Cardiovascular Risk from Smoking: Doubt or Absolute Certainty?

Abstract

alterations. These have shown to follow a typical course due to the effects of two main compounds of cigarette smoke, nicotine and carbon monoxide. The latter should not be considered as a product of tobacco leaf, but, on the contrary, as the combustion of manufactured tobacco and the paper of the cigarette. However, carbon monoxide has to be seen as the most dangerous chemical of smoking since it is mainly responsible of irreversible cardiovascular pathology in the time [2,3]. Nicotine causes primarily a functional and reversible damage to the heart and blood vessels in both active smokers and individuals passively exposed to tobacco smoking [4]. This substance, which reaches different concentrations according to the type of cigarettes smoked [5], exerts direct and mediated effects due to adrenergic and sympathetic stimulation of the heart with impaired cardiac performance and endothelium, which meets a dysfunction characterized by impaired endothelium-dependent vasodilatation due to reduced nitric oxide release and changes in platelet function. There is evidence that the alterations caused by nicotine and its metabolite cotinine are stably reproducible in those experiments exactly conducted with the same protocol of study. Therefore, this fact shows with no doubt the certainty of cardiovascular damage related to a smoking compound. In addition, nicotine burns at a temperature of 240°C below the boiling point of 247°C. Chemically, that means the alkaloid has an auto-ignition point less than that of boiling, allowing the cigarette to diffuse up to nicotine decomposition occurring at a boiling level with maximum of substance absorption. Thus, individuals anyway exposed to smoke feel the harmful effects at a high level of toxicity as well as to a prolonged addiction of the chemical.