2019
DOI: 10.1080/00015385.2019.1634333
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Acute hypoxic pulmonary hypertension associated with right heart failure

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Cited by 2 publications
(3 citation statements)
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“…The increase in LV afterload by an overload of pressure or volume is considered a determining cause of left heart failure (LHF). In contrast, pulmonary hypertension, pulmonary stenosis, chronic obstructive pulmonary disease, and tricuspid valve pathology produce similar consequences on the right side, inducing right heart failure (RHF) [ 100 102 ]. RHF could be acute or chronic.…”
Section: Distinctions Between Right and Left Ventricle Dysfunctionmentioning
confidence: 99%
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“…The increase in LV afterload by an overload of pressure or volume is considered a determining cause of left heart failure (LHF). In contrast, pulmonary hypertension, pulmonary stenosis, chronic obstructive pulmonary disease, and tricuspid valve pathology produce similar consequences on the right side, inducing right heart failure (RHF) [ 100 102 ]. RHF could be acute or chronic.…”
Section: Distinctions Between Right and Left Ventricle Dysfunctionmentioning
confidence: 99%
“…RHF could be acute or chronic. Acute RHF is caused by a suddenly increased RV afterload due to hypoxia or a pulmonary embolus [ 102 , 103 ] or decreased RV contractility in RV ischemia, myocarditis, or postcardiotomy shock [ 104 ]. On the other hand, chronic RHF results from the gradual increases in RV afterload produced by pulmonary hypertension [ 101 , 102 ], which promotes cardiac remodeling with increased RV mass, fibrosis, and hypertrophy of cardiomyocytes, analogous to the remodeling observed in LHF [ 105 ].…”
Section: Distinctions Between Right and Left Ventricle Dysfunctionmentioning
confidence: 99%
“…Hypoxia causes vascular endothelial cell damage, which in turn perturbs the synthesis and secretion of various vasodilator factors and leads to pulmonary vasoconstriction in the short term and pulmonary vascular remodeling in the longer term (1). Such vascular remodeling is characterized by thickening of the medial membrane due to proliferation of phenotypically altered smooth muscle cells, and endothelial cell dysfunction not only leads to intimal thickening and distal pulmonary artery dilatation, but also inflammation and infiltration of the outer membrane (2).…”
Section: Introductionmentioning
confidence: 99%