Cardiac adaptation to intensive training in prepubertal swimmers

BACKGROUND: Despite the increasing involvement of child athletes in intensive training regimens, little is known about the influence of such training on autonomic regulation and cardiac structure and function. PATIENTS AND METHODS: Twenty-five highly trained (12-14 h weekly for at least 4 years) swimmers (aged 11.9 +/- 1.6 years; 15 males, 10 females) and 20 non-training normal children who served as controls (aged 11.3 +/- 0.6 years; 14 males, 6 females) were studied. Heart rate variability analysis in the time and frequency domains was performed on 15 min resting heart rate acquisitions. Left ventricular morphology and systolic function was studied with two-dimensional guided M-mode echocardiography. The transmitral flow velocity profile was assessed with pulsed Doppler. Parameters measured included the peak early (E) and peak late (A) transmitral flow velocity and their ratio (E/A). Left atrial (LA) volumes were determined at mitral valve (MV) opening (maximal, Vmax), at onset of atrial systole (P wave of the ECG, Vp), and at MV closure (minimal, Vmin) from the apical 2- and 4-chamber views, using the biplane area-length method. LA systolic function was assessed with the LA active emptying volume (ACTEV) = Vp-Vmin and the LA active emptying fraction (ACTEF) = ACTEV/Vp. RESULTS: Average NN (967.1 +/- 141.8 vs. 768.4 +/-85.6 ms, P < 0.0001), logSDNN (1.89 +/- 0.14 vs. 1.80 +/- 0.17 ms, P < 0.05), logPNN 50% (1.66 +/- 0.23 vs. 1.46 +/- 0.35, p < 0.05), and logHF power (3.13 +/- 0.32 vs. 2.95 +/- 0.26 ms2, p < 0.05) were greater in swimmers than in controls. Left ventricular end-diastolic diameter was greater (32.3 +/- 3.3 vs. 29.5 +/- 3.3 mm m(-2), P < 0.02) in swimmers than in controls, whereas the left ventricular septal (5.9 +/- 1 vs. 5.6 +/- 0.8 mm m(-2), P = NS) and posterior wall thickness (5.7 +/-0.9 vs. 5.4 +/- 0.8 mm m(-2), P = NS) were similar in the two groups. The E/A ratio was greater (2.2 +/- 0.49 vs. 1.78 +/- 0.36, P < 0.003) whereas the A velocity was lower (0.41 +/- 0.09 vs. 0.50 +/- 0.13 m s(-1), P < or = 0.02) in swimmers than in controls. Vmax was greater (18.6 +/-4.8 vs. 14.9 +/-5.3 cm m(-2), P < 0.03), whereas ACTEF was lower (36 +/- 12% vs. 44.2 +/- 12%, P < 0.04) in swimmers than in controls. CONCLUSION: Cardiac adaptation to intensive training in prepubertal swimmers includes vagal predominance, a mild increase in left ventricular dimensions without significant changes in septal or posterior wall thickness, and increased LA size associated with depressed LA systolic function. Evaluation of LA size and systolic function may contribute to a better understanding of the characteristics of the 'athlete's heart' in children and to the differential diagnosis between left ventricular adaptive and pathologic changes.     

Mitral regurgitation following mitral balloon valvotomy. Differing mechanisms for severe versus mild-to-moderate lesions

BACKGROUND. This study was designed to evaluate the incidence and mechanisms of mitral regurgitation following mitral balloon valvotomy (MBV) in 40 consecutive patients with symptomatic tight pliable mitral stenosis. METHODS AND RESULTS. Transthoracic echocardiography with color flow mapping was performed before and 24 hours after the procedure. Patients who developed significant mitral regurgitation following MBV also underwent transesophageal echocardiography. The relation between increased mitral regurgitation and both valvular morphology and procedure-related factors was examined. Gorlin mitral valve area increased from 0.81 +/- 0.3 to 1.95 +/- 0.7 cm2 (p less than 0.001). No patient had more than 2+ mitral regurgitation by angiography and color Doppler prior to MBV. There was a moderate correlation between Doppler and angiographic increase in mitral regurgitation (r = 0.73, p less than 0.0001). By Doppler criteria 33 patients had no (n = 6) or mild (n = 27) increase in mitral regurgitation (group 1), and seven developed significant new mitral regurgitation (group 2). Baseline clinical, echocardiographic, and procedure-related data for the two groups were similar. Multiple regression analysis did not select any individual valve characteristic (valvular thickening, mobility, calcification, and subvalvular disease), total echocardiographic score, balloon diameter, or ratio of balloon to mitral annular diameter as disruption with a torn anterior or posterior mitral leaflet in six and a ruptured papillary muscle in one. Two of these patients have required mitral valve replacement (6 and 9 months following the procedure), whereas the remainder are significantly symptomatic. By contrast, mitral regurgitation in group 1 either occurred at the site of commissural split (n = 20) or was associated with prolapse of the anterior mitral leaflet (n = 6). CONCLUSIONS. Thus, severe new mitral regurgitation following MBV is due to noncommissural tearing of the mitral leaflet and confers an adverse long-term prognosis. A mild increase in mitral regurgitation following MBV is frequent and occurs at the site of commissural split or is associated with prolapse of the anterior leaflet. Furthermore, in this study, an increase in mitral regurgitation could not be predicted from any valvular or procedure-related factor.     

Heart failure with reduced,mildly reduced,or preserved left ventricular ejection fraction: Has reasoning been lost?

Left ventricular (LV) ejection fraction (LVEF), defined as LV stroke volume divided by end-diastolic volume, has been systematically used for the diagnosis, classification, and management of heart failure (HF) over the last three decades. HF is classified as HF with reduced LVEF, HF with midrange or mildly reduced LVEF, and HF with preserved LVEF using arbitrary, continuously changing LVEF cutoffs. A prerequisite for using this LVEF-based terminology is knowledge of the LVEF normal range, which is lacking and may lead to erroneous conclusions in HF, especially at the higher end of the LVEF spectrum.     

Impact of dopamine infusion on renal function in hospitalized heart failure patients: results of the Dopamine in Acute Decompensated Heart Failure (DAD-HF) Trial

BackgroundWorsening renal function (WRF) and hypokalemia related to diuretic use for acute decompensated heart failure (ADHF) are common and associated with poor prognosis. Low-dose dopamine infusion improves renal perfusion; its effect on diuresis or renal function specifically in ADHF is not known.Methods and ResultsSixty consecutive ADHF patients (age 75.7 ± 11.2 years; 51.7% female; left ventricular ejection fraction 35.3 ± 12.1%) were randomized, after receiving a 40 mg intravenous furosemide bolus, to either high-dose furosemide (HDF, 20 mg/h continuous infusion for 8 hours) or low-dose furosemide combined with low-dose dopamine (LDFD, furosemide 5 mg/h plus dopamine 5 μg kg^?1 min^?1 continuous infusion for 8 hours). Both strategies were compared for total diuresis, WRF (defined as a rise in serum creatinine of >0.3 mg/dL from baseline to 24 hours), electrolyte balance, and 60-day postdischarge outcomes. Mean hourly excreted urine volume (272 ± 149 mL in HDF vs 278 ± 186 mL in LDFD group; P = .965) and changes in dyspnea score (Borg index: ?4.4 ± 2.1 in HDF group vs ?4.7 ± 2.0 in LDFD group; P = .575) during the 8 hours of protocol treatment were similar in the two groups. WRF was more frequent in the HDF (n = 9; 30%) than in the LDFD group (n = 2; 6.7%; P = .042). Serum potassium changed from 4.3 ± 0.5 to 3.9 ± 0.4 mEq/L at 24 hours (P = .003) in the HDF group and from 4.4 ± 0.5 to 4.2 ± 0.5 mEq/L at 24 hours (P = .07) in the LDFD group. Length of stay and 60-day mortality or rehospitalization rates (all-cause, cardiovascular, and worsening HF) were similar in the two groups.ConclusionsIn ADHF patients, the combination of low-dose furosemide and low-dose dopamine is equally effective as high-dose furosemide but associated with improved renal function profile and potassium homeostasis.Clinical Trial Registration InformationClinicalTrials.gov Identifier: NCT00937092 (http://clinicaltrials.gov/ct2/show/NCT00937092)     

Global left atrial failure in heart failure

The left atrium plays an important role in the maintenance of cardiovascular and neurohumoral homeostasis in heart failure. However, with progressive left ventricular dysfunction, left atrial (LA) dilation and mechanical failure develop, which frequently culminate in atrial fibrillation. Moreover, LA mechanical failure is accompanied by LA endocrine failure [deficient atrial natriuretic peptide (ANP) processing‐synthesis/development of ANP resistance) and LA regulatory failure (dominance of sympathetic nervous system excitatory mechanisms, excessive vasopressin release) contributing to neurohumoral overactivity, vasoconstriction, and volume overload (global LA failure). The purpose of the present review is to describe the characteristics and emphasize the clinical significance of global LA failure in patients with heart failure.     

Excessive vasoconstriction in rheumatic mitral stenosis with modestly reduced ejection fraction.

OBJECTIVES. The primary hypothesis examined was that underfilling due to inflow obstruction accounts for modestly depressed ejection performance in mitral stenosis. Having found little evidence to support this hypothesis, we sought to determine other factors that might differentiate patients with different levels of ejection performance. METHODS. Ventricular load and performance were compared in two groups of patients before and immediately after successful balloon valvuloplasty that was not complicated by mitral regurgitation: those in whom prevalvuloplasty ejection fraction was > or = 0.55 (group I, n = 10) and those in whom it was < 0.55 (group II, n = 11). RESULTS. Before valvuloplasty, mitral valve area was less in group II (0.65 cm2) than in group I (0.84 cm2, p = 0.02), but end-diastolic pressure (12 vs. 12 mm Hg in group I), end-diastolic wall stress (46 vs. 44 kdynes/cm2 in group I) and end-diastolic volume (152 vs. 150 ml in group I) were not less in group II, nor were these variables significantly reduced compared with those of a normal control group. In group II, end-systolic volume was larger (77 vs. 55 ml in group I, p = 0.001) and cardiac output was less (3.1 vs. 3.6 liters/min in group I, p = 0.03), possibly owing to higher systemic vascular resistance (2,438 vs. 1,921 dynes.s.cm-5 in group I, p = 0.05) and end-systolic wall stress (273 vs. 226 kdynes/cm2 in group I, p = 0.06), although mean arterial pressure in the two groups was similar (91 vs. 84 mm Hg in group I, p = 0.22). Group II patients also had higher values for pulmonary vascular resistance (712 vs. 269 dynes.s.cm-5 in group I, p = 0.03) and mean pulmonary artery pressure (47 vs. 29 mm Hg in group I, p = 0.02) despite similar values for mean left atrial pressure (20 vs. 18 mm Hg in group I, p = 0.35). After valvuloplasty, mitral valve area increased by 2.5- and 3-fold, respectively, in group I (to 2.1 cm2) and group II (to 2.0 cm2). Modest increases in left ventricular end-diastolic pressure, end-diastolic stress and end-diastolic volume (+9%) after valvuloplasty were statistically significant only for group II. End-systolic wall stress did not decline in either group II (281 kdynes/cm2) or group I (230 kdynes/cm2), and ejection fraction failed to increase significantly (0.49 to 0.51 for group II and 0.62 to 0.61 for group I) after valvuloplasty. Contractile performance estimated with a preload-corrected ejection fraction-afterload relation was within or near normal limits in all 19 patients in whom it was assessed. CONCLUSIONS. Excessive vasoconstriction may account for the higher afterload, lower ejection performance and lower cardiac output observed in a subset of patients with mitral stenosis because contractile dysfunction could not be detected and left ventricular filling--which was not subnormal despite severe inflow obstruction--improved only modestly after valvuloplasty.