Review Article
Right Ventricular Heart Failure From Pulmonary Embolism: Key Distinctions From Chronic Pulmonary Hypertension

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Abstract

Background

The right ventricle normally operates as a low pressure, high-flow pump connected to a high-capacitance pulmonary vascular circuit. Morbidity and mortality in humans with pulmonary hypertension (PH) from any cause is increased in the presence of right ventricular (RV) dysfunction, but the differences in pathology of RV dysfunction in chronic versus acute occlusive PH are not widely recognized.

Methods and Results

Chronic PH that develops over weeks to months leads to RV concentric hypertrophy without inflammation that may progress slowly to RV failure. In contrast, pulmonary embolism (PE) results in an abrupt vascular occlusion leading to increased pulmonary artery pressure within minutes to hours that causes immediate deformation of the RV. RV injury is secondary to mechanical stretch, shear force, and ischemia that together provoke a cytokine and chemokine-mediated inflammatory phenotype that amplifies injury.

Conclusions

This review will briefly describe causes of pulmonary embolism and chronic PH, models of experimental study, and pulmonary vascular changes, and will focus on mechanisms of right ventricular dysfunction, contrasting mechanisms of RV adaptation and injury in these 2 settings.

Section snippets

PE—Acute Occlusive PH

PE is an acute, occlusive, thromboembolic disorder causing PH that may lead to RV damage.2, 3, 4, 12, 16 By far, most PE arises as a result of embolism from deep vein thrombosis, most commonly from veins in the legs.17 Furthermore, deep vein thrombosis and PE share the same predisposing risk factors, such as inherited hypercoagulable states and acquired factors such as reduced mobility, trauma, pregnancy, oral contraceptives, obesity, and malignancy.17 Acute PH and RV strain may also occur in

Conclusions and Future Directions

Similarities between pulmonary embolism (acute occlusive PH) and chronic PH include the fact that pulmonary circulatory resistance increases, RV tissue converts to the fetal gene profile, and RV function may decline. Furthermore, mortality and morbidity are correlated with the extent of RV dysfunction in both cases. Mechanisms of change within the lungs and heart, however, are drastically different between these 2 types of PH. Acute occlusive PH results from an abrupt blockage of pulmonary

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