Abstract-Exposure to diesel exhaust was recently identified as an important cardiovascular risk factor, but whether it impairs nitric oxide (NO)-mediated endothelial function and increases production of reactive oxygen species (ROS) in endothelial cells is not known. We tested these hypotheses in a randomized, controlled, crossover study in healthy male volunteers exposed to ambient and polluted air (n=12). The effects of skin microvascular hyperemic provocative tests, including local heating and iontophoresis of acetylcholine and sodium nitroprusside, were assessed using a laser Doppler imager. Before local heating, skin was pretreated by iontophoresis of either a specific NO-synthase inhibitor (L-N-arginine-methyl-ester) or a saline solution (Control). ROS production was measured by chemiluminescence using the lucigenin technique in human umbilical vein endothelial cells preincubated with serum from 5 of the subjects. Exposure to diesel exhaust reduced acetylcholine-induced vasodilation (P<0.01) but did not affect vasodilation with sodium nitroprusside. Moreover, the acetylcholine/sodium nitroprusside vasodilation ratio decreased from 1.51±0.1 to 1.06±0.07 (P<0.01) and was correlated to inhaled particulate matter 2.5 (r=−0.55; P<0.01). NO-mediated skin thermal vasodilatation decreased from 466±264% to 29±123% (P<0.05). ROS production was increased after polluted air exposure (P<0.01) and was correlated with the total amount of inhaled particulate matter <2.5 μm (PM2.5). In healthy subjects, acute experimental exposure to diesel exhaust impaired NO-mediated endothelial vasomotor function and promoted ROS generation in endothelial cells. Increased PM2.5 inhalation enhances microvascular dysfunction and ROS production.

PM2.5 and NO exposures incrementally increase the risk of STEMI. The risk related to PM appears to be greater in the elderly, while younger patients appear to be more susceptible to NO exposure.

Left bundle branch area pacing (LBBAP) has emerged as a novel pacing modality which aims to capture the left bundle branch area and avoids the detrimental effects of right ventricular pacing. Current approaches for LBBAP have been developed using lumen-less pacing leads (LLL). Expanding the tools and leads for LBBAP might contribute to a wider adoption of this technique. Standard stylet-driven pacing leads (SDL) differ from current LLL as they are characterized by a wider lead body diameter, are stylet-supported and often have a non-isodiametric extendable helix design. Although LBBAP can be performed safely with SDL, the implant technique of LBBAP differs compared to LLL. In the current overview we describe in detail how different types of SDL can be used to target a deep septal position and provide a practical guide on how to achieve LBBAP using SDL.

Air pollution has recently been associated with the development of acute decompensated heart failure, but the underlying biological mechanisms remain unclear. A pulmonary vasoconstrictor effect of air pollution, combined with its systemic effects, may precipitate decompensated heart failure. The aim of the present study was to investigate the effects of acute exposure to diesel exhaust (DE) on pulmonary vascular resistance (PVR) under resting and stress conditions but also to determine whether air pollution may potentiate acquired pulmonary hypertension. Eighteen healthy male volunteers were exposed to ambient air (AA) or dilute DE with a particulate matter of <2.5 μm concentration of 300 μg/m(3) for 2 h in a randomized, crossover study design. The effects of DE on PVR, on the coefficient of distensibilty of pulmonary vessels (α), and on right and left ventricular function were evaluated at rest (n = 18), during dobutamine stress echocardiography (n = 10), and during exercise stress echocardiography performed in hypoxia (n = 8). Serum endothelin-1 and fractional exhaled nitric oxide were also measured. At rest, exposure to DE did not affect PVR. During dobutamine stress, the slope of the mean pulmonary artery pressure-cardiac output relationship increased from 2.8 ± 0.5 mmHg · min · l (-1) in AA to 3.9 ± 0.5 mmHg · min · l (-1) in DE (P < 0.05) and the α coefficient decreased from 0.96 ± 0.15 to 0.64 ± 0.12%/mmHg (P < 0.01). DE did not further enhance the hypoxia-related upper shift of the mean pulmonary artery pressure-cardiac output relationship. Exposure to DE did not affect serum endothelin-1 concentration or fractional exhaled nitric oxide. In conclusion, acute exposure to DE increased pulmonary vasomotor tone by decreasing the distensibility of pulmonary resistive vessels at high cardiac output.

Disclosures: Dr. De Pooter reports speaker fees and honoraria from Medtronic and Biotronik. Dr. Peytchev and dr. Heggermont report that their research institution (CRI Aalst) receives consultancy fees on their behalf from Medtronic, Biotronik, St Jude Medical, Boston Scientific and Microport. Dr Wauters reports speaker and consultancy fees from Biotronik. Dr. le Polain de Waroux reports nonsignificant speaker fees and honoraria for proctoring and teaching activities from Medtronic, Boston Scientific, Abbott and Biotronik. The other authors report no disclosures. Dr. Tung reports speaker and consulting honoraria from Medtronic, Boston Scientific, Abbott, and Biotronik.