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PubMed2005

Delayed severe multivessel spasm and aborted sudden death after Taxus stent implantation.

Sudden cardiac arrest associated with major spasm of three coronary arteries was observed about 10 hours after Taxus stent insertion in a three vessel lesion and was successfully treated by intracoronary glyceryl trinitrate infusion. This case illustrates a potential risk associated with drug eluting stent and alerts clinicians to the life threatening risk of spasm when stenting multiple vessels with drug eluting stent (especially the Taxus stent).

Blood Vessel Prosthesis↗
PubMed1981

Prinzmetal's angina with documented coronary artery spasm. Treatment and follow-up.

Eighteen patients with Prinzmetal's angina were studied angiographically and 17 were followed for an average of 27 months. The were 12 men and six women, with a mean age of 46.3 years. The mean duration of symptoms before clinical diagnosis was 4.1 weeks. Four had had a previous myocardial infarction. Six patients had spontaneous cardiac arrests within 48 hours of diagnosis and hospital admission. At coronary arteriography, 10 patients had significant coronary artery disease; two of these had coronary artery spasm. The remaining eight patients had normal cornary arteries with significant coronary artery spasm at arteriography. Angiographic mitral valve prolapse was found in eight patients; seven of these had inferior ST segment elevation with pain. Six of the 10 patients with significant coronary artery disease had aortocoronary bypasses performed with good results. Ten of the remaining 11 patients who were treated medically had their symptoms controlled with oral isosorbide dinitrate alone or in combination with propranolol, nifedipine or perhexiline but propranolol may have an adverse effect. Though the initial clinical course in untreated patients was unfavourable, progress after starting treatment was good, with no further cardiac arrests, myocardial infarctions, or deaths.

Angina Pectoris↗
PubMed1976

Evidence for the presence of a vasoactive substance (possibly involved in the aetiology of cerebral arterial spasm) in cerebrospinal fluid from patients with subarachnoid haemorrhage.

Cerebrospinal fluid from patients with subarachnoid haemorrhage and cerebral arterial spasm contracted the isolated basilar artery and potentiated contractions produced by 5-hydroxytryptamine, noradrenaline, and six prostaglandins. The unidentified substance in cerebrospinal fluid probably plays a role in the aetiology of cerebral arterial spasm.

Adolescent↗
PubMed1996

Hemifacial spasm: a prospective long-term follow up of 83 cases treated by microvascular decompression at two neurosurgical centres in the United Kingdom.

OBJECTIVE: To evaluate the use of microvascular decompression (MVD) for the treatment of hemifacial spasm (HFS). METHODS: Eighty three patients with HFS who underwent MVD via a suboccipital craniectomy are presented. RESULTS: Seventy two out of seventy eight patients available for follow up remained free of any spasms at a mean follow up period of eight years. Two patients continued to have minor intermittent muscle twitches and three had recurrence of HFS. One patient's operation was not completed. Twenty had a transient complication and eight were left with permanent postoperative deficits, the commonest being unilateral sensorineural deafness. Seventy one patients declared themselves satisfied with the procedure. A causative vessel was found on the root exit zone of the seventh cranial nerve in 81 patients. CONCLUSION: The procedure seems to provide lasting relief for most patients. The correct operative technique is essential if complications are to be avoided.

Adult↗
PubMed2005

Middle cerebral artery spasm after subarachnoid hemorrhage: detection with transcranial color-coded duplex US.

PURPOSE: To prospectively determine the accuracy of transcranial color-coded duplex ultrasonography (US) used alone and in conjunction with carotid artery US for diagnosis of middle cerebral artery (MCA) spasm, with intraarterial digital subtraction angiography (DSA) used as the reference standard. MATERIALS AND METHODS: The institutional ethics committee approved the study. Each patient, or members of the patient's family, gave informed consent. One hundred twenty consecutive patients (64 women, 56 men; mean age, 45.5 years +/- 13.6 [standard deviation]) were routinely referred for DSA after subarachnoid hemorrhage. Vasospasm was graded as mild (< or =25% reduction in vessel diameter), moderate (>25% to 50% reduction), or severe (>50% reduction). US was performed 2 hours or less before angiography. The ratio of flow velocity in the middle cerebral artery (V(MCA)) to flow velocity in the ipsilateral extracranial internal carotid artery (V(ICA)) was calculated. Diagnostic accuracy was evaluated by calculating the area under the receiver operating characteristic curve (Az). The significance of the difference between the two Az values (for US vs DSA) was determined by using the z test with correction for correlated data. RESULTS: Nine of 120 patients were excluded because of inadequacy of acoustic windows in the squama of temporal bones. Spasm was mild in 17, moderate in 16, and severe in only nine of 222 arteries studied. Arteries with moderate or severe vasospasm were combined in one group. The best-performing parameters were peak systolic velocity and V(MCA)/V(ICA) ratio. Az values for these two parameters in diagnosis of moderate-to-severe vasospasm were 0.93 and 0.95, and in diagnosis of mild vasospasm, 0.90 and 0.91. Accuracy of the V(MCA)/V(ICA) ratio calculated on the basis of end-diastolic velocity for diagnosis of mild MCA narrowing was significantly better than that of end-diastolic MCA velocity alone (Az = 0.88 vs 0.84, P < .05). The stepwise approach with use of the V(MCA)/V(ICA) ratio after flow velocity measurements in the MCA resulted in a decreased number of false-negative findings in both vasospasm subgroups. The thresholds of highest efficiency were at a mean velocity of 94 and 108 cm/sec and a peak systolic V(MCA)/V(ICA) ratio of 3.6 and 3.9 for diagnosis of mild and moderate-to-severe vasospasm, respectively. CONCLUSION: Transcranial color-coded duplex US alone or in conjunction with carotid artery US has excellent accuracy for angiographic detection of vasospasm. Use of MCA velocity measurements and V(MCA)/V(ICA) ratio can increase the accuracy of Doppler US.

Adolescent↗
PubMed2001

Orbicularis oculi and orbicularis oris reflexes in blepharospasm and torticollis spasmodica during spasm-free intervals.

To investigate possible abnormalities of the blink reflex pathways, we analyzed the latencies and amplitudes of the blink reflex responses in the orbicularis oculi (Ooculi) muscle, following supraorbital nerve stimulation, in 19 patients with blepharospasm, 16 patients with torticollis spasmodica and 22 control subjects. Furthermore, in order to examine the suprasegmental control of the responses, the reflex responses were also evoked in the orbicularis oris (Ooris) muscle after stimulation of the ipsilateral supraorbital nerve. The responses were recorded only when subjects had no contractions of the eyelid muscles, either involuntarily, voluntarily or spontaneously; this could be controlled by a sound signal. The metrics of the reflex responses in the Ooculi and Ooris muscles in patient groups were comparable to those in controls. Our data indicate that the afferent and efferent pathways of the reflex arc and the suprasegmental control of the reflex are intact in patients with blepharospasm and torticollis spasmodica, at least during spasm-free intervals. Alterations of responses may occur during spasms due to either segmental or suprasegmental changes.

Adult↗
PubMedDate not supplied

Effects of Ginkgo biloba extract (EGb 761) on arteriolar spasm in a rat cremaster muscle preparation.

The effects of an extract of Ginkgo biloba (EGb 761) on arteriolar spasm were confirmed using a preparation of rat cremaster muscle. When vasospasm was induced by rat serum, arteriolar constriction reached 25-30% of the initial diameter after 10 min. Intravenous injection of EGb 761 (30 mg/kg) 5 min after inducing spasm inhibited about 80% of this serum-induced vasoconstriction. As previous studies have shown that EGb 761 has an antiaggregatory effect on platelets, thrombin, serotonin (platelet-derived compounds that are present in the serum) and a thromboxane analogue (U46619) were also used to induce vasospasm. Administration of EGb 761 (30 mg/kg) 5 min after exposure of the preparation to serotonin (10(-3) M) or 10 min after exposure to thrombin (20 units) did not affect vasospasm induced by these agents. In contrast, treatment with this same dose of EGb 761 5 min after exposure of the preparation to U46619 (10(-4) M) abolished the arteriolar constriction induced by this agent in 15 min. The thromboxane/prostaglandin H2 receptor antagonist SQ29548 antagonized serum-induced vasospasm, indicating an involvement of thromboxane. Other experiments indicated that the effects of EGb 761 of counteracting vasospasm may be mediated in part by ginkgolide B, a triterpene constituent of the extract that is an antagonist of platelet-activating factor and in part by an 'NO-like' action of its proanthocyanidin constituents. Taken together, these results have revealed that EGb 761 treatment can antagonize the vasoconstrictor effect of thromboxane on arterioles. As thromboxane is implicated in many cardiovascular disorders, this property of EGb 761 may explain some of its beneficial clinical effects in such pathologies.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1981

Coronary artery spasm during exercise: treatment with verapamil.

Six patients who had documented coronary spasm and no coronary artery with organic obstruction greater than 50% developed angina and ST-segment elevation on exercise testing. Oral verapamil, 160-480 mg/day, prevented exercise-induced ischemia in all patients and increased maximal work capacity from 611+/- 250 kpm to 808 +/- 160 kpm (p less than 0.02). In two patients, a relationship between the prevention of exercise-provoked ischemia and the plasma concentration of verapamil was demonstrated, and in one of these, the relationship had a diurnal pattern. Patients with variant angina may develop coronary spasm on effort and often respond to verapamil.

Angina Pectoris↗
PubMed1982

Morphologic evidence for coronary artery spasm in eclampsia.

Vascular spasm has been considered to be an important component of the eclamptic state. If this abnormal vascular reactivity affects the coronary arteries in eclampsia, one might expect to find areas of myocardial contraction band necrosis, a lesion secondary to coronary reflow after periods of no flow. We reviewed the cardiac findings in the 34 patients with fatal eclampsia (hypertension, edema, proteinuria, and convulsions without evident cause) autopsied at The Johns Hopkins Hospital since 1899, and compared each with the next pregnant or puerperal nontoxemic autopsied patient. The eclamptic patients were 15-45 years old (average 27 years). Convulsions began antepartum in 21 patients, intrapartum in eight, and postpartum in five. The hearts weighed 200-407 g (average 312 g). One heart had rheumatic valvular disease and one had myocarditis. Histologic study of heart sections showed the presence of contraction band necrosis in 12 cases (35%). The control cases included two patients with rheumatic valvular disease, two with endocarditis, two with myocarditis, two with pericarditis, and one with leukemic infiltration. Only one control patient (3%) had contraction band necrosis (p less than 0.001). The frequent occurrence of myocardial contraction band necrosis suggests that coronary artery spasm may be common in patients who die with eclampsia.

Adolescent↗
PubMed1982

Determinants of arrhythmic death due to coronary spasm: effect of preexisting coronary artery stenosis on the incidence of reperfusion arrhythmia.

Coronary spasm can occur in the presence or absence of coronary artery disease. We therefore determined the effect of preexisting coronary stenosis on the incidence of ventricular fibrillation during reperfusion after circumflex artery (CFX) occlusion. Twenty dogs underwent a 30-minute open-chest CFX occlusion. During reperfusion, CFX blood flow was restricted by a partial occluder. In dogs that survived reperfusion, peak CFX flow was 91 +/- 44% of baseline (mean +/- SD) compared with 163 +/- 68% in dogs that died of ventricular fibrillation (p less than 0.02). In another 17 dogs, the left anterior descending coronary artery was gradually occluded by an ameroid constrictor. After 17-39 days, the CFX was acutely occluded for 30 minutes and then reperfused. Collateral flow to the CFX, measured by microspheres, was 27.6 +/- 28.3 ml/min . 100 g-1 in dogs that died of reperfusion ventricular fibrillation, compared with 64.4 +/- 27.2 ml/min . 100 g-1 in surviving dogs (p less than 0.02). Thus, the risk of reperfusion ventricular fibrillation is greater in dogs with normal coronary arteries than in dogs with a flow-limiting partial stenosis of the artery undergoing transient occlusion, or chronic stenosis of a second coronary artery inducing collateralization to the artery subsequently undergoing transient occlusion. These results suggest that the risk of ventricular fibrillation during release of coronary spasm may be greater in patients without than in those with coronary artery disease.

Animals↗
PubMed1982

Postinfarction angina caused by coronary arterial spasm.

Recurrent ST-segment elevations in leads where new Q waves developed were repeatedly recorded in six patients during a recovery phase of acute myocardial infarction. Such ST-segment elevations were transient, occurred with or without chest pain, and returned to control levels. No enzymatic changes signifying recurrent myocardial necrosis were found after each episode. Selective coronary cineangiography in one patient demonstrated a mild segmental stenosis in the coronary artery perfusing the infarcted area; this artery became completely occluded after administration of i.v. ergonovine. Administration of calcium antagonists effectively reduced the frequency of postinfarction angina and ST-segment elevations. The clinical features suggest that the postinfarction angina in these patients is produced by coronary arterial spasm and that coronary arterial spasm may cause severe life-threatening dysrhythmias.

Adult↗
PubMed1982

Pathophysiology of coronary artery spasm.

Coronary arterial measurements were made from cineangiograms in patients with positive and negative ergonovine tests. In those with positive tests, normal segments of arteries adjacent to the site of spasm and arteries without spasm showed no greater sensitivity to ergonovine than arteries from control patients (20 +/- 13% constriction vs 17 +/- 12%, NS). In patients with positive and negative ergonovine tests, constriction was measured at lesion sites after ergonovine and compared with values predicted from a geometric theory. The measured constriction was always greater than predicted in patients with a positive ergonovine test, and frequently less than predicted in patients with a negative test. The increased sensitivity of arteries that show localized vasospasm at lesion sites after ergonovine administration is not explained by geometry alone.

Adult↗
PubMed1983

Transient collateral augmentation during coronary arterial spasm associated with ST-segment depression.

To examine the possible existence of collateral circulation during coronary artery spasm, we attempted to visualize the transient appearance of collateral vessels that could serve to salvage otherwise jeopardized ischemic areas. In three patients with vasospastic angina, total spastic obstruction of a major coronary artery was associated with transient collateral augmentation, which was supplied by the nonspastic artery during anginal period associated with ST-segment depression. These collateral vessels disappeared when the angina and ST changes resolved after nitroglycerin administration. These findings suggest that the collateral blood supply could transiently occur through preexisting vessels to perfuse the ischemic area during coronary artery spasm and that such collateral flow could have a role in preventing transmural myocardial ischemia, resulting in a lesser degree of ischemia associated with ST-segment depression.

Adult↗
PubMed1983

Coronary spasm and thrombosis associated with myocardial infarction in a patient with nearly normal coronary arteries.

A 37-year-old man presented with an evolving inferior myocardial infarction. Coronary angiography performed within 3 hours after the onset of the pain showed spasm of the right coronary artery and the presence of intracoronary thrombi. After resolution of spasm and the disappearance of thrombi, angiography revealed nearly normal coronary arteries. An ergonovine test was positive when the patient was not taking medication and became negative when he was taking diltiazem. The course was uncomplicated, and after 9 months the patient is free of angina.

Adult↗
PubMed1986

Histamine-induced coronary spasm in regions of intimal thickening in miniature pigs: roles of serum cholesterol and spontaneous or induced intimal thickening.

The pathogenesis of histamine-induced coronary spasm was examined angiographically and morphometrically in Göttingen miniature pigs. In five of 36 consecutive pigs that were 4 to 5 months of age, coronary spasm was provoked by the intracoronary administration of histamine, and the left coronary arteries were examined histologically without endothelial denudation (group 1). Endothelial balloon denudation of the major branch of the left coronary artery was performed in 31 of 36 pigs and five died during the procedure. The remaining 26 pigs were randomly allotted to one of two groups, one fed a cholesterol-supplemented (group 2, n = 13) and one fed a regular low-cholesterol diet (group 3, n = 13). After 3 months, serum cholesterol increased significantly from 57 +/- 6 to 222 +/- 27 mg/dl (p less than .01) in group 2, but remained unchanged (48 +/- 5 to 55 +/- 6 mg/dl) in group 3. Percent narrowing of the coronary diameter induced by 10 micrograms/kg ic histamine after administration of the H2 blocker cimetidine (60 mg/kg iv) was 39 +/- 3% and 24 +/- 2% (p less than .05 between groups 2 and 3) at the nondenuded site and 78 +/- 3% and 74 +/- 4% at the denuded site in groups 2 and 3, respectively (p less than .01 between nondenuded and denuded sites). Histamine-induced percent narrowing of the coronary diameter after cimetidine in group 1, 2, and 3 pigs correlated well with the degree of intimal thickness on an exponential curve (r = .92, p less than .001). Since percent narrowing at the intact site was 27% (n = 19) in all three groups, predicted histamine-induced percent narrowing at the spastic site, applying the geometric theory, was 33 +/- 3%. Accordingly, enhanced constriction of the coronary artery with intimal thickening in response to histamine can largely be explained by the acquired hyperresponsiveness of the vascular wall to autacoids. This phenomena, not related to the level of serum cholesterol, may be uniquely linked to the basic pathology of evolution of atherosclerosis.

Animals↗
PubMed1993

Cigarette smoking is a major risk factor for coronary spasm.

BACKGROUND: Although there have been many studies on the risk factors for coronary artery disease, the etiology of coronary artery spasm has not yet been determined. METHODS AND RESULTS: After diagnosis by coronary arteriography, various risk factors were compared between two groups of subjects using logistic regression analysis. The vasospasm group included 175 patients with angiographically determined coronary artery spasm but no coronary artery narrowing exceeding 25% of the luminal diameter. The control group comprised 176 subjects with completely normal coronary arteries and a negative response to ergonovine maleate. The adjusted odds ratio and 95% confidence interval for smoking as a risk factor for vasospasm was 2.41 and 1.53-3.82, respectively (p < 0.05). The adjusted odds ratios for total cholesterol, low density lipoprotein, high density lipoprotein, triglycerides, diabetes mellitus, and body mass index, calculated by multivariate logistic regression analysis, were not statistically nonsignificant. CONCLUSIONS: Smoking appears to be a major risk factor for vasospastic angina without significant coronary narrowing. The other risk factors for coronary artery disease may not contribute to coronary vasospasm.

Adult↗
PubMed1996

Relaxation of subarachnoid hemorrhage-induced spasm of rabbit basilar artery by the K+ channel activator cromakalim.

BACKGROUND AND PURPOSE: Cerebral vasospasm resulting from subarachnoid hemorrhage (SAH) is refractory to most vasodilators. However, despite evidence that a mechanism underlying the vasospasm may be smooth muscle cell membrane depolarization resulting from decreased K+ conductance, the ability of K+ channel activators to relax the spasm has not been thoroughly investigated. The purpose of this study, therefore, was to investigate whether K+ channel activation selectively relaxes SAH-induced vasospasm. METHODS: Three days after SAH in the rabbit, relaxation of the basilar artery in response to the K+ channel activator cromakalim as well as to staurosporine (protein kinase C antagonist), forskolin (adenylate cyclase activator), and sodium nitroprusside (guanylate cyclase activator) was measured in situ with the use of a cranial window. Relaxation in response to these agents was also investigated in control vessels contracted with serotonin. Membrane potential of the smooth muscle cells of the basilar artery from SAH and control rabbit was measured in vitro with the use of intracellular microelectrodes. RESULTS: Cromakalim completely relaxed the SAH-induced spastic basilar artery, while staurosporine, forskolin, and sodium nitroprusside were significantly less efficacious. In contrast, sodium nitroprusside and forskolin were more efficacious relaxants in serotonin-contracted control vessels than in SAH vessels. The K+ channel blocker glyburide and high [K+] prevented cromakalim-induced relaxation. Glyburide did not inhibit forskolin-induced relaxation of serotonin-contracted control vessels. Cromakalim concentration-dependently repolarized spastic basilar artery smooth muscle cells, and the repolarization was prevented by glyburide. CONCLUSIONS: These results suggest that K+ channel activation selectively relaxes SAH-induced vasospasm. We speculate that the ability of K+ channel activators to selectively relax the spasm may be due, at least in part, to the underlying inhibition of K+ channels after SAH.

Animals↗