Functional behavior and morphology of the coronary artery wall in patients with Kawasaki disease assessed by intravascular ultrasound

Objectives. To examine the development of coronary artery lesions in Kawasaki disease, we assessed the functional behavior and morphology of coronary arteries by intravascular ultrasound.Background. Long-term follow-up studies of patients with Kawasaki disease have demonstrated the development of localized coronary stenoses even after aneurysms have regressed. It is also possible that angiographically normal coronary segments in patients with this disease may retain histologic changes.Methods. Twenty-three patients followed up by serial coronary angiography were examined at a mean age ± SD of 14.9 ± 2.9 years. The thickness of the intima-media complex was measured by intravascular ultrasound (30 MHz; 3.5 or 4.3F; 1,800 rpm). Coronary reactivity to nitroglycerin was determined by measuring percent changes in cross-sectional coronary artery area after intracoronary injection (7 μg/kg body weight) of this agent.Results. A remarkably thickened intima-media complex was observed at the sites with persisting (0.54 ± 0.20 mm, n = 19) and regressed (0.84 ± 0.40 mm, n = 23) aneurysms. Mild thickening of the intima-media complex was often observed even in angiographically normal segments (0.22 ± 0.05 mm, n = 31), in the left main coronary artery (0.47 ± 0.15 mm, n = 20) and at normal branches (0.36 ± 0.09 mm, n = 13). Coronary reactivity to nitroglycerin was significantly lower at the sites of regressed aneurysms (12.8 ± 6.6%, n = 9) than in normal segments (32.8 ± 10.9%, n = 13, p < 0.01), indicating the presence of functional impairment at the sites with regressed aneurysms. Decreased nitroglycerin reactivity was also observed in some segments without evidence of aneurysm.Conclusions. These results indicate that in patients with Kawasaki disease the coronary disease accompanying impaired reactivity to nitroglycerin is present at the sites of regressed aneurysms as well as in angiographically normal coronary segments. We suggest that these sites with morphologic and functional abnormalities are related to the development of significant stenosis.     

三磷酸腺苷负荷超声心动图和冠状动脉造影在川崎病远期随访中的价值

目的探讨三磷酸腺苷（adenosinetriphosphate，ATP）负荷超声心动图及冠状动脉造影（coronaryangiography，CAG）在川崎病（Kawasakidisease，KD）冠状动脉损害远期随访中的应用价值。方法对临床确诊的156例KD患儿于恢复期行ATP负荷超声心动图检查，其中15例患儿同时进行CAG。随访时间为自急性期后6个月至10年，按急性期冠状动脉损害程度分为冠状动脉瘤组、冠状动脉扩张组及冠状动脉正常组。结果恢复期ATP负荷超声检查结果显示，3组均有部分患儿存在不同程度的冠状动脉血流储备下降和（或）出现节段性室壁运动异常，其在冠状动脉瘤组和冠状动脉扩张组的发生率高于冠状动脉正常组，差异有统计学意义[75．00％（30／40）vs.44．29％（31／70）vs．21．74％（10／46），P〉0．01]。15例同时进行CAG与负荷超声检查的患者结果显示，两种检查方法的符合率为93．33％（Kappa=0．04，P=0．70）。结论CAG能较清楚地显示冠状动脉形态，但不能准确地提供冠状动脉血流动力学信息及冠状动脉微循环的情况；ATP负荷超声心动图检查能安全、可靠地评估冠状动脉血流动力学，补充冠状动脉造影的不足，可用于KD患儿冠状动脉损害的长期追踪随访以及药物疗效的判断。     

Does Passive Smoking Impair Endothelium-Dependent Coronary Artery Dilation in Women?

Objectives. This study sought to examine whether passive smoking is associated with endothelial dysfunction in the coronary arteries.Background. Long-term exposure to cigarette smoking has been reported to suppress endothelium-dependent arterial dilation in humans. Endothelial dysfunction is an early feature of atherogenesis, and the impairment of acetylcholine (ACh)-induced coronary artery dilation indicates coronary endothelial dysfunction.Methods. We studied 38 women (40 to 60 years old) who had no known risk factors for coronary artery disease other than tobacco smoking: 11 nonsmokers who had never smoked and had never been regularly exposed to environmental tobacco smoke; 19 passive smokers with self-reported histories of exposure to environmental tobacco smoke of ≥1 h/day for ≥10 years; and 8 active smokers. We examined the response of the epicardial coronary artery diameters (proximal and distal segments of the left anterior descending [LAD] and left circumflex [LCx] coronary arteries) to the intracoronary injection of ACh into the left coronary artery by means of quantitative coronary angiography.Results. ACh significantly dilated the distal segment in nonsmokers (percent change from baseline diameter: LAD 13.7 ± 3.4%, p < 0.05; LCx 18.8 ± 2.9%, p < 0.01) but not the proximal segment (LAD 7.4 ± 3.5%; LCx 3.1 ± 5.0%). ACh significantly constricted all segments of the left coronary artery in passive smokers (LAD: proximal −20.3 ± 3.7%, p < 0.05; distal −22.3 ± 4.1%, p < 0.01; LCx: proximal −20.8 ± 3.1%, p < 0.05; distal −17.3 ± 2.9%, p < 0.01) and active smokers (LAD: proximal −14.8 ± 3.4%, p < 0.05; distal −27.2 ± 6.0%, p < 0.01; LCx: proximal −14.5 ± 6.6%, p < 0.05; distal −22.4 ± 4.0%, p < 0.01). Thus, ACh constricted most coronary arteries in both passive and active smokers and dilated the coronary arteries in nonsmokers.Conclusions. Impairment of ACh-induced coronary artery dilation, indicating coronary endothelial dysfunction, may occur diffusely in passive smokers as well as in active smokers.     

Vitamin C attenuates abnormal vasomotor reactivity in spasm coronary arteries in patients with coronary spastic angina

Objectives. This study sought to examine effect of vitamin C, an antioxidant, on the abnormal vasomotor reactivity in spasm coronary arteries.Background. Oxygen free radicals generated in the arterial walls have been shown to cause endothelial vasomotor dysfunction.Methods. Responses of the epicardial arterial diameters of the left coronary arteries to the intracoronary infusion of acetylcholine (ACh) (10 and 50 μg/min) were measured by quantitative coronary angiography before and during combined intracoronary infusion of vitamin C (10 mg/min) or saline as a placebo in 32 patients with coronary spastic angina and in 34 control subjects.Results. Vitamin C infusion suppressed the constrictor response of the epicardial diameter to ACh in spasm coronary arteries but had no significant effect in the control coronary arteries (percent change in distal diameter in response to 10 μg/min of ACh [constriction (−), dilation (+), mean ± SEM] before vitamin C: −8.2 ± 2.9% in spasm arteries, +8.4 ± 2.9%1 in control arteries; during vitamin C: +0.2 ± 3.8%1 in spasm arteries, +7.2 ± 1.3%1 in control arteries [1p < 0.01 vs. spasm arteries before vitamin C]). The coronary sinus–arterial difference in plasma thiobarbituric acid reactive substances during ACh infusion, an indicator of lipid peroxidation in coronary circulation, was higher in patients with coronary spastic angina than in control subjects (p < 0.01) but was suppressed in patients with coronary spastic angina to comparable levels in control subjects by combined infusion of vitamin C. Saline infusion had no effect.Conclusions. The results indicate that vitamin C attenuates vasomotor dysfunction in epicardial coronary arteries in patients with coronary spastic angina. Oxygen free radicals may at least in part play a role in the abnormal coronary vasomotor reactivity in response to ACh in spasm coronary arteries.     

Clinical manifestations of coronary aneurysms in the adult as possible sequelae of Kawasaki disease during infancy

Coronary artery aneurysms are rare findings usually diagnosed incidentally at necropsy or at angiography in patients with symptoms of myocardial ischaemia. Even if atherosclerosis is a common cause of coronary aneurysms in the adult, other acquired diseases with inflammatory pathogenesis are associated with coronary artery aneurysms. We present three cases of patients with low probability of coronary artery atherosclerotic disease, due to their age, risk factors profile and history, complaining of chest pain suggestive of myocardial ischaemia and angiographic documentation of one or more coronary aneurysms. In all cases, although no patient had had a previous diagnosis of Kawasaki disease (KD), an unexplained febrile syndrome had occurred in childhood, which is compatible with misdiagnosed episode of KD causing the aneurysmatic lesions. The present reports highlight the potential clinical relevance of previously misdiagnosed KD in patients with ischaemic chest pain, low probability of atherosclerosis and coronary aneurysms.     

Fate of coronary aneurysms in Kawasaki disease: Serial coronary angiography and long-term follow-up study

Between January 1973 and December 1979, 290 patients with Kawasaki disease were evaluated with coronary angiography after the acute stage of illness. Of these patients, 43 (15 percent) were diagnosed as having coronary aneurysms. Forty-two patients have been followed up for an average of 4 years (range 15 months to 8 years). One 8 month old girl died of myocardial infarction after 4 months of illness. Follow-up coronary angiography was performed in 42 patients 5 to 18 months after the acute illness. Four groups can be distinguished. Group I: In 21 (50 percent) of 42 patients angiography showed that the coronary aneurysms had regressed, so that no observable lesions were seen. During convalescence, none of these patients experienced cardiac symptoms, and results of electrocardiography, exercise stress testing and thallium scintigraphy were within normal limits. In the other 21 patients abnormal findings persisted on follow-up angiography. Group II: Ten patients showed persistent coronary aneurysms, although reduced in size. Group III: In seven patients the aneurysms had disappeared, but complete obstruction or marked stenosis of coronary arteries was found. Group IV: In four patients, irregularities of the coronary arterial wall without stenosis were seen. Among patients with abnormal angiographic findings myocardial infarction and mitral regurgitation were also seen. Early initiation of aspirin therapy remains the mainstay in the prevention of thrombus formation. Coronary aneurysms show regression on angiography in 1 or 2 years in about half of patients. The remaining patients are at risk for ischemic heart disease. Thus, Kawasaki disease should be considered an important cause of ischemic heart disease in children and a possible risk factor of premature coronary atherosclerosis.     

Long term consequences of regressed coronary aneurysms after Kawasaki disease: vascular wall morphology and function

OBJECTIVES: To investigate the long term consequences of regressed aneurysms after Kawasaki disease, using follow up coronary angiography; to assess the vascular wall morphology at the site of the aneurysms by intravascular ultrasound imaging; and to evaluate the function of the affected vessels using intracoronary infusions of acetylcholine and isosorbide dinitrate. DESIGN: 33 patients were studied, 27 with previous Kawasaki disease and six with congenital heart disease. All Kawasaki disease patients were followed for more than 10 years from disease onset. The 33 patients comprised four groups: group 1 included 13 Kawasaki disease patients with a total of 23 sites of regressed large sized (>/= 4 mm) coronary aneurysms; group 2 included 13 Kawasaki disease patients with 22 sites of regressed small sized (< 4 mm) coronary aneurysms (four patients had sites of both large and small sized aneurysms); group 3 included a further five Kawasaki disease patients with 25 normal coronary angiography sites in the acute stage of Kawasaki disease; and group 4 comprised the six patients with congenital heart disease as controls, with a total of 27 normal coronary angiography sites. During coronary angiography, 15 microg of acetylcholine and 0.5 mg isosorbide dinitrate were infused into the coronary artery. The luminal diameter at the sites was measured using a cine-videodensitometric analyser, to assess the distensibility of the coronary artery wall. RESULTS: Coronary angiography in all 22 patients in groups 1 and 2 and in all the patients in group 3 was normal, with no stenoses and no irregularity of the arterial wall. However, the intravascular ultrasound imaging in groups 1 and 2 showed various degrees of the intimal thickening. In groups 1 and 2, there was significantly more vascular constriction with acetylcholine, and poorer dilatation with isosorbide dinitrate than in groups 3 or 4 (each p < 0.05, respectively). There was no difference between group 3 and group 4 in response to either acetylcholine or isosorbide dinitrate, CONCLUSIONS: There is evidence of persisting abnormal vascular wall morphology and vascular dysfunction at the site of regressed coronary aneurysms in patients with previous Kawasaki disease. These patients should be counselled to avoid potential risk factors for atherosclerosis, and long term follow up is needed into adult life.     

Maladie de Kawasaki de l’adulte

Kawasaki disease (KD) is a multisystemic vasculitis affecting mainly the skin, mucosa, and lymph nodes. Coronary artery aneurysms occur in 25% of patients but their prevalence is reduced to 4% in those patients treated with intravenous immunoglobulin (IVIg) within 10 days of illness onset. Interesting data recently published relate to physiopathology and diagnosis of the disease. Investigations identified an antigen-driven IgA oligoclonal response directed against cytoplasmic inclusions in KD tissues. An algorithm using laboratory tests and echocardiography has been recently proposed to improve early detection of incomplete KD. Although KD predominantly affects children, it may be also of interest for adult physicians. First, patients may develop long-term cardiovascular event. Coronary artery aneurysms may lead to the development of coronary stenosis or thrombosis. Despite the absence of coronary lesions during the acute phase of the disease, patients may present morphological and functional sequelae of coronary and peripheral arteries at convalescent phase. These potential arterial sequelae require long-term follow-up and treatment of associated cardiovascular risk factors. Although the level of injury seems to be correlated with the severity of initial coronary lesions, long-term course of vascular injuries is poorly known. Second, KD may occur in adults with 91 cases reported in the literature. Twenty-one cases have been reported in HIV infected patients. Intravenous immunoglobulins appear to shorten the disease course. Recent studies highlight the existence of incomplete KD and symptomatic coronary aneurysms in adults. Overall, these data suggest that adult patients with biological or echocardiographic features suggestive of incomplete KD should receive prompt IVIg to prevent coronary artery sequelae.     

Difference Between Persistent Aneurysm,Regressed Aneurysm,and Coronary Dilation in Kawasaki Disease: An Optical Coherence Tomography Study

Background

Coronary artery (CA) aneurysms are a serious complication of Kawasaki disease (KD). Conventional imaging techniques often described segments with regressed aneurysms as normal, whereas studies have shown significant endothelial dysfunction.

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

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

Findings in the pulmonary vascular bed in the remote phase after Kawasaki disease

Kawasaki disease (KD) is a form of systemic vasculitis that causes chronic changes in arterial walls, including pulmonary arteries. The aim of this study was to test the hypothesis that pulmonary arterial wall properties and hemodynamics are abnormal after the resolution of KD. Pulmonary arterial input impedance was measured during cardiac catheterization (4.8 ± 4.5 years after disease onset) in 47 consecutive patients (mean age 7.8 ± 5.7 years) with KD and coronary artery lesions (CALs) in the acute phase and 42 control patients (mean age 6.7 ± 4.6 years). Patients with KD were subdivided into 2 groups: 28 with persistent CALs and 19 with regressed CALs. There were no significant differences in characteristic impedance and peripheral vascular resistance between patients with KD and controls. Compared with controls, patients with persistent CALs had significantly lower pulmonary arterial compliance, suggesting increased wall stiffness of the peripheral pulmonary vascular bed (p <0.05, analysis of variance). Patients with persistent CALs also exhibited increased wave reflection compared with other groups (p <0.05, analysis of variance). In conclusion, unlike patients with regressed CALs, patients with persistent CALs have abnormal mechanical properties and hemodynamics of the pulmonary artery after KD. Together with previous reports of abnormal properties of coronary and systemic arteries, these data suggest that KD vasculitis causes chronic changes in arterial wall properties in the entire arterial system to varying degrees and extent. The fate of these abnormalities in the pulmonary bed and other arterial systems and their potential adverse effects must be monitored in long-term follow-up.     

急性冠脉综合征患者血清血小板源性生长因子表达的临床研究

目的：探讨急性冠脉综合征患者外周血及冠状动脉局部血清PDGF浓度与冠状动脉疾病严重程度的关系。方法：纳入2012年9月至2013年12月在南京医科大学第一附属医院心血管科行冠状动脉造影的急性冠脉综合征患者,并纳入同期因胸痛住院行冠状动脉造影且冠脉未见狭窄者最为对照组,收集各组患者临床资料,计算SYNTAX积分,通过ELSIA方法测定患者外周血及冠状动脉局部血清PDGF浓度;分析非冠心病组与冠心病ACS组、ACS患者不同亚组间血清PDGF浓度的差异,利用Pearson相关性分析血清PDGF浓度与SYNTAX积分的相关性。结果：与对照组比较,冠心病ACS组外周血PDGF浓度显著升高（723.29±679.53 vs 369.12.0±292.39,P＜0.05）;冠心病ACS组中AMI组外周血PDGF浓度较UAP组显著升高（758.36±714.56 vs 614.11±600.39,P＜0.05）。冠状动脉局部PDGF浓度较外周血PDGF浓度显著升高（911.89±735.41 vs 723.29±679.53,P<0.01）。Person相关分析显示外周血PDGF浓度与冠脉狭窄程度(SYNTAX评分)呈正相关关系(rho= 0.233,p<0.05)。随着血清PDGF浓度的升高,平均Syntax积分逐步升高,高浓度组Syntax积分高于低PDGF浓度组。结论：急性冠脉综合征患者血清PDGF浓度显著升高,尤其在冠状动脉局部PDGF呈现浓聚,血清PDGF浓度可反应冠状动脉病变的严重程度。     

载脂蛋白M与冠状动脉病变的关系

目的探讨冠心病患者血清载脂蛋白M水平与冠状动脉病变的关系。方法根据冠状动脉造影结果,将120例受试者分为冠心病组(73例)和对照组(47例),应用酶联免疫吸附法检测受试者血清载脂蛋白M水平。比较冠心病组与对照组血清载脂蛋白M水平;比较不同冠状动脉病变数量和狭窄程度血清载脂蛋白M水平。结果冠心病组患者血清载脂蛋白M水平(10.12±1.79 mg/L)明显低于对照组(11.69±2.02 mg/L,P<0.01);冠心病患者多支病变组载脂蛋白M水平(9.19±1.22 mg/L)明显低于单支病变(11.22±1.69 mg/L)和双支病变(10.36±1.94 mg/L)组(P均<0.01);轻度狭窄组(11.39±1.58 mg/L)、中度狭窄组(10.14±1.46 mg/L)及重度狭窄组(9.04±1.30 mg/L)载脂蛋白M水平逐渐降低(P<0.05);冠状动脉病变数量(r=-0.485)和狭窄程度(r=-0.508)与血清载脂蛋白M水平呈负相关(P均<0.01)。结论载脂蛋白M可能是抑制动脉粥样硬化的保护因子。     

Coronary artery aneurysms in a young patient with acute myocardial infarction: a case report

Coronary artery aneurysms are not uncommon. They are usually arteriosclerotic in origin, and may be congenital or secondary to injury, dissection, infection, inflammation, or Kawasaki disease (KD). Herein, we report a case involving a 25-year-old male smoker with acute myocardial infarction (AMI). Coronary angiography showed triple-vessel disease, coronary artery aneurysms, and diffuse ectasia. Coronary artery bypass grafting was performed without complications. Based on his history, serologic examinations, and angiographic findings, we suspected that his coronary artery aneurysms and ectasia were the adult sequelae of KD. This case is a good reminder that KD victims may suffer from young-onset AMI.     

心电图有心肌缺血改变而冠状动脉造影正常者的冠状动脉血流的意义

目的　以计帧法评价心电图有心肌缺血改变而冠状动脉造影正常者的相关冠状动脉血流的意义。方法　静息心电图或踏板运动试验 (treadm ill test,TMT)有缺血改变 (连续 2个以上相关导联 ST段水平型或下斜型压低≥0 .0 5 m V或 T波深倒置 )但冠状动脉造影正常的 19例患者为缺血组。有心绞痛样症状而静息心电图、踏板运动试验以及冠状动脉造影正常的 5 2例为对照组。测定缺血相关性冠状动脉血流心肌梗死溶栓治疗试验 (thrombolysisin myocardial infarcton,TIMI)计帧值 (frame count,TIMI- FC)。结果　缺血组心电图示前壁心肌缺血者的冠状动脉前降支血流和下壁缺血者的右冠状动脉血流以及高侧壁缺血者的左回旋支血流的 TIMI- FC值显著大于对照组(分别为 35 .3± 16 .1vs19.9± 13.7,P<0 .0 5 ;38.9± 11.7vs2 1.7± 14 .1,P<0 .0 5及 35 .9± 16 .7vs.14 .1± 9.5 ,P<0 .0 1) ;TIMI- FC测定结果以 <2 7为血流正常 ,≥ 2 7为血流缓慢。血流缓慢 (slow coronary flow,SCF)者 2 2例 ,血流正常 (norm al coronary flow,NCF)者 4 9例。SCF者中心电图有缺血改变的患者 (15例 ,6 8.2 % )显著多于 NCF者中心电图有缺血的患者 (4例 ,8.2 % ) ;NCF者中心电图正常者 (4 5例 ,91.8% )显著多于 SCF者中心电图正常者(7例 ,     

冠状动脉病变程度与估算肾小球滤过率的相关性

【摘要】 目的 研究冠状动脉病变程度与估算肾小球滤过率的相关性。方法 将在煤炭总医院心内科行冠状动脉造影的425例患者根据冠状动脉造影结果分为非冠心病组、冠状动脉单支病变组、冠状动脉双支病变组和冠状动脉三支病变组,收集患者的临床资料和相关生化检查指标,采用改良MDRD公式计算估算肾小球滤过率(eGFR),探讨冠状动脉病变程度与估算肾小球滤过率的相关性。结果 冠状动脉三支病变组血肌酐明显高于冠状动脉单支病变组,差异有统计学意义(123.72±165.88 vs 73.26±21.18, P<0.05);冠状动脉三支病变组eGFR低于冠状动脉单支病变组和冠状动脉双支病变组,差异有统计学意义(85.23±34.73 vs 98.33±34.62, 85.23±34.73 vs 96.30±32.84, P<0.05)。logistic回归分析显示：与冠脉双支病变相比eGFR与冠脉三支病变呈负相关(OR=0.987,95％CI 0.977-0.997,P= 0.014);与冠脉单支病变相比,血肌酐与冠脉三支病变呈正相关(OR=1.022,95％CI 1.003-1.040,P= 0.021)。结论 与冠脉双支病变相比,eGFR降低为冠脉三支病变的独立危险因素。肾功能不全与冠状动脉病变严重程度密切相关。     

经皮桡动脉冠状动脉造影及冠状动脉成形术的临床应用

目的 :评价经皮桡动脉冠状动脉造影术与冠状动脉腔内成形术 (PTCA)的临床应用价值。方法 :有选择性的对 37例患者行经皮桡动脉途径冠状动脉造影及冠状动脉成形术 ,观察其疗效和血管并发症。结果 :1 桡动脉穿刺成功率为 93 8% (有 2例失败 )。 2 14例冠状动脉造影正常 ,17例冠状动脉造影显示 2 6处存在≥ 70 %的狭窄病变 ,适合行冠状动脉介入手术。 2 6处病变有 4处PTCA疗效满意 ,2 2处行PTCA +支架术 ,植入支架 31只。狭窄从 (81± 12 ) %降低至 (10 6± 7 4 ) % ,最小血管直径由 (0 86± 0 12 )mm增加至 (3 0 8± 0 32 )mm。 6例病人行冠状动脉旁路移植术。 3 所有患者术后即拔导管鞘 ,局部压迫 4h。术后并发症的发生率为 3 3% (1例术后的桡动脉闭塞 )。结论 :经桡动脉途径行冠状动脉造影及冠状动脉成形术安全可行 ,其具有穿刺部位出血少、住院时间短的特点 ,可选择性的应用于某些冠心病患者。     

Effects of chronic obstructive pulmonary disease on coronary atherosclerosis

The chronic systemic inflammation and oxidative stress are important features in chronic obstructive pulmonary disease (COPD). Atherosclerosis is accepted as an inflammatory disease. Both local and systemic inflammation and oxidative stress negatively affect the atherosclerotic process. Metabolic alterations, systemic inflammation, and neurohormonal activation frequently occur in patients with COPD. However, the impact of COPD on intensity and severity of atherosclerosis and morphology of stenotic lesions in patients with established coronary artery disease by coronary angiography is unknown. Eighty-eight patients who were diagnosed with COPD disease were enrolled in the study. Eighty-two patients without any pulmonary disease were included in the control group. Coronary angiography and blood gases analysis were performed in all patients. Gensini score and Extent score were used to evaluate the intensity and severity of atherosclerosis. Lesion morphologies were defined in all patients. The mean number of affected coronary arteries was 2.5 ± 0.6 in the COPD group and 2.1 ± 0.7 in the control group (P = 0.004). The mean Extent score was 37 ± 16 in the COPD group and 23 ± 11 in the control group (P = 0.001). The Gensini score in the COPD group was significantly higher than that in the control group (respectively 10.9 ± 6.3 vs 6.6 ± 4.1, P = 0.01). The number of critical lesions, and type B and C lesions were higher in the COPD group. Multivariate analysis demonstrated that COPD was independently predictive for Gensini score (odds ratio 1.371; 95% confidence interval 1.682–9.228; P = 0.002) and Extent score (odds ratio 1.648; 95% confidence interval 2.023–13.339; P = 0.001). Severity and intensity of atherosclerosis increases in COPD and atherosclerotic lesions have worse morphological properties in COPD.     

Aneurysms of the common trunk, anterior descending and right coronary artery in a 33 years old man with acute myocardial infarction. A case report

Coronary artery aneurysms are often incidental findings during coronary angiography; they are mostly secondary to atherosclerosis or vasculitis, they are rarely congenital. Right coronary circumflex and anterior descending arteries are usually involved but only few cases of aneurysms of left main coronary artery are reported. A case of coronary artery aneurysms is described involving left main, right and anterior descending coronary arteries, probably secondary to atypical Kawasaki disease in a 33 years old man with acute myocardial infarction.     

Repeated quantitative angiograms in coronary arterial aneurysm in Kawasaki disease

Accurate evaluation of the extent of coronary artery lesions complicating Kawasaki disease is clinically important in patient management. Based on a total of 188 coronary angiograms and retrospective follow-up observations, the condition of coronary aneurysms was quantitatively graded as: 0 (normal)—no significant enlargement in any portion of the coronary artery; I (mild)—aneurysmal dilatation of the coronary artery evident but localized, with a maximal diameter of less than 4.0 mm; II (moderate)—maximal diameter of coronary aneurysms between 4.0 and 8.0 mm, regardless of body size; III (severe)—giant aneurysms, with the maximal diameter greater than 8.0 mm. Most mild coronary aneurysms regressed to normal within a short time, and the patient's prognosis was good. The course of grade II aneurysms varied, depending on initial angiographic coronary diameter, but all were eventually reduced in coronary size. In contrast, grade III aneurysms usually progressed to become obstructive or stenotic coronary lesions, or the large aneurysm persisted. Follow-up observations revealed that the course of coronary artery disease depended on the size and distribution of aneurysms at initial angiography. This grading of the severity of coronary lesions may provide useful criteria for predicting the prognosis of patients with Kawasaki disease.