Left coronary artery-left ventricle fistula with right coronary artery spasm

A 72-year-old woman was admitted to our hospital for evaluation of chest pain. Coronary angiography showed a left coronary artery-left ventricle fistula. An acetylcholine provocation test induced vasoconstriction of the right but not the left coronary artery. Her chest pain was not relieved by combined therapy with isosorbide dinitrate, diltiazem and nicorandil. Because of the coronary spasm, beta-blockers could not be used. However, her chest pain was relieved after the administration of a minor tranquilizer. Thus, the patient's chest pain was unlikely to be associated with either the fistula or the coronary spasm.     

Effect of nitroglycerin and nicorandil on regional poststenotic quantitative coronary blood flow in coronary artery disease: a combined digital quantitative angiographic and intracoronary doppler study

The biophysical activity of lung surfactant depends, to a large extent, on the presence of the hydrophobic surfactant proteins B (SP-B) and C (SP-C). The role of these proteins in lipid adsorption and lipid squeeze-out under dynamic conditions simulating breathing is not yet clear. Therefore, the aim of this study was to investigate the interaction of spread hydrophobic surfactant proteins with phospholipids in a captive-bubble surfactometer during rapid cyclic area changes (6 cycles/min). We found that SP-B and SP-C facilitated the rapid transport of lipids into the air-water interface in a concentration-dependent manner (threshold concentration > or = 0.05:0.5 mol% SP-B/SP-C). Successive rapid cyclic area changes did not affect the concentration-dependent lipid adsorption process, suggesting that SP-B and SP-C remained associated with the surface film.     

Role of coronary artery spasm in progression of organic coronary stenosis and acute myocardial infarction in a swine model. Importance of mode of onset and duration of coronary artery spasm

BACKGROUND: Coronary spasm may play an important role in progression of organic coronary stenosis and myocardial infarction, but the mechanisms responsible for these complications are not known. This study aimed to examine whether the mode of onset and the duration of coronary spasm influenced progression of organic coronary stenosis and acute myocardial infarction in a swine model of coronary spasm. METHODS AND RESULTS: G?ttingen miniature pigs were subjected to cholesterol feeding, balloon-induced coronary arterial denudation, and x-ray irradiation. Five months later, coronary spasm was induced by intracoronary injection of serotonin. In 10 pigs, coronary spasm was provoked abruptly and maintained for 25 minutes by five repeated intracoronary injections of serotonin (10 micrograms/kg) every 5 minutes (group A, abrupt onset and short duration). In group B, coronary spasm was provoked gradually by intracoronary injections of serotonin at graded doses of 0.1, 0.3, and 0.6 microgram/kg every 5 minutes and was then maintained for 25 minutes in four pigs (group B1, gradual onset and short duration) and for 120 minutes in six pigs (group B2, gradual onset and long duration) by repeated intracoronary injections of serotonin (10 micrograms/kg) every 5 minutes. Intramural hemorrhage was noted histologically at the spastic site more frequently in group A with abrupt onset (nine of 10 pigs) than in group B with gradual onset (two of 10 pigs) (p < 0.01). Progression of organic coronary stenosis due to intramural hemorrhage was noted in seven pigs (six pigs in group A and one pig in group B), including three cases of total coronary occlusion. Evidence for the evolution of acute myocardial infarction (serial ECG findings, left ventriculograms, and histological findings) was noted in one pig (7%) of group A or B1 with short duration and in five of six pigs (83%) in group B2 with long duration (p < 0.01 versus group A and B1). CONCLUSIONS: These results indicate that: 1) intramural hemorrhage was frequently induced by coronary spasm of abrupt but not of gradual onset, 2) intramural hemorrhage resulted in acute progression of coronary stenosis and sometimes resulted in persistent total coronary occlusion leading to acute myocardial infarction, and 3) prolonged coronary spasm resulted in acute myocardial infarction without progression of organic coronary stenosis.     

Acute myocardial infarction during pregnancy caused by coronary artery spasm

A 33-year-old pregnant woman suffered from acute anteroseptal myocardial infarction at the 19th gestational week. Despite periodic attacks of myocardial ischaemia after admission, the coronary arteriograms under the use of nitroglycerin were normal. Thereafter, she remained free from the ischaemic events with diltiazem hydrochloride and delivered a healthy baby. The coronary arteriography at puerperium also showed no organic narrowing. However, the provocative test with acetylcholine chloride caused severe spasm of the left anterior descending coronary artery. These findings strongly suggest that acute myocardial infarction in this pregnant woman was caused by coronary artery spasm.     

Hyperventilation as a specific test for diagnosis of coronary artery spasm

Xanthomas may be associated with benign or malignant lymphoproliferative diseases, often with associated hypergammaglobulinema. In human immunodeficiency virus type 1 (HIV-1) disease, there is a high lymphoproliferative rate despite the immunodeficiency and increased cell death. We report three HIV-1-positive patients with facial papular xanthomatosis eruptions associated with hypergammaglobulinema, and an immunoglobulin A (IgA) gammopathy. Histopathologic features include lipid-laden macrophages, extracellular nuclear dust with phagocytosized nuclear debris, and hyalinization with areas of hyaline necrosis of collagen fibers. These distinctive papular xanthomas may be a marker of HIV-1 disease and of a pattern of immunodysregulation, immunodeficiency, and lymphoid proliferation seen in HIV-1 disease.     

Low prevalence of coronary artery spasm in patients with normal coronary angiograms and unexplained ventricular fibrillation

AIMS: The aetiology of ventricular fibrillation in patients without identifiable structural heart disease is unknown. Recently, high prevalence of silent ischaemia due to coronary artery spasm has been reported in such patients. However, in at least one report, all patients had non-critical coronary artery lesions. Identification of coronary artery spasm as the underlying aetiology of ventricular fibrillation has important therapeutic implications. METHODS AND RESULTS: We performed ergonovine provocation tests in 18 patients (14 males, and four females; mean age, 36 years) with documented ventricular fibrillation in the absence of identifiable structural heart disease who had undergone aborted sudden death. In group I (n = 7) ergonovine provocation tests were performed at a mean interval of 31 months (range 21-42 months) after the index episode. These patients had already received an implantable cardioverter defibrillator, after failed electrophysiologically guided antiarrhythmic therapy. In group II (n = 11) the ergonovine provocation test was performed prospectively as part of the diagnostic evaluation. All patients were off antiarrhythmic drugs, calcium entry or beta-adrenoceptor blockers at the time of the ergonovine provocation test. Ergonovine was administered intravenously as a bolus injection, beginning with 0.05 mg followed every 3 min by incremental doses up to a cumulative maximum dose of 0.45 mg. Predefined end-points were (1) recording of ischaemic ST segment shifts of > or = 1 mm in at least two corresponding leads of the 12-lead electrocardiogram; (2) induction of ventricular tachycardia or ventricular fibrillation; and (3) administration of a cumulative dose of 0.45 mg. A positive response to ergonovine was seen in only one patient (5%) in group I in whom there developed ST segment elevation without angina and a short burst of rapid ventricular tachycardia. CONCLUSIONS: This study found a low prevalence of coronary artery spasm in patients with aborted sudden death resulting from documented ventricular fibrillation and non-apparent underlying heart disease. All patients had normal coronary angiograms and a negative history for spontaneous episodes of chest pain. The mechanism of arrhythmogenesis in such patients remains largely unknown.     

Use of the radial artery graft in coronary artery bypass grafting: harvesting technique and spasm prevention

The use of radial artery (RA) in coronary artery bypass grafting (CABG) has been increasing recently as a revival. In this report, we describe several practical suggestions for improving patency rate of the graft. Between April of 1997 and February of 1998, 41 CABGs were performed using RA graft, totalling 56 anastomoses. The early patency rate of the graft has been 100% (graft: 38/38, anastomosis: 53/53). Harvesting technique: with the use of Harmonic Scalpel, it is possible to atraumatically harvest the vessel in a short time. Although longitudinal fasciotomy of the adventitia has been recently reported to be effective in releasing spasm, the nature of the vessel raise concern that the fasciotomy may even induce spasm. We hypothesize that leaving the adventitia intact, preserving vasa vasorum, rather than performing fasciotomy leads to improvement of long-term patency. Spasm prevention: we consider the body temperature to be the most important factor. Therefore, we utilize normothermic cardiopulmonary bypass (CPB). Another important factor is that the arterial CO2 is kept at a high level during CPB. For dilation of RA graft, milrinone is used instead of papaverine. For the intra- and postoperative management, intravenous continuous administration of diltiazem was changed to nicorandil. Technically, essential resolution for improvement of patency rate is either to allow for large proximal anastomosis, or to make sequential anastomosis with another coronary artery which has a good run off. For these purposes, the proximal anastomosis on the ascending aorta seems to have the advantage over placing it on ITA.     

Selective ergonovine-induced coronary artery spasm and ST-segment alternans after blunt thoracic trauma

A 24-year-old man was found to have angiographically normal coronary arteries shortly after suffering blunt thoracic trauma. Selective ergonovine administration into the left coronary artery induced total occlusion of the left anterior descending branch and electrical alternans of the ST-segment. This case demonstrates coronary artery spasm as a possible mechanism of coronary occlusion after blunt thoracic trauma.     

Evaluation of functional importance of coronary artery stenosis by intracoronary Doppler blood flow velocity measurement

Intracoronary doppler blood flow velocity measurements supply important information for clinical decision making during angioplasty, especially with regard to stenoses of ambiguous severity. In the presence of an intermediate stenosis of unknown physiological impact (40-60%), determination of normal flow parameters (coronary flow reserve: CFR, diastolic to systolic velocity ratio: DSVR and proximal to distal velocity ratio: P/D) will make deferment of treatment acceptable. Post-angioplasty success can be based on restoral of normal flowparameters. The inability to achieve normal CFR immediately after angioplasty does not indicate an unsuccessful procedure, it remains to be shown whether a lack of normalization of DSVR and/or P/D does so. Continuous post-lesional flow monitoring can show and quantify the existence of collateral flow.     

Scaffolding the coronary arteries: intracoronary stenting

Stenting is a new method for treating coronary artery stenosis. This article presents an overview of the rationale for the implantation of stents, the various types of stents available, and roles the home care nurse assumes in caring for these patients.     

Can intracoronary ultrasound correctly assess the luminal dimensions of coronary artery lesions? A comparison with quantitative angiography

In 62 patients with angina pectoris Canadian Class III and IV, the luminal dimensions of 25 pre-PTCA and 56 post-PTCA lesions without occlusion were examined with a 4.3 F 30 MHz mechanical ultrasound imaging catheter, and analysed off-line using ultrasound cross-sectional area (U-CSA) measurements from s-VHS video images (n = 81). In addition, 42 angiographically normal coronary segments were examined. At the site of the examination, the U-CSA was integrated centrally to the leading edge echo of the inner contour of the vessel wall and the corresponding angiographic cinefilm images were analysed by edge detection using the Cardiovascular Angiography Analysis System. The obstruction diameter (at the lesion) and the mean vessel diameter (at normal sites) were used to calculate the angiographic cross-sectional area (A-CSA) assuming a circular model. U-CSA values were compared with the corresponding A-CSA values using t-test and linear regression analysis. The study showed that larger CSA are measured with ultrasound than with angiography. (P < 0.0001). An acceptable correlation was found between U-CSA and A-CSA values in normal coronary segments (correlation coefficient: r = 0.73, mean diff. = 1.44 +/- 1.22 mm2). However, the correlation was poor at the site of pre-PTCA lesions (r = 0.62, mean diff. = 1.81 +/- 1.14 mm2) and deteriorated following PTCA (r = 0.47, mean diff. = 1.28 +/- 2.20 mm2). No correlation was found between the degree of lumen eccentricity measured with intracoronary ultrasound (ICUS) and the individual differences between U-CSA and A-CSA values.(ABSTRACT TRUNCATED AT 250 WORDS)     

Angina pectoris caused by coronary microvascular spasm

BACKGROUND: Microvascular angina can occur during exercise and at rest. Reduced vasodilator capacity of the coronary microvessels is implicated as a cause of angina during exercise, but the mechanism of angina at rest is not known. Our aim was to test the hypothesis that primary hyperconstriction (spasm) of coronary microvessels causes myocardial ischaemia at rest. METHODS: Acetylcholine induces coronary artery spasm in patients with variant angina. We tested the effects of intracoronary acetylcholine at graded doses in 117 consecutive patients with chest pain (at rest, during exertion, or both) and no flow-limiting (>50%) organic stenosis in the large epicardial coronary arteries. We also assessed the metabolism of myocardial lactate during acetylcholine administration in 36 of the patients by measurement of lactate in paired blood samples from the coronary artery and coronary sinus vein. FINDINGS: Of the 117 patients, 63 (54%) had large-artery spasm, 29 (25%) had microvascular spasm, and 25 (21%) had atypical chest pain. The 29 patients with microvascular spasm developed angina-like chest pain, ischaemic electrocardiogram (ECG) changes, or both spontaneously (two patients) or after administration of acetylcholine (27 patients) without spasm of the large epicardial coronary arteries. Testing of paired samples of arterial and coronary sinus venous blood showed that lactate was produced during angina attack in nine of 11 patients with microvascular spasm. There was more women (p<0.01) and fewer coronary risk factors (p<0.01) in patients with microvascular spasm than in those with large-artery spasm. INTERPRETATION: Coronary microvascular spasm and resultant myocardial ischaemia may be the cause of chest pain in a subgroup of patients with microvascular angina.     

Management of intracoronary thrombosis complicating percutaneous transluminal coronary angioplasty

With technological advances in equipment and increased experience of operators, the success rates of percutaneous transluminal coronary angioplasty (PTCA) now exceed 90%. However, acute periprocural occlusion continues to complicate approximately 6% of all procedures, and many of these occlusions are due to intracoronary (IC) thrombus. Patients at highest risk for this complication include those with acute ischemic syndromes or with angiographically apparent thrombus. These individuals may be candidates for the use of prolonged heparin infusions prior to dilatation, intracoronary thrombolytic therapy, or monoclonal antibody directed against the platelet glycoprotein IIb/IIIa receptor. All patients undergoing PTCA should receive adequate antiplatelet therapy, including aspirin, and heparin with dosing monitored by activated clotting times (ACT). In addition, some recommend the use of ionic contrast material. When IC thrombus accumulates following intervention, initial therapy should include IC nitroglycerin followed by a combination of redilatation and IC urokinase infusion. Prolonged balloon inflations may be useful, particularly with the use of autoperfusion catheters. Platelet glycoprotein IIb/IIIa receptor antagonists may prove to be beneficial in this situation as well. If the patient's clinical status deteriorates in spite of these measures, emergency coronary artery bypass graft surgery may be required.     

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

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

Therapy with nitroglycerin increases coronary vasoconstriction in response to acetylcholine

OBJECTIVES: The purpose of this study was to investigate whether therapy with nitroglycerin (GTN) would lead to abnormal coronary artery responses to the endothelium-dependent vasodilator acetylcholine. BACKGROUND: Nitroglycerin therapy is associated with specific biochemical changes in the vasculature that may lead to increased vascular sensitivity to vasoconstrictors. METHODS: Patients were randomized to continuous transdermal GTN, 0.6 mg/h (n = 8), or no therapy (n = 7), for 5 days prior to a diagnostic catheterization. Patients had similar risk factors for endothelial dysfunction. Quantitative angiography was performed in the morning to measure the mean luminal diameter of the left anterior descending coronary artery (LAD) in response to intracoronary acetylcholine (peak concentration, 10(-4) mol/liter). The transdermal preparation was removed from the GTN group, and 3 h later experimental procedures were repeated. RESULTS: In the morning, the GTN group experienced greater coronary constriction in response to acetylcholine infusion than those not receiving GTN (-19.6+/-4.2 vs. -3.8+/-3.0%; p = 0.01). Three hours later, the GTN group continued to display greater constriction to acetylcholine (-24.1+/-5.9%) as compared to the non-GTN group (-1.8+/-4.8%). When the morning and afternoon responses to acetylcholine were compared, the increase in coronary constriction in the GTN group was greater than the change observed in the non-GTN group (p < 0.05). CONCLUSIONS: This study demonstrates that therapy with GTN causes abnormal coronary vasomotor responses to the endothelium-dependent vasodilator acetylcholine, changes that were persistent for up to 3 hours after GTN discontinuation. This nitrate-associated vasomotor dysfunction has implications with respect to the development of nitrate tolerance and the potential for adverse events during nitrate withdrawal.     

Comparison of coronary microvascular response to nipradilol and nitroglycerin

Nitrovasodilators and beta-adrenoceptor antagonists are effective in the treatment of angina pectoris and hypertension, but each has side effects that may prevent their long-term use. In the present study responses of coronary arteries and arterioles to nipradilol, a beta-adrenoceptor antagonist with nitrovasodilator action, were compared to nitroglycerin in normal myocardium of the beating left ventricle in anesthetized dogs. Coronary arteries and arterioles were visualized using stroboscopic illumination of epicardial surface of the heart and intravital microscopy with fluorescence angiography. Diameters were measured under control conditions and during topical suffusion of nipradilol (10(-8)-10(-4) M) or nitroglycerin (10(-8)-10(-4) M). Nipradilol produced dose-dependent dilation of all size arteries and arterioles however, dilation was inversely related to vessel size. Arterioles less than 100 microns in diameter dilated more than arteries greater than 200 microns in diameter. In contrast, dilation to nitroglycerin was directly related to vessel size. Arteries larger than 200 microns dilated more than arterioles less than 100 microns. In conclusion, although nipradilol and nitroglycerin are both nitrovasodilators the microvascular response to these agents is different.     

Effect of intracoronary estrogen on coronary collateral blood flow velocity

The effect of estrogen on collateral circulation has not been previously investigated. We assessed the acute effect of estradiol on collateral blood flow velocity with the Flowire during percutaneous transluminal coronary angioplasty and found that intracoronary estradiol decreased collateral blood flow velocity compared with controls.     

Enhanced myosin light chain phosphorylations as a central mechanism for coronary artery spasm in a swine model with interleukin-1beta

BACKGROUND: Although coronary artery spasm plays an important role in a wide variety of ischemic heart diseases, the intracellular mechanism for the spasm remains to be clarified. We examined the role of myosin light chain (MLC) phosphorylations, a key mechanism for contraction of vascular smooth muscle, in our swine model with interleukin-1beta (IL-1beta). METHODS AND RESULTS: IL-1beta was applied chronically to the porcine coronary arteries from the adventitia to induce an inflammatory/proliferative lesion. Two weeks after the operation, intracoronary serotonin repeatedly induced coronary hyperconstrictions at the IL-1beta-treated site both in vivo and in vitro, which were markedly inhibited by fasudil, an inhibitor of protein kinases, including protein kinase C and MLC kinase. Western blot analysis showed that during serotonin-induced contractions, MLC monophosphorylation was significantly increased and sustained in the spastic segment compared with the control segment, whereas MLC diphosphorylation was noted only in the spastic segment. A significant correlation was noted between the serotonin-induced contractions and MLC phosphorylations. Both types of MLC phosphorylation were markedly inhibited by fasudil. In addition, MLC diphosphorylation was never induced by a simple endothelium removal in the normal coronary artery, whereas enhanced MLC phosphorylations in the spastic segment were noted regardless of the presence or absence of the endothelium. CONCLUSIONS: These results indicate that enhanced MLC phosphorylations in the vascular smooth muscle play a central role in the pathogenesis of coronary spasm in our swine model.