Activation of the “Splenocardiac Axis” by electronic and tobacco cigarettes in otherwise healthy young adults

Abstract

The “Splenocardiac Axis” describes an inflammatory signaling network underlying acute cardiac ischemia, characterized by sympathetic nerve stimulation of hematopoietic tissues, such as the bone marrow and spleen, which then release proinflammatory monocytes that populate atherosclerotic plaques, thereby promoting ischemic heart disease. Electronic (e) cigarettes, like tobacco cigarettes trigger sympathetic nerve activation, but virtually nothing is known about their influence on hematopoietic and vascular tissues and cardiovascular risks. The objective of this study was to determine if the Splenocardiac Axis is activated in young adults who habitually use either tobacco or e‐cigarettes. In otherwise healthy humans who habitually use tobacco cigarettes or e‐cigarettes (not both), we used 18F‐flurorodeoxyglucose positron emission tomography/computer tomography (FDG‐PET/CT) to test the hypothesis that tobacco or e‐cigarettes increased metabolic activity of the hematopoietic and vascular tissues. FDG uptake in the spleen increased from nonuser controls (1.62 ± 0.07), to the e‐cigarette users (1.73 ± 0.04), and was highest in tobacco cigarette smokers (1.82 ± 0.09; monotone P = 0.05). Similarly, FDG uptake in the aorta increased from the nonuser controls (1.87 ± 0.07) to the e‐cigarette users (1.98 ± 0.07), and was highest in tobacco cigarette smokers (2.10 ± 0.07; monotone P = 0.04). FDG uptake in the skeletal muscle, which served as a control tissue, was not different between the groups. In conclusion, these findings are consistent with activation of the Splenocardiac Axis by emissions from tobacco cigarettes and e‐cigarettes. This activation suggests a mechanism by which tobacco cigarettes, and potentially e‐cigarettes, may lead to increased risk of future cardiovascular events.

The Evolving Landscape of e-Cigarettes

“…There are conflicting reports as to whether e-cigarette use is associated with cardiovascular disease in population studies 60,61 . Although a very small study in humans (n=9) suggested that e-cigarette use does not affect the metabolic activity of aortic wall tissue 62 , another showed that e-cigarette use increased arterial stiffness 63 . Murine models have shown that e-cigarette exposure leads to increased aorta stiffness and constrictor responses 64 , increased angiogenesis in heart tissue 65 , increased endothelial cell markers 63 and decreased vasodilation 64 .…”

E-Cigarettes or Heat-not-Burn Tobacco Products: Advantages or Disadvantages for the Lungs of Smokers

“…Oxidative stress develops following direct action of toxic compounds on the airways and alveolar epithelial cells [71]. Moreover, e-liquid decreases antioxidant activity [72]. Neutrophils and macrophages are probably the largest source of reactive oxygen species.…”

“…Similarly to smoke, e-cigarettes have elevated nicotine-depending blood presure and heart rate in acute observational or experimental studies [87]. Some authors have postulated activation of sympathetic central outflow as a part of "splenocardiac axis" [72]. However, the influence of these cardiac parameters is weaker than acute smoke exposure [87].…”

Mit tudunk az e-cigaretta káros hatásairól?

“…Magas vérnyomásos dohányosokon e-cigarettára váltás után 12 hónapos követéssel mind a szisztolés, mind a diasztolés vérnyomás kisebb lett [40]. FDG-PET/CT szerint a nem dohányzókhoz viszonyítva e-cigaretta-használókon magasabb volt a lép és az aorta FDG-felvétele, de még magasabbnak bizonyult hagyományos cigarettát szívóknál [49]. Adatbázist feldolgozva a soha nem dohányzókhoz viszonyítva mindennapos e-cigaretta-használat esetén a szívinfarktus-rizikó hányadosa 2,25, mindennapos dohányzás esetén 2,95 [50].…”