Pd > or = 32.5 ms and Pmax > or = 103.0 ms predict the recurrence of PAF after ablation with acceptable positive and negative predictive values. Pd > or = 32.5 ms is an independent predictor of recurrence of PAF after catheter ablation in patients with WPW syndrome.
Background: Imbalance in autonomic nervous system and impaired myocardial repolarization has been shown to increase the risk for arrhythmias in patients with coronary artery disease. This study evaluated the effects of coronary artery bypass grafting (CABG) on heart rate variability and QT interval dynamicity in subjects with coronary artery disease undergoing elective CABG surgery. Methods: The study group consisted of 68 consecutive patients (mean age ±SD: 61 ± 9 years) with coronary artery disease who underwent elective CABG. Twenty-four-hour Holter monitoring was performed 2–5 days before cardiac surgery and was repeated 10 days after CABG. ELATEC holter software was used to calculate heart rate variability and QT dynamicity parameters. All subjects had a complete history, laboratory examination and transthoracic echocardiography. Results: All patients had beta-blocking agent medication pre- and postoperatively. Standard deviation of all NN intervals for a selected time period, square root of the mean of the sum of the squares of differences between adjacent RR intervals, the proportion of differences in successive NN intervals greater than 50 ms, normalized low-frequency power, and normalized high-frequency power were significantly decreased after CABG surgery, whereas low-frequency/high-frequency ratio was significantly increased after CABG. QT/RR slopes over 24 h were significantly increased after CABG surgery for QT end and QT apex (QTapex/RR: 0.16 ± 0.13 vs. 0.28 ± 0.19, p < 0.001; QTend/RR: 0.18 ± 0.13 vs. 0.36 ± 0.23, p < 0.001). Conclusion: This prospective study showed for the first time that CABG was associated with a significant worsening of heart rate variability and QT dynamicity parameters in the postoperative period.
We demonstrated that myocardial velocities, were affected in patients with BD. Therefore, we conclude that right and left ventricular function is impaired in patients with BD.
It is thought that high MPV levels may be an effective marker in determining the severity of CAD in patients with DM. And the high MPV level may be related with CAD pathophysiology in DM patients.
Obesity-associated alterations in coagulation and fibrinolytic factors in favor of thrombosis are well known. Observations suggest that leptin, a recently discovered obesity gene product, in addition to being a satiety factor, induces platelet aggregation, accelerates formation of firm thrombi, and is associated with abnormal fibrinolysis. The authors studied the influence of plasma leptin concentrations on admission within 6 hours of acute myocardial infarction (MI) on the outcome of thrombolytic therapy (TT). Forty-one patients with acute MI who underwent TT were enrolled into the study. Levels of plasma leptin were determined with radioimmunoassay method in samples obtained just before initiation of TT. Patients were initially classified according to the admission plasma leptin concentrations, and it was observed that failure of reperfusion therapy with streptokinase was significantly higher in patients with admission plasma leptin concentrations > or =14 ng/mL (group 2) as compared to patients with admission plasma leptin concentrations <14 ng/mL (group 1). Final failure of TT, identified both by reinfarction and absence of early reperfusion as assessed noninvasively, was observed in 11 patients (39%) in group 1 and in 10 patients (77%) in group 2 (p=0.025). Left ventricular ejection fraction was slightly but significantly higher in group 1 than in group 2 (p=0.031). High plasma leptin concentrations on admission in patients within 6 hours after the onset of acute MI are associated with less TT efficacy. The authors suggest that admission leptin levels may play a role in the management of patients with acute MI.
Protein Z is a vitamin-K-dependent plasma protein that serves as a cofactor for the inhibition of factor Xa. Although the precise physiologic function of protein Z is still unknown, abnormal plasma protein Z concentrations have been associated with a number of thrombotic disease states. There is the evidence of universal activation of the hemostatic system in Behçet's disease (BD), which represents a hypercoagulable/prothrombotic state. Circulating protein Z levels in patients with BD were evaluated. Plasma protein Z concentrations were assayed in 24 patients with BD (male/female: 13/11, mean age 35.4 years) and in 24 healthy controls (males/females: 14/10, mean age 59.8 years). The disease duration was 10.6 years (range, 1-30 years). None of the subjects in either group had received anticoagulants within 3 weeks before the study, and none of them had liver dysfunction. Patients complicated with vascular disease were also excluded from the study. Mean plasma concentrations of protein Z were 141 ng/mL (range, 56.8-257) in healthy controls and 107.8 ng/mL (range, 21.2-202) in BD patients (p<0.05). There was a positive correlation between the disease duration and protein Z levels in the study group (p<0.05, r=0.448). Alterations of protein Z concentrations could complicate the pathobiology of the prothrombotic state of BD. Furthermore, the tendency of increment in the protein Z with the passage of time may reflect the diminution of the disease activity.
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