A high admission RDW level in patients with STEMI undergoing primary PCI was associated with increased risk for in-hospital and long-term cardiovascular mortality.
Left ventricular (LV) systolic and diastolic parameters derived from Doppler echocardiography have been used widely to predict functional capacity but diastolic filling is affected by various factors. Tissue Doppler imaging (TDI) that records systolic and diastolic velocities within the myocardium and at the corners of the mitral annulus, has been shown to provide additional information about regional and global LV function. The goal of this study was to examine whether TDI-derived parameters add incremental value to other standard Doppler echocardiographic measurements in predicting exercise capacity. The study enrolled 59 consecutive patients with stable congestive heart failure (CHF). The etiology of heart failure was coronary artery disease in 42 patients and dilated cardiomyopathy in 17. Twenty-three age-matched healthy subjects were recruited as controls. Conventional echocardiographs and TDI were obtained. Early (Ea) and late (Aa) diastolic and systolic (Sa) mitral annulus velocities, the Ea/Aa and E/Ea ratios, were measured by pulsed wave TDI placed at the septal side of the mitral annulus and results were compared with results of cardiopulmonary exercise testing. Systolic and early diastolic velocities of mitral annulus were decreased and the E/Ea ratio was increased in the restrictive group as compared to controls (P = 0.02, P = 0.03, P < 0.001, respectively) but there was no significant difference in late diastolic velocity and the Ea/Aa ratio between the restrictive group and controls. The average peak VO2 of the patients were 14.9 +/- 4.9 ml/min per kg. Achieved peak VO2 of the patients with E/Ea ratio
SUMMARYAn attenuated heart rate recovery (HRR) immediately after exercise has been shown to be predictive of mortality. It is not known whether HRR predicts mortality when measured in patients with heart failure. The present study was undertaken to evaluate the ability of HRR to predict mortality in patients with heart failure.We studied 84 NYHA class II or III chronic congestive heart failure patients who had a left ventricular ejection fraction ≤ 40%. All patients underwent symptom limited cardiopulmonary exercise testing. The value for the HRR was defined as the difference in heart rate between peak exercise and one-minute later; a value ≤ 18 beats per minute was considered abnormal. The patients were divided into 2 groups according to the value of HRR. Those with abnormal HRR were assigned to group I and those with normal HRR were assigned to group II. The 2 groups were compared with each other regarding baseline characteristics and exercise capacity assessed by peak VO 2 .There were 26 patients (31%) in group I and 58 patients (69%) in group II. Group II patients had better performance on treadmill exercise testing than group I patients. They had greater exercise duration (7.5 ± 3.8 minutes versus 5 ± 3.5 minutes, P = 0.006), better heart-rate reserve (79 ± 25% versus 63 ± 27%, P = 0.01), and higher values of maximal heart-rate (141 ± 18 beats/min versus 132 ± 17 beats/min, P = 0.04). Group II patients also had higher peak VO 2 values (16.8 ± 4.4 mL/kg/min versus 14.4 ± 3.6 mL/ kg/min, P = 0.01). When we separated the groups according to beta-blocker usage, betablockers had no prominent effect on HRR.In the follow-up period (mean 14.1 ± 6.1 months), the presence of abnormal HRR and lower peak VO 2 (≤ 14 mL/kg/min) were the only significant predictors of mortality in our patient population (adjusted hazard ratio [HR] 5.2, 95% CI, 1.3 to 24, P = 0.03 and adjusted HR 13, 95% CI, 2.1 to 25.6, P = 0.005, respectively).It seems that the attenuated HRR value one minute after peak exercise appears to be a reliable index of the severity of exercise intolerance in heart failure patients and this study supports the value of HRR as a prognostic marker among heart failure patients referred for cardiopulmonary exercise testing for prediction of prognosis. (Int Heart J 2006; 47: 431-440)
Background/Aims: The timing of GpIIb/IIIa inhibitor administration may be important in achieving early epicardial and myocardial reperfusion. We evaluated the effect of early tirofiban on myocardial salvage and cardiovascular outcome in patients with acute myocardial infarction (AMI) undergoing infarct-related artery stenting. Methods: Patients (n = 66) with a first AMI presenting <6 h from onset of symptoms were randomized to either early administration of tirofiban in the emergency room (n = 32) or later administration in the catheterization laboratory (n = 34) (tirofiban bolus dose of 10 µg/kg, followed by 0.15 µg/kg for 24 h). The primary end-point was the degree of myocardial salvage, determined by means of serial scintigraphic studies with technetium-99m sestamibi. Thirty-day major adverse cardiac events were also assessed. Results: There were no significant differences in patient characteristics or in their presentation. The mean door-to-balloon time was similar in both groups (43 ± 12 and 53 ± 9 min, p = 0.08). The early and late treatment groups received tirofiban 18 ± 4 and 52 ± 10 min after admission, respectively. Angiographic analysis revealed a higher initial frequency of TIMI grade 3 flow in the early group (31% vs. 12%, p = 0.04). Procedural success was achieved in all patients. Myocardial risk area were comparable between early and late treatment groups (35.6 ± 12.2% vs. 39.3 ± 14.0%, p = 0.6). Scintigraphic outcomes demonstrated a significant reduction in the final infarction size (11.8 ± 5.2% vs. 22.4 ± 6.2%, p = 0.01), and improvement in salvage index (0.68 ± 0.22 vs. 0.44 ± 0.18, p = 0.003) in favor of the early tirofiban group. The thirty-day composite end-point of death, recurrent MI or rehospitalization also favored the early group (6% early, 15% late, p = 0.06). Conclusion: Early tirofiban administration enhanced the degree of myocardial salvage and clinical outcome in patients with AMI undergoing infarct-related artery stenting.
SUMMARYLeft atrial (LA) function is associated with left ventricular (LV) diastolic filling and cardiac output response to exercise. But the relation between LA function and exercise performance has not been adequately evaluated.The aim of this study was to investigate the relation between LA function and exercise capacity in dilated cardiomyopathy (DCM) with cardiopulmonary exercise testing.Forty-four patients with a left ventricular end-diastolic dimension (LVDd) ≥ 60 mm and an ejection fraction (EF) ≤ 40%, and in normal sinus rhythm were included in this study. Patients were divided into group 1 and group 2 according to their exercise peak oxygen uptake (VO 2 ) (group 1: peak VO 2 >14 mL/kg/min, group 2: peak VO 2 ≤ 14 mL/ kg/min). LA function indices were defined as follows: LA end-systolic diameter (LASd), end-diastolic diameter (LADd), LA systolic volume (LASV), LA diastolic volume (LADV), LA ejection volume (LAEV), and LA ejection fraction (LAEF).LASd, LADd, LASV, and LADV were significantly increased in group 2 (P < 0.001, P < 0.001, P < 0.05, P < 0.005). Group 1 had significantly higher LAEF (P < 0.001 ) and LVEF (P < 0.05). Group 2 had significantly shorter exercise duration, and decreased anaerobic threshold levels and minute ventilation volumes (P < 0.001, P < 0.001, P < 0.005 ). There was a positive correlation between peak VO 2 and LVEF (r = 0.46, P = 0.002), and LAEF (r = 0.61, P < 0.001), peak A wave velocity (r = 0.39, P = 0.009), E wave deceleration time (r = 0.56, P < 0.001), and isovolumic relaxation time (IVRT) (r = 0.35, P = 0.04). There was a negative correlation between peak VO 2 and LASd (r = -0.53, P < 0.001) LADd (r = -0.59, P < 0.001), LASVI (r = -0.34, P = 0.027), LADVI (r = -0.37, P = 0.001), and the E/A ratio (r = -0.41, P = 0.006), Decreased LAEF and increased LA sizes were associated with decreased peak VO 2 . The results clearly demonstrate that LA functions at rest are related to exercise performance in patients with heart failure. (Int Heart J 2005; 46: 123-131)
Effect of hormone replacement (HRT) therapy on plasma lipoproteins and apolipoproteins, endothelial function and myocardial perfusion in postmenopausal women with estrogen receptor-α (ER-α) IVS1–397 C/C genotype and established coronary artery disease. Background/Aims: Associations between various ER-α polymorphisms and clinical phenotypes have been studied, including lipid levels and coronary atherosclerosis. We studied 48 postmenopausal women to determine the effect of ER-α IVS1–397 polymorphism on the response to treatment with HRT. Methods: The study had a randomized, double-blind, placebo-controlled and crossover design. Patients were divided into two groups according to ER-α IVS1–397 polymorphism: CC genotype (n = 9); CT or TT genotype (n = 39). HRT was given continuously for 4 weeks, with 4-week washout periods between the treatment periods. Brachial artery Doppler and Tl-201 scintigraphy were performed at the end of each treatment period. Results: HRT lowered total cholesterol, LDL-c and Apo-B levels from baseline values (all p < 0.05) and to a similar degree in CC and CT/TT genotype patients. HRT increased estradiol, HDL-c and Apo A-1 levels relative to baseline values, but to a greater degree in CC patients (p = 0.04, 0.05 and 0.04 by ANOVA, respectively). HRT increased peak forearm blood flow, brachial artery diameter during reactive hyperemia and endothelium-dependent dilation in both groups, but to a greater degree in CC patients (p = 0.03, 0.03 and 0.04 by ANOVA, respectively). Summed stress and rest scores were also more markedly reduced in CC patients (p = 0.04 and 0.05, respectively). The increase in estradiol levels was strongly correlated with the improvement in endothelium-dependent dilation (r = 0.66, p < 0.01), which in turn showed negative correlation with summed stress (r = –0.62, p < 0.01) and rest scores (r = –0.52, p < 0.05) in the CC genotype group. Conclusion: These data suggest that the improvement in endothelium-dependent dilation and the reduction in perfusion abnormalities by increasing estradiol levels with HRT in postmenopausal women with coronary artery disease may differ with respect to different genotypes, the effect being more prominent in those patients with ER-α IVS1–397 CC genotype.
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