Percutaneous closure of atrial septal defect type ostium secundum using the new Intrasept occluder: initial experience.

We report the first experience obtained with the new Intrasept device. We attempted to treat 35 patients with a mean age of 43 +/- 21 years. The mean size of the defect was 17/15 mm. It was successfully closed in 31 patients. In the remaining four the device could not be stabilized because of excessive defect size. A small residual shunt was present immediately following implantation in three patients. No complications occurred during the procedure and at 6 months, 31 patients had an uneventful outcome. Only one patient had a small residual shunt. No thrombus, embolization, or device fracture was documented during a mean follow-up of 17 +/- 11 months. Percutaneous closure of ASD ostium secundum is feasible with the Intrasept device with a high success rate and very good medium-term outcome. Our initial experience and results were excellent with small to medium size defects, however, large defects (>20 mm) remain challenging.

[Percutaneous closure of patent foramen ovale: preliminary experience with the PFO Star]. / Fermeture percutanée de foramen ovale perméable: expérience préliminaire avec le PFO Star.

This article reports the experience of percutaneous closure of patent foramen ovale with the PFO Star device. Between January 2000 and December 2002, 44 consecutive patients with a mean age of 53 years were included in this registry. The implantation of the prosthesis was successful in 43 patients (98%): in 1 patient the atrial septum could not be crossed at operation. An early complication was observed in 3 patients (7%): one had transient amnesia and two patients had temporary ST elevation in the inferior ECG leads. Four patients (7%) had late complications: there was one case of spontaneously regressive atrial fibrillation, two recurrences of stroke (one in the patient without an implanted prosthesis and the other in a patient in whom the patent foramen ovale had been closed). Finally, one patient developed a fistula between the aorta and right atrium which occluded spontaneously when the anticoagulants were stopped. Complete closure of the patent foramen ovale was confirmed at 1 year in 92% of patients. The authors conclude that this preliminary experience shows that closure of patent foramen ovale with this device is effective and safe.

[Endocarditis due to HACEK bacteria. A case report of endocarditis due to Kingella kingae]. / Les endocardites dues aux germes du groupe HACEK. A propos d'un cas d'endocardite native à Kingella kingae.

Endocarditis is a common disease in hospital practice. Identification of the microorganism responsible for the valvular damage is essential to establish the prognosis and to determine the optimal antibiotic treatment. In some cases of endocarditis the diagnosis is laborious, especially when the responsible microorganism is difficult to detect using standard culture techniques. Here we report a case of native aortic valve endocarditis due to Kingella kingae, a Gram negative organism of the HACEK group. In addition we review 6 other cases of endocarditis caused by organism belonging to this group, treated in our hospital between 1983 and 1999. Epidemiological studies show that less than 5% of all cases of endocarditis are caused by organisms of the HACEK group. The diagnosis is often delayed because their slow growth on a standard culture medium. We describe clinical and microbiological characteristics of this group of endocarditis.

Haemodynamic and sympathetic effects of inhibition of nitric oxide synthase by systemic infusion of N(G)-monomethyl-L-arginine into humans are dose dependent.

BACKGROUND: In several animal species, nitric oxide (NO) buffers central neural sympathetic outflow, but data concerning humans are sparse and conflicting. We hypothesized that these conflicting results could be related to large differences in the dose of N(G)-monomethyl-L-arginine, a stereospecific inhibitor of NO synthase, infused in these human studies. OBJECTIVE: To investigate the haemodynamic and sympathetic effects of systemic inhibition of NO synthase by intravenous infusion of two different doses of N(G)-monomethyl-L-arginine into healthy humans and compare these effects with those of an equipressor dose of the non-endothelium-dependent vasoconstrictor phenylephrine. METHODS: Muscle sympathetic nerve activity was measured by microneurography and blood flow by venous occlusion plethysmography. N(G)-monomethyl-L-arginine was infused over 15 min at a rate of 50 microg/kg per min into members of one group (n = 8) and at a rate of 450 microg/kg per min into members of another group (n = 7). An equipressor dose of phenylephrine was infused into four subjects from each group. RESULTS: Infusions of N(G)-monomethyl-L-arginine and of phenylephrine at the higher dose similarly suppressed sympathetic activity. In contrast, infusions of N(G)-monomethyl-L-arginine and of an equipressor dose of phenylephrine at the lower dose had different sympathetic effects. Burst frequency of muscle sympathetic nerve activity remained unchanged during infusion of N(G)-monomethyl-L-arginine but decreased by roughly 50% during infusion of phenylephrine. Infusion of N(G)-monomethyl-L-arginine at both doses did not alter forearm blood flow. Only infusion of N(G)-monomethyl-L-arginine at the higher dose increased forearm vascular resistance. CONCLUSIONS: Haemodynamic and sympathetic effects of inhibition of NO synthase by infusion of N(G)-monomethyl-L-arginine into humans are dose dependent. At higher doses, N(G)-monomethyl-L-arginine exerts sympathoinhibitory effects that are comparable to those evoked by a non-specific vasoconstrictor drug, whereas at lower doses, it exerts sympatho-excitatory effects.

Cardiovascular and sympathetic effects of nitric oxide inhibition at rest and during static exercise in humans.

BACKGROUND: Nitric oxide (NO) regulates vascular tone and blood pressure, and studies in animals suggest that it does so, at least in part, by modulating sympathetic neural outflow. Loss of NO-induced vasodilator tone and restraint on sympathetic vasoconstrictor outflow could lead to exaggerated vasoconstrictor and pressor responses to physical stress in humans. METHODS AND RESULTS: To determine the role of NO in the modulation of central sympathetic outflow and vascular tone at rest and during a physical stress, we tested effects of systemic inhibition of NO synthase by N(G)-monomethyl-L-arginine (L-NMMA) infusion (a stereospecific inhibitor of NO synthase) on sympathetic nerve activity (microneurography), regional vascular resistance, and blood pressure at rest and during static handgrip. The major new findings are that (1) under resting conditions, L-NMMA infusion, which increased mean arterial pressure by approximately 10%, did not have any detectable effect on muscle sympathetic nerve activity, whereas a similar increase in arterial pressure evoked by phenylephrine infusion (an NO-independent vasoconstrictor) decreased the rate of sympathetic nerve firing by approximately 50%; (2) during static handgrip, the exercise-induced sympathetic nerve responses were preserved during L-NMMA infusion but markedly attenuated during phenylephrine infusion; and (3) the L-NMMA-induced loss of vasodilator tone did not result in exaggerated exercise-induced pressor and calf vasoconstrictor responses. CONCLUSIONS: These findings indicate that NO is involved in the central regulation of sympathetic outflow in humans and suggest that both neuronal and endothelial NO synthesis may contribute to the regulation of vasomotor tone.

Body fat and sympathetic nerve activity.

Obesity, a major health problem in industrialized societies, is associated with a high incidence of cardiovascular complications such as hypertension, ischemic heart disease and stroke. However, the underlying mechanism relating obesity and these cardiovascular events is not clear. In lean subjects even slight elevations in plasma insulin concentration exert marked effects on the cardiovascular system, and these effects are directly related to insulin (rather than to insulin-induced stimulation of intermediary metabolism). Moreover, insulin's vascular effects are mediated both by the sympathetic nervous system and the L-arginine nitric oxide pathway. Obesity is characterized by sustained sympathetic activation (possibly related to chronic hyperinsulinemia) and an impaired vasodilator responsiveness to insulin. Although, undoubtedly many factors contribute to the increased incidence of cardiovascular complications in overweight subjects, sympathetic activation could be one important mechanism and either trigger acute events or--possibly in conjunction with an impairment in insulin-induced vasodilation--contribute to sustained elevation of arterial pressure.

Insulin-induced sympathetic activation and vasodilation in skeletal muscle. Effects of insulin resistance in lean subjects.

Insulin-induced stimulation of blood flow and sympathetic nerve activity in skeletal muscle tissue is impaired in obesity, but the underlying mechanism is unknown. To determine whether insulin resistance alters sympathetic and vasodilatory responses to euglycemic hyperinsulinemia, in eight healthy subjects we measured calf blood flow and muscle sympathetic nerve activity (MSNA) (n = 5) during insulin/glucose infusion (euglycemic hyperinsulinemic [6 pmol.kg-1.min-1] clamp) performed alone and performed during concomitant fat emulsion infusion, a maneuver designed to induce insulin resistance. The major new finding is that fat emulsion infusion, which attenuated insulin-induced stimulation of carbohydrate oxidation by 39 +/- 7% (P < 0.01), did not have any detectable effect on insulin-induced vasodilatory and sympathetic responses: at the end of the 2-h clamp, blood flow and MSNA had increased by 35 +/- 6% (P < 0.01) and 152 +/- 58% (P < 0.01), respectively, during insulin infusion alone and by 35 +/- 7% (P < 0.01) and 244 +/- 90% (P < 0.01), respectively, during insulin infusion superimposed on free fatty acid infusion. These observations in lean healthy subjects indicate that induction of resistance to the stimulatory effects of insulin on carbohydrate metabolism does not attenuate muscle blood flow and MSNA responses evoked by acute euglycemic hyperinsulinemia. These findings provide further evidence that hyperinsulinemia per se is the primary stimulus that triggers stimulation of muscle blood flow and MSNA during insulin/glucose infusion in humans and suggest that the impaired insulin-induced vasodilation in obese subjects is not related primarily to impaired stimulation of muscle carbohydrate metabolism.