[Effects of air pollution on cardiovascular events in cardiac intensive care units]. / Effets de la pollution de l'air sur les évènements cardiovasculaires en unité de soins intensifs cardiologiques.

Many environmental factors influence the occurrence of cardiovascular events. Among these, air pollution is certainly the most harmful, due to its dual composition and effects. Air pollution is both particulate and gaseous, and can vary in concentration and composition according to its source and type of emission. Moreover, clinical effects are not only observed at long-term but also at short-term, following rapid deterioration in air quality. Air pollution must therefore be seen both as a risk factor for atherosclerotic disease, and as a trigger for cardiovascular events. These acute effects are essentially mediated by an increased risk of acute coronary syndromes and heart failure. The effects of air pollution on admissions for ventricular arrhythmias and arterial hypertension are also possible. The cardiotoxicity of pollution is mainly mediated by sympatho-vagal imbalance, by the initiation and amplification of an oxidative, inflammatory and pro-aggregatory cascade, and by endothelial dysfunction and activation of metalloproteinases. Although now well established, the consequences of air pollution on acute cardiovascular events require further investigation. Environmental cardiology is an emerging discipline whose current vision still fails to integrate qualitative aspects, such as the oxidative potential of particulate matter, and the joint effects of multiple environmental exposures.

Ecology of the cardiovascular system: Part II - A focus on non-air related pollutants.

An integrated exposomic view of the relation between environment and cardiovascular health should consider the effects of both air and non-air related environmental stressors. Cardiovascular impacts of ambient air temperature, indoor and outdoor air pollution were recently reviewed. We aim, in this second part, to address the cardiovascular effects of noise, food pollutants, radiation, and some other emerging environmental factors. Road traffic noise exposure is associated with increased risk of premature arteriosclerosis, coronary artery disease, and stroke. Numerous studies report an increased prevalence of hypertension in people exposed to noise, especially while sleeping. Sleep disturbances generated by nocturnal noise are followed by a neuroendocrine stress response. Some oxidative and inflammatory endothelial reactions are observed during experimental session of noise exposure. Moreover, throughout the alimentation, the cardiovascular system is exposed to persistent organic pollutants (POPs) as dioxins or pesticides, and plastic associated chemicals (PACs), such as bisphenol A. Epidemiological studies show positive associations of exposures to POPs and PACs with diabetes, arteriosclerosis and cardiovascular disease incidence. POPs and PACS share some abilities to interact with nuclear receptors activating different pathways leading to oxidative stress, insulin resistance and angiotensin potentiation. Regarding radiation, survivors of nuclear explosion have an excess risk of cardiovascular disease. Dose-effect relationships remain debated, but an increased cardiovascular risk at low dose of radiation exposure may be of concern. Some emerging environmental factors like electromagnetic fields, greenspace and light exposure may also require further attention. Non-air related environmental stressors also play an important role in the burden of cardiovascular disease. Specific methodologies should be developed to assess the interactions between air and non-air related pollutants.

Air pollution and ST-elevation myocardial infarction: A case-crossover study of the Belgian STEMI registry 2009-2013.

BACKGROUND: Previous studies have shown that air pollution particulate matter (PM) is associated with an increased risk for myocardial infarction. The effects of air pollution on the risk of ST-elevation myocardial infarction (STEMI), in particular the role of gaseous air pollutants such as NO2 and O3 and the susceptibility of specific populations, are still under debate. METHODS: All patients entered in the Belgian prospective STEMI registry between 2009 and 2013 were included. Based on a validated spatial interpolation model from the Belgian Environment Agency, a national index was used to address the background level of air pollution exposure of Belgian population. A time-stratified and temperature-matched case-crossover analysis of the risk of STEMI was performed. RESULTS: A total of 11,428 STEMI patients were included in the study. Each 10µg/m3 increase in PM10, PM2.5 and NO2 was associated with an increased odds ratio (ORs) of STEMI of 1.026 (CI 95%: 1.005-1.048), 1.028 (CI 95%: 1.003-1.054) and 1.051 (CI 95%: 1.018-1.084), respectively. No effect of O3 was found. STEMI was associated with PM10 exposure in patients ≥75y.o. (OR: 1.046, CI 95%: 1.002-1.092) and with NO2 in patients ≤54y.o. (OR: 1.071, CI 95%: 1.010-1.136). No effect of air pollution on cardiac arrest or in-hospital STEMI mortality was found. CONCLUSION: PM2.5 and NO2 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 NO2 exposure.

[Renal denervation: new treatment for refractory hypertension?]. / Dénervation rénale: nouveau traitement de l'hypertension artérielle résistante?

Sympathetic renal hyperactivity is involved hypertension and in its progression towards organ damages. Using femoral access, a dedicated ablation catheter can be inserted into the renal vessels to deliver high frequency energy in the arterial wall. This therapy leads to a focal heating, which ablates the renal nerve fibers running in the adventitia. First clinical results (Simplicity HTN 1 and HTN 2 trials) have demonstrated a significant and sustained decrease in office blood pressure. The response rate to this therapy was about 85 to 90%. This procedure did not cause serious adverse event and seems to have also positive impact on glucose metabolism and exercise capacity. Based on these first results, renal denervation appears as a new interesting therapy, which requires further studies to better define its place in the antihypertensive therapeutic arsenal. Actually, it should not be considered as an alternative to pharmacological therapy and renal denervation should be only proposed to patients with resistant hypertension. Prior to renal denervation, an upstream work has to be done to ensure an adequate patient selection. The mandatory point is to ensure that patient scheduled for this therapy respond to the definition of arterial resistant hypertension. Because of the narrowed limit between the very common situation of "uncontrolled" hypertension and the "true resistant" group, we proposed a 3 steps algorithm that can help for patient selection.

Acute effect of sidestream cigarette smoke extract on vascular endothelial function.

Acute exposure to passive smoking adversely affects vascular function by promoting oxidative stress and endothelial dysfunction. However, it is not known whether tobacco sidestream (SS) smoke has a greater deleterious effect on the endothelium than non-tobacco SS smoke and whether these effects are related to nicotinic endothelial stimulation. To test these hypotheses, endothelial-dependent relaxation and superoxide anion production were assessed in isolated rat aortas incubated with tobacco SS smoke, non-tobacco SS smoke, or pure nicotine. Tobacco SS smoke decreased the maximal relaxation to acetylcholine (Ach) from 79 +/- 6% to 57 +/- 7.3% (% inhibition of phenylephrine-induced plateau, P < 0.001) and increased superoxide anion production from 31 +/- 9.7 to 116 +/- 24 count/10 sec/mg (P < 0.01, lucigenin-enhanced chemiluminescence technique). The non-tobacco SS smoke extract had no significant effect on the response to Ach but increased superoxide anion production in the aortic wall to 133 +/- 2 count/10 sec/mg (P < 0.001). Furthermore, concentration-response curves to Ach and superoxide production remained unaltered with nicotine (0.001, 0.01, or 0.1 mM). In conclusion, despite similar increases in vascular wall superoxide production with tobacco and non-tobacco SS smoke, only the tobacco SS smoke extracts affected endothelium-dependent vasorelaxation. Nicotine alone does not reproduce the effects seen with tobacco SS smoke, suggesting that the acute endothelial toxicity of passive smoking cannot simply be ascribed to a nicotine-dependent mechanism.

Facial cooling and peripheral chemoreflex mechanisms in humans.

AIM: Reductions in arterial oxygen partial pressure activate the peripheral chemoreceptors which increase ventilation, and, after cessation of breathing, reduce heart rate. We tested the hypothesis that facial cooling facilitates these peripheral chemoreflex mechanisms. METHODS: Chemoreflex control was assessed by the ventilatory response to hypoxia (10% O2 in N2) and the bradycardic response to voluntary end-expiratory apnoeas of maximal duration in 12 young, healthy subjects. We recorded minute ventilation, haemoglobin O2 saturation, RR interval (the time between two R waves of the QRS complex) and the standard deviation of the RR interval (SDNN), a marker of cardiac vagal activity throughout the study. Measurements were performed with the subject's face exposed to air flow at 23 and 4 degrees C. RESULTS: Cold air decreased facial temperature by 11 degrees C (P < 0.0001) but did not affect minute ventilation during normoxia. However, facial cooling increased the ventilatory response to hypoxia (P < 0.05). The RR interval increased by 31 +/- 8% of the mean RR preceding the apnoea during the hypoxic apnoeas in the presence of cold air, compared to 17 +/- 5% of the mean RR preceding the apnoea in the absence of facial cooling (P < 0.05). This increase occurred despite identical apnoea durations and reductions in oxygen saturation. Finally, facial cooling increased SDNN during normoxia and hypoxia, as well as during the apnoeas performed in hypoxic conditions (all P < 0.05). CONCLUSION: The larger ventilatory response to hypoxia suggests that facial cooling facilitates peripheral chemoreflex mechanisms in normal humans. Moreover, simultaneous diving reflex and peripheral chemoreflex activation enhances cardiac vagal activation, and favours further bradycardia upon cessation of breathing.