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)

Glycoprotein IIb/IIIa inhibitor therapy during primary percutaneous coronary intervention (PCI) decreases the incidence of major adverse cardiac events. These effects directly result from the level of platelet inhibition. It was shown that standard dosing of tirofiban is insufficient for optimal platelet inhibition. We sought to determine the efficacy and safety of single high-dose bolus (HDB) tirofiban with high-dose clopidogrel loading in primary PCI in acute ST elevation myocardial infarction. A total of 100 patients (mean age 55.2 +/- 9.9 years, male/female = 86/14) undergoing primary PCI, pretreated with clopidogrel (450 mg) and aspirin (325 mg), were consecutively randomized into two groups. Group I (n = 50) received a standard dose bolus of tirofiban (10 microg/kg/3 min) with 24-h infusion at a rate of 0.15 microg/kg/min. Group II received single HDB tirofiban (25 microg/kg/3 min). The assessed angiographic, clinical, and echocardiographic endpoints were: initial and final Thrombolysis in Myocardial Infarction (TIMI) grade flow (TGF), corrected TIMI frame count (CTFC), ST-segment resolution (STR) at 90 min, in-hospital bleeding complications, echocardiographic left ventricular ejection fraction (LVEF), death, reinfarction, and repeat target vessel revascularization at 1 month. Platelet function inhibition was measured using PFA-100 (Behring-Dade, Liederbach, Germany) with a test cartridge unit containing a membrane coated with 2 microg of equine Type I collagen and 50 microg adenosine diphosphate before, and 10 min, 2, 4, 6, 12, and 24 h after the bolus of the tirofiban in the first 10 cases of each group. There were no significant differences in baseline characteristics between groups. Initial TGF III was more frequent (24% vs 8%, P = 0.029) and the value of CTFC was lower (75 +/- 34 vs 89 +/- 25, P = 0.03) in group II. Postprocedural TGF, CTFC, STR, bleeding complications, and LVEF at 1 month were not different between the two groups. There was a higher rate of reinfarction in group II (8%) compared with group I (2%), but this difference was not statistically significant (P > 0.05). The results of platelet function analyses showed that group II patients had significantly prolonged platelet function assay closure times (299 +/- 6 s) compared with group patients (236 +/- 97 s) at 10 min after the bolus dose (P = 0.04). However, after the first dose between 2 and 24 h, PFA closure times were significantly prolonged in patients with tirofiban infusion. High-dose bolus of tirofiban seems to be safe and more effective than conventional dose at the periprocedural time, whereas continuous infusion of tirofiban may be necessary in the first 24 h before stable and safe antiplatelet status is reached with clopidogrel. However, safety and efficacy of HDB tirofiban and high-loading-dose clopidogrel together with tirofiban infusion requires further studies with a larger population.

Neurofibromatosis is a rare cause of coronary aneurysm. We present a case of multiple coronary artery aneurysms in a patient with neurofibromatosis. Coronary angiography was performed because of postmyocardial infarction angina. Coronary angiography revealed multiple coronary aneurysms in the left anterior descending and circumflex arteries, and diffuse irregularities in the right coronary artery. None of the coronary arteries showed critical stenosis. The patient was successfully managed with aspirin, clopidogrel, and beta-blocker therapy.