Left ventricular biomechanics in professional football players.

Chronic exercise induces adaptive changes of left ventricular (LV) ejection and filling capacities which may be detected by novel speckle-tracking echocardiography (STE) and tissue Doppler imaging (TDI)-based techniques. A total of 103 consecutive male elite Norwegian soccer players and 46 age-matched healthy controls underwent echocardiography at rest. STE was used to assess LV torsional mechanics and LV systolic longitudinal strain (LS). Diastolic function was evaluated by trans-mitral blood flow, mitral annular velocities by TDI, and LV inflow propagation velocity by color M-mode. Despite similar global LS, players displayed lower basal wall and higher apical wall LS values vs controls, resulting in an incremental base-to-apex gradient of LS. Color M-mode and TDI-derived data were similar in both groups. Peak systolic twist rate (TWR) was significantly lower in players (86.4±2.8 vs controls 101.9±5.2 deg/s, P<.01). Diastolic untwisting rate (UTWR) was higher in players (-124.5±4.2 vs -106.9±6.7 deg/s) and peaked earlier during the cardiac cycle (112.7±0.8 vs 117.4±2.4% of systole duration, both P<.05). Untwisting/twisting ratio (-1.48±0.05 vs -1.11±0.08; P<.001) and untwisting performance (=UTR/TW; -9.25±0.34 vs -7.38±0.40 s-1 , P<.01) were increased in players. Augmented diastolic wall strain (DWS), a novel measure of LV compliance in players, was associated with improved myocardial mechanical efficiency. The described myocardial biomechanics may underlie augmented exertional cardiac function in athletes and may have a potential role to characterize athlete's heart by itself or to distinguish it from hypertensive or hypertrophic cardiomyopathy.

Diuretic use in heart failure and outcomes.

Diuretics are frequently administered to relieve congestive symptoms in patients with heart failure (HF). Despite their widespread use, prospective data on the potential of diuretics to modulate HF-related morbidity and mortality are scarce. Diuretic efficacy may be limited by adverse neurohormonal activation and by "congestion-like" symptoms that may occur in the absence of fluid overload. Herein, we review the current knowledge on diuretic use and outcomes in HF.

Induction of myocardial connective tissue growth factor in pacing-induced heart failure in pigs.

AIMS: Connective tissue growth factor (CTGF) is a secreted, heparin-binding, and extracellular matrix associated protein shown to stimulate many of the cellular events underlying fibrosis. Previous investigations have revealed that myocardial CTGF is substantially induced in ischaemic heart failure, particularly in the ischaemic and peri-ischaemic region. The purpose of the present study was to investigate to what extent myocardial induction of CTGF is a general response to congestive heart failure (CHF) and to what extent CTGF is a decisive effector of fibrosis. METHODS: Experimental heart failure in pigs was induced by rapid pacing at 220-240 beats min(-1) for 3 weeks (CHF pigs; n = 12). RESULTS: The CHF pigs exhibited significant left ventricular (LV) dilatation, reduced contractility, and increased cardiac filling pressures. Northern blot analysis demonstrated that myocardial CTGF mRNA levels in CHF pigs were fivefold higher (P < 0.05) than those in control pigs (n = 10). Similar elevations of immunoreactive CTGF (sixfold; P < 0.05) were observed in myocardial tissue samples prepared for Western blot analysis. Immunohistochemical analysis of myocardial tissue sections revealed predominant expression in interstitial and perivascular fibroblasts and endothelial cells. Myocardial procollagen alpha1(I) mRNA levels were also significantly elevated (sixfold; P < 0.05) in CHF pigs compared with controls, whereas myocardial tissue contents of collagen were not statistically different between the groups. CONCLUSION: Induction of myocardial CTGF in heart failure is not just a response to ischaemia, but rather a general response to evolving heart failure. Yet, induction of myocardial CTGF was clearly not a sufficient effector of fibrosis.