Pulmonary Hypertension in Heart Failure Patients: Pathophysiology and Prognostic Implications

Marco Guazzi, Valentina Labate

Research output: Contribution to journalArticlepeer-review


Pulmonary hypertension (PH) due to left heart disease (LHD), i.e., group 2 PH, is the most common reason for increased pressures in the pulmonary circuit. Although recent guidelines incorporate congenital heart disease in this classification, left-sided heart diseases of diastolic and systolic origin including valvular etiology are the vast majority. In these patients, an increased left-sided filling pressure triggers a multistage hemodynamic evolution that ends into right ventricular failure through an initial passive increase in pulmonary artery pressure complicated over time by pulmonary vasoconstriction, endothelial dysfunction, and remodeling of the small-resistance pulmonary arteries. Regardless of the underlying left heart pathology, when present, PH-LHD is associated with more severe symptoms, worse exercise tolerance, and outcome, especially when right ventricular dysfunction and failure are part of the picture. Compared with group 1 and other forms of pulmonary arterial hypertension, PH-LHD is more often seen in elderly patients with a higher prevalence of cardiovascular comorbidities and most, if not all, of the features of metabolic syndrome, especially in case of HF preserved ejection fraction. In this review, we provide an update on current knowledge and some potential challenges about the pathophysiology and established prognostic implications of group 2 PH in patients with HF of either preserved or reduced ejection fraction.

Original languageEnglish
Pages (from-to)1-14
Number of pages14
JournalCurrent Heart Failure Reports
Publication statusAccepted/In press - Nov 17 2016


  • Heart failure
  • Pulmonary hypertension

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)
  • Emergency Medicine


Dive into the research topics of 'Pulmonary Hypertension in Heart Failure Patients: Pathophysiology and Prognostic Implications'. Together they form a unique fingerprint.

Cite this