Author + information
- Elias B. Hanna, MD∗ (, )
- Frank W. Smart, MD and
- Eliana Hanna Deschamps, MD
- ↵∗Department of Medicine, Cardiovascular Section, Louisiana State University, CSRB Building, Room 346, 433 Bolivar Street, New Orleans, Louisiana 70112
We read with great interest the article by Mascherbauer et al. (1), in which the relationship between mean pulmonary artery wedge pressure (PAWP) and left ventricular end-diastolic pressure (LVEDP) was analyzed in heart failure with preserved ejection fraction (HFpEF).
We offer the following 4 comments regarding the mechanisms of discrepancy between mean PAWP and LVEDP:
1. PAWP is sometimes equated with pulmonary capillary hydrostatic pressure, but as we described previously, this scenario is not always true (2, Online Ref. 1). In alveolocapillary obstruction, pulmonary capillary hydrostatic pressure exceeds left atrial (LA) pressure, but PAWP remains comparable to LA pressure, which contrasts with the authors’ speculation. Wedging the pulmonary arterial catheter leads, in most cases, to a static column of blood between the catheter tip and an equally large pulmonary vein, even when the alveolocapillary membrane is thickened or the venular bed is obstructed (2). Therefore, PAWP corresponds to the pressure in the large pulmonary veins and, consequently, to the LA pressure rather than the pressure in the capillaries and the pulmonary venules. When the obstruction is at the capillary or post-capillary level, PAWP may be damped and featureless with attenuated A and V waves, because the LA pressure gets retrogradely transmitted through this obstruction, but still correlates with the LA pressure.
2. The discrepancy between mean PAWP and LVEDP may rather be explained by the discrepancy between mean LA pressure and LVEDP, which depends on the size of the V-wave and, therefore, on the degree of clinical decompensation of HFpEF (Figure 1) (3–5). In left ventricular (LV) diastolic dysfunction with normal LA pressure, LV pressure is normal throughout diastole but increases after A-wave, a result of impaired LV compliance; similarly, PAWP is overall normal and only increases in end-diastole after A-wave, explaining why mean PAWP (averaged throughout the cardiac cycle) may be lower than end-diastolic PAWP and LVEDP.
In the more decompensated stage of LV diastolic dysfunction with elevated LA pressure, there is a mismatch between the LA compliance and the overwhelming LA volume, leading to PAWP elevation throughout the cardiac cycle, X-descent flattening, and V-wave enlargement, even in the absence of mitral regurgitation (3,4). Mean PAWP may exceed LVEDP by an amount proportional to the amplitude and duration of V-wave.
This hemodynamic relationship may explain why PAWP is a strong prognostic marker yet potentially a weaker diagnostic marker than LVEDP in clinically compensated patients. It also explains why the sole determination of PAWP may misclassify a significant subset of pulmonary venous hypertension as pre-capillary pulmonary hypertension, as shown in a large series (Online Ref. 2).
3. The reduced carbon monoxide diffusion capacity may be the result of the elevated PAWP and the aforementioned pathophysiology, rather than the cause of it. In fact, the alveolocapillary congestion that results from the elevated pulmonary venous pressure may reduce the carbon monoxide diffusion capacity.
4. Atrial fibrillation (AF), which is highly prevalent in this study, further alters the PAWP–LVEDP relationship. In AF, atrial compliance is reduced. Moreover, in AF, the loss of atrial contraction reduces end-diastolic emptying and, thus, the atrial volume increases in systole and overwhelms the reduced atrial compliance, leading to V-wave augmentation (Online Ref. 3). Consequently, PAWP more readily exceeds LVEDP. In fact, a recent study has shown that, in patients undergoing cardiac catheterization for the evaluation of pulmonary hypertension, PAWP generally surpasses LVEDP in AF, whereas the opposite is true in sinus rhythm (Online Ref. 4).
In summary, PAWP may be higher or lower than LVEDP in HFpEF, and the discrepancies may be explained by the rhythm and the LV and LA compliances.
Please note: The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- 2018 American College of Cardiology Foundation
- Mascherbauer J.,
- Zotter-Tufaro C.,
- Duca F.,
- et al.
- Hanna E.B.