[Premature ventricular complexes: what to do?] / Extrasystoles ventriculaires : que faire ?

Premature ventricular complexes (PVCs) are frequently encountered arrhythmias in the general population. They can occur in the context of an underlying structural heart disease (SHD) of ischemic, hypertensive or inflammatory cause and therefore be a prognostic factor. Some PVCs can appear in the context of inherited arrhythmic syndromes while others are seen as idiopathic in the absence of an underlying heart condition and are considered benign. Those idiopathic PVCs often arise from the ventricular outflow tracts, mostly from the right ventricle outflow tract (RVOT). The PVCs burden even with no underlying SHD can be associated with PVC-induced cardiomyopathy which is a diagnosis of exclusion.

Les extrasystoles ventriculaires (ESV) sont fréquentes dans la population générale. Elles peuvent résulter d'une cardiopathie sous-jacente d'origine ischémique, hypertensive ou inflammatoire, et représentent alors un facteur pronostique défavorable. Certaines ESV sont l'expression de syndromes arythmiques héréditaires, alors que d'autres sont qualifiées d'idiopathiques lorsqu'elles surviennent en l'absence de cardiopathie structurelle et sont généralement considérées comme bénignes. Elles prennent le plus souvent leur origine dans les chambres de chasse ventriculaires, majoritairement la chambre de chasse droite. Une charge élevée en ESV peut engendrer une cardiomyopathie rythmique avec dysfonction ventriculaire progressive en l'absence de cardiopathie structurelle. Cette entité constitue néanmoins toujours un diagnostic d'exclusion.

[Pacemakers and defibrillators: what the non-specialist needs to know]. / Pacemakers et défibrillateurs: ce que le non-spécialiste doit savoir.

Cardiologists are in charge of the follow-up of patients equipped with pacemakers and defibrillators. In many situations, however, the non-specialist will have to take care of these patients. It is therefore essential that the practitioner understands the basics of how these devices work, the potential complications and the situations in which the cardiologist's intervention is necessary. This article summarizes implantation techniques, post-operative follow-up and potential complications of implantable devices. It recapitulates the differences between pacemaker, defibrillator and resynchronization therapy. It explains the stimulation modes and reminds the reader how the magnet works and the precautions to be taken in the operating theatre, during magnetic resonance imaging or in situations of emergency.

Le suivi des patients porteurs de pacemakers et de défibrillateurs incombe au cardiologue. Dans de nombreuses situations néanmoins, le non-spécialiste devra prendre en charge ces patients. Il demeure donc essentiel que le praticien soit familier avec les bases du fonctionnement de ces dispositifs, les potentielles complications et les situations pour lesquelles l'intervention du cardiologue s'avère nécessaire. Cet article résume les techniques d'implantation, le suivi postopératoire et les complications potentielles de ces dispositifs médicaux; il rappelle également les différences entre pacemaker, défibrillateur et thérapie de resynchronisation. Il revient finalement sur les modes de stimulation, le fonctionnement de l'aimant ainsi que sur les précautions à prendre au bloc opératoire, lors d'examens par résonance magnétique ou en situation d'urgence.

Implications of the local hemodynamic forces on the formation and destabilization of neoatherosclerotic lesions.

OBJECTIVE: To examine the implications of endothelial shear stress (ESS) distribution in the formation of neoatherosclerotic lesions. METHODS: Thirty six patients with neoatherosclerotic lesions on optical coherence tomography (OCT) were included in this study. The OCT data were used to reconstruct coronary anatomy. Blood flow simulation was performed in the models reconstructed from the stent borders which it was assumed that represented the lumen surface at baseline, immediate after stent implantation, and the estimated ESS was associated with the neointima burden, neoatherosclerotic burden and neointima characteristics. In segments with neointima rupture blood flow simulation was also performed in the model representing the lumen surface before rupture and the ESS was estimated at the ruptured site. RESULTS: An inverse association was noted between baseline ESS and the incidence and the burden of neoatherosclerotic (ß = -0.60, P < 0.001, and ß = -4.05, P < 0.001, respectively) and lipid-rich neoatherosclerotic tissue (ß = -0.54, P < 0.001, and ß = -3.60, P < 0.001, respectively). Segments exposed to low ESS (<1 Pa) were more likely to exhibit macrophages accumulation (28.2% vs 10.9%, P < 0.001), thrombus (11.0% vs 2.6%, P < 0.001) and evidence of neointima discontinuities (8.1% vs 0.9%, P < 0.001) compared to those exposed to normal or high ESS. In segments with neointima rupture the ESS was high at the rupture site compared to the average ESS over the culprit lesion (4.00 ±â€¯3.65 Pa vs 3.14 ±â€¯2.90 Pa, P < 0.001). CONCLUSIONS: Local EES is associated with neoatherosclerotic lesion characteristics, which suggests involvement of ESS in the formation of vulnerable plaques in stented segments.

Neointima and neoatherosclerotic characteristics in bare metal and first- and second-generation drug-eluting stents in patients admitted with cardiovascular events attributed to stent failure: an optical coherence tomography study.

AIMS: The aim of this study was to assess neoatherosclerotic plaque morphology in bare metal (BMS) and first- and second-generation drug-eluting stents (DES) in patients presenting with an event attributed to stent failure. METHODS AND RESULTS: Thirty-five patients (11 implanted with BMS, 13 with a first-generation and 11 with a second-generation DES) admitted with an event due to stent failure who had neoatherosclerotic lesions on optical coherence tomography were included in the analysis. The lumen and stent borders were detected and the lipid and calcific tissue were identified in the neointima and their burden was estimated. The neointima attenuation and backscatter indices were computed and compared between the different stent types. Although there were no differences in the neointima burden, the BMS group exhibited thinner fibrous caps (p<0.001), and a numerically increased incidence of lipid-rich plaques (p=0.052) and macrophage accumulation (p=0.012). Neointima discontinuities (p=0.009) and thrombus (p=0.032) were seen more often in first-generation DES. In all stent types, neoatherosclerosis had focal manifestations. In neoatherosclerotic lesions the attenuation and backscatter indices were increased in BMS (p=0.031 and p=0.018, respectively) compared to DES; however, there were no differences between stents in the attenuation indices in subsegments located distally to neoatherosclerotic lesions which had low values in all stent types. CONCLUSIONS: Although there are differences in lipid burden and neointima characteristics in different stent types, in all stents neoatherosclerosis has focal manifestations indicating that, irrespective of the stent type, focal triggers are involved in the generation of vulnerable neolesions.

Intravascular multimodality imaging: feasibility and role in the evaluation of coronary plaque pathology.

Coronary artery disease remains the leading cause of death in the developed world. Over recent years, research has been focused on the development of diagnostic intravascular imaging techniques that enable assessment of plaque composition and morphology, and allow identification of vulnerable, high-risk lesions. Nevertheless recent studies of coronary atherosclerosis have shown that invasive modalities have a limited accuracy in detecting lesions that will progress and cause events, whilst histology-based studies also highlighted the limitations of invasive imaging in assessing plaque characteristics. To overcome these drawbacks, multimodality imaging has been proposed. Although it is apparent that coronary imaging with two or three imaging modalities is time consuming and is associated with a risk of complications, evidence from small clinical studies demonstrated that it provides incremental information about plaque pathology and biology and underscored the need to develop dual-probe hybrid imaging catheters that would enable complete and comprehensive assessment of plaque morphology. This paper reviews the current clinical evidence that supports the use of multimodality intravascular imaging in the study of atherosclerosis, summarizes the key findings of the first invasive imaging studies that utilize hybrid dual-probe catheters, and discusses the limitations of combined intravascular imaging that restrict its broad application in both the clinical and research arena.

Insulin modulation of luteinizing hormone secretion in normal female volunteers and lean polycystic ovary syndrome patients.

BACKGROUND/AIMS: Endocrine features of polycystic ovary syndrome (PCOS) include altered ovarian steroidogenesis, hyperinsulinemia and abnormal luteinizing hormone (LH) secretion. This study was undertaken to further evaluate the role of insulin to modulate LH secretion in lean PCOS patients with normal insulin sensitivity and normal volunteers. METHODS: The study was performed in five nonobese patients diagnosed with PCOS on the basis of amenorrhea and a polycystic morphology at ovarian ultrasound, and 5 normal controls in early to mid-follicular phase and matched for weight and age. All subjects were phenotyped, and then admitted for 12 h of frequent (q 10') blood sampling on two separate occasions, once for a baseline study and the other time for a hyperinsulinemic and euglycemic clamp study. LH was measured in samples obtained throughout each admission in order to perform LH pulse analysis. RESULTS: Baseline LH secretion in PCOS subjects was significantly different from controls: they had higher LH levels, higher LH/FSH ratios as well as a faster LH pulse frequency than normal women. Insulin administration did not affect the pattern of LH secretion of PCOS patients, whereas it significantly increased the LH pulse frequency while decreasing the LH interpulse intervals in the controls. CONCLUSIONS: These data confirm that an abnormal pattern of LH secretion characteristic of PCOS can be observed in lean patients, and appears independent of peripheral insulin levels. Furthermore, our results in lean controls provide the first direct evidence that peripheral insulin can modulate the activity of hypothalamic gonadotropin-releasing hormone (GnRH) neurons in the human.

A 4-wk high-fructose diet alters lipid metabolism without affecting insulin sensitivity or ectopic lipids in healthy humans.

BACKGROUND: High fructose consumption is suspected to be causally linked to the epidemics of obesity and metabolic disorders. In rodents, fructose leads to insulin resistance and ectopic lipid deposition. In humans, the effects of fructose on insulin sensitivity remain debated, whereas its effect on ectopic lipids has never been investigated. OBJECTIVE: We assessed the effect of moderate fructose supplementation on insulin sensitivity (IS) and ectopic lipids in healthy male volunteers (n = 7). DESIGN: IS, intrahepatocellular lipids (IHCL), and intramyocellular lipids (IMCL) were measured before and after 1 and 4 wk of a high-fructose diet containing 1.5 g fructose . kg body wt(-1) . d(-1). Adipose tissue IS was evaluated from nonesterified fatty acid suppression, hepatic IS from suppression of hepatic glucose output (6,6-2H2-glucose), and muscle IS from the whole-body glucose disposal rate during a 2-step hyperinsulinemic euglycemic clamp. IHCL and IMCL were measured by 1H magnetic resonance spectroscopy. RESULTS: Fructose caused significant (P < 0.05) increases in fasting plasma concentrations of triacylglycerol (36%), VLDL-triacylglycerol (72%), lactate (49%), glucose (5.5%), and leptin (48%) without any significant changes in body weight, IHCL, IMCL, or IS. IHCL were negatively correlated with triacylglycerol after 4 wk of the high-fructose diet (r = -0.78, P < 0.05). CONCLUSION: Moderate fructose supplementation over 4 wk increases plasma triacylglycerol and glucose concentrations without causing ectopic lipid deposition or insulin resistance in healthy humans.

Interaction between dietary lipids and physical inactivity on insulin sensitivity and on intramyocellular lipids in healthy men.

OBJECTIVE: To assess the effect of a possible interaction between dietary fat and physical inactivity on whole-body insulin sensitivity and intramyocellular lipids (IMCLs). RESEARCH DESIGN AND METHODS: Eight healthy male volunteers were studied on two occasions. After 2 days of an equilibrated diet and moderate physical activity, participants remained inactive (bed rest) for 60 h and consumed either a high-saturated fat (45% fat, of which approximately 60% was saturated fat [BR-HF]) or a high-carbohydrate (70% carbohydrate [BR-HCHO]) diet. To evaluate the effect of a high-fat diet alone, six of the eight volunteers were restudied after a 2-day equilibrated diet followed by 60 h on a high-saturated fat diet and controlled physical activity (PA-HF). Insulin sensitivity was measured by hyperinsulinemic-euglycemic clamp and IMCL concentrations by (1)H-magnetic resonance spectroscopy. RESULTS: Insulin-mediated glucose disposal was decreased by BR-HF condition (-24 +/- 6%, P < 0.05) but did not change with BR-HCHO (+19 +/- 10%, NS). BR-HF and BR-HCHO increased IMCL levels (+32 +/- 7%, P < 0.05 and +17 +/- 8%, P < 0.0011, respectively). Although the increase in IMCL levels with PA-HF (+31 +/- 19%, P = 0.12) was similar to that during BR-HF, insulin-mediated glucose disposal (-7 +/- 9%, NS) was not decreased. CONCLUSIONS: These data indicate that physical inactivity and a high-saturated fat diet may interact to reduce whole-body insulin sensitivity. IMCL content was influenced by dietary lipid and physical inactivity but was not directly associated with insulin resistance.