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PubMed1996

Treatment choices of 119 patients with hemifacial spasm over 11 years.

A retrospective study of patients with hemifacial spasm (HFS) was performed in order to determine long-term treatment choices: local botulinum toxin, type A, injections, oral pharmacologic agents, and surgery (neurosurgical decompression of the seventh nerve at the brainstem level and upper eyelid blepharoplasty). Of 119 patients with diagnosed hemifacial spasm in the Oculoplastics Division of the Department of UMD-New Jersey Medical School, Newark, NJ from September, 1983, to June 1, 1994, 108 were initially treated with 735 botulinum toxin injections. Forty-seven of the 108 patients (43.5%) initially treated at our institution received 459 injections for a median treatment period of 59 months per patient. Eight patients (7.4%) continued treated elsewhere and four other patients were injected at our institution until their death from other causes. Twenty-two patients (20.4%) were lost to followup after receiving 117 injections. Five patients (4.6%) had spontaneous resolution of their condition after botulinum toxin therapy and nine patients (8.3%) chose not to receive any additional injections or other treatment. Thirteen patients (12.0%) did not respond adequately to botulinum injections and 10 such patients obtained relief from treatments other than botulinum toxin: oral pharmacologic agents (two patients), neurosurgical decompression of the seventh nerve (two patients), and upper eyelid blepharoplasty (one patient). In addition to botulinum injections, 15 patients required adjunctive minor tranquilizers and/or antiseizure medications. Botulinum A toxin is an excellent long-term treatment of hemifacial spasm. This condition may occasionally spontaneously resolve after botulinum therapy.

Age of Onset↗
PubMed1993

Coronary artery spasm and no spasmogens?

Traditionally coronary artery spasm, which is implicated in the pathogenesis of angina, myocardial infarction and sudden death, has been perceived as involving either a powerful spasmogen or larger quantities of a less potent stimulant. The present essay proposes that spasm may occur in the complete absence of any inciting chemical or spasmogen. Sudden intense coronary artery constriction may reflect an abnormality in an intrinsic system of tone regulation involving pacemaker cell discharge, intercellular conduction through gap junctions to adjacent cells, and the cycling of extracellular and bound calcium. Defects in spontaneous tone generation and recovery, may be primary factors in the causation of clinically occurring coronary artery spasm and its sequela.

Aging↗
PubMed2006

The mystery of coronary artery spasm.

Coronary artery spasm is an important cause of chest pain and myocardial ischaemia. It can be defined as an exaggerated contractile response of epicardial coronary artery smooth muscle to various stimuli but the underlying mechanism is not well understood. Recent studies have shown that the loss of endothelial vasodilatory function in conjunction with an increase in vascular smooth muscle constrictor sensitivity to calcium are the likely predisposing conditions for coronary spasm. This review highlights current understanding of the pathophysiology, predisposing factors, diagnostic and therapeutic approaches for coronary spasm.

Coronary Vasospasm↗
PubMed2005

Is there a role for provocation testing to diagnose coronary artery spasm?

Spontaneous coronary artery spasm is an important cause of morbidity both in patients with coronary artery disease and in those with variant angina. A number of pharmacological agents have been identified which can provoke coronary artery spasm in susceptible patients. The role of provocation testing in the clinical diagnosis of coronary spasm is controversial. This is reflected by variations in the clinical use of provocation testing between specialist cardiac centres. Provocation testing appears to be a sensitive method of identifying patients with variant angina and active disease but such patients can often be diagnosed clinically. The specificity is less clear. There is little evidence that altering patient therapy on the basis of a positive test modifies prognosis. There may be a role for provocation testing in rare patients with refractory disease to identify a target site for coronary stenting. A more widespread use of these tests in patients with undiagnosed chest pain syndromes would not currently be recommended.

Coronary Vasospasm↗
PubMed2004

Brachytherapy: potential therapy for refractory coronary spasm.

OBJECTIVES: We sought to demonstrate that brachytherapy reduces coronary spasm in refractory and highly symptomatic variant angina. BACKGROUND: In some patients with variant angina due to extensive vasoconstriction, intensive drug therapy fails to sufficiently relieve symptoms. METHODS: In 18 patients with frequent angina episodes despite triple anti-anginal therapy, coronary spasm was induced by intracoronary acetylcholine (ACh) infusion. Five patients had spasm in a second vessel. Intracoronary radiation (20 Gy) was applied to vasospastic segments using a beta-emitting ((32)P) wire source centered within a Galileo balloon. Parameters of vessel function before and after brachytherapy were investigated. RESULTS: Before brachytherapy, artery diameters decreased (p < 0.0001) from 2.8 +/- 0.4 mm to 1.0 +/- 0.4 mm for the first vessels and from 3.1 +/- 0.3 mm to 1.0 +/- 0.2 mm for the second vessels. After brachytherapy (143 +/- 106 and 80 +/- 52 days for first and second vessels, respectively), ACh-induced vasoconstriction was significantly reduced. The ACh-induced changes in artery diameter before and after brachytherapy were -1.5 +/- 0.5 mm and -0.5 +/- 0.3 mm (p < 0.0001) for the first vessels and -1.4 +/- 0.3 mm and -0.4 +/- 0.2 mm (p < 0.01) for the second vessels, respectively. In non-irradiated spastic vessels, ACh-induced vasoconstriction remained unchanged (e.g., -1.7 +/- 0.6 mm, -1.6 +/- 0.3 mm, and -1.5 +/- 0.5 mm for second vessels, at first investigation, first follow-up, and immediately before brachytherapy, respectively). Angina frequency decreased from 15.6 +/- 6.0 to 2.2 +/- 2.4 angina episodes/week (p < 0.001) in treated patients. CONCLUSIONS: Brachytherapy is a potential therapy in patients with highly symptomatic variant angina.

Adult↗
PubMed2006

JMF2-1, a lidocaine derivative acting on airways spasm and lung allergic inflammation in rats.

BACKGROUND: Prior reports show that nebulized lidocaine might be an effective treatment for asthma. OBJECTIVE: We sought to determine the anti-inflammatory and spasmolytic effects of lidocaine and its analogue, JMF2-1, which we have synthesized for reduced local anesthetic activity. METHODS: Blockade of Na(+) currents was assayed in cultured GH(3) cells by using the patch-clamp technique, whereas anesthesia was assessed in a cutaneous pinching test in rats. Lidocaine and its analogue were nebulized into sensitized rats for evaluation of their effectiveness on airways spasm and inflammation induced by methacholine and allergen, respectively. Tissue histamine release and tracheal spasm triggered by allergen challenge in the absence and presence of these treatments were also examined in vitro. RESULTS: The 50% inhibitory concentration values for blockade of Na(+) currents after treatment with JMF2-1 (25.4 mM) was remarkably higher than that of lidocaine (0.18 mM), which is consistent with the weak anesthetic capacity of this analogue. In contrast, JMF2-1 was more potent than lidocaine in inhibiting allergen-induced histamine release and tracheal spasm. In in vivo settings methacholine-induced increase in lung resistance (145%) significantly reduced to 72% and 47% after lidocaine and JMF2-1 treatment, respectively. Both treatments inhibited by about 81% allergen-evoked eosinophil accumulation into the lung tissue. CONCLUSION: Replacement of the 2,6-dimethyl radicals by the 2-trifluormethyl group on the benzene ring of lidocaine significantly reduces anesthetic activity, preserving its ability to prevent key aspects of the allergic inflammatory response in the lung. CLINICAL IMPLICATIONS: Nebulized JMF2-1 might be a means of achieving the antiasthmatic effects of lidocaine without the anesthetic effects.

Anesthetics↗
PubMed2005

Masseter spasm after succinylcholine administration.

We report the case of a 20-year-old woman who developed masseter spasm after receiving succinylcholine for rapid sequence intubation. Sometimes referred to as "jaws of steel," masseter spasm secondary to anesthetic administration may progress to malignant hyperthermia. Although succinylcholine-induced masseter spasm is uncommon, it is important to be prepared to deal with this entity when administering succinylcholine.

Adult↗
PubMed1990

The value of exercise testing in patients with coronary artery spasm.

To analyze the usefulness of a single exercise test to predict the presence of fixed obstructive coronary artery disease in patients with active coronary spasm, 91 consecutive patients with angiographically proven symptomatic coronary artery spasm who had performed a symptom-limited exercise test within the week before diagnostic coronary angiography were studied. Coronary angiography revealed significant coronary obstructions in 61 patients (67%). According to the type of angina, the prevalence of significant coronary stenosis was 53% for patients with angina at rest, 68% for those with effort angina, and 92% for those with mixed angina. Exercise-induced ST segment elevation was present in eight patients (9%), ST segment depression was seen in 37 patients (41%), and no ST abnormalities in 46 (50%). There was not a significant relationship between the ST segment response to exercise and the clinical variables assessed except for coronary anatomy. Abnormal exercise test results were significantly more frequent in patients with significant coronary obstructions than in those without significant coronary occlusions (62% versus 23%; p less than 0.01). ST elevation was not useful to predict the presence of fixed coronary lesions. However, ST depression strongly suggested the presence of underlying coronary lesions with a sensitivity of 54%, a specificity of 87%, and a positive predictive value of 89%. Using this criterion, 65% of the patients were correctly classified. The results indicate that despite the functional component of ischemia in patients with coronary spasm, ST segment depression with exercise is still a highly specific sign with a high positive predictive value for the presence of significant coronary artery disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1982

Diltiazem for long-term therapy of coronary arterial spasm.

The first 36 patients with coronary arterial spasm treated with diltiazem and followed up at the Stanford University Coronary Artery Spasm Clinic for 6 months or longer are described. There were 13 men and 23 women with a mean age of 50.2 years; the mean duration of angina was 36.1 months. All patients had angina at rest with a good or fail response to sublingual nitroglycerin. During a mean of 17.5 months of diltiazem therapy, the frequency of angina was reduced from a mean of 21.5 to 1.3 attacks/week. This 94 percent reduction in pain frequency occurred when either 240 or 360 mg of diltiazem was administered daily. Sixteen patients required the addition of isosorbide dinitrate to achieve a painfree state. Pain breakthrough occurred a mean of 1.7 times during the 17.5 month follow-up period but tended to be of short duration. Six patients had trace to 1+ pedal edema and no other adverse effects occurred. It is concluded that diltiazem is highly effective and well tolerated for the long-term prophylaxis and treatment of angina in patients with coronary spasm.

Adult↗
PubMed1998

Ergonovine-induced alterations in coronary flow velocity preceding onset of occlusive spasm in patients without significant coronary artery stenoses.

This study examined serial changes in coronary flow velocity to elucidate the dynamic change of coronary circulation during coronary spasm. Twenty patients with variant angina and 27 control patients were studied. Coronary flow velocity was monitored using a Doppler guidewire following intracoronary ergonovine administration. In the control group, diastolic flow velocity either did not change or increased slightly in response to ergonovine. However, in patients with variant angina, 2 patterns of flow velocity alterations were observed. In the first pattern, flow initially increased and then suddenly decreased (16 of 20 patients). In the second pattern, flow gradually decreased (3 of 20 patients). In the remaining patient, the coronary flow alteration could not be detected because of branch spasm. When abnormally high flow velocity was defined as a 100% increase in flow after ergonovine administration within 1 minute, and abnormally low flow velocity was defined as a 50% decrease in flow to diagnose variant angina, sensitivities of 35%, 75%, and 85% were noted if flow was measured 1.0, 2.0, and 3.0 minutes after ergonovine administration, respectively. These abnormal flow velocities were observed before ischemic ST changes appeared. In conclusion, in patients with variant angina, characteristic serial changes in coronary flow velocity occur before occlusive spasm. Variant angina may be diagnosed earlier by monitoring flow velocity rather than by monitoring for ischemic electrocardiographic changes.

Aged↗
PubMed1998

Lethal postoperative coronary artery spasm.

BACKGROUND: Coronary artery spasm in the immediate postoperative period after a coronary operation is recognized infrequently. Its severity is variable and manifestations unpredictable. The diagnosis is usually made by an awareness of the possibility and thereafter by exclusion of other causes of myocardial ischemia. An opportunity for a positive diagnosis is rarely available. METHODS: The case reports of 3 patients with similar presentations of ischemic heart disease and with severe manifestations of coronary artery spasm in the postoperative period are presented. RESULTS: All 3 patients were women aged 55 to 60 years. All had single-vessel coronary artery disease involving the left anterior descending artery and underwent a left internal mammary artery bypass graft. Severe manifestations of myocardial ischemia of abrupt onset developed approximately 7 hours postoperatively in each patient. One patient died of severe hemodynamic deterioration from which resuscitation was unsuccessful. Another sustained a large anterior myocardial infarction despite graft patency. The third patient was supported by an intraaortic balloon pump and made a full recovery. CONCLUSIONS: The early diagnosis of coronary artery spasm is achieved by an awareness of the condition. The institution of early appropriate management may prevent its consequences.

Adult↗
PubMed1999

Rho-kinase-mediated pathway induces enhanced myosin light chain phosphorylations in a swine model of coronary artery spasm.

OBJECTIVE: We recently demonstrated in our swine model of coronary artery spasm that enhanced myosin light chain (MLC) phosphorylations (both MLC mono- and diphosphorylations) play a central role in the pathogenesis of the spasm. However, the molecular mechanism for and the phosphorylation sites for the enhanced MLC phosphorylations were unknown. In the present study, we addressed these points using hydroxyfasudil, a novel inhibitor of protein kinases, which we found preferentially inhibits Rho-kinase. METHODS: The specificity of the inhibitory effects of hydroxyfasudil on Rho-kinase, MLCK, MRCK beta and PKC were examined by kinase assay in vitro. The left porcine coronary artery was chronically treated with interleukin-1 beta (IL-1 beta, 2.5 micrograms). Two weeks after the operation, coronary artery vasomotion was examined both in vivo and in vitro. MLC phosphorylations were examined by Western blot analysis and the sites for the phosphorylations by anti-phosphorylated MLC antibodies that identified the monophosphorylation site as Ser19 and diphophorylation sites as Ser19/Thr18 of MLC. RESULTS: Inhibitory effects of hydroxyfasudil was at least 100 times more potent for Rho-kinase as compared with other protein kinases tested. Intracoronary serotonin (10 micrograms/kg) caused coronary hyperconstriction at the IL-1 beta-treated site in vivo, which was dose-dependently inhibited by hydroxyfasudil (p < 0.01). The coronary segment taken from the spastic site also showed hypercontractions to serotonin in vitro, which were again dose-dependently inhibited by hydroxyfasudil (p < 0.01). Western blot analysis showed that MLC monophosphorylation was significantly greater in the spastic segment than in the control segment, while MLC diphosphorylation was noted only at the spastic segment (p < 0.01). The sites for the mono- and diphosphorylated MLC were identified as the monophosphorylated site Ser19 and diphosphorylated sites Ser19/Thr18 of MLC, respectively. Both types of MLC phosphorylations at the spastic segment were markedly inhibited by hydroxyfasudil (p < 0.01). CONCLUSION: These results indicate that hydroxyfasudil-sensitive Rho-kinase-mediated pathway appears to mediate the enhanced MLC phosphorylations (on Ser19 and Ser19/Thr18 residues) and plays a central role in the pathogenesis of coronary artery spasm.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1985

Spasm in ectatic coronary arteries.

Patients with ectatic coronary arteries often have occlusion of the affected arteries. Because ectatic arteries are considered to have medial damage, they are normally assumed to have little capacity to constrict; therefore, spasm has not been considered a factor in the occlusive process. In two patients who had diffuse coronary ectasia, no appreciable stenosis, and angina pectoris, we found that the ectatic arteries indeed had an augmented vasoconstrictor response to ergonovine. This finding indicates that some ectatic arteries have a sufficient amount of smooth muscle to cause coronary spasm and may produce symptoms of coronary disease by causing recurrent arterial spasm.

Aged↗
PubMed1985

Spasm of the coronary arteries: causes and consequences (the scientist's viewpoint).

Both beta 1- and alpha 1-adrenoceptors are present on canine coronary arteries, and they are accessible to norepinephrine released from the sympathetic nerves. Under normal conditions, these arteries relax because of the predominance of the beta 1-adrenoceptors, whereas constriction prevails in the presence of beta 1-adrenoceptor antagonists. The coronary arteries also have cholinergic nerves. When activated, these nerves release acetylcholine, which acts on muscarinic receptors on the sympathetic nerve terminals to reduce the output of norepinephrine and thereby lessen the relaxation mediated by beta 1-adrenoceptors. Thus, muscarinic agonists can precipitate coronary artery spasm. If the smooth muscle cells of the coronary arteries become hypoxic, their responsiveness to beta-adrenergic stimulation is lost and constrictor responses are exaggerated. Cardiac glycosides prevent the predominance of the beta-adrenergic effects of norepinephrine. Therefore, after treatment with ouabain, release of norepinephrine from the sympathetic nerves leads not to relaxation but to further contraction of coronary arteries. The endothelium of the coronary arteries inhibits platelet aggregation by the formation and release of prostacyclin, and it reacts to platelet products by causing relaxation of the underlying smooth muscle. In addition, if any thrombin is formed, it also causes endothelium-mediated relaxation. If the endothelium is damaged, these protective mechanisms are lost. Patients with coronary artery spasm usually have morphologic changes in the artery at the site of the spasm. Platelets can aggregate at this site and release vasoactive substances, which--aided by formation of thrombin--cause contraction. Thus, the blood supply to the myocardium is reduced; the ensuing hypoxia augments the constriction. Acute myocardial ischemia caused by coronary vasospasm may precipitate acute cardiac rhythm disturbances and sudden death by ventricular tachycardia or fibrillation.

Adrenergic beta-Agonists↗
PubMed2004

Atrial septal defect in apical hypertrophic cardiomyopathy associated with coronary spasm.

Apical hypertrophic cardiomyopathy (HCM) is a well-known myocardial disease, but the additional coexistence of an atrial septal defect (ASD) and coronary spasm is quite rare. We report here on a 62-year-old man suffering from congestive heart failure due to apical HCM complicated by coronary spasm and secundum-type ASD. The transthoracic, transesophageal echocardiography and cardiac catheterization were useful for diagnosing and evaluating of the patient's status. A calcium channel blocker was given to prevent coronary spasm, and a surgical patch closure operation was successfully performed. Afterwards, his symptoms were alleviated.

Calcium Channel Blockers↗
PubMed2001

Multiple endothelial injury in epicardial coronary artery induces downstream microvascular spasm as well as remodeling partly via thromboxane A2.

OBJECTIVES: The study was undertaken to develop a coronary microvascular spasm model in pigs by repeated epicardial coronary artery endothelial injury. BACKGROUND: The pathophysiologic mechanisms responsible for coronary microvascular spasm remain unclear, in large part because a suitable animal model has yet to be found. METHODS: Balloon endothelial denudation was done just distal to the site of an implanted Doppler flowmeter in the left anterior descending coronary artery (LAD) every two weeks for a total of four times. Changes in LAD blood flow by intracoronary administration of vasoactive agents were assessed before each denudation. RESULTS: In the epicardial LAD endothelial denudation pigs, decreases in LAD blood flow caused by acetylcholine were augmented. Before denudation, it was - 15 +/- 4%, and at week 8 (i.e., two weeks after the fourth denudation) it was -100% (i.e., zero flow [p < 0.01]). The LAD flow changes in response to 5-hydroxytryptamine (5-HT) changed from an increase to a decrease, accompanied by medial thickening of microvessels in the LAD perfusion area. These flow responses were observed without significant changes in LAD diameter. In contrast, the LAD blood flow responses to acetylcholine and 5-HT did not change throughout the experiment in pigs given aspirin and a thromboxane A2 (TXA2) synthase inhibitor orally. CONCLUSIONS: This microvascular spasm model indicates that hypersensitivity to vasoactive substances in the microvascular beds as well as microvascular remodeling are brought about partly through TXA2. This model should be useful for examining the pathophysiology and treatment of microvascular angina.

Animals↗
PubMed2002

ST-segment elevation and ventricular fibrillation without coronary spasm by intracoronary injection of acetylcholine and/or ergonovine maleate in patients with Brugada syndrome.

OBJECTIVES: The study examined whether patients with Brugada syndrome are sensitive to vagal stimulation or ischemia. BACKGROUND: Experimental studies have suggested that a prominent transient outward current (I(to))-mediated action potential notch and a subsequent loss of the action potential dome in the epicardium, but not in the endocardium, give rise to ST-segment elevation and subsequent ventricular fibrillation (VF). METHODS: We evaluated the frequency of coronary spasm, augmentation (> or =0.1 mV) of ST-segment elevation in leads V(1) to V(3), and induction of VF by intracoronary injection of acetylcholine (ACh) and/or ergonovine maleate (EM) in 27 symptomatic patients with Brugada syndrome and 30 control subjects. RESULTS: The coronary spasm was induced in 3 (11%) of the 27 patients with Brugada syndrome and in 13 (43%) of the 30 control subjects. ST-segment elevation was augmented by 11 (33%) of the 33 right coronary injections (ACh: 6/11 [55%]; EM: 5/22 [23%]), without coronary spasm, but not by any of the left coronary injections in patients with Brugada syndrome. Ventricular fibrillation was induced by 3 (9%) of the 33 right coronary injections (ACh: 2/11 [18%]; EM: 1/22 [5%]), but not by any of the left coronary injections. In contrast, neither ST-segment elevation nor VF was observed in any of the control subjects. CONCLUSIONS: Our results support the hypothesis that mild ischemia and vagal influences act additively or synergistically with the substrate responsible for the Brugada syndrome to elevate the ST-segment and precipitate VF. These observations suggest that Brugada patients may be at a higher risk for ischemia-related sudden death.

Acetylcholine↗
PubMed1983

Coronary artery spasm at the site of angioplasty in the first 2 months after successful percutaneous transluminal coronary angioplasty.

The clinical course of five patients manifesting coronary artery spasm at the site of previous successful percutaneous coronary angioplasty is reviewed. All patients showed this spasm on hemodynamically insignificant (less than 50% diameter narrowing) obstruction. Four patients did not respond to therapy with calcium channel antagonists and nitrates and subsequently developed recurrent stenosis. One patient died 2 months after angioplasty and 1 day after coronary bypass surgery. Pathologic study at the site of angioplasty revealed new artherosclerotic disease. Coronary spasm may occur during the healing period after coronary angioplasty and should be distinguished from fixed obstruction.

Adult↗