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At least 433 records · Page 24Linked to original sources
PubMed1979

The mechanism of coronary artery spasm: roles of oxygen, prostaglandins, sex hormones and smoking.

A reduced oxygen supply to the heart causes coronary vasodilatation in the first instance. But if the hypoxia is severe or prolonged, the dilatation passes off and coronary vasospasm develops leading to a vicious circle with a further reduction of myocardial oxygenation. The spasm is associated with increased outflow of prostaglandin (PG)-like material and can be prevented or reversed by inhibitors of PG synthesis such as indomethacin or antagonists of PG action such as chloroquine. The spasm does not appear to be caused by thromboxane (TX) A2 since selective inhibitors of TXA2 synthesis enhance the hypoxic spasm and by themselves can cause spasm even in oxygenated hearts. The mechanism may be related to loss of negative feedback control of the PG pathway by TXA2. Oxygen may enhance TXA2 production and reduce formation of vasoconstrictor PGs, while smoking, because of the formation of carboxyhaemoglobin, may have the opposite effect. Oestradiol and testosterone do not influence the hypoxic spasm but progesterone at physiological concentrations blocks it completely. Progesterone may be the protective female hormone and the increased susceptibility to myocardial infarction in women on oral contraceptives may be related to reduced formation of endogenous progesterone.

Coronary Circulation↗
PubMed1988

Sensitivity and specificity of intracoronary injection of acetylcholine for the induction of coronary artery spasm.

Intracoronary injection of acetylcholine has been shown to induce coronary spasm in patients with variant angina. To examine its sensitivity and specificity, incremental doses of acetylcholine (20, 50 and 100 micrograms into the left coronary artery and 20 and 50 micrograms into the right coronary artery) were injected into the coronary artery or arteries in 70 patients with variant angina (Group 1) (mean age 57 years) and 93 patients without variant angina or angina at rest (Group 2) (mean age 54 years). Forty patients of the latter group had atypical chest pain, 16 cardiomyopathy, 14 arrhythmia, 11 valvular disease, 7 stable effort angina due to advanced coronary artery disease, 3 congenital heart disease and 2 hypertension. A temporary cardiac pacemaker set at 40 to 50 beats/min was positioned in the right ventricle. Coronary spasm was defined as total occlusion or severe vasoconstriction associated with chest pain or ischemic ST changes on the electrocardiogram or both. In Group 1, acetylcholine induced spasm in 63 (90%) of the 70 patients in the artery or arteries predicted to be responsible for spontaneous attacks. In Group 2, acetylcholine induced coronary spasm only in one patient with effort angina and advanced coronary artery disease although lesser degrees of vasoconstriction (less than or equal to 75% of the luminal diameter) occurred in most patients after acetylcholine (specificity of acetylcholine thus was 99%). In conclusion, intracoronary injection of acetylcholine is sensitive and reliable for the induction of coronary spasm.

Acetylcholine↗
PubMed2004

Genetic risk and gene-environment interaction in coronary artery spasm in Japanese men and women.

AIMS: The aim of the study was to identify genes that confer susceptibility to coronary artery spasm and clarify the interaction between genetic and environmental factors in this condition. METHODS AND RESULTS: The study population comprised 2188 Japanese individuals, including 593 subjects with coronary artery spasm (453 men, 140 women) and 1595 controls (762 men, 833 women). The genotypes for 35 polymorphisms of 29 candidate genes were determined with an allele-specific DNA primer-probe assay. Multivariable logistic regression analysis adjusted for age, body mass index, and the prevalence of smoking, hypertension, diabetes mellitus, hypercholesterolaemia, and hyperuricaemia revealed a significant association with coronary artery spasm of one polymorphism (242C-->T in the NADH/NADPH oxidase p22 phox gene) in men and two polymorphisms (-1171/5A-->6A in the stromelysin-1 gene and -634C-->G in the interleukin-6 gene) in women. A stepwise forward selection procedure revealed that smoking was the most important risk factor for coronary artery spasm and that the effects of these polymorphisms on this condition were statistically independent of smoking. CONCLUSION: The NADH/NADPH oxidase p22 phox gene is a susceptibility locus for coronary artery spasm in men, and the stromelysin-1 and interleukin-6 genes are susceptibility loci in women.

Coronary Vasospasm↗
PubMed1999

Frequency of provoked coronary vasospasm in patients undergoing coronary arteriography with spasm provocation test of acetylcholine.

This study examines the incidence of spasm by intracoronary injection of acetylcholine in Japanese patients who underwent coronary angiography. The subjects were 685 consecutive patients (477 men, mean age 63.2 +/- 7.5 years) who were studied with an acetylcholine test. Acetylcholine was injected in incremental doses of 20, 50, and 80 microg into the right coronary artery and 20, 50, and 100 microg into the left coronary artery. Spasm was defined as total or subtotal occlusion. Coronary vasospasm was determined in 221 patients (32.3%). Spasm occurred often during effort and rest in patients with angina (25 of 51, 49.0%), exertional angina (25 of 74, 33.8%), recent myocardial infarction (30 of 80, 37.5%), healed myocardial infarction (14 of 37, 37.8%), and especially in patients with rest angina (83 of 124, 66.9%), whereas spasm was relatively uncommon in patients with nonischemic heart disease (23 of 252, 9.1%). Spasm was superimposed on significant atherosclerotic lesions in 35.9% of patients as well as on nonfixed atherosclerotic lesions in 30.8% of patients. We conclude that >9% of Japanese patients may have coronary vasospasm with intracoronary injection of acetylcholine and recommend the provocation test for evaluating coronary vasospasm if coronary angiography is undertaken.

Acetylcholine↗
PubMed1983

Intraoperative coronary artery spasm successfully treated with nitroglycerin and nifedipine.

Coronary artery spasm is recognized as a major cause of angina and may coexist with fixed coronary artery disease. This report presents the case of a patient who developed recurrent coronary artery spasm in the operating room following effective coronary artery bypass grafting. The coronary artery spasm was manifested by sudden ST segment elevation, hypotension, and decreased cardiac output. Direct injection of nitroglycerin into each coronary artery graft was necessary to reverse the coronary artery spasm. Peripheral intravenous nitroglycerin plus nifedipine administered through a nasogastric tube prevented further recurrence of coronary artery spasm.

Angina Pectoris↗
PubMed1982

Coronary artery spasm following coronary artery revascularization.

Coronary artery spasm is a well-documented phenomenon in patients undergoing medial treatment. We describe coronary artery spasm occurring in the immediate postoperative period following coronary artery bypass operation. The spasm occurred in a vessel that was not operated on and that had no apparent lesion. The diagnosis of spasm was made by coronary angiography immediately after operation. Complications associated with this spasm are discussed. Emphasis is placed on early postoperative angiography for patients whose condition is inexplicably unstable after operation.

Amyl Nitrite↗
PubMed1999

Possible role of high susceptibility of high-density lipoprotein to lipid peroxidative modification and oxidized high-density lipoprotein in genesis of coronary artery spasm.

Recent study demonstrated high susceptibility of plasma LDL to lipid peroxidative modification in patients with variant angina. Oxidized stress state, especially oxidized LDL, may induce coronary artery spasm by its impairing effect of endothelium-dependent arterial relaxation, but precise mechanisms remain unclear. Study subjects included 93 patients who underwent coronary angiographic examination: 12 patients with coronary artery spasm provoked by ergonovine without organic stenosis (group I), 11 patients who did not demonstrate coronary artery spasm or organic stenosis (group II) and 70 patients with organic coronary artery stenosis (group III). Levels of plasma HDL-cholesterol and apoA-I in group I were similar to those in III but were significantly lower than those in II, although the other plasma lipid parameters were not different among the three groups. The levels of TBARS in plasma and HDL were significantly higher in group I than in II or III (2.94+/-1.56 vs. 1.91+/-0.35 or 2.23+/-0.89 nmol MDA/ml and 1.23+/-1.00 vs. 0.54+/-0.37 or 0.70+/-0.63 nmol MDA/mg protein; P < 0.05), although the levels of TBARS in LDL were not significantly different. In the monitoring curve of diene production during copper-induced lipid peroxidation of HDL, its propagation slope was steeper and levels of maximum diene absorbance was higher in group I as compared with that in II or III, but not found in those of LDL. These results suggested that high susceptibility of HDL to lipid peroxidative modification in group I may contribute to the genesis of coronary artery spasm, and oxidized HDL rather than oxidized LDL is more likely to be related to coronary artery spasm.

Copper↗
PubMed1985

A model for the study of coronary spasm induced changes in cardiac metabolism.

A model is described which permits the study of localized and generalized arterial spasm in the intact working perfused rabbit heart with a perfluorochemical (FC-43) as perfusate. Coronary arteries were visualized by intraatrial injection of Patent Blue Dye with gated photography. Localized spasm resulted from topical spray of histamine (40 mumols) on the epicardial surface overlying an obtuse marginal artery. Before and following topical administration of histamine, regional coronary flow was determined using radioisotope-labeled microspheres. Generalized arterial spasm was initiated by intraatrial injection of histamine (10 mumols). After topical administration, abtuse marginal artery diameter decreased by 57%; large vessel resistance rose 32 fold; 20% rise of total coronary resistance resulted in a slight reduction of total coronary flow (16%). Heart rate, cardiac output, dP/dtmax and myocardial oxygen consumption did not change. However, regional coronary flow in the myocardium supplied by the affected artery diminished 21% resulting in ischemic changes in redox pairs. After intraatrial injection of histamine, changes were more pronounced. Obtuse marginal artery diameter declined by 88% resulting in 3300-fold rise of large vessel resistance. Total coronary resistance increased 150%, coronary flow and cardiac output diminished (56% and 24%). Both heart rate and dP/dtmax increased (16% and 17%). Generalized coronary spasm after intraatrial histamine injection resulted in severe metabolic effects: Myocardial oxygen consumption (-48%); ATP (-29%); creatine phosphate (-34%); redox ratios, alpha-glycerophosphate/dihydroxyacetone phosphate and lactate/pyruvate, increased by 449% and 114%, respectively. The findings illustrate that localized and generalized coronary spasm can be produced and quantitated in a working heart model.

Animals↗
PubMed1998

Heparin-releasable endothelial cell-associated tissue factor pathway inhibitor (TFPI) is increased in the coronary circulation after coronary spasm in patients with coronary spastic angina.

Tissue factor pathway inhibitor (TFPI) is a physiological regulator of the extrinsic coagulation cascade. Coronary spasm can alter endothelial cell properties in the coronary artery with resultant thrombosis. To determine whether coronary spasm affects plasma TFPI level, we measured the heparin-releasable endothelial cell-associated TFPI (heparin-releasable TFPI) (ng/ml) in the coronary sinus and the aortic root before and after coronary spasm induced by an injection of acetylcholine in 18 patients with coronary spastic angina, and before and after myocardial ischemia induced by rapid atrial pacing in 18 patients with stable exertional angina, and in 17 control subjects with normal coronary arteries and no coronary spasm. Heparin-releasable TFPI level in the coronary spastic angina group significantly increased in the coronary sinus (1 22+/-46 to 147+/-63, p<0.001) after the ischemic event but not in the aortic root (113+/-44 to 121+/-58). The level in the coronary sinus and the aortic root remained unchanged after the ischemic event in the stable exertional angina group and after the injection of acetylcholine in the control group. The coronary sinus-arterial difference in the amount of the heparin-releasable TFPI significantly increased after the ischemic event only in the coronary spastic angina group (10+/-18 to 26+/-18, p<0.002). Our result suggested that heparin-releasable TFPI is increased in the coronary circulation after coronary spasm.

Aged↗
PubMed2001

Three-year follow-up of the Japanese patients with microvascular angina attributable to coronary microvascular spasm.

BACKGROUND: We recently reported that coronary microvascular spasm could cause angina in patients with chest pain and normal coronary arteriograms. However, the long-term prognosis of these patients or the effect of calcium channel blockers is not known. METHODS: Of consecutive 283 patients who underwent acetylcholine testing for the evaluation of chest pain, we identified 68 patients with microvascular angina attributable to coronary microvascular spasm. All patients were discharged on calcium channel blockers and followed up for an average period of 3.3 years. RESULTS: As compared with those having epicardial spasm (n=169), there was a female predominance in the microvascular spasm group (P<0.01), and 81% of the female patients were postmenopausal. During the follow-up, no patient died and one patient (1%) developed non-Q wave myocardial infarction. The frequency of chest pain was unchanged or increased in 24 patients (36%) and decreased or disappeared in 42 patients (64%). The angina status was improved only in 16 of 33 patients treated with calcium channel blockers alone. By contrast, it was improved in 18 of 21 patients on the combination of calcium channel blockers and angiotensin converting enzyme inhibitors (P<0.05). CONCLUSIONS: Patients with microvascular angina in the present study were more women and had a different risk factor profile as compared with those having epicardial spasm. Long-term prognosis was excellent with regard to mortality, but angina persisted in many patients even on calcium channel blockers. The result warrants prospective studies to evaluate the efficacy of angiotensin converting enzyme inhibitors as adjunct to calcium channel blockers in this population.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1987

Louis F. Bishop lecture. Role of coronary artery spasm in symptomatic and silent myocardial ischemia.

The revival of the concept of coronary spasm has stimulated research into coronary artery disease. Observations in patients with variant angina have substantially contributed to the appreciation of painless myocardial ischemia. However, the presence or absence of pain during ischemic episodes is not related to the cause of ischemia, because painless ischemia can be observed in variant angina (caused by spasm), in effort-induced angina (caused by increased myocardial demand) and in myocardial infarction (caused by thrombosis). Continuous monitoring initially of patients with variant angina and subsequently of patients with unstable and stable angina proved that often painful and painless ischemic episodes are caused by a transient impairment of regional coronary blood flow rather than by an excessive increase of myocardial demand. The transient impairment of coronary flow appears to be caused by dynamic stenosis of epicardial coronary arteries. This most often occurs at the site of atherosclerotic plaques encroaching on the lumen to a variable extent. Dynamic stenosis can be caused by 1) "physiologic" increase of coronary tone, as in stable angina, 2) spasm, as in variant angina, and 3) thrombosis, usually in combination with "physiologic" changes in tone or with spasm, or both, as in unstable angina. The mechanisms of spasm, as typically observed in variant angina, are different from those of "physiologic" increase of tone; they appear to be related to a local alteration that makes a segment of coronary artery hyperreactive to a variety of constrictor stimuli causing only minor degrees of constriction in other coronary arteries. The nature of this abnormality, which may remain stable for months and years, is yet unknown.

Angina Pectoris, Variant↗
PubMed1996

Evaluation of the long-term effectiveness of extraluminal and intraluminal vasodilators in an in vitro porcine model of arterial graft spasm.

OBJECTIVE: Postoperative graft spasm is a concern when arterial conduits are used because there may be insufficient arterial graft flow. Intraoperatively, vasodilators are used to increase flow and prevent spasm, but little is known about their duration of effectiveness. METHODS: To examine this we attached porcine gastroepiploic and internal thoracic arteries (GEA, n = 48; ITA, n = 24, 10-12 cm long) to a computer-controlled perfusion system (constant inflow pressure 80 mm Hg) with a fixed outflow resistance. Norepinephrine (10(-9)-10(-5) M) was incrementally added to the perfusate at baseline (B), then immediately (h+0) and 2 h (h+2) after the vessels were treated with 30 min of extraluminal or intraluminal nitroglycerin, nitroprusside, verapamil or papaverine. RESULTS: At (B), norepinephrine caused a dose-dependent decrease in flow in both the ITAs and GEAs. In the ITAs, at (h+0), both extraluminal and intraluminal papaverine and, to a lesser extent nitroprusside, increased initial flow and decreased graft sensitivity to norepinephrine. At (h+2), only extraluminal papaverine sustained this maximal effect (ED50 for extraluminal papaverine at (B) 2.6 E(-7) vs. (h+2) 1.3 E(-6), P = 0.01). For the GEAs, at (h+0), both extraluminal and intraluminal verapamil, papaverine, nitroprusside and nitroglycerin attenuated flow reduction due to norepinephrine. At (h+2), only extraluminal papaverine, extraluminal verapamil and intraluminal verapamil were effective in preventing norepinephrine-induced spasm (ED50 for extraluminal papaverine at (B) 1.0 E(-7) vs. (h+2) 6.4 E(-6) (P = 0.004); extraluminal verapamil at (B) 1.2 E(-7) vs. (h+2) 4.0 E(-6); intraluminal verapamil at (B) 5.8 E(-7) vs. (h+2) 5.7 E(-6), P = 0.005). CONCLUSION: Verapamil-and papaverine-treated arteries have a greater duration of efficacy in resisting spasm than arteries treated with nitroglycerin and nitroprusside. In the ITA, extraluminal administration of papaverine is most efficacious, possibly due to the prolonged exposure afforded by this route of administration. The effects of verapamil and papaverine are more prolonged in the GEA when administered extraluminally, potentially due to absorption in the perivascular fat-pad and subsequent slow release. The results of this study suggest that extraluminally administered verapamil and papaverine appear to be the preferred vasodilators for preventing arterial graft spasm in the postoperative period. This may be especially important when multiple arterial grafts are used.

Animals↗
PubMed1983

Percutaneous lumbar rhizotomy for spasms in paraplegia.

Twenty-one patients with myelopathy causing uncontrollable spasms of the legs underwent percutaneous lumbar rhizotomy. There were two groups: active, otherwise healthy people with spinal lesions whose rehabilitation was hampered by spasms of flexion or extension of the hips and knees; and a second group of hospitalised, debilitated paraplegic patients with unhealing decubitus ulcers. Fourteen of the 16 active patients had excellent results initially, as did all five of the patients with pressure sores. Six have undergone repeat procedures in 7 to 18 months for recurrences of some component of the spasms. All have had at least minor recurrences. Of six patients with significant sensory preservation pre-operatively, four found the resulting numbness disturbing and two did not achieve good relief from the spasms. The procedure is recommended when uncontrollable spasms interfere with rehabilitation or healing of pressure sores in patients with spinal lesions with complete motor and sensory loss.

Electrocoagulation↗
PubMed2002

Is there a role of a small dose of propofol in the treatment of laryngeal spasm?

BACKGROUND: Propofol has been found to depress the laryngeal reflexes. We studied whether this property could be utilized to relieve laryngeal spasm. METHODS: This study was conducted over a period of 3 years, and included children aged 3-10 years, ASA status I and II. Most of the children were undergoing minor surgical procedures, under general anaesthesia with Laryngeal Mask Airway (LMA trade mark ) and caudal epidural analgesia. RESULTS: During this period, 20 patients developed laryngeal spasm on removal of the LMA at the end of surgery. Initially, they all were treated with 100% O2, with gentle positive pressure ventilation. Out of 20 patients, seven responded well with 100% O2 and gentle positive pressure ventilation. The remaining 13 were treated with a small dose of propofol (0.8 mg.kg-1 body weight). Laryngeal spasm was relieved successfully in 10 patients and three patients required intubation to improve their oxygenation. CONCLUSIONS: Propofol in a small dose (0.8 mg.kg-1 body weight) was a useful drug to relieve laryngeal spasm in most children (76.9%) following the removal of the LMA. Because it was not found to be effective in all patients, succinylcholine still has a role to play in critical conditions. However, we recommend propofol as a suitable alternative for relieving laryngeal spasm in situations where succinylcholine is contraindicated.

Anesthesia, General↗
PubMed2001

Fully endoscopic vascular decompression of the facial nerve for hemifacial spasm.

Hemifacial spasm is an uncommon disorder manifesting as a unilateral, involuntary, sporadic contraction of the musculature innervated by the seventh cranial nerve. Although debated, the etiology of hemifacial spasm is generally accepted as compression of the facial nerve by vessels of the posterior circulation. Early surgical techniques were ineffective and fraught with morbidity. Over the past 25 years microvascular decompression surgery has allowed the safe and effective treatment of hemifacial spasm. Recent reports combining microsurgical and endoscopic techniques have documented the advantages of the endoscope in exposing the anatomy of this region. Enhanced visualization allows a less traumatic dissection and increases the surgeon's ability to locate nerve-vessel conflicts often difficult to identify through the limited view of the microscope. This article reviews the history of hemifacial spasm and describes the first three cases of fully endoscopic vascular decompression for hemifacial spasm, emphasizing the advantages of this novel surgical approach.

Case Reports↗
PubMed2001

Hyperventilation and cold-pressor stress echocardiography for noninvasive diagnosis of coronary artery spasm.

We report the usefulness of 2-dimensional echocardiography during the cold-pressor test immediately after hyperventilation for noninvasive diagnosis of coronary vasospasm in 43 patients with suspected vasospastic angina. The stress test consisted of hyperventilation for 6 minutes, followed by cold water pressor stress for 2 minutes under continuous electrocardiographic and echocardiographic monitoring. Coronary angiography with an intracoronary injection of acetylcholine was performed within 2 weeks after the stress test. Coronary spasm was observed in 33 patients by angiography. Multivessel spasm was diagnosed in 26 patients by stress echocardiography and in 23 patients by angiography. The stress-induced wall motion abnormalities occurred earlier than the ST-segment changes and chest pain. The wall motion abnormalities shown on the echocardiogram correlated well with the vascular territories of the coronary artery that had the spasm. The sensitivity, specificity, and diagnostic accuracy of hyperventilation and cold-pressor stress echocardiography for detecting vasospastic angina against coronary angiography with an intracoronary injection of acetylcholine were 91%, 90%, and 91%, respectively. However, the sensitivity, specificity, and diagnostic accuracy of hyperventilation and cold-pressor stress electrocardiography for detecting vasospastic angina were 48%, 100%, and 60%, respectively. No major side effects were observed during or after the stress test. Echocardiographic monitoring during the stress test detected spasm unaccompanied by either ST- segment changes or chest pain and revealed the location of multivessel coronary spasm. Hyperventilation and cold-pressor stress echocardiography is thus a noninvasive and useful tool for the diagnosis of vasospastic angina.

Aged↗
PubMed1983

The provocation of coronary arterial spasm in patients with recent transmural myocardial infarction.

Provocative tests for coronary spasm were performed in a group of 131 patients (124 men and 7 women) with recent (less than 6 weeks) transmural myocardial infarction. Coronary arteriography was performed 27 +/- 9 days after the onset of the infarction. The provocative test was performed using a single IV bolus of 0.4 mg of ergometrine. Aortic pressure, ECG and arteriograms of the two coronary vessels were repeated 3 and 5 min later. Provoked spasm was observed in 27 (21%) of the patients. In 13 (48%) the coronary spasm occurred in a vessel presumed to be responsible for the myocardial infarction, while it was observed in coronary artery unrelated to the area of the infarct in 14 (52% of the cases with spasm). Thus, this study demonstrates a high degree of reactivity of the coronary tree of patients with recent transmural myocardial infarction suggesting the likelihood of a role for spasm in the infarction process and offering some explanation for subsequent recurrent ischemic events.

Adult↗
PubMed2000

Increased expression of L-type calcium channels in vascular smooth muscle cells at spastic site in a porcine model of coronary artery spasm.

Coronary artery spasm is caused primarily by increased contractility of vascular smooth muscle. Excessive Ca2+ entry into vascular smooth muscle cells (VSMCs) may be one of the key mechanisms for the spasm, but no study has ever directly examined the possible alterations of Ca2+ channels in the spastic coronary artery. Here we show that L-type Ca2+ channels are excessively expressed at the spastic site of the coronary artery. In a porcine model of coronary spasm with balloon injury, both receptor-mediated stimulation of L-type Ca2+ channels by serotonin and direct stimulation of the channels by Bay K 8644 (a dihydropyridine Ca2+ channel agonist) repeatedly induced coronary spasm in vivo, which was abolished by pretreatment with nifedipine, a dihydropyridine Ca2+ channel antagonist. In a single VSMC freshly dispersed from coronary arteries in vitro, patch-clamp experiments showed that current density of L-type Ca2+ channel current was significantly increased in VSMCs from the spastic site compared with that from the control site even when the channels were maximally stimulated by Bay K 8644. There was no difference in the sensitivity of the channels to Bay K 8644. These results indicate that functionally available L-type Ca2+ channels are excessively expressed at the spastic site of the coronary artery in our porcine model, suggesting that increased expression of L-type Ca2+ channels and concomitant increase in Ca2+ entry into VSMCs through the channels may contribute, at least in part, to the pathogenesis of coronary artery spasm.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗