His bundle pacing for newly acquired pacing needs in patients implanted with a subcutaneous implantable cardioverter defibrillator : a feasibility study based on the automated screening score and clinical cases

Introduction: Management of subcutaneous implantable cardioverter defibrillator (S-ICD) patients with newly acquired pacing needs remains problematic. His bundle pacing (HBP) allows for cardiac pacing without significant changes in the QRS morphology. We hypothesized that HBP does not alter S-ICD sensing and functions. Methods: Twenty consecutive patients were implanted with a HB pacemaker. Among them, 17 demonstrated successful His recruitment and were prospectively screened with the automated screening tool (AST). Results of screenings performed immediately after implant and during follow-up, during intrinsic rhythm and while pacing from all available pacing configurations, were compared using the AST score. Positive-screening tests were defined by greater than or equal to 1 positive vector. Results: Among the 17 patients successfully implanted (male: 41%; mean age: 73), 13 presented an indication of ventricular pacing and four of cardiac resynchronization. Absolute AST scores during both HBP (all configurations) and intrinsic rhythm were similar (p: NS). Due to left bundle branch block correction, HBP resulted in higher number of positive vectors (AST >= 100). AST scores were higher during HBP when compared with right ventricular pacing (RVP) (primary vector: 272 [16; 648] vs 4.6 [0.8; 16.2]; P = .003; secondary vector: 569 [183; 1186] vs 1.5 [0.7; 8.3]; P < .0001; alternate vector: 44 [2;125] vs 4.8 [0.9; 9.3]; P = .02) and resulted in a much higher number of positive vectors. Up to 90% of the patients had a positive-screening test during HBP. This passing rate was higher when compared RVP (17%; P < .0001). Conclusion: HBP restores normal intrinsic conduction and minimally modifies the surface electrocardiograph and subcutaneous electrograms. When ventricular pacing is needed, HBP might represent an ideal pacing option for patients implanted with a S-ICD

Pro-atherothrombotic effects of acute diesel exhaust exposure: vascular and hemostatic insights

Résumé Responsable de près de 7 millions de décès prématurés par an à travers le monde, la pollution atmosphérique représente un problème sanitaire mondial majeur. L’exposition humaine à la pollution particulaire dont les émissions de diesel représentent la principale source, est responsable d’une élévation de la mortalité et de l’incidence d’événements cardiovasculaires. Les mécanismes physiopathologiques sous-tendant cette toxicité aigue restent à ce jour largement méconnus. A l’aide d’une méthodologie d’exposition standardisée aux émissions de diesel, nous avons exploré les effets vasculaires périphériques et pulmonaires ainsi que les effets hémostatiques et plaquettaires secondaires à l’inhalation particulaire chez des sujets sains. L’étude dynamique de la microcirculation périphérique par Laser Doppler Imager nous a permis de démontrer une altération de la vasomotricité endothélium-dépendante induite par l’exposition aux émissions de diesel. La dysfonction observée est associée à une diminution de la biodisponibilité locale du NO ainsi qu’à une production radicalaire accrue au sein de la cellule endothéliale. Au cours d’une épreuve dynamique d’élévation du débit cardiaque par infusion de dobutamine, l’exposition aiguë aux émissions de diesel entraîne une élévation de la résistance vasculaire pulmonaire et une diminution de la distensibilité vasculaire pulmonaire mesurées par échocardiographie. Enfin, l’expression de surface des marqueurs d’activation plaquettaire CD62p (P-selectine) et CD63 est augmentée après exposition aux émissions de diesel, en corrélation avec la quantité de particules inhalées et constitue ainsi un état d’activation plaquettaire accru sans toutefois de modification de l’agrégation plaquettaire. A travers ces effets vasculaires systémiques et pulmonaires ainsi que ces effets hémostatiques, l’exposition aux émissions de diesel entraîne une toxicité cardiovasculaire aiguë, agissant en synergie, capable de déclencher la survenue d’événements cardiovasculaires.Abstract Responsible for up to 7 million deaths/year, air pollution is a major worldwide health burden. Particulate human exposure mainly originates from diesel exhaust and is associated with an increased cardiovascular mortality and an increased onset of cardiovascular events. Physiopathologic mechanisms underlying this acute toxicity remain largely unknown. We used a standardized diesel exhaust exposure protocol to explore not only the peripheral and pulmonary vascular effects, but also the hemostatic and platelet modifications in healthy subjects after particulate inhalation. Diesel exhaust exposure impairs the endothelium-dependant vasodilation during a dynamic evaluation of the peripheral microcirculation assessed by Laser Doppler Imager, whilst the endothelial independent vasodilatation remains unaffected. Vascular dysfunction is associated to a decreased local NO bioavailability and an increased endothelial reactive oxygen species production. During a dynamic cardiac stress test using continuous dobutamine infusion, acute diesel exhaust exposure induces an increased pulmonary vascular resistance associated to a decreased pulmonary vascular distensibility, both evaluated by echocardiography. Finally, platelet activation is modified after diesel exhaust exposure with an increased CD62p (P-selectin) and CD63 platelet surface expression, correlated with the total amount of inhaled particles. We observed a state of platelet activation without change in platelet aggregation. Through these multiples effects, combining systemic and pulmonary vascular impairment with platelet prothrombotic modifications, diesel exhaust exposure induces an acute cardiovascular toxicity, which can synergistically trigger acute events.Doctorat en Sciences médicales (Médecine)info:eu-repo/semantics/nonPublishe

Pacemaker lead rupture in a patient with subacute endocarditis: a case report

no abstract availabl

Effects of HeartWare ventricular assist device on the von Willebrand factor: Results of an academic Belgian center

Background: Left Ventricular Assist Device (LVAD) is a promising therapy for patients with advanced heart failure (HF), but bleeding complications remain an important issue. Previous series show that acquired von Willebrand syndrome was present in up to 100 % of first generation LVAD recipients. We report the effects of new generation LVADs on vW factor (vWF) metabolism and activity in our center. Methods: Fifteen LVAD recipients (HeartWare®, Framingham, MA, USA) were compared to 12 HF patients, matched for age and body mass index. vWF antigen and activity, as well as D-dimers, were measured on hemostasis analyzers. A vWF LVAD-induced alteration was evocated when the/[vWF antigen] ratio was <0.6. ADAMTS13 and high molecular weight multimers of vWF were also assessed. Results: LVAD recipients had similar levels of endothelial vWF production than the HF subjects (137 ± 14.5 vs. 147 ± 11.7 %; respectively, p = 0.611) but a decreased vWF activity (90 ± 11 vs. 132.6 ± 13 %; respectively, p = 0.017)./[vWF antigen] ratio was 0.65 ± 0.02 in the LVAD recipients and 0.92 ± 0.06 in the subjects with HF (p = 0.001). ADAMTS13 activity was 80.3 ± 4.7 % in LVAD recipients and 96.2 ± 3.5 % in the HF patients (p = 0.016). LVAD patients disclosed markedly elevated D-dimers (3217.7 ± 735 vs. 680.6 ± 223.2 ng/mL FEU in the HF patients, p = 0.006). The LVAD patients experienced one major hemorrhagic event and one systemic thrombotic event during the median follow-up of 345 days. Conclusions: LVAD recipients achieved a new hemostatic equilibrium characterized by infrequent major hemorrhagic and thrombotic events, despite a mildly impaired vWF function and a markedly enhanced thrombin formation. Trial registration:ISRCTN39517567SCOPUS: ar.jinfo:eu-repo/semantics/publishe

L-NAME iontophoresis: a tool to assess NO-mediated vasoreactivity during thermal hyperemic vasodilation in humans.

Decreased endothelial Nitric oxide (NO) bioavailability is one of the earliest events of endothelial dysfunction. Assessment of microvascular blood flow using a Laser Doppler Imager during local noninvasive administration of L-N-Arginine-Methyl-Ester (L-NAME) by skin iontophoresis may help discriminate the relative contributions of NO and non-NO pathways during a skin thermal hyperemic test.info:eu-repo/semantics/publishe

Pro-thrombotic effect of exercise in a polluted environment: A P-selectin-and CD63-related platelet activation effect

Exposure to diesel exhaust is an important cardiovascular risk factor and may promote atherothrombotic events. Some data suggest that polluted air exposure could affect haemostasis through platelet activation. The aim of the study was to investigate the effects of acute exposure to diesel exhaust on platelet activation and platelet function. We tested the hypothesis in a randomised, crossover study in 25 healthy men exposed to ambient and polluted air; 11 of the subjects also performed exercise during exposure sessions. Platelet activation was evaluated by surface expression of CD62P (P-selectin) and CD63 (dense granule glycoprotein) using flow cytometry of labelled platelets. Platelet function was measured using the PFA-100 platelet function analyser and by Multiplate whole blood impedance platelet aggregometry. Acute diesel exhaust exposure had no effect on platelet activation at rest, but exercise in polluted air increased the collagen-induced expression of CD62P and CD63 (both p< 0.05). The increase in the expression of CD62P and CD63 was related to the total amount of PM2.5 inhaled during the exercise sessions (r=+0.58 and +0.60, respectively, both p< 0.05). Platelet aggregation was not impaired after polluted air exposure at rest or during exercise. In conclusion, in healthy subjects, diesel exhaust exposure induces platelet activation as illustrated by a dose-response increase in the release of CD62P and CD63. This platelet priming effect could be a contributor to the triggering of atherothrombotic events related to air pollution exposure.SCOPUS: ar.jinfo:eu-repo/semantics/publishe

Does third generation left ventricular assist device alter heart failure-related microvascular dysfunction?

Background Left ventricular assist device (LVAD) is a promising new therapy in patients with advanced heart failure. Previous studies suggested that continuous blood flow impairs endothelial function. Whether the third-generation LVAD (HeartWare®, HeartWare Inc. Framingham, MA, USA) system affects endothelial regulation of microvascular flow, endothelial nitric oxide (NO) bioavailability and endothelial production of vWF is not known. Methods Fifteen LVAD-supported heart failure patients and 13 age/body mass index matched heart failure patients (HF) were included. The microvascular endothelial function of skin vessels was assessed with laser Doppler imager (LDI) using 3 different hyperaemic challenges: acetylcholine (Ach) iontophoresis, sodium nitroprusside (SNP) iontophoresis and local heating to 44°C. NO-mediated vasodilation was further evaluated by comparing heating hyperaemic response in skin area pretreated either by a saline solution (control) or a specific NO-synthase inhibitor (L-N-arginine-methyl-ester, L-NAME). vWF antigen was also measured in LVAD and HF patients. Results SNP-induced vasodilation did not differ between LVAD and HF patients, and we observed a trend towards an increased vasodilator response to Ach in LVAD patients (P = 0.06). Compared to HF patients, skin thermal hyperaemia was increased in LVAD patients in both control and L-NAME pretreated skin (all P < 0.001). The hyperaemic reaction attributable to NO-mediated vasodilation correlated negatively with HF duration (r = –0.50, P < 0.01, n = 28), but did not differ between LVAD and HF patients. Both groups disclosed also similar vWF antigen serum levels. Conclusion This case-control study indicates that third-generation LVAD therapy does not alter skin microvascular endothelial function and vWF production of patients with HF.SCOPUS: ar.jinfo:eu-repo/semantics/publishe