[Physical reproduction of cardiac sutures. A new field of investigation in cardiology]. / Reproduction physique des structures cardiaques. Une nouvelle voie d'exploration en cardiologie.

A new technique of physical reproduction of cardiac anatomy has been developed from volumetric data and its practical value assessed in cardiological practice. The acquisition of the volumetric data was by 3D echocardiography. Parallel and equidistant 2D views were selected from this information. The images were printed at a scale adjusted to the true dimensions of the structures of interest and then stuck on a support, the thickness of which was identical to the distance between the views, and the slices were superimposed while respecting the initial orientation. This technique has been adapted secondarily to modern industrial processes of rapid prototyping (3D printing and powdering) allowing automatic tooling of models. Several physical models have been made: whole heart in end diastole, mitral valve stenosis and prolapse, atrial septal defect with insertion of a percutaneous prosthetic device, great vessels at the base of the heart. There are many possible cardiological applications of physical models: investigation of complex cardiac disease, pre- and per-operative simulation of surgical procedures, elaboration of prosthetic material, physiopathological studies, teaching and training, patient information.

[Three-dimensional echocardiography. Principles and applications]. / Echocardiographie tridimensionnelle. Principes et applications.

Three-dimensional echocardiography is based on two methods of retrospective reconstruction from two-dimensional echocardiographic images. The acquisition of the two-dimensional images may be free or imposed, the transducer either carrying an emission-reception system or fixed to an articulated support providing data about its position. In the first system, manual tracing of the contours of the region of interest performed on each frame are superimposed after time sequencing (using the ECG) and spatial repositioning, so enabling three-dimensional visualisation of the contours of the cardiac structures: this approach provides reliable quantitative information (volumes, mass and ejection fractions) and has led to the redefinition of the echocardiographic criteria of mitral valve prolapse. The second system is based on equidistant sections obtained by progressive, controlled two-dimensional scanning (parallel, arc of a circle and rotational) of the structure of interest: a value of grey scale is assigned to the space between two adjacent pixels, enabling the formation of voxels which, when superimposed, give the required effects of volume and surface for three-dimensional imaging. It is then possible to obtain any section of the volume and simulate surgical views of the beating heart. This approach may significantly improve diagnostic accuracy compared with two-dimensional echocardiography and provides access to new quantitative and qualitative parameters.

[Value and limitations of methods for measuring left ventricular mass]. / Intérêts et limites des méthodes de mesure de la masse ventriculaire gauche.

M-mode echocardiographic measurement of the left ventricular mass is inaccurate when the hypertrophy is asymmetric and the ventricule very deformed. The routine calculation of the mass is based on several hypotheses, verified in normal and hypertensive subjects: the standard error (SEE) is 30-40 g, 10-15% (r > 0.9). The standard deviation of inter-examination differences (> 25 +/- 30 g with a variation coefficient c = 10-15%) makes it difficult to appreciate variations of mass in a given patient. Two-dimensional echocardiographic measurement of left ventricular mass requires the use of geometric formulae which have not been validated in the cardiomyopathies. The absence of a consensus on the models used has favorized the use of MRI and of ultrafast computed tomography. MRI measurement of mass has been validated in normal and ischaemic hearts (r > 0.97, SEE < 8 g, c = 15%) but the times of acquisition are long. Using ultrafast CT, not universally available, this measurement has been validated in vivo and in vitro, including in cardiomyopathy for which the SEE is low (6%) and reproducibility excellent (c = 4-8%), comparable with results in normal subjects.

[Three-dimensional echocardiography: methodology trial]. / Echocardiographie tridimensionnelle: essai de méthodologie.

A method has been developed for systematic and reproducible exploration by three-dimensional echocardiography. An associated technical terminology has also been introduced, and the application principles have been examined together with a number of useful clinical examples. After a period of technical and clinical validation, three-dimensional echocardiography has now entered the stage of practical clinical application, in particular for mitral valve disorders and intraauricular communications. The methodology that has been proposed is intended to provide user training, facilitate communication with teams working in the field, and also between echography operators and surgeons, and catheter or clinical staff.

Clinical study of the effects of latissimus dorsi muscle flap stimulation after cardiomyoplasty.

BACKGROUND: Beneficial hemodynamic effects after dynamic cardiomyoplasty have been inconsistently demonstrated, and the effects seen may be due to the wrap itself, to flap stimulation, or both. The aim of this study was to determine whether flap stimulation per se acts as a systolic active process after cardiomyoplasty. METHODS AND RESULTS: Catheterizations were performed in 13 patients 14.4 +/- 7 months after cardiomyoplasty. New York Heart Association functional class decreased from 3.3 to 2.1 after the procedure (P = .0005). Hemodynamic evaluations were first performed with the stimulator on in the 2:1 mode and then after the stimulator had been off for at least 24 hours. Left ventricular (LV) ejection fraction increased from 25.1 +/- 6% before surgery to 28.2 +/- 6.7% with the stimulator on after cardiomyoplasty (P = .04). When stimulation was stopped, there was no change (P > .05) in indexes of systolic or diastolic LV function (peak systolic LV pressure, LV ejection fraction, peak positive dP/dt, peak negative dP/dt, or tau). Pulmonary capillary wedge pressure and cardiac index were unchanged when stimulated and nonstimulated settings were compared (P > .05). However, a remarkable heterogeneity of individual responses was observed. Ejection fraction and cardiac index decreased with the stimulator off in 3 patients, but peak positive dP/dt decreased in 6 patients; diastolic function deteriorated in 2 patients, but a slight improvement was noted in 3 patients. Cardiothoracic ratio, echocardiographic LV end-diastolic dimension, and fractional shortening remained unchanged between immediate (< 1 month) and long-term (36.7 +/- 25.9 months) postoperative evaluations. CONCLUSIONS: In the majority of our patients, there was no short-term hemodynamic benefit of flap stimulation; therefore, we conclude that the efficacy of cardiomyoplasty may be a consequence of a passive "girdling effect," which limits the progression of ventricular enlargement and further deterioration of ejection fraction.

Does transplantation of cardiomyocytes improve function of infarcted myocardium?

BACKGROUND: The feasibility of successfully grafting fetal cardiomyocytes into infarcted myocardium is now established, but the functional effects of such a procedure still remain elusive. METHODS AND RESULTS: Twenty-three female rats underwent 45 minutes of coronary artery occlusion followed by 30 minutes of reperfusion. At this time point, 13 animals received intramyocardial injections of fetal cardiomyocytes (6 x 10(6) cells in 60 microL of culture medium) in the once ischemic area, whereas the 10 control rats were injected with an equivalent volume of culture medium alone. One month after transplantation, left ventricular function was assessed by two-dimensional (2D) and Doppler echocardiography using a short focus 10- to 13-MHz transducer, and a numeric acquisition of 2D images up to 65.5 frames/second. Explanted hearts were then processed for histological assessment of infarct size. The presence of male donor cells into female recipient myocardium was detected by fluorescent in situ hybridization using a deoxyribonucleic acid probe specific for Y chromosome. Cellular transplantation resulted in an improved left ventricular function, as demonstrated by significantly higher 2D ejection fraction and cardiac output (P<.02 and P<.02 versus control hearts, respectively). The histological sections of female recipient myocardium were Y-positive in all but one heart, thereby suggesting that this improvement of function was causally related to the presence of transplanted cells. CONCLUSIONS: These data suggest that transplantation of cardiomyocytes might be an effective means of improving function of infarcted myocardium.

Can cellular transplantation improve function in doxorubicin-induced heart failure?

BACKGROUND: Transplantation of fetal cardiomyocytes has been shown to improve function of regionally infarcted myocardium, but its effects on global heart failure are still unknown. METHODS AND RESULTS: Heart failure was induced in female mice by intraperitoneal injection of doxorubicin (2 mg/kg twice per week over 2 cycles of 2 weeks separated by a 2-week drug-free period). One week after the end of treatment, left ventricular function was assessed by transthoracic echocardiography (baseline). Animals were then randomized into 3 groups: The treated group (n = 12) received an intramyocardial injection of fetal cardiomyocytes (1 x 10(6) in 10 microL) harvested from transgenic mice expressing the gene of beta-galactosidase, the control group (n = 15) received an equivalent volume of culture medium alone, and 10 sham mice had no surgery. Two weeks and 1 month after transplantation, function was again assessed echocardiographically. At baseline, fractional shortening was not significantly different between the 3 groups. It then significantly increased in cell-treated mice at 2 weeks and 1 month after transplantation (P < 0.002 and P < 0.03 versus baseline, respectively), whereas it did not change in untreated animals. Transplanted cells could not be identified by beta-galactosidase activity or presence of Y chromosome (with 1 exception). CONCLUSIONS: Cellular transplantation can improve function of globally failing hearts by a mechanism that might not necessarily involve the sustained presence of transplanted cells but rather the effects of cardioprotective factors released by them.