Endothelial function in conduit and resistance arteries in men with coronary disease

The aims of this study were to determine whether non-invasive measurement of endothelial function in conduit arteries reflects that of subcutaneous resistance arteries measured in vitro and to examine whether there is an endothelial dysfunction also in resistance arteries in patients with a previous myocardial infarction. The brachial artery diameter responses to a hyperemic flow stimulus and an in vitro method, pressure myography, to directly evaluate flow-mediated responses in arteries obtained from biopsies of subcutaneous fat were measured in 25 patients with a previous myocardial infarction and in 8 aged matched healthy subjects. Flow-mediated dilatation of the brachial artery was more pronounced in the healthy group compared with the group with coronary disease, 5.1 +/- 2.5% and 2.6 +/- 2.1%, respectively (p < 0.05). The flow-mediated dilatation in subcutaneous arteries from CHD patients was significantly reduced compared to control subjects (e.g. percent change from initial preconstriction at maximum flow rate of 204 microl/min: 42 +/- 7% CHD (n = 25) versus 84 +/- 24% control (n = 8), ANOVA, p = 0.03). There was a significant correlation between flow-mediated dilatation of the brachial artery and maximum flow-mediated dilatation at microvascular level, (p < 0.01). In conclusion this study demonstrates endothelial dysfunction in both conduit and resistance circulation in patients after myocardial infarction compared to an aged-matched healthy control group. Furthermore, a significant and independent relationship between endothelial function by means of flow-mediated dilatation in large conduit arteries and resistance arteries was observed.     

Brachial reactivity and extent of coronary artery disease in patients with first ST-elevation acute myocardial infarction

We examined peripheral endothelial function, as measured by brachial artery reactivity, in 49 stable patients with a first episode of acute ST-segment elevation myocardial infarction to examine the relation between extent of coronary disease and peripheral vascular reactivity. Brachial artery reactivity was assessed by ultrasound and flow-mediated dilation (FMD) was calculated as the change in brachial artery diameter after release of suprasystolic blood pressure cuff inflation. FMD was classified as abnormal in (< or =6%) 19 patients (group 1) and as normal in 30 patients (group 2). Average FMDs were 2 +/- 2% in group 1 and 11 +/- 4% in group 2. Patients in group 1 were older (62 +/- 5 vs 54 +/- 11 years, p = 0.02) and more often had a history of hypertension (n = 10, 52%, vs 6, 20%, p = 0.017). Patients with abnormal endothelial function (group 1) had a larger number of coronary obstructive (>or =50%) lesions (3.6 +/- 2.4 vs 2.0 +/- 1.7, p = 0.01) and more extensive coronary disease (1.9 +/- 0.8 vs 1.4 +/- 0.8 vessel disease, p = 0.05). In patients with 3-vessel disease, FMD was lower (4.0 +/- 1.8% vs 8.2 +/- 0.8%, p = 0.04) than in those with lesser coronary involvement. In conclusion, in patients with a first episode of ST-segment elevation myocardial infarction, there was a strong correlation between extent of coronary artery disease and brachial artery reactivity. Patients with localized coronary disease had relatively normal brachial reactivity, whereas those with diffuse coronary disease had more severe abnormal brachial artery reactivity.     

The effects of atorvastatin on coronary endothelial function in patients with recent myocardial infarction

BACKGROUND: Endothelial dysfunction is a key early event in atherosclerosis that occurs in acute coronary syndrome. It was reported that atorvastatin improves the endothelial function of skeletal muscle vessels, but the effect on the coronary artery is unknown. HYPOTHESIS: The purpose of this study is to determine the effects of atorvastatin on coronary endothelial function in humans. METHODS: Non-infarct-related coronary arteries of 48 patients with acute myocardial infarction who had undergone successful percutaneous transluminal coronary angioplasty were examined. Three groups were studied: hyperlipidemia with use of atorvastatin (Group 1, n=17), hyperlipidemia without statin use (Group 2, n=18), and normal cholesterol level controls (Group 3, n=13). Statin treatment was started at discharge. Acetylcholine (Ach) was infused into the coronary artery and the diameter was assessed by quantitative angiography at baseline and after 6 months. RESULTS: Acetylcholine given in doses of 1, 3, 10, and 30 mg/min increased the coronary artery diameter change in a dose-dependent manner. In the initial study, patients in the three groups had similar responses to Ach. The mean diameter change after 6 months was significantly improved in Group 1 compared with Groups 2 and 3 (-11 +/- 3% vs. -20 +/- 7% and -21 +/- 6%, respectively; p < 0.01 in each case). Multivariate regression analysis showed that atorvastatin (p < 0.01) was the significant determinant for improvement of endothelial function. CONCLUSIONS: These findings suggest that atorvastatin improves endothelial function of the coronary artery in patients with myocardial infarction.     

Relation of vasodilator response of the brachial artery to inflammatory markers in patients with coronary artery disease

Endothelial dysfunction of the coronary artery is closely related to elevated levels of systemic inflammatory markers and cardiovascular events in patients with coronary artery disease (CAD). We hypothesized that patients with CAD may have a higher risk of endothelial dysfunction of the peripheral artery than patients without evidence of CAD, and that endothelial dysfunction of the peripheral artery also may be related to elevated levels of inflammatory markers. Using high resolution ultrasound, we assessed the brachial vasodilator response to reactive hyperemia (endothelium-dependent) and sublingual nitroglycerin (endothelium-independent). As inflammatory markers, serum C-reactive protein (CRP), erythrocyte sedimentation rate (ESR) levels, and lipid profiles were measured in patients with CAD (n = 30, 16 male and 14 female) and normal subjects without evidence of CAD (n = 45, 23 male and 22 female). Patients with CAD (Group II) showed a significantly reduced endothelium-dependent vasodilation as compared with normal subjects (Group I) (4.4 +/- 3.6 vs 7.4 +/- 6.1%, P < 0.05). However, endothelium-independent vasodilation was not significantly different between the two groups (7.7 +/- 7.1 vs 9.7 +/- 8.0%, P > 0.05). In Group II, CRP level was inversely related to endothelium-dependent vasodilation (r = -0.398, P = 0.029). In contrast, ESR level was not significantly associated to endothelium-dependent vasodilation (r = -0.113, P = 0.552). On multivariate analysis, CRP and low density lipoprotein cholesterol levels were significant independent predictors of a blunted endothelium-dependent vasodilation in Group II. Our study showed that elevated CRP level was associated with blunted endothelium-dependent vasodilation of the brachial artery in patients with CAD. Thus, identification of elevated CRP levels combined with demonstration of endothelial dysfunction of the brachial artery may have a possible clinical application for the detection of high risk CAD patients.     

Cardiovascular risk factor profiles and endothelial function in coronary artery disease patients treated with statins.

Although endothelial dysfunction is associated with cardiovascular risk factors and is improved by cholesterol-lowering therapy, the relationship between endothelial function and cardiovascular risk factor profiles has not been fully investigated in coronary artery disease patients who have been treated with statins. We investigated endothelial function in male hypercholesterolemic patients (n=53) who underwent statin therapy over 6 months in a cross-sectional study. Patients were classified into three groups based on the results of coronary angiography: a normal coronary artery group (n=15), an angina pectoris group (n=20) and a myocardial infarction group (n=18). Endothelial function was assessed by measuring flow-mediated dilatation after reactive hyperemia in the brachial artery, and serum lipid, lipoprotein (a), glucose and insulin levels were measured. Significant associations were observed between the status of coronary disease and systolic blood pressure, lipoprotein (a), glucose and insulin levels (p <0.05, respectively), and the levels of these risk factors in the myocardial infarction group were higher than those in the other groups. Flow-mediated dilatation was also associated with the status of coronary disease (p <0.05), and the myocardial infarction group showed the lowest levels of flow-mediated dilatation (p <0.05). Flow-mediated dilatation was negatively correlated with systolic and diastolic blood pressures, serum levels of lipoprotein (a), glucose and insulin, and the status of coronary disease. Stepwise multiple regression analysis also revealed that lipoprotein (a), diastolic blood pressure and the status of myocardial infarction were significantly correlated with impaired vasodilatation. Serum lipids, age and smoking habit were independent of flow-mediated dilatation. In conclusion, even after cholesterol-lowering treatment, male patients with myocardial infarction still had endothelial dysfunction, and higher levels of lipoprotein (a) may be associated with endothelial dysfunction in such patients.     

Involvement and function of the right ventricle in acute myocardial infarct. Hemodynamic, echocardiographic and angioscintigraphic correlations

To assess the acute effects of myocardial infarction on right ventricular function 22 patients were studied utilizing right heart catheterization, radionuclide angiography and two dimensional echocardiography. Thirteen patients had inferior myocardial infarction (Group I) and 9 anteroseptal or anterior (Group II). Hemodynamic findings suggesting right ventricular infarction were present in 3 patients of Group I. Mean radionuclide right ventricular ejection fraction was lower in inferior myocardial patients (38.2 +/- 7.6-Group I vs 50.3 +/- 11.4-Group II, p less than 0.005), while left ventricular ejection fraction in anteroseptal, and anterior myocardial infarction patients (36.8 +/- 10.5-Group II vs 55.9 +/- 7.6-Group I, p less than 0.001). Six patients in Group I presented a depressed radionuclide right ventricular ejection fraction (less than 40%): moreover right ventricular ejection fraction correlated with left ventricular ejection fraction in Group II (r = 0.79, p less than 0.001) but not in Group I (r = 0.55, p = NS). By mean of 2 dimensional echocardiography Group I patients had an increased right ventricular end diastolic area (15.3 +/- 3.8 vs 12.1 +/- 1.2 cm2, p less than 0.05) while Group II an increased right ventricular free wall motion (47.3 +/- 10.7 vs 32.4 +/- 14.1%, p less than 0.005); right ventricular end diastolic area correlated with right ventricular ejection fraction only in Group I (r = 0.60, p less than 0.05). Five patients in Group I and no patients in Group II had an enlarged right ventricular end diastolic area. Therefore, radionuclide and echocardiographic evidence of right ventricular involvement were not always associated with abnormal hemodynamics. Thus, the damaged right ventricular chamber dilates to allow an adequate stroke volume in presence of low ejection fraction; hemodynamic significant right ventricular myocardial infarction becomes evident only in patients with more severe right ventricular compromise; the increase in right ventricular free wall motion in anterior myocardial infarction patients compensates the loss of contribution of interventricular septum contraction.     

Impact of left ventricular ejection fraction on endothelial function in patients with coronary artery disease

BACKGROUND: Endothelial dysfunction is present in patients with coronary artery disease (CAD) or with congestive heart failure. HYPOTHESIS: This study was performed to evaluate the impact of systolic heart function on endothelial function in patients with CAD. METHODS: The study population consisted of 283 consecutive patients (mean age 59 years, 176 men) undergoing coronary angiography. Endothelial function was assessed by measuring flow-mediated vasodilation (FMD) of the brachial artery. RESULTS: Patients (n = 236) with an ejection fraction (EF) > or = 55% on routine echocardiogram were younger (mean age 58 vs. 62 years), showed a lower prevalence of diabetes (15 vs. 38%) and myocardial infarction (13 vs. 66%), and showed a higher FMD (4.8 +/- 2.4 vs. 4.0 +/- 2.0%, p < 0.05) than patients (n = 47) with an EF < 55%. The correlation coefficient between FMD/endothelial function and EF/systolic heart function was 0.149 (p < 0.02) in the overall study population. Multivariate analysis showed that of age, gender, frequency of diabetes mellitus, myocardial infarction, and CAD extent, EF was the only significant independent parameter correlating with FMD in patients with CAD. CONCLUSIONS: Compared with the other tested risk factors, EF surprisingly was the only significant independent parameter correlating with endothelial function in patients with CAD. Our results support the view that endothelial function is an independent prognostic factor in patients with CAD.     

TNF-alpha blockade induces a reversible but transient effect on endothelial dysfunction in patients with long-standing severe rheumatoid arthritis

Considerable evidence indicates that patients with rheumatoid arthritis (RA) are at greater risk of developing atherosclerosis and cardiovascular disease. Recent studies support the predictive ability of endothelial function measures for subsequent atherosclerotic events. We have investigated the effects of infliximab, a chimeric monoclonal anti-tumor necrosis factor (TNF) antibody, on endothelial vasodilation, measured by brachial ultrasonography and on the levels of inflammatory biomarkers and adhesion molecules in ten consecutive patients with severe long-standing RA, despite methotrexate therapy, during the loading phase of infliximab therapy. Flow-mediated dilation (FMD) in RA patients at baseline was significantly impaired compared with healthy controls (7.71 +/- 2.78% vs 14.91 +/- 6.41%; p = 0.008) and improved significantly after infliximab infusion (12.63 +/- 1.63% vs 7.71 +/- 2.78%; p = 0.005). At baseline, a statistically significant correlation between C-reactive protein levels and FMD was found (r = -0.69, p = 0.026). However, this improvement was transitory, as FMD values returned to baseline values before each infliximab infusion at weeks 2, 6 and 14. There were no significant differences in baseline brachial artery diameter between visits, although at each time, the diameter was increased. According to European League Against Rheumatism response criteria, all ten patients were good responders. No significant differences were observed in intercellular cell adhesion molecule-1, vascular cell adhesion molecule-1, vascular endothelial growth factor and E-selectin plasma levels before and after each infusions. This study demonstrates that endothelial dysfunction is a reversible phenomenon in RA. The addition of anti-TNFalpha treatment reduces inflammatory symptoms in patients with severe RA. The improvement of endothelial function during the loading phase of therapy is transitory, suggesting an enhanced and persistent TNF-alpha generation within the arterial wall.     

Impaired endothelial function in patients with rapidly stabilized unstable angina: assessment by noninvasive brachial artery ultrasonography.

BACKGROUND: Endothelial dysfunction may contribute to symptoms of instability in patients with acute coronary syndromes. High-resolution external ultrasound assessment of the brachial artery responses allows noninvasive determination of endothelial function. HYPOTHESIS: This study was conducted to assess endothelial function in patients with unstable angina using a noninvasive technique. METHODS: We studied 189 patients who were subdivided into three groups. Group 1: 60 apparently healthy subjects with no cardiovascular risk factors or symptoms of coronary artery disease; Group 2: 105 subjects with cardiovascular risk factors--arterial hypertension, hypercholesterolemia, cigarette smoking, diabetes, and obesity, but no evidence of coronary artery disease; and Group 3: 24 patients with unstable angina (chest pain at rest within the 24 h preceding study entry). All patients underwent pre- and postischemic brachial artery test evaluation with measurements of internal arterial diameters and blood flow. RESULTS: Results are expressed as percentage change from basal values. Subjects in Groups 1 and 2 showed a diameter increase of 19.1 and 11.9%, respectively, whereas patients in Group 3 showed a diameter change of 1.2% (p < 0.002 and < 0.0001, respectively). Calculated blood flow did not differ significantly in Groups 1 or 2 (74.4 and 56.4%), but was notably lower in Group 3 (18.4%, p < 0.005 vs. Groups 1 and 2). In nine patients of Group 3, the brachial studies were repeated 4 weeks after symptom stabilization and showed values comparable with those in Group 2. CONCLUSIONS: Patients with unstable angina showed endothelial dysfunction compared with control individuals. It is of interest that in patients whose symptoms were stabilized by medical therapy, endothelial function was restored 4 weeks after hospital discharge.     

Predictive value of noninvasively determined endothelial dysfunction for long-term cardiovascular events and restenosis in patients undergoing coronary stent implantation: a prospective study

BACKGROUND: Endothelial dysfunction plays a key role in atherosclerosis and predicts future cardiovascular events in individuals with or without coronary artery disease and improves with risk reduction therapy. We sought to determine the predictive value of endothelial dysfunction for long-term cardiovascular events and in-stent restenosis in patients undergoing percutaneous coronary intervention (PCI). METHODS: Using high-resolution ultrasound, we assessed endothelial function by using the brachial artery flow-mediated dilation (FMD) method in 135 patients with coronary artery disease before elective coronary stenting. Patients were prospectively followed up for an average of 12 months after PCI. RESULTS: Thirty patients had an event during follow-up including cardiac death (four patients), myocardial infarction (nine patients), unstable angina/non-ST elevation myocardial infarction (15 patients), and stroke (two patients) and in-stent restenosis was determined in 16 of these patients. Endothelium-dependent FMD was significantly lower in patients who had an event compared with those without an event (4.7+/-1.9 vs. 6.0+/-2.0%, P=0.007), whereas endothelium-independent vasodilation to nitroglycerin was similar in both groups. FMD was the only predictor of cardiovascular events (P=0.03). Impaired endothelial function was associated with a significantly higher incidence of cardiovascular events and in-stent restenosis by Kaplan-Meier analysis. When a cutoff point of 7.5% was used, flow-mediated dilation had a sensitivity of 93%, specificity of 37%, and negative predictive value of 95% for cardiovascular events. CONCLUSION: Impaired brachial artery FMD is associated with long-term cardiovascular events and in-stent restenosis in patients undergoing PCI. Noninvasive assessment of endothelial function may serve as a surrogate marker for the estimation of future cardiovascular event risk and long-term follow-up in these patients.     

Myocardial infarction in young women: apropos of 22 cases. Pathogenic and prognostic approach]

The authors report 22 cases of myocardial infarction documented by selective left ventriculography and coronary angiography in women under 45 years of age. The average age in this series was 36 +/- 6.8 years. Two patient groups were identified: Group I (n = 16) with the cardiovascular risk factor of oral contraception (mean age 33.9 +/- 5 years); and Group II (n = 6) comprising older patients (43.8 +/- 1.8 years) with a high prevalence of other risk factors (hyperlipidaemia, hypertension, diabetes). Myocardial infarction tended to be the inaugural event in Group I (9 out of 16 cases, 56.2%) whereas symptoms of effort angina were commonly observed in Group II (5 out of 6 cases, 83.3%). Coronary angiography showed more severe coronary lesions in Group II (score 1.5) than in Group I (score 0.75) in which isolated, single vessel disease mainly affecting the left anterior descending artery or normal coronary angiography was observed. Thrombolytic therapy was performed in 8 patients: percutaneous transluminal angioplasty was performed in 4 patients in the first month with a primary success in 3 cases. Coronary bypass surgery was performed in 1 case. The outcome during follow-up lasting 44.5 +/- 4.2 months was mainly favourable as 15 of the 20 patients had no secondary complications. Nevertheless, 2 patients died in the hospital period (1 from cardiogenic shock and 1 from complications of transluminal coronary angioplasty), 2 patients died less than 1 year after acute myocardial infarction (1 sudden death, 1 cardiogenic shock). Although oral contraception was withdrawn in all cases, many women continued to smoke.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of folic acid on endothelial function following acute myocardial infarction

The aim of this study was to test the influence of high-dose folic acid (10 mg/d) on endothelial function in patients referred for coronary intervention after an acute myocardial infarction (AMI) and determine its relation to homocysteine levels. Flow-mediated dilation (FMD) of the brachial artery was performed in 40 patients after AMI (16 with normal homocysteine levels and 24 patients with elevated levels [>11 micromol/L]). Subjects were randomized to receive first folic acid (10 mg/day; group A) or placebo (group B) for 6 weeks in a double-blind crossover trial with a 2-week washout. Plasma folate, total homocysteine and its subtypes (oxidized, reduced, and protein-bound), FMD, and nitroglycerin-mediated dilation were assessed at baseline and at 6 and 14 weeks. In group A, folic acid improved FMD from 3.98 +/- 0.35% to 6.44 +/- 0.56% (p <0.001). This effect persisted after the crossover with placebo (5.42 +/- 0.59, p = 0.13). In group B, placebo did not increase FMD (4.01 +/- 0.34% vs 4.46 +/- 0.38, p = 0.38); however, a significant increase was observed in the second active treatment period (6.49 +/- 0.56%, p = 0.005). In both groups, improved FMD neither correlated with basal levels of homocysteine and its subtypes nor with changes induced during the folate treatment. Nitroglycerin-mediated dilation did not change significantly in either group. Folic acid increased FMD in both normo- and hyperhomocysteinanemic groups (p = 0.006 and p <0.001). In conclusion, 6-week treatment with high-dose folic acid improves endothelial function in post-AMI patients, independent from homocysteine status. Folic acid can be recommended to improve postinfarction endothelial dysfunction in patients with normo- and hyperhomocysteinemia.     

Effects of exercise rehabilitation on endothelial reactivity in older patients with peripheral arterial disease

Peripheral arterial disease (PAD) is a major cause of morbidity and mortality. Endothelial function, which is a measure of vascular health, is impaired in patients with PAD. We examined the effects of 6 months of aerobic exercise rehabilitation on brachial artery endothelial function, assessed using high-frequency ultrasonography, and calf blood flow in 19 older PAD patients (age 69 +/- 1 years, mean +/- SEM) with intermittent claudication (ankle to brachial artery index of 0.73 +/- 0.04). After exercise, the time to onset of claudication pain increased by 94%, from 271 +/- 49 to 525 +/- 80 seconds (p <0.01), and the time to maximal claudication pain increased by 43%, from 623 +/- 77 to 889 +/- 75 seconds (p <0.05). Exercise rehabilitation increased the flow-mediated brachial arterial diameter by 61%, from 0.18 +/- 0.03 to 0.29 +/- 0.04 mm (p <0.005), as well as the relative change in brachial arterial diameter from the resting state by 60%, from 4.81 +/- 0.82% to 7.97 +/- 1.03% (p <0.005). Maximal calf blood flow (14.2 +/- 1.0 vs 19.2 +/- 2.0 ml/100 ml/min; p = 0.04), and postocclusive reactive hyperemic blood flow (9.8 +/- 0.8 vs 11.3 +/- 0.7 ml/100 ml/min; p = 0.1) increased 35% and 15%, respectively. In conclusion, exercise rehabilitation improved ambulatory function, endothelial-dependent dilation, and calf blood flow in older PAD patients with intermittent claudication.     

Patency of the artery responsible for myocardial infarction: role on ventricular function and long-term outcome]

Out of 3,171 consecutive patients referred for coronary angiography, 240 were selected on the following criteria: recent primary myocardial infarction, single vessel coronary disease, no angioplasty or coronary surgery after the angiography which was performed 20 to 90 days after the onset of myocardial infarction. The patients were divided into 2 groups according to whether the artery responsible for infarction was patent (Group I: 115 patients) or not (Group II: 125 patients). The left ventricular ejection fraction was significantly higher in Group I (58 +/- 10.8%) than in Group II (53.7 +/- 11.3%) and end systolic and end diastolic left ventricular volumes were greater in Group II (51.8 +/- 22 ml/m2 and 88 +/- 22 ml/m2 respectively). Long-term follow-up (56 +/- 25 months in Group I and 61 +/- 26 months in Group II) was possible in 112 patients in Group I and 123 patients in Group II. Of the 7 patients who died in group II, 4 deaths were of cardiac origin; in addition, 2 cases of sustained ventricular tachycardia were observed in this group. None of the 6 deaths observed in Group I was of cardiac origin and there were no cases of ventricular tachycardia (p = 0.05). The functional status was identical in the two groups at the end of the study. These results suggest that the patency of the coronary artery responsible for myocardial infarction at a distance from the acute event is associated with better left ventricular function and a better long term prognosis.     

Evaluation by high-resolution ultrasonography of endothelial function in brachial artery after Kawasaki disease and the effects of intravenous administration of vitamin C.

Previous studies in patients with a history of Kawasaki disease (KD) have focused on the endothelial function of the coronary arteries and that of the systemic arteries is not fully understood. Furthermore, the effect of vitamin C on systemic vascular endothelial function after KD has not yet been elucidated. In the present study, 39 patients (age, 7.1 +/- 2.7 years) at 1-10 years after acute KD were compared with 17 matched healthy subjects (7.0 +/- 3.1 years). High-resolution ultrasonography was used to analyze brachial artery responses to reactive hyperemia (with increased flow causing endothelium-dependent dilation) and sublingual nitroglycerin (causing endothelium-independent dilation) after KD, and to investigate whether the acute administration of vitamin C can restore systemic endothelial dysfunction. The percent change in diameter of the brachial artery induced by reactive hyperemia in the patients with a history of KD (6.2 +/- 3.9%) was significantly less than that in the control group (14.1 +/- 6.8%, p < 0.0001). No significant difference could be found in the percent change in diameter induced by sublingual nitroglycerin between the controls (33.2 +/- 13.7%) and the patients (30.6 +/- 9.2%, p = 0.49). There was no significant difference in percent change in diameter of the brachial artery induced by reactive hyperemia between the patients who received gamma globulin (6.0 +/- 4.0) and those who did not (7.9 +/- 3.3, p = 0.33). Intravenous infusion of vitamin C significantly increased the percent change in diameter of the brachial artery induced by reactive hyperemia in 19 patients with history of KD (6.6 +/- 3.5% to 13.0 +/- 5.5%, p < 0.0001). After placebo administration in 20 patients with history of KD there was no significant increase in the percent change in the diameter of the brachial artery induced by reactive hyperemia (6.5 +/- 4.5% to 7.3 +/- 4.9%, p = 0.20). The decreased percent change in the diameter of the brachial artery induced by reactive hyperemia in patients with a history of KD compared with the healthy children indicates that systemic endothelial dysfunction exists after KD. Although it is not influenced by early treatment with high-dose gamma globulin in the acute stage of KD, systemic vascular endothelial function can be restored by acute intravenous administration of vitamin C.     

Convalescent stage coronary flow reserve and late myocardial morphologic outcomes in patients with first anterior acute myocardial infarction.

BACKGROUND: Microvascular damage immediately after reperfusion therapy is an independent predictor of left ventricular function in patients with acute myocardial infarction (AMI). However, its recovery may vary among individuals and the relationship between convalescent stage microvasculature and late myocardial morphologic change is unclear. METHODS AND RESULTS: Patients treated with coronary angioplasty within 12 h of their first anterior AMI were enrolled in this study. Coronary flow reserve (CFR) was measured 3 weeks post AMI, in both branches of the left coronary artery: culprit (left anterior descending artery: LAD) and non-culprit (left circumflex artery: LCX). Left ventriculography was performed at 3 weeks and 6 months post AMI and compared. Seventeen patients showed abnormal CFR in the LAD (Group 1: CFR<2), whereas 20 patients showed normal CFR (Group 2: CFR >/=2). Percent changes of end-diastolic volume tended to be higher in Group 1 than in Group 2 (11.8+/-21.6% vs -1.3+/-14.4%, p=0.056), and %changes of end-systolic volume was significantly smaller in Group 2 (11.8+/-22.1% vs -8.7+/-25.1%, p<0.05). A statistically significant correlation was found between absolute and relative CFR in the LAD and %change of end-systolic volume (r=-0.58: p<0.001, and r=0.40: p<0.05, respectively). CONCLUSIONS: Microvascular function in the convalescent stage may be related to these favorable changes.     

"Smoker's paradox" in patients with acute myocardial infarction receiving primary coronary intervention

OBJECTIVES: Smokers with acute myocardial infarction have lower mortality rates than non-smokers despite increased risk for coronary artery disease. This study assessed the effects of smoking on complications and outcomes after acute myocardial infarction, and investigated the relationship between the clinical factors and the paradoxical effects of smoking in patients receiving primary coronary intervention. METHODS: Subjects were 367 consecutive patients with acute myocardial infarction who were admitted within 24 hr of onset and underwent successful coronary intervention, 165 (45%) of whom were smokers. RESULTS: The smoking group contained significantly more male patients, and the smoking group was significantly younger than the non-smoking group (p < 0.0001). The value of acute phase brain natriuretic peptide (BNP) and atrial natriuretic peptide (ANP) were significantly lower (BNP: 250 +/- 366 vs 448 +/- 513pg/ml, p = 0.0002; ANP: 48 +/- 77 vs 74 +/- 82pg/ml, p = 0.005) in the smoking group. Peak creatine kinase time from onset was significantly earlier (12.9 +/- 9.3 vs 16.1 +/- 10.0 hr, p = 0.049) in the smoking group. Left ventricular ejection fraction in the chronic phase was significantly better in the smoking group (58 +/- 13% vs 52 +/- 14%, p = 0.03). The early ST-segment resolution rate was higher in the smoking group (81% vs 67%, p = 0.003), and there were significantly fewer patients with heart failure in the smoking group than in the non-smoking group (28% vs 41%, p = 0.01). The cardiac mortality rate during 6 months was significantly lower in the smoking group (3% vs 9%, p = 0.01). The beneficial effects of smoking on the prognosis were related with the differences in sex and age of the study group. CONCLUSIONS: The reason why smokers with acute myocardial infarction have lower mortality rates than non-smokers, the "smoker's paradox", may be related to less damage to the microvascular function after primary coronary intervention, with lower BNP and better left ventricular ejection fraction.     

The effect of ST resolution on QT dispersion after interventional treatment in acute myocardial infarction

BACKGROUND: It has been reported that reperfusion treatment reduces QT dispersion (QTD) in cases of acute myocardial infarction (AMI). Successful myocardial perfusion is not synonymous with Thrombolysis in Myocardial Infarction (TIMI) III flow. It has been demonstrated that in AMI, the grade of ST-resolution correlates strongly with left ventricular (LV) function, enzyme elevation, and mortality after primary angioplasty. HYPOTHESIS: This study investigated the relation between ST-resolution grade and QTD and the feasibility of using QTD as a determinant of successful myocardial tissue perfusion in patients in whom TIMI III flow in the infarct-related artery (IRA) is restored by interventional treatment for AMI. METHODS: The study included 57 patients (38 men, 19 women, average age 54.4 +/- 11.6 years), whose IRA was perfused by primary angioplasty after the diagnosis of anterior AMI with ST elevation. Electrocardiograms of patients were taken 45 +/- 12 min post procedure, and patients were divided into three groups depending on the grade of ST resolution: Group 1, full ST resolution; Group 2, partial ST resolution; and Group 3, unsuccessful ST resolution. RESULTS: Full ST resolution was seen in 19 cases (33%), partial resolution in 26 cases (47%), and unsuccessful resolution in 12 cases (20%). There were no differences among groups in terms of risk factors, stent diameters, symptom onset-balloon time, LV function, and preprocedure corrected QTD (QTcD) (p = 0.274). After the procedure, a significant reduction in QTcD was found within the groups (p = 0.0001 in Group 1, p = 0.004 in Group 2, and p = 0.011 in Group 3). Reductions in QTcD post procedure were 24.21 +/- 14.27, 11.85 +/- 16.18, and 12.50 +/- 11.58 ms in Groups 1, 2, and 3, respectively. There was a statistically significant difference of p = 0.015 between Groups 1 and 2 and a difference of p = 0.028 between Groups 1 and 3. There was no statistically significant difference between Groups 2 and 3 (p = 0.916). CONCLUSION: In acute MI, TIMI III flow led to a reduction in QTcD, and full myocardial perfusion made an additional contribution to the electrical stability of the myocardium.     

Brachial endothelial function is impaired in patients with systemic lupus erythematosus

OBJECTIVE: To verify if endothelial function is impaired in pre-menopausal women with systemic lupus erythematosus (SLE) and whether endothelial dysfunction is related to disease duration, cumulative prednisone dose, antimalarial use, anticardiolipin antibody (aCL), hypertension, Raynaud's phenomenon, disease activity score, and vasculitis. METHODS: Using high-resolution ultrasound, we measured the diameter of brachial artery at rest, during reactive hyperemia, and after glyceryl trinitrate (GTN). We compared 69 pre-menopausal female patients with SLE (mean age 29 +/- 8 years) with 35 age and sex-matched controls (mean age 29 +/- 6 years), The mean disease duration was 72 months. RESULTS: There was no significant difference in baseline brachial artery diameter. The flow-mediated dilation (endothelial dependent dilation) was significantly impaired in SLE patients when compared to controls (5.0 +/- 5.0% vs 12.0 +/- 6.0%, p < 0.001), even in the subgroup of patients without coronary artery disease risk factor (4.5 +/- 4.0% vs 12.0 +/- 6.0%, p < 0.001). The GTN induced dilation (endothelial independent dilation) was significantly lower in the aCL positive SLE patients when compared to the controls (11.9 +/- 4.0% vs 16.3 +/- 6.0%, p < 0.05). The endothelium-dependent dilation was not related to disease duration, cumulative prednisone dose, antimalarial use, anticardiolipin antibody, hypertension history, Raynaud's phenomenon, SLE disease activity score or vasculitis. CONCLUSION: This is the first study using brachial artery ultrasound imaging to evaluate endothelium function in SLE. Patients with SLE presented lower flow mediated dilation (endothelium dependent dilation) than sex and age-matched controls, even in patients without traditional cardiovascular risk factors and this may represent an early atherosclerotic process.     

Association between endothelial dysfunction and major cardiovascular events in peripheral arterial disease

BACKGROUND: Patients with peripheral arterial disease (PAD) are characterized by a high mortality for cardiovascular events. An impairment of endothelial function, expressed as brachial-artery flow-mediated vasodilation (FMV), has been described in PAD patients. Aim of this study was to investigate the association between FMV and cardiovascular events in patients with PAD. PATIENTS AND METHODS: Thirty-eight patients with intermittent claudication (71% men, mean age 71 years) were divided into two groups according to the presence or absence of previous major cardiovascular events (myocardial infarction or stroke). RESULTS: Brachial FMV was significantly lower in patients with a history of myocardial infarction or stroke (n = 16) than in patients without cardiovascular events (3.2 +/- 3.6% vs. 5.7 +/- 3.6%; p = 0.042). In the group with cardiovascular events there was a significantly higher proportion of subjects in the lower FMV tertile (56% vs. 18%), and a lower proportion of subjects in the upper tertile (25% vs. 41%; chi 2 test, p = 0.047). CONCLUSION: We conclude that FMV of the brachial artery is significantly reduced in PAD patients with a history of stroke and myocardial infarction. These cross-sectional results suggest a potential role of FMV as a marker of major cardiovascular events.