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[Prognostic significance of typical immune reactions in myocardial infarction].

AIM
To ascertain the role of typical reactions of the immune system in early prognostication of congestive cardiac failure (CCF) in patients with primary transmural anterior myocardial infarction (MI) in the postinfarction period.


MATERIAL AND METHODS
Typical immune reactions were studied for a year after the disease onset. A total of 228 males aged 40-60 years (mean age 53.8 +/- 4.1 years) with primary Q-wave MI of anterior location without accompanying diseases or allergy, with comparable volumes of myocardial necrosis were included in the trial. The control group consisted of 35 healthy men aged 40 to 60 years (mean age 52.9 +/- 4.3 years). Morphofunctional characteristics of the heart were studied by Doppler echocardiography within a month since MI onset and a year after MI. Immunological examination performed on MI day 1, 15 and 25 included determination by tests of the first-second level by R. V. Petrov of the count of leukocytes, lymphocytes, T-cells, T-helpers, T-suppressors (CD3+, CD4+, CD9+), zero lymphocytes, immunoglobulins, circulating immune complexes, complement by 50% hemodialysis, phagocyte index and count. Statistical processing included parametrical and non-parametrical criteria, correlation-regression analysis, criterion chi-square. The index of diagnostic significance Kj was calculated. Also, frequency and graphic analyses were made.


RESULTS
The analysis of immunological disorders in patients with five variants of primary Q-wave MI (LV aneurism with moderate dilatation of the cavity, aneurism of the heart in combination with L V cavity dilation with CDR >60 mm and development of mitral regurgitation >2 degrees, prevalence of LV diastolic dysfunction, progressive dilatation of the heart cavities with development of mitral of degree 2-3 and tricuspidal of degree 1-2 insufficiency, compensated hemodynamics without essential changes of the LV and LA) has established the same type of immune reactions to the pathological process manifesting with a fall in the count of absolute and relative count of lymphocytes, T-cells, T-helpers, B-lymphocytes, complement, phagocytic index, suppression index. These changes were accompanied with increased count of T-suppressors, zero-lymphocytes, CIC, immunoglobulins, leucointoxication index. The immunological examination of the patients showed that all morphofunctional variants of the myocardium correlated with suppression of immune reaction in the following order: compensated aneurism of the LV (18 parameters), diastolic dysfunction of the LV (11), progressive dilatation of the heart cavities (8), aneurism of the LV (6), marked dilatation of the heart cavities (4). Patients with pronounced dynamics of the regenerative processes had suppression of cellular immunity of the second degree, in positive hemodynamics there were characteristic changes in T-suppressor link of immunity in accumulation of zero lymphocytes. Patients with poor outcome of primary Q-MI had the same formula of immune parameters: reduced count of T-helpers, high values of T-suppressors and CIC. Thus, the data show that low count of T-helpers, common T-cells, high level of T-suppressors or zero-cells during post-MI month 1 are related with compensated regeneration of the cardiac muscle. If the patients have deviation of the regulatory index and accumulation of CIC, they have poor prognosis. Regarding the time since MI (1, 15 or 25 days), the following regulation was seen: patients with compensated hemodynamics have 4 decreased and 1 increased parameters of immune status; patients with pathological myocardial remodeling have stimulation of at least 5-6 parameters of the immune status.


CONCLUSION
Myocardial remodeling of the LV proceeds within the first year after development of myocardial necrosis; outcomes of myocardial restoration correlate with severity of immune disorders forming 2-3 weeks after MI, suppression of cell reactions agrees with compensated hemodynamics; accumulation of CIC in blood points to the risk of pathological remodeling of the left ventricle and post-MI cardiac failure.