Clinical-functional peculiarities of stable angina of different functional classes considering myocardial infarction in an anamnesis
Keywords:stable angina pectoris, Q-myocardial infarction, nonQ-myocardial infarction, echocardiography, bicycle ergometry, coronary angiography, amino-terminal propeptide of natriuretic peptide, C-reactive protein, uric acid, testosterone
Aim. To study clinical-functional peculiarities of stable angina pectoris (SAP) of different functional classes (FC) with post-infarction and diffuse cardiosclerosis.
Materials and methods. In total, 120 patients with SAP involved in the study, and a written informed consent was obtained from all of them. The patients were distributed into the groups according to angina severity, experienced Q-myocardial infarction (Q-MI) in the anamnesis, nonQ-myocardial infarction (nonQ-MI) and diffuse cardiosclerosis.
Results. Q-MI in the anamnesis was found to promote the development of more severe SAP (Р < 0.01), unlike nonQ-MI. Coronary angiography findings were indicative of the hemodynamically significant damage of the coronary arteries among the patients with FC III SAP. Higher FC SAP was associated with a considerable increase in total cholesterol (Р < 0.05) rather than increase in triglyceride levels (Р > 0.05), irrespective of experienced MI in the anamnesis. The levels of amino-terminal propeptide of natriuretic peptide and C-reactive protein were higher in FC III SAP (Р < 0.01 and Р < 0.001, respectively) regardless of MI in the anamnesis. An increased level of uric acid caused more severe SAP (Р < 0.001) among patients who had experienced myocardial infarction Q-MI (Р < 0.01).
According to the echocardiography findings, patients with FC III SAP presented larger size of the left ventricle (Р < 0.05), irrespective of experienced MI in the anamnesis. The bicycle ergometry results revealed lower indices of the threshold load and tolerance to physical exercise (in both cases Р < 0.001) and more pronounced test-induced ischemia (Р < 0.001) due to FC III SAP.
Conclusions. Higher FC SAP is caused by more hemodynamically significant damage of the coronary arteries with increased levels of amino-terminal propeptide of natriuretic peptide and C-reactive protein, irrespective of experienced Q-MI and nonQ-MI in the anamnesis.
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