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PubMed1980

Preoperative arteriographic spasm and outcome from aneurysm operation.

The timing of intracranial operation for the treatment of ruptured cerebral aneurysm remains controversial. To find objective parameters to guide us, we performed angiography 24 to 72 hours before contemplated operation in 35 Grade I patients in whom subarachnoid hemorrhage had occurred at least 1 week earlier. Operation in the presence of angiographic vasospasm in Grade I patients over 1 week after SAH was associated with increased morbidity and mortality rates. Only 1 of 28 patients in whom spasm was absent or mild at the time of operation had an unsatisfactory outcome from operation (P less than 0.003). There was no correlation between clinical grade and significant spasm; 17 patients who were clinically Grade I over 1 week after SAH had moderate or severe angiographic spasm. These data suggest that all patients should undergo angiography just before contemplated operation and that operation should be postponed if vasospasm is present.

Carotid Artery, Internal↗

PubMed2002

Tetrahydrobiopterin improves coronary endothelial function, but does not prevent coronary spasm in patients with vasospastic angina.

Reduced bioavailability of tetrahydrobiopterin (BH4), an essential cofactor for nitric oxide (NO) synthase, and the resulting decrease in NO in the coronary circulation may be involved in the pathogenesis of coronary spasm. The present study investigated the effects of BH4 on the vascular response to acetylcholine (ACh) in 28 patients with vasospastic angina (VA) using quantitative angiography. After recording the vascular responses to ACh (3 and 30 microg/min), either BH4 (1 mg/min) or saline was infused into the coronary artery for 2 min before and during a subsequent infusion of ACh. With the 3 microg/min dose of ACh, BH4 attenuated the ACh-induced decrease in coronary diameter in both the nonspastic segments (-1.1 +/- 2.2% ACh vs 6.0 +/- 2.8% ACh+BH4) and spastic segments (-6.3 +/- 2.7% ACh vs 2.9 +/- 2.7% ACh+BH4), but did not influence the ACh-induced coronary spasm at 30 microg/min (-57.3 +/-2.4% ACh vs -55.3 +/- 2.4% ACh+BH4). In the control patients, saline did not influence either the spastic or nonspastic vasoconstrictor responses to ACh. Acute administration of BH4 improves coronary endothelial function, but does not prevent coronary spasm in patients with VA.

Acetylcholine↗

PubMed2003

Acetylcholine-induced coronary spasm with a history of Kawasaki disease: case report.

A 21-year-old woman without any known coronary risk factors was found at coronary catheterization to have normal coronary angiograms, but demonstrated acethylcholine (ACh)-induced coronary spasm. She had a history of Kawasaki disease (KD) at 19 months of age and, although coronary angiography was not performed at that time, no coronary aneurysms were detected by echocardiography. To the best of our knowledge, this is the first case report of ACh-induced coronary spasm associated with normal coronary angiograms in a young person with a history of KD. The findings suggest that subclinical, persistent coronary endothelial dysfunction may exist in this patient; furthermore, the dysfunction appears diffuse and might be unrelated to coronary aneurysm formation. The long-term significance of coronary endothelial dysfunction in patients with KD, as suspected by coronary spasm, remains unknown but may be an important risk factor for future atherosclerosis.

Acetylcholine↗

PubMed1985

Significant role of alpha 2-adrenoceptors in coronary artery spasm.

Ergonovine, methoxamine and clonidine were administered intravenously in order to clarify the mechanism of coronary artery spasm in canine experiments. After these administrations, 27.5% of the dogs treated with ergonovine, 59.5% of the dogs treated with methoxamine and 72.7% of the dogs treated with clonidine showed ST segment elevation. The combined application of propranolol with ergonovine or methoxamine could more easily induce ST segment elevation than a single application of ergonovine or methoxamine. Most cases of elevated ST segment returned to the normal after the administration of nitroglycerin and phentolamine. Yohimbine was completely effective for the restoration of normal ST segment. Plasma norepinephrine decreased to 20 +/- 8.0% of the control when ST segment elevation was induced. This is a significantly greater decrease than that seen without ST segment elevation (p less than 0.001). Concomitant with the restoration of normal ST segment, plasma norepinephrine increased after the administration of yohimbine. Methoxamine and clonidine increased (p less than 0.01) and yohimbine decreased (p less than 0.01) coronary vascular resistance. Coronary spasm was visualized on coronary arteriogram after the application of clonidine; also coronary vasodilation was visualized after the administration of yohimbine. These results confirm the hypothesis that coronary artery spasm is mediated by pre- and postsynaptic alpha 2-adrenoceptors.

Animals↗

PubMed1992

Role of electrophysiologic testing and coronary spasm provocation test in survivors of cardiac arrest.

Twenty-one patients were successfully resuscitated from cardiac arrest. Electrocardiograms (ECG) during cardiac arrest were recorded in 14 patients with ventricular fibrillation in 7, ventricular tachycardia in 4, cardiac standstill in three, Torsade de Points in one and atrial fibrillation with rapid ventricular response in 1. Thirteen patients (group I) had structural heart disease or primary ECG abnormality and 8 patients (group II) had no apparent heart disease. Electrophysiologic study (EPS) was performed in 12 patients of group I and 5 of group II. In group I, ventricular tachycardia was induced in 7, and His-ventricular conduction disturbance was demonstrated in 2, and 2 patients with Wolff-Parkinson-White (WPW) syndrome had an effective refractory period of the antegrade accessory pathway less than 250 msec. No patients in group II showed abnormal EPS findings. Spasm provocation test was performed in 8 patients (2 in group I and 6 in group II). Coronary spasm was induced in 5 patients (1 in group I and 4 in group II). Two patients in group II had positive results of upright-tilt testing. During the follow-up period, 2 patients died suddenly in group I and 1 patient whose cause of cardiac arrest was unknown had a recurrence of cardiac arrest. In group II, all patients whose etiology could be demonstrated by serial examinations had good prognosis. In conclusion, EPS is useful in evaluation of the cause of cardiac arrest especially when patients have structural heart disease, and coronary spasm may be involved in patients with cardiac arrest without apparent heart disease.

Adolescent↗

PubMed1993

Coronary spasm in two sisters.

Coronary spasm was observed in two sisters. Neither of them had significant atheromatous stenosis in the coronary arteries. The 41-year-old elder sister presented with resting morning angina. The stress electrocardiogram showed marked depression of the ST-segment in precordial leads. Diffuse vasospasm in the left anterior descending artery was induced by the intracoronary administration of acetylcholine. The 38-year-old younger sister suffered from acute inferior myocardial infarction after taking methylergonovine following an abortion. Emergent coronary angiography disclosed a thrombus in the proximal right coronary artery which was dissolved with intracoronary administration of urokinase. There was no residual stenosis in the culprit vessel. Although the sisters do have risk factors for coronary spasm, an inherited factor may contribute to the mechanism of the spasm.

Adult↗

PubMed2000

Elevated levels of soluble intercellular adhesion molecule-1 in the coronary circulation of patients with coronary organic stenosis and spasm.

The cell surface expression of intercellular adhesion molecule-1 (ICAM-1) is upregulated following activation during inflammatory responses, mediating both cell migration and activation. The involvement of inflammation in unstable angina is suggested by the presence of activated circulating leukocytes. To examine whether plasma soluble ICAM-1 (sICAM-1) levels increase in the coronary circulation of patients with coronary organic stenosis and coronary spasm, plasma sICAM-1 levels were measured in the coronary sinus (CS) and the aortic root (Ao) simultaneously in 10 patients with 90% or more coronary narrowing and coronary spasm (coronary spastic angina (CSA) with organic stenosis), in 11 patients with coronary spasm and no significant coronary narrowing (CSA without organic stenosis), in 16 patients with stable exertional angina, and in 13 control subjects. The plasma sICAM-1 levels (ng/ml) in the CS increased in CSA with organic stenosis (230+/-26) as compared with CSA without organic stenosis (158+/-14), stable exertional angina (130+/-9) and control subjects (121+/-10) (p<0.01). The levels in the Ao also increased in CSA with organic stenosis (208+/-24) as compared with CSA without organic stenosis (149+/-13), stable exertional angina (130+/-11) and control subjects (121+/-10) (p<0.01). Furthermore, the plasma sICAM-1 levels were higher in the CS than in the Ao only in CSA with organic stenosis. These results suggest that activation of leukocytes occurs through the induction of ICAM-1 in the coronary circulation in the patients with CSA with organic stenosis.

Aged↗

PubMed2000

Changes in autonomic nervous activity prior to spontaneous coronary spasm in patients with variant angina.

Although the autonomic nervous system has been implicated in the genesis of coronary spasm, the precise mechanism by which it serves as the trigger of coronary spasm remains unclear. The aim of this study was to investigate changes in autonomic nervous activity associated with ischemic episodes in patients with variant angina (VA). Heart rate variability (HRV) on Holter monitoring was analyzed during 17 ischemic episodes in 11 patients with VA. The parameters of HRV were measured during a 2-min period at various time intervals prior to the onset of ST-segment elevation. The low frequency (LF) and high frequency (HF) components of the HRV, LF/HF ratio, mean RR interval, and the coefficient of the RR interval variation (CV) were calculated for each time interval. Both the HF and the CV increased significantly in the 2 min prior to the onset of ST-segment elevation, suggesting heightened vagal activity. The LF/HF ratio, a measure of cardiac sympatho-vagal balance, did not change. The LF, a measure of sympathetic activity with vagal modulation, also did not change. The RR interval decreased significantly in the 2 min prior to the onset of ST-segment elevation. These results suggest that enhancement of both the vagal and the sympathetic nervous activity plays an important role in the initiation of coronary spasm.

Adult↗

PubMed1981

Experience with ergonovine provocative testing for coronary arterial spasm.

We reviewed our experience with the ergonovine provocative test for coronary arterial spasm in 40 patients with pain in the chest believed to be angina pectoris and in one patient with a myocardial infarction and normal coronary arteries. Twenty-nine patients had normal coronary arteries, while 12 had mild to moderate lesions. Ergonovine maleate was administered incrementally in total cumulative doses of 0.25 mg to 1.2 mg. The effect of ergonovine on coronary arterial caliber was determined by comparing the arterial diameter from the angiogram obtained after administration of ergonovine with that from the control. Measurements were made at the same preselected points in both films and also at points of greatest response. Excluding the three cases with complete occlusion, the mean reduction in coronary arterial diameter at preselected points was 12 +/- 15 percent. When the points of greatest response were examined, the maximum reduction in coronary arterial diameter was less than 25 percent in 13 patients, 25 to 50 percent in 20 patients, and more than 50 percent in eight patients. The patterns of response included complete occlusion of a vessel in the three patients with variant angina, diffuse narrowing in 16, diffuse and focal narrowing in six, and spasm at the catheter tip in three patients. All patients with maximum reductions of more than 50 percent in coronary arterial diameter and six of those with maximum reductions of 25 to 50 percent had pain in the chest, but only the three with complete occlusion had associated changes in the S-T segment. Thus, the response in patients with variant angina represents one end of a spectrum of responses to administration of ergonovine. In addition, a large number of patients may have ergonovine-induced pain in the chest without electrocardiographic changes and only an intermediate degree of coronary arterial spasm.

Adult↗

PubMed2005

Cefuroxime-induced coronary artery spasm manifesting as Kounis syndrome.

Allergic angina and allergic myocardial infarction (Kounis syndrome) occurring during the course of a drug-induced allergic reaction in the absence of angiographically stenosed coronary arteries, is rare in clinical practice. This paper reports the case of a 70-year-old woman with no significant risk factors for coronary artery disease who developed coronary artery spasm after intravenous injection of cefuroxime. A subsequent coronary angiogram revealed normal coronary arteries (type I variant of the syndrome). The allergic reaction following cefuroxime administration seems to have triggered the development of coronary artery spasm. Susceptible individuals expressing an amplified mast cell degranulation effect may be more vulnerable to coronary artery spasm. The clinical implications of this syndrome are also discussed.

Aged↗

PubMed2004

Heart failure with silent coronary artery spasm exhibiting microscopic focal myocardial necrosis and amyloid-deposition.

We report a 67-year-old Japanese man who presented with worsening heart failure with asymptomatically transient ischemic ST-segment depression. Left ventriculography showed diffuse hypokinesis; asymptomatic coronary artery spasm was evoked by the acetylcholine provocation test. Endomyocardial biopsy exhibited hypertrophic cardiomyocytes and scattered microscopic focal myocardial necrosis with amyloid-deposition. Transient ST-segment depression improved after treatment with a calcium antagonist, but cardiac contraction was still impaired. We hypothesize that asymptomatic coronary spasm may cause irreversible cardiac damage and heart failure with amyloid-deposition; the presence or absence of coronary spasm in heart failure patients should be clarified in order to determine therapeutic strategy.

Acetylcholine↗

PubMedDate not supplied

Coronary artery spasm demonstrated by coronary angiography in a patient with acute myocarditis resembling acute myocardial infarction; a case report.

A 59-year-old male with acute myocarditis presenting symptoms resembling acute myocardial infarction underwent urgent coronary angiography due to difficulties in determining a diagnosis. Coronary artery spasm was demonstrated in the proximal right and left anterior descending coronary arteries. The spasm varied from time to time and lesion to lesion. But no fixed occluded lesion was observed. Predischarge coronary angiography showed no abnormal findings. Histological findings of the biopsy specimen from the left ventricle were consistent with myocarditis. The findings of this case indicate that a coronary artery spasm may aggravate the myocardial damage occurring in acute myocarditis. Urgent coronary angiography and endomyocardial biopsy are important to make the diagnosis of myocarditis in patients presenting symptoms resembling acute myocardial infarction.

Coronary Angiography↗

PubMed1996

Hemifacial spasm due to compression of the facial nerve by vertebral artery-posterior inferior cerebellar artery aneurysm and elongated vertebral artery--case report.

A 62-year-old female presented with rapid aggravation of long-standing facial spasm occurring within a few months. Neuroimaging and angiography demonstrated compression of the root exit zone (REZ) of the facial nerve by an ipsilateral saccular aneurysm at the left vertebral artery (VA)-posterior inferior cerebellar artery bifurcation, in addition to the elongated VA. Neck clipping of the aneurysm and decompression of the REZ from the elongated VA and clipped aneurysm resulted in complete disappearance of the facial spasm. The aneurysm had very thin walls and was apparently about to rupture. Aggravation of long-standing hemifacial spasm may be a warning sign for rapid growth and rupture of a causative aneurysm.

Facial Nerve Diseases↗

PubMed1993

Hemifacial spasm: early postoperative normalization of blink reflex latency.

Electrophysiological improvement in the blink reflex latency after neurovascular decompression of the facial nerve in patients with hemifacial spasm is believed to be related to remyelination and occurs 2-8 months after surgery. We report a patient with hemifacial spasms for 3 years, in whom the increased blink reflex latency returned to normal within a week after surgery. This suggests that compression without demyelination may be responsible for increased blink reflex latency in some of the patients with hemifacial spasms.

Adult↗

PubMed1975

Chronic cerebral arterial spasm. The role of intracranial pressure.

The author used isolated rabbit common carotid and femoral arteries perfused at a constant pressure of 90 mm Hg to examine the variation of flow (F) with transmural pressure (TMP). When the TMP was reduced below 50 to 60 mm Hg in arteries with normal smooth muscle tone, arterial resistance increased significantly causing a reduction in flow. It is suggested that the diffuse arterial narrowing that occurs in patients with severe intracranial hypertension may be the result of a similar reduction in TMP. In the presence of active vasoconstriction, any increase in extraluminal (intracranial) pressure (ICP) resulted in a substantial increase in arterial resistance and subsequent reduction of flow. This F-TMP relationship depended only on the initial degree of constriction and was independent of the vasoconstrictor used to achieve this constriction and of the artery in which this constriction was produced. A review of the literature suggests that human cerebral arteries normally exhibit only mild constrictions in response to subarachnoid blood during the chronic phase of spasm. In the present study, a mild constriction in the absence of increased ICP or a moderate increase in ICP (45 mm Hg) in the absence of constriction produced minor reductions in arterial diameter and an average flow reduction of only 5% to 10%. However, when ICP was increased to 45 mm Hg in the presence of a mild constriction, severe arterial narrowing resulted and flow was reduced by 50%. Therefore, it is suggested that chronic arterial spasm is the result of a mild constriction which is amplified by the simultaneous occurrence of increased ICP. Phenoxybenzamine was found to be effective in reversing and preventing these contractions. The improvement in flow produced by phenoxybenzamine decreased as the TMP was reduced below 60 mm Hg. The effects of both diffuse and local spasm on cerebral blood flow are discussed.

Animals↗

PubMed1978

Vertebrobasilar spasm: a significant cause of neurological deficit in head injury.

Cerebral vasospasm in the anterior circulation has been recognized as a significant factor in the sequelae of head injury; however, vertebrobasilar spasm resulting from trauma has received much less attention. In the past year we have observed six patients where spasm in the major vessels of the posterior circulation was primarily or in part responsible for the neurological deficit. In such cases, the neurological examination may suggest a supratentorial mass with herniation and, in three of our cases, burr holes or carotid angiography were performed first. However, in every instance neurological signs present on admission indicated primary brain-stem dysfunction. In each of the six cases vertebral angiography demonstrated significant spasm in either the vertebral or basilar arteries. Intracranial pressure was monitored in each of the six patients and did not exceed 25 mm Hg in any. In cases of head injury where the neurological examination indicates brain-stem dysfunction inconsistent with or after a supratentorial mass has been excluded, vertebral angiography may aid in the diagnosis and subsequent management of such patients.

Adolescent↗

PubMed1989

Relaxant effect of calcitonin gene-related peptide on cerebral arterial spasm induced by experimental subarachnoid hemorrhage in dogs.

This study examines the relaxant effect of calcitonin gene-related peptide (CGRP), a 37-amino acid peptide with a potent vasodilator action, on cerebral arterial spasm after subarachnoid hemorrhage (SAH). The spasm was induced by injecting autologous arterial blood percutaneously into the cisterna magna in adult mongrel dogs. The single-injection model of SAH was produced by injection of 1.0 ml/kg body weight of blood (on Day 0), and the double-injection model involved two successive injections of 0.5 ml/kg body weight of blood made 48 hours apart (on Day 0 and Day 2). On vertebral angiograms, arterial narrowing of the major cerebral arteries was most prominent on Day 3 after SAH in the single-injection model and on Day 7 in the double-injection model. When 10(-10) mol/kg of CGRP was administered intracisternally in the single-injection model on Day 3, the diameter of the spastic cerebral arteries, as determined by angiography, recovered to normal. After intracisternal administration of 10(-11) to 2 X 10(-10) mol/kg of CGRP on Day 7 in double-injection models, spastic cerebral arteries dilated in a dose-dependent manner. The dilatory effect of CGRP continued for a few hours after administration. The results suggest that CGRP injected intracisternally may reverse cerebral arterial spasm after SAH.

Animals↗

PubMed2006

An increased monocyte count predicts coronary artery spasm in patients with resting chest pain and insignificant coronary artery stenosis.

BACKGROUND: Coronary atherosclerosis with inflammation gives rise to coronary vasospasm in the patients with coronary vasospastic angina. We have postulated that the peripheral leukocyte count and the differential count are associated with vasospastic angina. METHODS: 144 patients who underwent intracoronary ergonovine provocation testing between January 2002 and December 2004 were divided into two groups: Group I (72 patients with provoked spasm, mean age: 54.8 +/- 10.7 years, males: 75%) and Group II (72 without spasm, mean age: 55.3 +/- 10.2 years, males: 35%). Blood sampling was done to measure the lipid profiles and inflammatory markers, including the high sensitive C-reactive protein (hsCRP) levels and the monocyte counts. We compared the angiographic findings and laboratory data between the two groups. RESULTS: There were no significant differences in the levels of serum lipid and hsCRP between the two groups. The white blood cell count and the monocyte count were higher in Group I than with Group II (7496.4 +/- 2622.28 vs. 6703.2 +/- 1768.37/mm3, respectively, p = 0.035; 627.5 +/- 270.70 vs. 426.9 +/- 205.76/mm3, respectively, p < 0.001). Gensini's score was higher in Group I than in Group II (2.2 +/- 2.88 vs. 0.5 +/- 1.03, respectively, p < 0.001). Multivariate analysis showed that the monocyte count and Gensini's score were independent factors affecting coronary spasm (p = 0.047 and p = 0.018, respectively). According to a receiver operating characteristics curve analysis, the area under the curve of the monocyte count was 0.738, that of the neutrophil count was 0.577 and that of the WBC count was 0.572. The cut-off value of the monocyte count was 530/mm3; the sensitivity and specificity of this cut-off value were 64% and 76%, respectively. CONCLUSIONS: The peripheral monocyte count is an independent marker for predicting vasospastic angina in the patients with resting chest pain and insignificant coronary artery stenosis.

Adult↗