IntroductionContinued adverse remodeling of myocardium after infarction may lead to progressive ventricular dilation and heart failure. We tested the hypothesis that exercise training in a healed myocardial infarction-dysfunction rat model can favorably modify the adverse effects of ventricular remodeling including attenuation of abnormal myosin gene expression. Sprague-Dawley rats were subjected to either proximal LAD ligation or sham operation. At 5 wk after the operation, animals were randomly assigned to sedentary conditions or 6 wk of graduated swim training, creating four experimental groups: infarct sedentary (IS), infarct exercise (IE), sham sedentary (SS), and sham exercise (SE). At 11 wk all rats were sacrificed and analyzed.Compared to sedentary infarct controls, exercise training attenuated left ventricular (LV) dilation and allowed more hypertrophy of the non infarct wall. The exercisetrained hearts also showed a reduction in the estimated peak wall tension. Northern blot analysis showed an increase in f8-myosin heavy chain expression in the hearts of the sedentary infarction group soon after infarction when compared to sham controls. However, with exercise training, there was a significant attenuation of the I8-myosin heavy chain expression in the myocardium.Exercise training in a model of left ventricular dysfunction after healed myocardial infarction can improve the adverse remodeling process by attenuating ventricular dilation and reducing wall tension. The abnormal f8-myosin expression was also attenuated in the exercise trained group. This is evidence that abnormal gene expression following severe myocardial infarction dysfunction can be favorably modified by an intervention. (J. Clin. Invest. 1995. 96:858-866 and slower speeds of contraction, and is often a marker of pathological hypertrophy (5-9). Continued late ventricular remodeling along this molecular pathway beyond the period of infarct expansion and scar formation accompanies the transition from ventricular dilation and dysfunction to frank heart failure (2, 10-14). It is known that aerobic exercise training creates a physiologic form of hypertrophy in the myocardium without systolic or diastolic dysfunction (15-18) or abnormal MHC gene expression in animal models (19). It follows that an intriguing possibility exists that suitably timed exercise training post myocardial infarction may overcome the abnormal fetal gene expression and morphological remodeling, and alter the natural course towards heart failure.Exercise training acutely postmyocardial infarction is controversial, as it may aggravate infarct expansion (20)(21)(22). Exercise training in chronic stages of heart failure on the other hand has been shown to improve peripheral metabolism (23, 24) and oxygen consumption (25-27), but its effects on ventricular remodeling are unknown (28).To investigate the effects of exercise training in postmyocardial infarction remodeling, we compared exercise by swim training with sedentary controls in a rat healed infarction model wi...

Background: Among individuals with nonvalvular atrial fibrillation (AF), the prevalence of obstructive sleep apnea (OSA) can be as high as 85%. Continuous positive airway pressure treatment for moderate or severe OSA might improve AF outcomes and quality of life, so early identification of OSA might be of value. However, screening questionnaires for OSA are suboptimal because they are weighted toward tiredness and loud snoring, which might be absent in AF patients.

After the introduction of Smart-TouchÔ, 421 procedures were performed with 3 tamponade events (3/421, 0.7%, P¼0.148). Analysis of other potential predictors is shown in Table 1. The only factor that was statistically significant was use of bridging heparin (P¼0.021). On multivariate analysis this became non-significant (P¼0.078). CONCLUSION: There was no significant difference in frequency of tamponade before and after introduction of contact force sensing catheters (1.9% v.s 0.7%, P¼0.148).

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