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Pulmonary hypertension in significant aortic valve disease: a dive into real-world data
  1. Dana Cramariuc1,2,
  2. Stig Urheim1,2
  1. 1 Department of Heart Disease, Haukeland University Hospital, Bergen, Norway
  2. 2 Department of Clinical Science, University of Bergen, Bergen, Norway
  1. Correspondence to Dr Dana Cramariuc, Heart Disease, Haukeland University Hospital, 5021 Bergen, Norway; dana.cramariuc{at}helse-bergen.no

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Left heart disease is the most common cause of pulmonary hypertension (PHT) accounting for over 65% of all diagnosed cases.1 In over half of these patients, PHT is the consequence of valve dysfunction, predominantly mitral regurgitation.2 However, echocardiographic evidence of PHT is not infrequent in the setting of aortic valve disease, particularly in patients with severe aortic stenosis (AS) in whom an estimated systolic pulmonary arterial pressure (eSPAP) >60 mm Hg has previously been reported in up to 34%.3 Data on PHT due to significant aortic regurgitation (AR) has up to now been much scarcer, with one study finding severe PHT in 16% of cases of severe AR.4

The chronic pressure overload generated by AS and pressure/volume overload caused by AR result in differential patterns of left ventricular (LV) remodeling, with more often a thick-walled, concentric remodeled LV in AS, and a dilated, eccentrically hypertrophied LV in AR. Both types of LV remodeling become maladaptive during the AS/AR progression and initiate the same pathway of elevated LV end-diastolic pressure and consequently elevated left atrial pressure (figure 1). The high pressure is further on transmitted backwards to the pulmonary veins, causing over time isolated postcapillary PHT. In advanced disease stages, due to pulmonary vascular remodeling and increasing pulmonary vascular resistance, a combined precapillary and postcapillary PHT might develop.

Figure 1

The pathophysiological link between left ventricular (LV) remodeling and development of pulmonary hypertension in aortic valve disease.

By echocardiography and using eSPAP >60 mm Hg as a surrogate of severe PHT, previous studies have documented higher mortality risk in patients with combined severe AS–PHT.3 5 The …

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Footnotes

  • Contributors DC and SU have written the manuscript and created the figure. They both approved the final version to be published.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests None declared.

  • Provenance and peer review Commissioned; internally peer reviewed.

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