This is the first experience in France of telemedicine consultation for pediatric and congenital cardiology. These videoconferences allowed patients in the south of Réunion to benefit from a specialist opinion on optimal therapeutic strategy, with no delay or need to travel a long distance.

SUMMARY. The early adaptation to aortic stenosis was studied in eight conscious dogs previously instrumented with a left ventricular micromanometer and ultrasonic crystals measuring left ventricular minor equator, left ventricular major axis, and ventricular wall thickness. Data were compared during control, acute inflation of a supravalvular aortic cuff ocduder and 24 hours after aortic stenosis with and without jS-blockade. Acute aortic stenosis increased peak systolic pressure and end-systolic pressure with a decrease of percent systolic shortening of minor diameter (%AL). Twenty-four hours after aortic constriction for heart rates, end-diastolic dimensions, and systolic pressures similar to those measured during acute aortic stenosis, %AL was significantly increased, compared with acute aortic constriction, and was close to control values. End-systolic diameter was not significantly different from control during sustained pressure overload, although end-systolic stress was increased by 26.7 ± 6.1% (P < 0.01 with control), representing a leftward shift of the end-systolic stress-diameter relation. Similar results were obtained under /J-blockade. We conclude that there is, in this model of moderate pressure overload, a nonsympathetic increased inotropic state very early after aortic constriction. (Circ Res 54: 21-29, 1984)

Factors determining peak velocity of fibre lengthening (dL/dtmax) were examined in 12 conscious dogs previously instrumented with a left ventricular pressure micromanometer and ultrasonic crystals measuring internal left ventricular diameter and myocardial segment length. dL/dtmax was studied during control state, atrial pacing, volume loading and methoxamine injection. The behaviour of dL/dtmax was similar in diameters and in segments. A significant correlation was found during control in each dog between dL/dtmax and the extent of systolic shortening (delta L). The effect of filling pressure on dL/dtmax appeared by comparing moderate volume loading and maximal volume loading where deltaL were similar while dL/dtmax was increased by 7.1% in segments and 20.2% in diameters. However, the effect of filling pressure on dL/dtmax was less pronounced that the effect of delta L since, for matched delta L during control and during volume loading, dL/dtmax increased by 37.9% while a 25% increase of delta L increased dL/dtmax by 55.6%. Heart rate and afterload changes did not appear as influencing dL/dtmax for matched deltaL. In conclusion, although and increased filling pressure does increased significantly dL/dtmax, the extent of systolic shortening, and thus restoring forces, appear as the primary determinant of peak velocity of fibre lengthening in basal conditions.

In La Réunion, the total prevalence of congenital heart defects is far inferior to that found in Europe. The difference can be attributable to lower prevalences of mild congenital heart defects.

The behavior of the end-systolic ventricular diameter was examined during control state, atrial pacing, and acute volume loading (VL) followed by methoxamine infusion in conscious dogs instrumented with a left ventricular micromanometer and ultrasonic crystals measuring internal diameter and wall thickness. Heart rate and systolic pressure were markedly increased by maximal VL but for moderate VL were minimally modified. Moderate VL increased end-diastolic diameter by 5% and end-systolic diameter by 2.9% with a significant increase of systolic stress. There was no common final pathway of shortening in the force-velocity-length diagram for different preloads. During methoxamine infusion, the end-systolic pressure-diameter points described a linear regression but points obtained during atrial pacing before VL were significantly shorter. We conclude that VL increases the total loading of the heart producing a lengthening of the end-systolic diameter when end-diastolic diameter is increased. This reduces the expression of the Starling mechanism and suggests caution when interpreting end-systolic pressure-diameter relations and derived indices for significantly different end-diastolic diameters.