Left Ventricular Heart Failure and Pulmonary Hypertension

Rosenkranz S, Gibbs JS, Wachter R, De Marco T, Vonk-Noordegraaf A, Vachiéry JL.
Left Ventricular Heart Failure and Pulmonary Hypertension. Eur Heart J 2015;Oct 27:[Epub ahead of print].

Among patients with left heart failure (HF), pulmonary hypertension (PH) and right ventricular (RV) dysfunction are common, and have substantial prognostic and therapeutic implications. This very well written review of the interaction between left-sided HF and PH is worth reading in its entirety. The following are key points to remember:

  1. Regardless of the origin, PH is defined as a mean pulmonary artery pressure (PAP) ≥25 mm Hg. Current terminology and classification defines post-capillary PH (left ventricular end-diastolic pressure [LVEDP] or pulmonary capillary wedge pressure [PCWP] >15 mm Hg) as either isolated post-capillary PH (diastolic pressure gradient [the difference between PAP and PCWP] <7 mm Hg and/or pulmonary vascular resistance [PVR] ≤3 Woods units [WU]) or combined post- and pre-capillary PH (diastolic pressure gradient ≥7 mm Hg and/or PVR >3 WU).
  2. Among patients with HF with reduced LV ejection fraction (EF), the prevalence of PH (based on right heart catheterization) is 40-75%. Among patients with HP with preserved EF (HFpEF), the prevalence (based on echocardiography or catheterization) is 36-83%. Numerous studies have demonstrated an inverse correlation between PH in left-sided HF and survival.
  3. The pathophysiology of PH in left-sided HF is complex and heterogeneous. PH results primarily from backward transmission of elevated left-sided filling pressures occurring as a consequence of systolic or diastolic LV dysfunction. Increases in pulmonary pressures and PVR result in maladaptive remodeling of the right atrium and RV, ultimately with RV dysfunction and failure.
  4. Both the susceptibility for pulmonary vascular disease (presumably related to genetic and environmental factors) and the chronicity of left-sided HF play roles in determining which patients with left-sided HF subsequently develop PH.
  5. Both PCWP and LVEDP can be used to diagnose post-capillary PH. However, PCWP measurements are prone to error. In discriminating pulmonary artery hypertension (PAH) from PH due to left-sided heart disease, the following should be considered:
    • The zero reference level should be set at the mid-thoracic level.
    • The threshold to discriminate between pre- and post-capillary PH should be 15 mm Hg, but suspicion for PH due to HFpEF should be raised at values between 12 and 15 mm Hg, especially after treatment with diuretics.
    • PCWP should be measured at end-expiration (without breath-hold or Valsalva maneuver).
    • Direct measurement of LVEDP should be considered if PCWP is not reliably measured, or if significant left-sided heart disease is suspected.
  6. When performing right heart catheterization, there are three main goals:
    • The presence of PH should be confirmed, using a threshold mean PAP ≥25 mm Hg.
    • Obtain complete pulmonary hemodynamics, including PAP, right atrial pressure, cardiac output/cardiac index, mixed venous oxygen saturation, and calculation of the transpulmonary pressure gradient, diastolic pressure gradient, and PVR.
    • PH should be characterized as pre-capillary, isolated post-capillary, or combined pre- and post-capillary.
  7. Some clinical features suggestive of PH caused by left-sided heart disease include: older age, hypertension, diabetes, coronary artery disease, obesity; evidence of LV hypertrophy, systolic or diastolic dysfunction; and elevated B-type natriuretic peptide.
  8. One consideration in the treatment of patients with PH and underlying left-sided heart disease includes optimizing treatment of the underlying left-sided heart disease using medical and interventional therapies (including cardiac resynchronization therapy, LV assist device, and mitral valve intervention).
  9. Another consideration is targeted treatment of PAH using endothelin receptor antagonists, prostanoids, phosphodiesterase type 5 inhibitors, and stimulators of soluble guanylate cyclase are not approved for the treatment of PH caused by left-sided heart disease.
  10. Despite significant achievements, important evidence gaps remain that need to be addressed in future studies.

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