Q-myocardial Infarction on the Background of Undifferentiated Connective Tissue Dysplasia: Pathogenetic “Paradoxes” and “Crossovers”

Abstract

Acute myocardial infarction (MI) is an important public health problem. Modern cardiology studies the role of such a premorbid background as undifferentiated connective tissue dysplasia (UCTD) in the pathogenesis of coronary heart disease (CHD) and MI in particular. Despite a large number of studies, the biochemical pathogenetic links of MI development against the background of UCTD remain unexplored. That is why our study aimed to analyze the stigmas of dysembryogenesis, coagulogram parameters, and platelet and uric acid (UA) levels as the most expected factors in the pathogenesis of MI with UCTD. The level of platelets in the peripheral blood of patients with UCTD (182.0 [161.0–265.0] x 109/l) did not differ reliably (but it was still significantly lower) from that in patients without UCTD [230.0 [206.0–309.0] x 109/l) (p>0.05). In particular, in 26 patients (57.8%) with UCTD, it was below the reference value. In those patients, who also have a large number of UCTD markers (10 or more), the stigma of “easy hematoma formation with insignificant damage” was most common. The level of UA in patients with Q-IM with UCTD was higher than normal and reliably higher than in the group without dysplasia (383.60 ± 33.82 vs. 292.11 ± 28.56, p<0.05). Increasing the level of UA provokes the activation of inflammatory processes in the coronary arteries, and leukocyte lymphocytic infiltration of their tunica media, which, even at a low platelet level, leads to a cascade of mutually aggravating pathological changes that converge at the level of multivector endothelial damage.