Dr Girard has critiqued my commentary in which I introduced the studies by Erkens et al. & Kovacs et al. in the Journal . The purpose of my brief commentary was not to provide an expert comment on pulmonary hypertension but to highlight these two important studies and provide the context for implementation of the findings of these studies. Patients with pulmonary embolus are in a precarious state and clinicians rightly worry that sudden death may occur. It is for this reason that patients with pulmonary embolus are traditionally treated as inpatients. However, as I indicated, this practise is changing and the studies by Erkens et al. & Kovacs et al. are helpful in providing a simple risk stratification model for selection of patients for treatment as outpatients.
My comments in relation to obstruction of the pulmonary vasculature related directly to the referenced report by McIntyre and Sasahara . Furthermore, my comments were obviously specifically in relation to patients with pulmonary embolus. Clearly, pulmonary hypertension does not result simply from a reduction in the cross-sectional area of the pulmonary vasculature, which is why patients with a 50% reduction due to removal of a lung do not develop it. In contrast, in patients with pulmonary emboli pulmonary hypertension occurs due to a combination of physical obstruction of the vascular bed and other factors such as shunting, as I stated. In the seminal study by McIntyre and Sasahara patients were studied by pulmonary angiography. In their study pulmonary hypertension was defined as a mean pulmonary artery pressure > 20 mmHg. The study identified the very different effects of pulmonary emboli in patients with and without pre-existing cardiac or lung disease. Dr Girard states that in patients with acute pulmonary embolism and without associated cardiac or respiratory disease clinically detectable hemodynamic compromise (i.e. shock) only occurs when the pulmonary arterial obstruction is above 60%. This is in keeping with the findings of McIntyre and Sasahara and my comments. However, I would caution against the definition of hemodynamic compromise being dependent on the presence of shock. For example, I consider a patient without shock but with right ventricular impairment to be compromised.
Dr Girard is quite correct in stating that pulmonary hypertension is now strictly defined as a mean pulmonary artery pressure > 25 mmHg. His comments on replacement of terms related to the size of thrombus burden with terms relating to risk is partly a semantic consideration but in the context of the commentary ‘size does matter’.
The relationship between pulmonary embolus and pulmonary hypertension remains intriguing, not least regarding the development of chronic thromboembolic pulmonary hypertension in some patients. Just as vasoreactivity contributes to acute pulmonary hypertension, a proportion of patients with chronic thromboembolic pulmonary hypertension sustain vasoreactivity, indicating that this also is not simply an obstructive disease .