Biomedical subjects

M Grobéty

Publications and source records attributed to M Grobéty.

8 recordsLinked to original sources

PubMed1999

Corrective use of the 2.5-mm GFX stent for suboptimal angioplasty results in small coronary arteries.

To evaluate the clinical efficacy of endoluminal stenting in the setting of percutaneous intervention for small coronary artery lesions, we reviewed our results on stenting with the 2.5-mm GFX stent (Arterial Vascular Engineering, Santa Rosa, CA) during an 18-month study period. A total of 120 patients with significant coronary artery disease in vessels </=2.6 mm were followed up clinically. Procedural success (defined as angiographic residual stenosis <20% without clinical complications) was obtained in 94% of cases. In-hospital complications were death (1%), non-Q-wave myocardial infarction (5%), and urgent repeat percutaneous intervention because of stent thrombosis (3%). During a mean follow-up of 9.8 months (range, 6-23 months), the following complications were noted: myocardial infarction (1%), clinical need for repeat intervention (13%) requiring repeat percutaneous treatment (12%) and surgical revascularization (1%). In conclusion, transcatheter application of a specifically designed stent for coronary artery disease in small vessels seems safe and efficient with a low incidence of adverse events during follow-up. Cathet. Cardiovasc. Intervent. 48:157-161, 1999.

Adult↗

PubMed1999

The chick embryo heart as an experimental setup for the assessment of myocardial remodeling induced by pacing.

The mechanisms regulating remodeling of the heart are not well understood and only rarely investigated for pacing. We therefore developed a model based on the well-established chick embryo heart preparation. Hamburger Hamilton 21 stage Leghorn chick embryos were used. Access to the heart was obtained after having dissected the shell membranes. The electrodes (platinum wires) were placed in ovo: the anode on the vitelline membrane and the cathode at different sites of the heart (sinus venosus, base/apex of the ventricle). Sensing and stimulation thresholds were measured. Survival of the paced chick was studied. Among 30 chick embryonic hearts, the stimulation thresholds were 1.4 mV +/- 0.5 SD for the atrium, 2.6 V +/- 1.4 SD at the base, and 3.2 V +/- 1.5 SD at the apex of the ventricle, while the sensing signals were 1.3 mV +/- 0.5 SD at the atrium, 19.6 mV +/- 4.1 SD at the base, and 21.6 mV +/- 3.9 SD at the apex of the ventricle. Continuous pacing (pacing rate = intrinsic rate + 10%) could be maintained for 1.5 hours +/- 0.5 SD at the atrium, 8.9 hours +/- 0.7 SD at the base of the ventricle, and 7.9 hours +/- 1 SD at the apex of the ventricle up to death of the embryos. By using intermittent electrical stimulation, the association of 5 minutes on/5 minutes off pattern during 18 hours and 5 minutes on/15 minutes off, during 30 hours resulted in an effective pacing period of 19 hours in 60% of the experiments, reflecting 15 cell turnover cycles. This experimental setup will allow the study of morphological, metabolic, and molecular bases of ventricular remodeling induced by electrical stimulation.

Animals↗

PubMed1999

Pacing-induced ventricular remodeling in the chick embryonic heart.

Chronic ectopic pacing in the adult heart induces myocardial hypotrophy close to the pacing site. We have recently described a similar localized decrease of compact myocardium thickness in the chick embryonic heart after 48 h of intermittent apical ventricular pacing. Here we analyze the cellular mechanisms underlying the response of the embryonic heart to pacing. Because the developing heart had been found to adjust its morphology according to functional demands by undergoing cellular hyperplasia or hypoplasia, we hypothesized that the stimulation should result in hypoplasia of the apical ventricular compartment. Morphologic analysis of hearts submitted to 18 h of effective pacing during 48 h showed a mild to moderate ventricular dilatation, a 28% decrease in the apical compact layer thickness with no changes in other ventricular locations, and atrial wall thickening. These modifications were caused by changes in the number of cell layers, whereas cell size was similar between paced and control hearts. Analysis of proliferative activity after 24 h of pacing showed a decrease of 32% in the rate of cell proliferation limited to the apical compact layer exposed to stimulation. No ultrastructural injury or increased cell death was found. These changes were accompanied by down-regulation of the myocardial growth factor fibroblast growth factor-2 but no differences were found in the expression of platelet-derived growth factor. Thus, chronic intermittent ventricular pacing induces myocardial remodeling in the chick embryonic heart, on the basis of locally regulated rates of cell proliferation.

Animals↗

PubMed1997

[Sudden death in hypertrophic obstructive and non-obstructive cardiomyopathy: can it be prevented?].

Sudden cardiac death constitutes the most devastating aspect of obstructive and non-obstructive hypertrophic cardiomyopathy. Loss of consciousness and family history of sudden cardiac death should alert the physician to the risk of sudden death. ECG, morphological and hemodynamic assessment, and exploration of central nervous activity are of little use in stratifying the risk of sudden cardiac death. Loss of consciousness associated with nonsustained ventricular tachycardia and inducible sustained ventricular arrhythmia identify patients at very high risk of sudden cardiac death. Nevertheless, many variable factors are involved in the pathophysiology of sudden cardiac death, and hence risk stratification of sudden cardiac death in patients with hypertrophic cardiomyopathy remains a very difficult clinical challenge.

Adolescent↗

PubMed1996

[Value of Doppler ultrasonic studies in the diagnosis of deep venous thrombosis of the lower limbs].

To compare the operating characteristics of the venous echo-doppler and that of venous phlebography in our setting, 90 consecutive patients admitted on suspicion of deep vein thrombosis of one leg underwent both examinations. Phlebography confirmed the diagnosis in 46 patients (51%). The sensitivity, specificity, and positive and negative predictive values of the echo-doppler were 91, 92, 94 and 90% respectively. For the subgroup of patients with proximal deep vein thrombosis, these values were 97, 97, 97 and 97%, respectively; for the subgroup with distal deep vein thrombosis, these values were 60, 95, 75 and 90%, respectively. This study confirms the excellent performance of the venous echo-doppler for the diagnosis of deep vein thrombosis of the leg in our hospital. However, in the subgroup of patients with distal deep vein thrombosis, only the sensitivity of the venous echo-doppler is relatively low and the diagnosis may still require color echo-doppler or phlebography.

Diagnosis, Differential↗

PubMed1996

[Cardiac pacemaker dysfunction secondary to outside interference: a review].

Electromagnetic signals from various sources may cause interference with pacemakers. The safety systems developed by manufacturers are generally effective. Nevertheless, some electromagnetic sources, particularly those found in the medical environment, can induce transitory or permanent pacemaker dysfunction. This paper presents the various sources of electromagnetic signals to which a pacemaker may be exposed. Taking into account the available literature, it attempts to clarify those which are really deleterious for the pacemaker and how to avoid them.

Biophysical Phenomena↗

PubMed1995

[Malfunction of a mitral bioprosthesis, hemolysis and acute renal insufficiency].

Intravascular hemolysis is a rare complication following valvular replacement, particularly with bioprostheses. It is generally secondary to prosthetic malfunction and is the cause of anemia. We report a rare case of acute renal insufficiency and severe hemolysis caused by malfunction of a bioprosthesis in the mitral position.

Acute Kidney Injury↗

PubMed1992

[Rhabdomyolysis, acute renal insufficiency and hypercalcemia].

Acute renal failure is a severe and frequent complication of rhabdomyolysis. During the early polyuric phase, hypercalcemia is observed in around 30% of cases. The principal mechanism is the liberation of calcium from areas of muscular necrosis. Two cases of toxic rhabdomyolysis with secondary hypercalcemia are described.

Acute Kidney Injury↗