Telemedicine and Cardiology in the Elderly in France: Inventory of Experiments.

Telemedicine is now in vogue, allowing through computer and communication tools to be deployed in the field of health, such as cardiology, area in which it has shown interest, in international studies. As the population ages, older people are increasingly concerned with this innovative practice. We take a look at telemedicine projects in France concerning the elderly, in the field of cardiology.

Telemedicine and Geriatrics in France: Inventory of Experiments.

Telemedicine is now in vogue, being deployed through computer and communication tools in various health fields, such as diabetology, nephrology, dermatology, neurology, and cardiology. With population ageing, geriatrics is coming into sharp focus. Telemedicine practices differ for home-based or institutionalized patients in long-term care homes. We take a look at telemedicine projects in France concerning the elderly.

[Experimentation of an e-platform to detect situations at risk of cardiac impairment (platform E-care) in an internal medicine unit]. / Expérimentation d'une plateforme de détection automatisée des situations à risque de décompensation cardiaque (plateforme E-care) dans une unité de médecine interne.

INTRODUCTION: Monitoring patients with heart failure by telemedicine systems is a potential means susceptible to optimize the management of these patients and avoid life-threatening emergencies. In this context, we experimented in internal medicine unit an e-platform E-care dedicated to automated, intelligent detection of situations at risk of heart failure. METHODS: The E-care platform based on medical sensors (blood pressure, heart rate, O2, weight), communicating (Bluetooth), to go up, in real time, to an intelligent physiological information and an analysis of the ontology medical, leading ultimately to the generation of alerts. After a development phase (proof of concept), the E-care platform has been deployed and tested by health professionals and patients in an internal medicine unit with 20 beds, opened on emergencies to the Strasbourg University Hospitals. RESULTS: One hundred and eighty patients were included and 1500 measurements were obtained. The patient profile included in this experiment was an elderly patient, with comorbidity in 90% of cases, with a loss of autonomy in 25%. Health professionals were using E-care platform every day to their great satisfaction. This experiment made it possible to validate the technology choices, to consolidate the system, and to test the robustness of the platform E-care. The collection continuously allowed us to have the critical number of patients for more detailed analysis of the relevance of alerts related to heart impairment. A preliminary analysis showed the relevance of the generated alerts. CONCLUSION: Preliminary results following the deployment of E-care platform in hospitals appear to show the relevance of technological choices, tools and solutions developed and adopted. This telemedicine system allows automatic, non-intrusive, generate alerts related to the detection of situations at risk for heart failure. Ultimately, E-care was capable of preventing hospitalization. A home deployment is currently underway.

Changes in renal haemodynamics induced by indomethacin in the rat involve cytochrome P450 arachidonic acid-dependent epoxygenases.

A significant renal vasodilation was observed previously after an acute cyclo-oxygenase (COX) inhibition induced with indomethacin. Because this effect could be due to COX-dependent intrarenal metabolization of arachidonic acid through cytochrome P450 (CYP450) pathways, the aim of the present study was to investigate, in vivo, possible interactions between COX and CYP450 mono-oxygenases. Mean arterial pressure (MAP) and renal blood flow (RBF), using an electromagnetic flow transducer for RBF evaluation, were measured continuously in 71 anaesthetized euvolaemic rats. Appropriate solvents (vehicle), 3 mg/kg indomethacin, 17-octadecynoic acid (17-ODYA; 2 mmol/L), either miconazole (MI; 1.5 mmol/L) or N-methylsulphonyl-6-(2-propargyloxyphenyl)hexanamide (MS-PPOH; 5 mg/kg) and N'-hydroxyphenylformamidine (HET0016; 5 or 10 mg/kg) were administered to inhibit either COX, CYP450 mono-oxygenases, epoxygenases or hydroxylase, respectively. The CYP450 and COX inhibitors were also combined as follows: 17-ODYA/indomethacin, MI (or MS-PPOH)/indomethacin, HET0016/indomethacin and indomethacin/HET0016. Mean arterial pressure and RBF were not modified by vehicle, 17-ODYA or MI (or MS-PPOH). However, MAP decreased slightly (P < 0.05; paired t-test, 5 d.f.) and RBF increased transiently (P < 0.05; anova, 5 d.f.) after HET0016. In contrast, MAP decreased by 10 mmHg (P < 0.05) and RBF increased by 10% (P < 0.05) after indomethacin. This enhancement was prevented by 17-ODYA or MI (or MS-PPOH), but not by HET0016. Moreover, RBF increased step-wise to 21% in the indomethacin/HET0016 experiment (P < 0.05). Consequently, changes from baseline in renal vascular resistance differed among treatments, averaging -2 +/- 3 (vehicle), -13 +/- 3 (indomethacin; P < 0.05 vs vehicle), -4 +/- 3 (17-ODYA/indomethacin), -3 +/- 4 (MI or MS-PPOH/indomethacin), -15 +/- 3 (HET0016/indomethacin; P < 0.05) and -22 +/- 4% (indomethacin/HET0016; P < 0.05). In conclusion, these results demonstrate that the renal vasodilation induced by indomethacin can be prevented by prior inhibition of CYP450 mono-oxygenases and further suggest that the CYP450 epoxygenases pathway may prevail.

Effects of Ca(2+) channel activity on renal hemodynamics during acute attenuation of NO synthesis in the rat.

In cultured vascular muscle cells, nitric oxide (NO) has been shown to inhibit voltage-dependent Ca(2+) channels, which are involved in renal blood flow (RBF) autoregulation. Therefore, our purpose was to specify in vivo the effects of this interaction on RBF autoregulation. To do so, hemodynamics were investigated in anesthetized rats during Ca(2+) channel blockade before or after acute NO synthesis inhibition. Rats were treated intravenously with vehicle (n = 10), 0.3 mg/kg body wt N(G)-nitro-L-arginine-methyl ester (L-NAME; n = 7), 4.5 microg. kg body wt(-1). min(-1) nifedipine (n = 8) alone, or with nifedipine infused before (n = 8), after (n = 8), or coadministered with L-NAME (n = 10). Baseline renal vascular resistance (RVR) averaged 14.0 +/- 1.2 resistance units and did not change after vehicle. RVR increased or decreased significantly by 27 and 29% after L-NAME or nifedipine, respectively. Nifedipine reversed, but did not prevent, RVR increase after or coadministered with L-NAME. RBF autoregulation was maintained after L-NAME, but the autoregulatory pressure limit (P(A)) was significantly lowered by 15 mmHg. Nifedipine pretreatment or coadministration with L-NAME limited P(A) resetting or suppressed autoregulation at higher doses. Results were similar with verapamil. Intrarenal blockade of Ca(2+)-activated K(+) channels also prevented autoregulatory resetting by L-NAME (n = 8). These findings suggest NO inhibits voltage-dependent Ca(2+) channels and thereby modulates RBF autoregulatory efficiency.