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      Assessment of Atrial Conduction in Patients with Scleroderma by Tissue Doppler Echocardiography and P Wave Dispersion


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          Background: Atrial conduction abnormalities in patients with scleroderma have not been evaluated in terms of P wave duration, P wave dispersion (P<sub>d</sub>) and electromechanical coupling measured by tissue Doppler echocardiography. Methods: Twenty-four patients with scleroderma and 24 control subjects underwent resting electrocardiogram (ECG), M mode and tissue Doppler echocardiography. The P wave duration was calculated in all leads of the surface ECG. The difference between the maximum (P<sub>max</sub>) and minimum P wave duration was calculated and defined as P<sub>d</sub>. Interatrial and intraatrial electromechanical delays were measured with tissue Doppler tissue echocardiography. Results: The left ventricular dimensions, fractional shortening, and left atrial diameter did not differ between the patients and the controls. P<sub>d</sub> and P<sub>max</sub> were significantly higher in patients with scleroderma compared with controls: 51 ± 17 versus 28 ± 7 ms (p < 0.01) and 109 ± 10 versus 93 ± 6 ms (p < 0.01), respectively. There was a delay between the onset of the P wave on surface ECG and the onset of the late diastolic wave (A wave; PA) obtained by tissue Doppler echocardiography in patients with scleroderma compared with controls measured at lateral septal annulus (lateral PA; 122 ± 8 vs. 105 ± 7 ms, p = 0.001), septal mitral annulus (104 ± 11 vs. 93 ± 10 ms, p = 0.01) and tricuspid annulus (right ventricular PA; 71 ± 9 vs. 64 ± 7 ms, p = 0.05). Interatrial conduction time (lateral PA – right ventricular PA) was delayed in patients with scleroderma compared with controls (88 ± 13 vs. 76 ± 11 ms, p = 0.01). A positive correlation was detected between interatrial electromechanical delay (lateral PA – right ventricular PA) and P<sub>d</sub> (r = 0.5, p = 0.03). Conclusion: Atrial conduction abnormalities as estimated with P<sub>d</sub> and P<sub>max</sub> are significantly higher in patients with scleroderma compared with controls. There is a delay in both intraatrial and interatrial electromechanical coupling intervals in patients with scleroderma.

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          Most cited references 19

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          A population-based study of the long-term risks associated with atrial fibrillation: 20-year follow-up of the Renfrew/Paisley study.

          To describe the effect of atrial fibrillation on long-term morbidity and mortality. The Renfrew/Paisley Study surveyed 7052 men and 8354 women aged 45-64 years between 1972 and 1976. All hospitalizations and deaths occurring during the subsequent 20 years were analyzed by the presence or absence of atrial fibrillation at baseline. Lone atrial fibrillation was defined in the absence of other cardiovascular signs or symptoms. Cox proportional hazards models were used to adjust for age and cardiovascular conditions. After 20 years, 42 (89%) of the 47 women with atrial fibrillation had a cardiovascular event (death or hospitalization), compared with 2276 (27%) of the 8307 women without this arrhythmia. Among men, 35 (66%) of 53 with atrial fibrillation had an event, compared with 3151 (45%) of 6999 without atrial fibrillation. In women, atrial fibrillation was an independent predictor of cardiovascular events (rate ratio [RR] = 3.0; 95% confidence interval [CI]: 2.1-4.2), fatal or nonfatal strokes (RR = 3.2; 95% CI: 1.0-5.0), and heart failure (RR = 3.4; 95% CI: 1.9-6.2). The rate ratios among men were 1.8 (95% CI: 1.3-2.5) for cardiovascular events, 2.5 (95% CI: 1.3-4.8) for strokes, and 3.4 (95% CI: 1.7-6.8) for heart failure. Atrial fibrillation was an independent predictor of all-cause mortality in women (RR = 2.2; 95% CI: 1.5-3.2) and men (RR = 1.5; 95% CI: 1.2-2.2). However, lone atrial fibrillation (which occurred in 15 subjects) was not associated with a statistically significant increase in either cardiovascular events (RR = 1.5; 95% CI: 0.6-3.6) or mortality (RR = 1.8; 95% CI: 0.9-3.8). Atrial fibrillation is associated with an increased long-term risk of stroke, heart failure, and all-cause mortality, especially in women.
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            P-wave dispersion: a novel predictor of paroxysmal atrial fibrillation.

             Polychronis E Dilaveris (corresponding) ,  John E Gialafos (2006)
            The prolongation of intraatrial and interatrial conduction time and the inhomogeneous propagation of sinus impulses are well known electrophysiologic characteristics in patients with paroxysmal atrial fibrillation (AF). Previous studies have demonstrated that individuals with a clinical history of paroxysmal AF show a significantly increased P-wave duration in 12-lead surface electrocardiograms (ECG) and signal-averaged ECG recordings. The inhomogeneous and discontinuous atrial conduction in patients with paroxysmal AF has recently been studied with a new ECG index, P-wave dispersion. P-wave dispersion is defined as the difference between the longest and the shortest P-wave duration recorded from multiple different surface ECG leads. Up to now the most extensive clinical evaluation of P-wave dispersion has been performed in the assessment of the risk for AF in patients without apparent heart disease, in hypertensives, in patients with coronary artery disease and in patients undergoing coronary artery bypass surgery. P-wave dispersion has proven to be a sensitive and specific ECG predictor of AF in the various clinical settings. However, no electrophysiologic study has proven up to now the suspected relationship between the dispersion in the atrial conduction times and P-wave dispersion. The methodology used for the calculation of P-wave dispersion is not standardized and more efforts to improve the reliability and reproducibility of P-wave dispersion measurements are needed. P-wave dispersion constitutes a recent contribution to the field of noninvasive electrocardiology and seems to be quite promising in the field of AF prediction.
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              A population-based study of mortality among patients with atrial fibrillation or flutter.

              To determine the mortality associated with atrial flutter and atrial fibrillation in the general population. Using the Marshfield Epidemiologic Study Area, a database that captures nearly all medical care and deaths among its 58,820 residents, we identified patients diagnosed with atrial flutter or atrial fibrillation from July 1, 1991, through June 30, 1995. Patients were followed prospectively and compared with a group of controls without these arrhythmias. A total of 4775 person-years of follow-up were completed in 577 patients and 577 controls. Compared with controls, mortality among patients with atrial fibrillation or flutter was nearly 7.8-fold higher at 6 months (95% confidence interval [CI]: 4.1 to 15) and 2.5-fold higher (95% CI: 2.0 to 3.1; P < 0.0001) at the last follow-up (mean [+/- SD] of 3.6 +/- 2.3 years; range, 1 day to 7.3 years). At 6 months, mortality among patients with atrial flutter alone was somewhat greater than in controls and less than one third that of those with atrial fibrillation (with or without atrial flutter) (P = 0.02). At the last follow-up, however, mortality was greater among patients with atrial flutter (hazard ratio [HR] = 1.7; 95% CI: 1.2 to 2.6; P = 0.007), atrial fibrillation (HR = 2.4; 95% CI: 1.9 to 3.1; P < 0.0001), or both atrial arrhythmias (HR = 2.5; 95% CI: 1.9 to 3.3; P < 0.0001) when compared with controls in models that adjusted for cardiovascular risk factors. In the general population, both atrial flutter and atrial fibrillation are independent predictors of increased late mortality. The relatively benign course during the 6-month period after the initial diagnosis of atrial flutter suggests that early diagnosis and treatment of these patients may improve their long-term survival.

                Author and article information

                S. Karger AG
                November 2007
                12 February 2007
                : 108
                : 4
                : 317-321
                Departments of aCardiology and bRheumatology, Hacettepe University, Ankara, and cDepartment of Rheumatology, Gaziantep University, Gaziantep, Turkey
                99102 Cardiology 2007;108:317–321
                © 2007 S. Karger AG, Basel

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                Page count
                Figures: 2, Tables: 3, References: 28, Pages: 5
                Original Research


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