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On an annual basis, 13.2% of all deaths are attributable to coronary artery disease (CAD), which makes CAD - with 7.4 million deaths - the leading cause of death in the world. In this review, we discuss current knowledge in the pathophysiology of atherosclerosis with its progression to stable CAD and its destabilization and complication with thrombus formation - myocardial infarction (MI). Next, we describe mechanisms of myocardial cell death in MI, the ischemia-reperfusion injury, leftventricular remodeling and complications of MI. Furthermore, we add acute management strategies concentrating on medical therapy, a decision on the reperfusion strategy, timing and cardiac protection by ischemic preconditioning, post-conditioning and remote ischemic conditioning.

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Background: Many studies have reported increased serum levels of vascular endothelial growth factor (VEGF) in patients with acute coronary syndromes. We searched for the association between either the –634 C/G or the insertion/deletion (I/D) polymorphism of the VEGF gene and myocardial infarction (MI) in subjects with type 2 diabetes. Methods: 143 subjects with type 2 diabetes and MI were compared to 228 diabetic subjects without coronary artery disease (CAD). VEGF serum levels were analyzed in 94 subjects with type 2 diabetes without CAD. Results: A significantly higher frequency of the CC genotype of the –634 C/G VEGF polymorphism was found in the patients with MI compared to the patients without CAD (17.5 vs. 9.2%; p = 0.019), whereas the insertion/deletion VEGF polymorphism failed to yield an association with MI. Significantly higher VEGF serum levels were demonstrated in subjects with the CC genotype compared to those with the other (CG + GG) genotypes (60.4 ± 32.1 vs. 44.1 ± 23.5 ng/l; p < 0.01). Conclusions: The present study demonstrates that the CC genotype of the –634 C/G VEGF gene might be a risk factor for MI in Caucasians with type 2 diabetes of duration of more than 10 years.

Aim: Substantial data indicate that oxidative stress is involved in the development of diabetic retinopathy (DR). The aim of the present study was to investigate whether the genetic polymorphisms: polymorphic deletions of glutathione S-transferases M1 (GSTM1) and T1 (GSTT1) and Ile105Val of the GSTP1 are associated with DR in Slovenian patients with type 2 diabetes.Methods: In this cross sectional case-control study 604 unrelated Slovene subjects (Caucasians) with type 2 diabetes mellitus were enrolled: 284 patients with DR (cases) and the control group of 320 subjects with type 2 diabetes of more than 10 years’ duration who had no clinical signs of DR. Genotypes were determined by polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP). Results: In our study, the deletion of the GSTM1 was found less frequent in cases with DR than in the controls (27.5% versus 44.4%; P < 0.001), whereas the deletion of GSTT1 was found significantly more often in cases than in the controls (49.3% versus 29.7%;P < 0.001). We did not find statistically significant differences in the genotype distribution in GSTP1 (Ile105Val) polymorphism between cases and controls (40.5% versus 46.0%). Conclusions: We may conclude that individuals homozygous for the deletion of GSTT1 are at an ≈ 2-fold-greater risk of DR, whereas the GSTM1 deficiency is associated with lower frequency of DR in type 2 diabetics.

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