Key result
Pathophysiological interactions between cardiomyocytes and pulmonary vascular cells, involving systems such as RAS, ROS, ET-1, VEGF, and BMP, play a crucial role in the development of pulmonary arterial hypertension following myocardial infarction.
Why the study?
The pathological mechanisms underlying vascular remodeling and exacerbation of PAH following MI remain unclear.
This review summarizes the pathophysiological interactions between cardiomyocytes and pulmonary vascular cells in the context of pulmonary arterial hypertension following myocardial infarction.
Left heart disease is the main cause of clinical pulmonary arterial hypertension (PAH). Common types of left heart disease that result in PAH include heart failure, left ventricular systolic dysfunction, left ventricular diastolic dysfunction and valvular disease. It is currently believed that mechanical pressure caused by high pulmonary venous pressure is the main cause of myocardial infarction (MI) in individuals with ischemic cardiomyopathy and left ventricular systolic dysfunction. In the presence of decreased cardiac function, vascular remodeling of pulmonary vessels in response to long‑term stimulation by high pressure in turn leads to exacerbation of PAH. However, the underlying pathological mechanisms remain unclear. Elucidating the association between the development of MI and PAH may lead to a better understanding of potential risk factors and better disease treatment. In this article, the pathophysiological effects of multiple systems in individuals with MI and PAH were reviewed in order to provide a general perspective on various potential interactions between cardiomyocytes and pulmonary vascular cells.
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Ye et al. (2020) conducted a review in Pulmonary arterial hypertension following myocardial infarction. Pathophysiological interactions between cardiomyocytes and pulmonary vascular cells, involving systems such as RAS, ROS, ET-1, VEGF, and BMP, play a crucial role in the development of pulmonary arterial hypertension following myocardial infarction.
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