The impact of arterial load on left ventricular performance: An invasive haemodynamic study in severe mitral stenosis
2015 (English)In: Journal of Physiology, ISSN 0022-3751, E-ISSN 1469-7793, Vol. 593, no 8, 1901-1912 p.Article in journal (Refereed) Published
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. 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 cm2) 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 (E<inf>es</inf>) was employed for LV contractility measurements. Effective arterial elastance (E<inf>a</inf>) and LV diastolic stiffness were measured. MS patients demonstrated significantly elevated afterload (E<inf>a</inf>: 3.0 ± 1.3 vs. 1.5 ± 0.3 mmHg ml-1; P < 0.001) and LV contractility (E<inf>es</inf>: 4.1 ± 1.6 vs. 2.4 ± 0.5 mmHg ml-1; P < 0.001) as compared to controls, with higher E<inf>a</inf> in subjects with smaller mitral valve area (≤ 0.8 cm2) and pronounced subvalvular fusion. Stroke volume (49 ± 16 to 57 ± 17 ml; P < 0.001) and indexed LV end-diastolic volume (LVEDV<inf>index</inf>: 57 ± 16 to 64 ± 16 ml m-2; P < 0.001) increased following PTMC while E<inf>es</inf> and E<inf>a</inf> 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.
Place, publisher, year, edition, pages
2015. Vol. 593, no 8, 1901-1912 p.
adult, arterial load, arterial pressure, artery compliance, Article, blood vessel parameters, brachial artery, cardiovascular parameters, controlled study, disease association, disease severity, female, heart afterload, heart catheterization, heart left ventricle compliance, heart left ventricle contractility, heart left ventricle diastolic stiffness, heart left ventricle ejection fraction, heart left ventricle enddiastolic volume, heart left ventricle failure, heart left ventricle function, heart preload, heart right ventricle enddiastolic volume, heart stroke volume, heart valve surgery, human, invasive procedure, major clinical study, male, mitral valve stenosis, percutaneous transvenous mitral commisurotomy, priority journal, sphygmomanometry, transthoracic echocardiography, treatment outcome
IdentifiersURN: urn:nbn:se:kth:diva-167782DOI: 10.1113/jphysiol.2014.280404ISI: 000353044300023ScopusID: 2-s2.0-84927692750OAI: oai:DiVA.org:kth-167782DiVA: diva2:814095
QC 201505262015-05-262015-05-222016-08-29Bibliographically approved