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Left Atrial Stenosis Induced Pulmonary Venous Arterialization and Group 2 Pulmonary Hypertension in Rat
Published on: November 18, 2018
CLINICAL PECULIARITIES AND PATHOGENETIC DETERMINANTS OF DEVELOPMENT AND PROGRESSION OF CHRONIC PULMONARY HEART WITH
Vitaliy N Seredyuk1, Igor P Vakaliuk1, Nestor M Seredyuk1
1IVANO-FRANKIVSK NATIONAL MEDICAL UNIVERSITY, IVANO-FRANKIVSK, UKRAINE.
Objective:
The aim: To investigate the clinical and pathogenetic peculiarities of formation and course of CCP and the relationship between clinical, hemodynamic and neurohumoral factors of comorbidity development in COPD combined with arterial hypertension (AH).
Patients And Methods:
Materials and methods: The object of the study were 484 patients with COPD. Among them, 350 patients with CCP as a result of cardiac insufficiency/severe congestive heart failure (COPD III-IV) out of aggravation, combined with AH II stage (non-symptomatic organ damage) and 1 - 3 grades, including 55 patients (43 men, 12 women) with compensated CCP (average age 43.7 ± 3.4 years), and 295 patients (212 men and 83 women) with decompensated CCP and chronic heart failure (CHF), average age 63.2 ± 8.9 years.
Results:
Results: It was found that the development and progression of the left and right CHF in patients with CCP combined with AH occurs due to the disorders of the central hemodynamic, progression of pulmonary hypertension, bronchial obstruction syndrome, neurohumoral and systemic immunoinflammatory activation, disorders of endothelial regulation of vascular tension, overproduction of epithelial and mitogenic growth factors, inducers of apoptosis, and is accompanied by increasing levels of natriuretic peptides.
Conclusion:
Conclusions: The main pathogenetic formation mechanisms of the heart failure on the background of CCP combined with AH are: neurohumoral and systematic immune-inflammatory activation with the development of endothelial dysfunction and (neo)angiogenesis, induction of pathological apoptosis, increase in the intrathoracic pressure, and deposition of blood in the extrathoracic tissues, which result in pulmonary and systemic hypertension, metabolic and hemodynamic remodelling and heart dysfunction.
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