Bogdan T. Violations of humoral and cellular immunity, platelets and lymphocytes membranes fatty acid spectrum, blood plasma amino acid spectrum in stable and unstable angina patients and possibilities of their drug correction

Українська версія

Thesis for the degree of Doctor of Science (DSc)

State registration number

0518U000048

Applicant for

Specialization

  • 14.01.11 - Кардіологія

01-02-2018

Specialized Academic Board

Д 26.003.08

Essay

In this work revealed complex pathogenetic links of lymphocyte and platelet membrane structure violations, cellular and humoral immunity, plasma amino acid spectrum imbalance, as important factors in the coronary circulation destabilization pathogenesis. As was established, these violations are directly correlated with ischemia and myocardial ectopic activity in CHD chronic and acute course. In stable angina patients myocardial ischemia directly correlated with myristic acid relative content in lymphocytes phospholipids membranes, sulfur amino acids plasma level and branched side chain amino acids plasma levels; silent myocardial ischemia duration directly correlated with myristic acid lymphocytes phospholipid membranes relative content and linoleic acid platelets phospholipid membranes relative content, arginine and branched side amino acids plasma levels. In unstable angina patients myocardial ischemia duration depends of circulating immune complexes level, myristic acid relative content in lymphocytes membranes phospholipids, arachidonic acid and linoleic acids relative content in platelet membranes phospholipids, sulfur amino acids plasma level; silent myocardial ischemia duration depends of arachidonic acid relative content in lymphocytes membranes phospholipids and plasma arginine level; group ventricular extrasistoles level increasing depends of lymphocytes and platelet membranes phospholipid arachidonic acid relative content, branched side chains amino acids level. Usage of nebivolol, rosuvastatin, clopidogrel and aspirin combination and additional L-arginine is pathogenetically reasonable for stable and unstable angina patients.

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