The impact of arterial load on left ventricular performance: an invasive haemodynamic study in severe mitral stenosis.

KEY POINTS: A hallmark of mitral stenosis (MS) is the markedly altered left ventricular (LV) loading. As most of the methods used to determine LV performance in MS patients are influenced by loading conditions, previous studies have shown conflicting results. The present study calculated LV elastance, which is a robust method to quantify LV function. We demonstrate that LV loading in MS patients is elevated but normalizes after valve repair and might be a result of reflex pathways. Additionally, we show that the LV in MS is less compliant than normal due to a combination of right ventricular loading and the valvular disease itself. Immediately after valve dilatation the increase in blood inflow into the LV results in even greater LV stiffness. Our findings enrich our understanding of heart function in MS patients and provide a simple reproducible way of assessing LV performance in MS. ABSTRACT: Left ventricular (LV) function in rheumatic mitral stenosis (MS) remains an issue of controversy, due to load dependency of previously employed assessment methods. We investigated LV performance in MS employing relatively load-independent indices robust to the altered loading state. We studied 106 subjects (32 ± 8 years, 72% female) with severe MS (0.8 ± 0.2 cm(2) ) and 40 age-matched controls. MS subjects underwent simultaneous bi-ventricular catheterization and transthoracic echocardiography (TTE) before and immediately after percutaneous transvenous mitral commisurotomy (PTMC). Sphygmomanometric brachial artery pressures and TTE recordings were simultaneously acquired in controls. Single-beat LV elastance (Ees ) was employed for LV contractility measurements. Effective arterial elastance (Ea ) and LV diastolic stiffness were measured. MS patients demonstrated significantly elevated afterload (Ea : 3.0 ± 1.3 vs. 1.5 ± 0.3 mmHg ml(-1) ; P < 0.001) and LV contractility (Ees : 4.1 ± 1.6 vs. 2.4 ± 0.5 mmHg ml(-1) ; P < 0.001) as compared to controls, with higher Ea in subjects with smaller mitral valve area (≤ 0.8 cm(2) ) and pronounced subvalvular fusion. Stroke volume (49 ± 16 to 57 ± 17 ml; P < 0.001) and indexed LV end-diastolic volume (LVEDVindex : 57 ± 16 to 64 ± 16 ml m(-2) ; P < 0.001) increased following PTMC while Ees and Ea returned to more normal levels. Elevated LV stiffness was demonstrated at baseline and increased further following PTMC. Our findings provide evidence of elevated LV contractility, increased arterial load and increased diastolic stiffness in severe MS. Following PTMC, both LV contractility and afterload tend to normalize.

The pulmonary capillary wedge pressure accurately reflects both normal and elevated left atrial pressure.

BACKGROUND: Pulmonary capillary wedge pressure (PCWP) is routinely used as an indirect measure of the left atrial pressure (LAP), although the accuracy of this estimate, especially under pathological hemodynamic conditions, remains controversial. OBJECTIVES: The aim of this prospective study was to investigate the reliability of PCWP for the evaluation of LAP under different hemodynamic conditions. METHODS: Simultaneous left and right heart catheterization data of 117 patients with pure mitral stenosis, obtained before and immediately after percutaneous mitral comissurotomy, were analyzed. RESULTS: A strong correlation and agreement between PCWP and LAP measurements was demonstrated (correlation coefficient = 0.97, mean bias ± CI, 0.3 ± -3.7 to 4.2 mm Hg). Comparison of measurements performed within a 5-minute interval and those performed simultaneously revealed that simultaneous pressure acquisition yielded better agreement between the 2 methods (bias ± CI, 1.82 ± 1.98 mm Hg). In contrast to previous observations, the discrepancy between the 2 measures did not increase with elevated PCWP. Multiple regression analysis failed to identify hemodynamic confounders of the discrepancy between the 2 pressures. The ability of PCWP to distinguish between normal and elevated LAP (cutoff set at 12 and 15 mm Hg, respectively), as tested by receiver operating characteristics analysis, demonstrated a remarkably high diagnostic accuracy (area under the curve: 0.989 and 0.996, respectively). CONCLUSIONS: Although the described limits of agreement may not allow the interchangeability of PCWP and LAP, especially at lower pressure ranges, our data support the clinical use of PCWP as a robust and accurate estimate of LAP.