Sustained cardiac programming by short-term juvenile exercise training in male rats.

KEY POINTS: Cardiac hypertrophy following endurance-training is thought to be due to hypertrophy of existing cardiomyocytes. The benefits of endurance exercise on cardiac hypertrophy are generally thought to be short-lived and regress to sedentary levels within a few weeks of stopping endurance training. We have now established that cardiomyocyte hyperplasia also plays a considerable role in cardiac growth in response to just 4 weeks of endurance exercise in juvenile (5-9 weeks of age) rats. The effect of endurance exercise on cardiomyocyte hyperplasia diminishes with age and is lost by adulthood. We have also established that the effect of juvenile exercise on heart mass is sustained into adulthood. ABSTRACT: The aim of this study was to investigate if endurance training during juvenile life 'reprogrammes' the heart and leads to sustained improvements in the structure, function, and morphology of the adult heart. Male Wistar Kyoto rats were exercise trained 5 days week-1 for 4 weeks in either juvenile (5-9 weeks of age), adolescent (11-15 weeks of age) or adult life (20-24 weeks of age). Juvenile exercise training, when compared to 24-week-old sedentary rats, led to sustained increases in left ventricle (LV) mass (+18%; P < 0.05), wall thickness (+11%; P < 0.05), the longitudinal area of binucleated cardiomyocytes (P < 0.05), cardiomyocyte number (+36%; P < 0.05), and doubled the proportion of mononucleated cardiomyocytes (P < 0.05), with a less pronounced effect of exercise during adolescent life. Adult exercise training also increased LV mass (+11%; P < 0.05), wall thickness (+6%; P < 0.05) and the longitudinal area of binucleated cardiomyocytes (P < 0.05), despite no change in cardiomyocyte number or the proportion of mono- and binucleated cardiomyocytes. Resting cardiac function, LV chamber dimensions and fibrosis levels were not altered by juvenile or adult exercise training. At 9 weeks of age, juvenile exercise significantly reduced the expression of microRNA-208b, which is a known regulator of cardiac growth, but this was not sustained to 24 weeks of age. In conclusion, juvenile exercise leads to physiological cardiac hypertrophy that is sustained into adulthood long after exercise training has ceased. Furthermore, this cardiac reprogramming is largely due to a 36% increase in cardiomyocyte number, which results in an additional 20 million cardiomyocytes in adulthood.

Phasic Compression of Left Circumflex Coronary Artery during Atrial Systole.

Phasic coronary artery compression is typically associated with spasm or myocardial bridging. Compression caused by acquired anatomic changes to the surrounding heart chambers has been reported only infrequently. We present a possibly unique case of phasic compression of the proximal left circumflex coronary artery during atrial contraction in association with a dilated left atrium. A 55-year-old man with multiple cardiac risk factors presented with worsening exertional dyspnea. An electrocardiogram and echocardiogram revealed marked left atrial dilation and a left ventricular ejection fraction of 0.15 to 0.20 with elevated filling pressures. Angiograms showed compression of the proximal segment of the left circumflex coronary artery during late ventricular diastole: the compression occurred in phase with atrial systole, whereas good flow without compression was present during atrial diastole. We attributed this phenomenon to ballooning of the lateral region of the atrial wall toward the atrioventricular groove during atrial systole. The patient complied with antihypertensive therapy, and his status improved after one year. To identify coronary artery compression in the presence of abnormal chamber geometry and to guide the treatment of the contributing medical conditions, we recommend careful analysis of angiographic results.

Favourable effects of exercise-based Cardiac Rehabilitation after acute myocardial infarction on left atrial remodeling.

BACKGROUND: Left atrial enlargement is an important predictor of cardiovascular outcomes in patients after acute myocardial infarction. While the favourable effect of exercise exercise-based Cardiac Rehabilitation (CR) on postinfarction LV remodeling has been well documented, those on LA remodeling have yet to be defined. This study investigated the effects of CR on LA remodeling in postinfarction patients with moderate left ventricular (LV) dysfunction. METHODS: Sixty postinfarction patients were randomised randomized into two groups, each composed of 30 patients: group T (LV ejection fraction (EF) 43.7+/-4.2%, mean+/-SD) entered a 6-month CR program, whereas group C (EF 44.7+/-4.4%, P=ns) did not. Doppler echocardiography and cardiopulmonary exercise test were performed upon enrolment and at 6-month. RESULTS: At 6-month, trained patients showed a significant (P<0.001) improvement in peak oxygen consumption (DeltaVO(2peak)=+5.2+/-2.1 ml/kg/min) and a reduction in LA (DeltaLAV(MAX)=-1.9+/-3.7 ml/m(2)) and in LV volumes (DeltaLVEDV=-3.6+/-4.4 ml/m(2)). At 6-month, untrained patients showed LAV(MAX) (+3.6+/-4.4 ml/m(2), P<0.001) and LV dilation (+4.2+/-5.1 ml/m(2), P<0.001; group T vs. C, P<0.001); whereas no significant changes in VO(2peak) were observed. Multiple linear regression analysis showed that age (beta=0.442, P<0.001), inclusion in the training group (beta=-0.599, P<0.001), E/A ratio (beta=-0.210, P=0.038), LVEDV (beta=0.376, P<0.001), and LVEF (beta=-0.279, P=0.007) are significant predictors of LA remodeling. CONCLUSIONS: Six-month exercise-based CR in postinfarction patients with mild to moderate LV dysfunction induced a favourable LA remodeling.