed 1) to reproduce coronary spasm similar to that seen in patients with variant angina, 2) to determine whether hypercontraction of the vascular smooth muscle occurs at the site of the spasm, 3) to document the relationship between functional and structural changes of the vascular wall and 4) to characterize the pathophysiological features of coronary spasm. After balloon de-endothelialization and feeding of a high cholesterol diet in mongrel dogs and Göttingen miniature pigs, there was evidence of vascular hypercontraction associated with arteriosclerotic changes. Coronary spasm of more than 75% narrowing of the artery was provoked with ischemic signs in miniature swine. These events could be repeatedly provoked by an intracoronary injection of histamine following pretreatment with cimetidine. The site of hypercontraction corresponded well with the site of the de-endothelialization, an area where the basal vascular tone was increased and was related to histamine activity. Thus, the present animal model will shed light on mechanism involved in vasoactive angina pectoris and aid in clarifying the pathophysiology of vascular smooth muscle.

Animals↗
PubMed1988

Plaque rupture possibly induced by coronary spasm--an autopsy case of acute myocardial infarction.

The histological picture of sites of coronary spasms has not yet been made sufficiently clear. A histopathological examination was performed on the coronary artery of a patient who died of acute myocardial infarction after a refractory coronary spasm was identified by coronary arteriography. In the site of the coronary spasm, intimal bleeding as well as infiltration by lymphocytes and plasma cells in the adventitia were seen. In the same region, fracture of intimal collagen fibers and rupture of atheromatous plaque were observed. Although it is very difficult to prove in individual cases of acute myocardial infarction that spasms played a part, some cases involving spasms may possibly exist among the cases of acute myocardial infarction showing atheromatous plaque rupture--thrombus formation.

Coronary Angiography↗
PubMed1993

Incidence of acetylcholine-induced spasm of coronary arteries subjected to balloon angioplasty.

To examine the vasospastic activity of coronary arteries which have been subjected to previous balloon angioplasty, we conducted an acetylcholine provocative test at diagnostic catheterization in 147 consecutive patients. All patients underwent successful elective angioplasty and had follow-up angiography 1 to 6 months after the procedure. Sixty-two patients had a history of prior myocardial infarction and 43 patients had multivessel coronary artery disease. Angioplasty was performed on 176 vessels. Incremental doses of acetylcholine (25 micrograms, 50 micrograms, 100 micrograms) were injected into the right and left coronary arteries over a period of 1 min. The incidence of coronary spasm of arteries which had been subjected to angioplasty was 44%. Angiographic restenosis was observed in 59 patients (40%). There was no correlation between the occurrence of coronary spasm and the presence of restenosis. The maximal dose of injected acetylcholine was smaller in patients with positive evidence of spasm than in patients with negative evidence of spasm (55 +/- 27 micrograms vs 82 +/- 28 micrograms, p < 0.01). In patients with single vessel coronary artery disease, the incidence of spasm of the contralateral artery, i.e. the artery without angioplasty, was lower than that of the artery subjected to angioplasty (22% vs 46%, p < 0.01). Thus, the data suggest that coronary arteries which have been previously subjected to angioplasty have enhanced vasospastic activity in response to acetylcholine.

Acetylcholine↗
PubMed2000

Successful management of intractable coronary spasm with a coronary stent.

Although the long-term survival of patients suffering from coronary spasm is usually excellent, serious complications can develop, such as disabling pain, myocardial infarction, ventricular tachyarrhythmias, atrioventricular block and sudden cardiac death. A 40-year-old man who had intractable chest pain from coronary artery spasm suffered ventricular fibrillation and an acute anterior myocardial infarction upon first admission. The patient underwent a coronary angiogram, which revealed a spontaneous focal spasm at the proximal left anterior descending coronary artery (LAD). He was treated by the combination of nitrate and calcium channel blocker, but continued to complain of severe chest pain despite intensive medical therapy and he had to be treated in the emergency room 5 times during an 8-month follow-up period. An ergonovine coronary angiogram was performed and an intracoronary ultrasound examination, which revealed a focal spasm at the same site of the proximal LAD with a small amount of localized eccentric atheromatous plaque. A coronary artery stent was placed in the proximal LAD and his symptoms resolved. A follow-up coronary angiogram was performed 3 years after stenting and the stent remained patent without any in-stent restenosis or spasm.

Adult↗
PubMed2001

Circadian variation of autonomic nervous activity in patients with multivessel coronary spasm.

The present study investigated whether the circadian rhythm of sympathovagal activity is related to the severity of coronary spasm or multivessel coronary spasm. Heart rate variability was examined in 22 consecutive patients with vasospastic angina provoked by intracoronary injection of acetylcholine, who had either multivessel spasm (Group M, n=11 ) or single vessel spasm (Group S, n= 11), in 20 subjects without coronary artery disease (Group C) and 20 patients with effort angina who had organic coronary artery stenosis (Group E). The frequency domain indices were analyzed, including low frequency (LF: 0.04-0.15 Hz) and high frequency (HF: 0.15-0.4Hz), the latter being an index of efferent parasympathetic activity, and the ratio (L/H) as an index of sympathovagal balance. The circadian variation of the parameters was analyzed by its pattern and was quantified by the difference of the mean values between daytime and nighttime. Although the HF power increased during nighttime in Groups C and S, this increase was attenuated in Groups E and M. The circadian variation of the L/H ratio (ie, a drop during nighttime) was smaller in the S and M groups than in Groups C and E. Accordingly, in Group M, the circadian variation of both sympathetic and parasympathetic nervous activity was attenuated, but in Group S, the variation of sympathetic nervous activity, but not parasympathetic nervous activity, was decreased. These data suggest that relatively enhanced sympathetic nervous activity at night may be involved in the mechanism underlying multivessel coronary spasm.

Acetylcholine↗
PubMed1985

Coronary spasm and allergy. Retrospective study of the incidence of allergic history in patients with variant angina.

Despite a large number of papers concerning coronary spasm, its mechanism still remains unsolved. Several cases have been reported in which coronary spasm was triggered by allergy. Since histamine is one of the causative substances released in allergic reactions, we speculated on some involvement of an allergic mechanism in the pathogenesis of coronary spasm. We retrospectively examined by questionnaire the incidence of allergic history in patients with variant angina (n = 47) and compared it with that in patients with non-ischemic heart diseases (n = 83). We could not find any relationship between coronary spasm and allergy. Furthermore, we have not experienced any case in which myocardial ischemia was provoked by an allergic reaction. Accordingly, allergy could not be a major cause of coronary spasm in our present experience.

Adult↗