| Abstract | Cilj je ovog istraživanja utvrditi je li povišena razina Lp(a) u serumu rizični čimbenik koji pridonosi povećanju IMT i broja plakova karotidnih arterija, a i s time povezanog povećanog rizika od kardiovaskularnog pobola i smrtnosti u osoba s tipom 2 šećerne bolesti. Analizirano je 146 bolesnika s tipom 2 šećerne bolesti bez znakova cerebrovaskularne i ishemičke bolesti srca. Na početku istraživanja određena je razina Lp(a), IMT i broj plakova karotidnih arterija. Nakon četiri godine praćenja mjerili smo IMT i broj plakova karotidnih arterija. Ispitanici su podijeljeni u dvije skupine s obzirom na razinu Lp(a) u serumu. Jednu skupinu su sačinjavali bolesnici s razinom Lp(a)≤30 mg/dL, a drugu skupinu bolesnici s razinom Lp>30mg/dL. IMT prikazan je ultrazvučnim sustavom visoke rezolucije tehnikom B-moda. Razina Lp(a) u serumu određena je imunoturbidimetrijskom metodom. Ispitivane skupine bolesnika s visokom i niskom razinom Lp(a) u serumu nisu se značajno razlikovale u IMT na početku istraživanja (p=0,112). Nakon četiri godine praćenja IMT u bolesnika s razinom Lp(a)>30 mg/dl iznosila je 1,24 + 0,22 mm i bila je značajno viša od IMT bolesnika s razinom Lp(a)30 mg/dl koja je iznosila 1,15+0,17 mm (p=0,005). Prosječno povećanje IMT u četiri godine u skupini s niskom razinom Lp(a) iznosilo je 0,12 mm (0,030 mm/god.), dok je prosječno povećanje IMT u skupini s viskom razinom Lp(a) iznosilo 0,17 mm (0,043 mm/god.). Multivarijatna analiza ukazuje da vrijednost IMT ovisi o Lp(a) a ne ovisi o razini triglicerida i HDL-kolesterola. U ispitivanim skupinama bolesnika nije bilo značajne razlike u broju plakova na početku istraživanja (p=0,276). Nakon četiri godine u objema skupinama bolesnika prati se značajan porast broja plakova u odnosu na početne vrijednosti (p<0,001), no među njima nije bilo značajne razlike (p=0,355). U ispitivanim skupinama bolesnika nismo našli značajane razlike u pobolu i smrtnosti od kardiovaskularnih bolesti. Udio bolesnika s preboljelim infarktom miokarda, moždanim udarom, umrlih od kardiovaskularnih bolesti i kombiniranim ishodom (infarkt mokarda, moždani udar i kardivaskularna smrt) nije se statistički značajno razlikovao među ispitivanim skupinama (p>0,05). Ovi rezultati sugeriraju da je Lp(a) neovisni, genetski određen čimbenik rizika koji je povezn s progresijom IMT u osoba s tipom 2 šećerne bolesti. |
| Abstract (english) | The aim of this study was to establish whether increased serum Lp(a) level is a risk factor which significantly contributes to an increase in intima-media thickness (IMT) and the number of carotid artery plaques, and the related increased risk of cardiovascular morbidity and mortality in patients with type 2 diabetes mellitus. The study included 146 type 2 diabetic patients without signs of cerebrovascular and ischaemic heart disease. The levels of Lp(a) and IMT, as well as the number of carotid artery plaques were determined at the beginning of the study. IMT and the number of carotid artery plaques were again determined after four years of follow-up. Subjects were divided into two groups according to their serum Lp(a) levels: patients with Lp(a) level of ≤30 mg/dL and those with Lp level >30 mg/dL. IMT was assessed by high-resolution B-mode ultrasound. Serum Lp(a) level was determined using immunoturbidimetric method. The studied groups of patients with high and low serum Lp(a) levels did not reveal significant differences in baseline IMT (p=0.112). After a 4-yr follow-up IMT was significantly greater in patients with Lp(a) level >30 mg/dL as compared to those with Lp(a) level of ≤30 mg/dL (1.24 + 0.22 mm vs. 1.15+0.17 mm, respectively ; p=0.05). Mean increase in IMT over four years in the group with low Lp(a) level was 0.12 mm (0.030 mm/yr.), whereas in the group with high Lp(a) level it was 0.17 mm (0.043 mm/yr.). Multivariate analysis indicated that IMT value depended on Lp(a), and not on triglyceride and HDL-cholesterol levels. The studied patients from both groups did not show significant difference in baseline number of plaques (p=0.276). A significant increase in the number of plaques (p<0.001) was found after the 4-yr follow-up as compared to baseline values. There were no significant differences in the number of plaques between the two groups at the end of the study (p=0.355). No statistically significant between-group differences were established either in cardiovascular morbidity and mortality or in the proportion of patients who had myocardial infarction or stroke, those who died from cardiovascular diseases or a combined outcome (myocardial infarction, stroke and cardiovascular death) (p>0.05). These results point to Lp(a) as an independent, genetically determined risk factor associated with IMT progression in type 2 diabetes mellitus. |
