| Abstract | Konzumiranje duhanskih proizvoda pušenjem među vodećim je svjetskim čimbenicima rizika za bolesti koronarnih arterija, vodeći čimbenik rizika malignih oboljenja dušnika, bronha i pluća, te najprisutniji spriječivi uzročnik među svim bolestima, posebice oboljenjima povezanim s duhanom.
Maligno djelovanje kao i glavnina štetnosti za organizam ne proizlazi iz samog nikotina, čiji je nootropni učinak poticaj na tu zdravstveno neodgovornu aktivnost, već iz mnogobrojnih nusproizvoda pušenja. Nikotin u razvoju novotvorina ima pomagačku funkciju, osim adrenergičnim djelovanjem, kroz svoj angiogenetski i neovaskularizacijski efekt koji novotvorinama pomaže u stvaranju kapilarne mreže radi opskrbe hranjivim tvarima. Taj isti angiogenetski efekt u cijelom tijelu imitira funkciju prirodnog zgušnjavanja kapilarne mreže kojim se tijelo prilagođava na kvantitativno nepovoljan udio kisika koji dobiva izmjenom plinova u plućima. Kroz taj slučajan fenomen, uslijed dugogodišnje izloženosti nikotinu, tijelo postaje spremno boriti se s lokalnim tkivnim hipoksijama u slučaju iznenadnog događaja u krvožilnom sustavu.
Akutni infarkt miokarda, kao posljedica djelomičnog ili potpunog prestanka dotoka krvi srčanom mišićju, svoj pozitivan ili negativan ishod nalazi u što bržoj ponovnoj uspostavi dotoka krvi zahvaćenom tkivu. Uz prisutnost gušće kapilarne mreže no što je prirodno prisutna, uslijed dugotrajnog unosa nikotina kao i prolongirane hipoksije izazvane nusproizvodima pušenja, šteta prouzročena infarktom se mitigira bolje i brže nego u nepušača.
U kohorti od 156 ispitanika, od kojih je 43,6% pušača, akutni infarkt miokarda preživjelo je 81,4% oboljelih. Omjer muškaraca i žena koji su imali pozitivan ishod je podjednak, iako unutar pojedinačne grupe žene preživljavaju češće. U grupi nepušača pozitivan ishod bolesti ima 69,3% oboljelih, a u grupi pušača 97,1%. U realnom omjeru taj broj pokazuje 1.4 puta veće šanse u korist pušača, odnosno pušači imaju 40,1% više šanse za preživljavanje. Takav rezultat je očekivan i u skladu s pretpostavkom postavljenom na poznatim biokemijskim učincima nikotina kao i patofiziološkim mehanizmima akutnog infarkta miokarda. |
| Abstract (english) | Consumption of tobacco products by smoking is among the world's leading risk factors for coronary artery disease, the leading risk factor for malignant diseases of the trachea, bronchi and lungs, and the most common preventable cause among all diseases, especially tobacco-related diseases.
Malignant action, as well as most of the harm to the body, does not come from nicotine itself, whose nootropic effect is an incentive for this health-irresponsible activity, but from numerous by-products of smoking. Nicotine in the development of neoplasms has an auxiliary function, apart from its adrenergic effect, through its angiogenic and neovascularizing effect, which helps neoplasms to create a capillary network for their supply of nutrients. This same angiogenic effect throughout the body imitates the function of natural thickening of the capillary network by which the body adapts to the quantitatively unfavorable proportion of oxygen that it receives through gas exchange in the lungs. Through this accidental phenomenon, as a result of long-term exposure to nicotine, the body becomes ready to fight local tissue hypoxia in the event of a sudden interruption in the circulatory system.
Acute myocardial infarction, as a result of partial or complete cessation of blood flow to the heart muscle, finds its positive or negative outcome in the fastest possible re-establishment of blood flow to the affected tissue. With the presence of a denser capillary network than occurs naturally, due to long-term nicotine intake as well as prolonged hypoxia caused by smoking by-products, the damage caused by a heart attack is mitigated better and faster than in a non-smoker.
In a cohort of 156 subjects, 43.6% of whom were smokers, 81.4% of patients survived acute myocardial infarction. The ratio of men and women who had a positive outcome is equal, although within the single group women survive more often. In the group of non-smokers, 69.3% of patients had a positive outcome, and in the group of smokers, 97.1%. In real terms, this number shows a 1.4 times greater chance of survival in favor of smokers, that is, smokers have a 40.1% greater chance of survival. Such a result is expected and in accordance with the thesis based on the known biochemical effects of nicotine as well as the pathophysiological mechanisms of acute myocardial infarction. |
