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Is it time to discard outdated notions of pulmonary hypertension in constrictive pericarditis?
  1. Brian D Hoit
  1. Medicine, Case Western Reserve University and University Hospitals of Cleveland, Cleveland, Ohio, USA
  1. Correspondence to Dr Brian D Hoit, Medicine, Case Western Reserve University and University Hospitals of Cleveland, Cleveland, OH 44106, USA; bdh6{at}case.edu

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Constrictive pericarditis (CP) is the result of scarring and the consequent loss of pericardial elasticity, which constrains ventricular filling; attenuates of the inspiratory decrease in intrathoracic pressure that is normally transmitted to the cardiac chambers and enhances ventricular interaction. CP can occur after virtually any pericardial disease process. The aetiology varies widely depending on the population studied, with idiopathic and post-treatment (postoperative or post-radiation) causes being more common in developed countries and infectious aetiologies (tuberculous or purulent) being more prominent in developing countries.

While echocardiography is the first-line diagnostic tool for suspected CP, invasive haemodynamic evaluation is sometimes necessary to confirm the diagnosis, particularly in those with suboptimal or non-diagnostic echocardiographic findings in whom imaging with cardiac magnetic resonance or cardiac CT is either unavailable or non-diagnostic. Cardiac catheterisation in patients with surgically confirmed CP shows the following time-honoured invasive diagnostic findings: an elevated mean right atrial pressure; an early diastolic dip followed by a plateau during diastasis (square root sign); diastolic equalisation of pressures and respiratory variation in the right ventricular and left ventricular (RV–LV) pressures (mirror image discordance). Classically, pulmonary arterial (PA) systolic pressure is mild (usually no greater than 50 mm Hg), a finding used to distinguish CP from its haemodynamic doppelganger, restrictive cardiomyopathy.

Recently, elevated PA pressures owing to both isolated post-capillary pulmonary hypertension (PH) (ie, passive transmittal of elevated left-sided filling pressures) and combined pre-capillary and post-capillary pressures (ie, additional pulmonary vasoconstriction and pulmonary vascular remodelling) have been reported in patients with increased LV filling pressure, including CP.1 2 In these patient subsets, increased systolic PH has been associated with increased mortality and …

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Footnotes

  • Contributors BDH is the sole author of this editorial.

  • 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.

  • Patient and public involvement Patients and/or the public were not involved in the design, or conduct, or reporting, or dissemination plans of this research.

  • Provenance and peer review Commissioned; internally peer reviewed.

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