10th March 2024

Group 2: Left heart disease

Left-sided heart failure is the most common cause of pulmonary hypertension, and this can happen in patients with both HF-pEF and HF-rEF. Recognising that pulmonary hypertension is present in these patients is essential as it carries an increased morbidity and mortality, though there are no specifically targeted therapies.

When considering pathophysiology, the first hemodynamic insult in this group of patients is an increase in left atrial or ventricular filling pressures. This, in turn, can reduce pulmonary arterial compliance, causing the pulmonary vasculature to become stiffer and increasing the pressure against which the RV needs to contract. Patients with left heart disease with both post- and pre-capillary pulmonary hypertension can develop pulmonary hypertension due to ongoing vasoconstriction and chronic remodelling of the pulmonary vascular beds. The increase in pulmonary pressures will cause an increased resistive afterload and, ultimately, dilatation, hypertrophy, and failure of the right ventricle (cor pulmonale).

Signs that raise the suspicion of pulmonary hypertension in these patients are: clinical signs (loud P2, RV heave), PASP>35mmHg on TTE, or right ventricular structural abnormalities or tricuspid regurgitation on cardiac imaging.

The initial diagnostic evaluation includes a TTE, which is the cornerstone to determine type and severity of heart failure, additional valvular abnormalities, and PASP. Right heart catheterisation is considered if PASP>35mmHg, and there is evidence of RV dysfunction, the cause of PH is unclear, and/or advanced therapies for heart failure are being considered. Right heart catheterisation is the gold standard for confirming the diagnosis and further categorising pulmonary hypertension.

The cornerstone of treatment is management of the underlying left heart disease with all evidence-based medical and surgical therapies available. Treatment for left heart disease aims to reduce left-sided filling pressures, which should consequently lead to an improvement in pulmonary pressures. Adequate decongestion with diuretics is essential to reduce left-sided pressures and improve pulmonary vascular function.

Systemic vasodilator challenge is only indicated for some candidates for heart transplantation to assess the reversibility of pulmonary hypertension. PH- targeted therapy is not indicated for routine use in group 2 PH as there is not sufficient evidence, and it may occasionally worsen pulmonary oedema.