Excessive left ventricular hypertrophy in moderate degenerative aortic stenosis: an ineffective compensatory mechanism triggered by primary myocardial dysfunction and enhanced by concomitant mild renal impairment?

Długosz, Dorota; Bolt, Klaudiusz; Sam, Wai S.; Nawara, Tomasz; Kruszelnicka, Olga; Chyrchel, Bernadeta; Surdacki, Andrzej

doi:10.5603/kp.a2018.0196

Cited by 9 publications

(5 citation statements)

References 12 publications

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“…In addition, the incidence of all study end-points, including all-cause death, CV death or sudden cardiac death was similar according to the use of RAS antagonists [61]. Finally, potential clinical benefits of ACEI/ARB in less than severe AS could also be linked to their capability to slow down the progression of renal function decline, recently shown to contribute to the development of excessive LVH in moderate AS, as described by our group [62].…”

Section: Renin-angiotensin System Blockade In As – a Tool To Inhibit mentioning

confidence: 89%

Is left ventricular hypertrophy a friend or foe of patients with aortic stenosis?

Davies

Zerebiec

Rożanowska

et al. 2018

pwki

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Left ventricular hypertrophy (LVH) is traditionally considered a physiological compensatory response to LV pressure overload, such as hypertension and aortic stenosis (AS), in an effort to maintain LV systolic function in the face of an increased afterload. According to the Laplace law, LV wall thickening lowers LV wall stress, which in turn would be helpful to preserve LV systolic performance. However, numerous studies have challenged the notion of LVH as a putative beneficial adaptive mechanism. In fact, the magnitude of LVH is associated with higher cardiovascular morbidity and mortality, especially when LVH is disproportionate to LV afterload. We have briefly reviewed: first, the importance of non-valvular factors, beyond AS severity, for total LV afterload and symptomatic status in AS patients; second, associations of excessive LVH with LV dysfunction and adverse outcome in AS; third, prognostic relevance of the presence or absence of pre-operative LVH in patients referred for aortic valve surgery; fourth, time course, determinants and prognostic implications of LVH regression and LV function recovery after surgical valve replacement and transcatheter aortic valve implantation (TAVI) with a focus on TAVI-specific effects; fifth, the potential of medical therapy to modulate LVH before and after surgical or interventional treatment for severe AS, a condition perceived as a relative contraindication to renin-angiotensin system blockade.

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Section: Renin-angiotensin System Blockade In As – a Tool To Inhibit mentioning

confidence: 89%

Is left ventricular hypertrophy a friend or foe of patients with aortic stenosis?

Davies

Zerebiec

Rożanowska

et al. 2018

pwki

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“…Beyond more than mild aortic regurgitation or disease of another valve, significant (≥50%) epicardial coronary narrowings, a history of acute coronary syndromes or coronary revascularization [ 10 , 11 ], exclusion criteria included any abnormalities which could potentially contribute to low SV index: atrial fibrillation, relevant mitral stenosis, mitral insufficiency or tricuspid regurgitation and right ventricular dysfunction [ 1 ]. We also excluded subjects with diabetes or chronic kidney disease because we had previously demonstrated subtle impairment of LV contractility in AS with concomitant type 2 diabetes [ 12 ] or renal dysfunction [ 13 ].…”

Section: Methodsmentioning

confidence: 99%

“…Routine echocardiography during the index hospitalization had been performed by an experienced sonographer. From in-hospital echocardiographic records (LV internal diameters and wall thickness) and average in-hospital cuff systolic blood pressure, we calculated LV systolic performance and circumferential systolic wall stress at the midwall level as previously described, assuming a simplified cylindrical two-shell LV model [ 14 , 15 , 16 ], similar to our earlier reports [ 10 , 11 , 12 , 13 ]. The model is based on a constant volume of each of two concentric shells representing the LV myocardium throughout the cardiac cycle and allows the quantification of systolic epicardial migration of a theoretical midwall fiber which is located at the midpoint of the LV wall at end-diastole [ 17 ] ( Figure 1 ).…”

Section: Methodsmentioning

confidence: 99%

Impaired Left Ventricular Circumferential Midwall Systolic Performance Appears Linked to Depressed Preload, but Not Intrinsic Contractile Dysfunction or Excessive Afterload, in Paradoxical Low-Flow/Low-Gradient Severe Aortic Stenosis

Długosz¹,

Surdacki

Zawiślak³

et al. 2022

JCM

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Paradoxical low-flow/low-gradient aortic stenosis (P-LFLG-AS) occurs in about one-third of patients with severe AS and preserved left ventricular (LV) ejection fraction (EF). Our aim was to differentiate between altered LV loading conditions and contractility as determinants of subtle LV systolic dysfunction in P-LFLG-AS. We retrospectively analyzed medical records of patients with isolated severe degenerative AS and preserved EF (30 subjects with P-LFLG-AS and 30 patients with normal-flow/high-gradient severe AS (NFHG-AS)), without relevant coexistent diseases (e.g., diabetes, coronary artery disease and chronic kidney disease) or any abnormalities which could account for a low-flow state. Patients with P-LFLG-AS and NFHG-AS did not differ in aortic valve area index and most clinical characteristics. Compared to NFHG-AS, subjects with P-LFLG-AS exhibited smaller LV end-diastolic diameter (LVd) (44 ± 5 vs. 54 ± 5 mm, p < 0.001) (consistent with lower LV preload) with pronounced concentric remodeling, higher valvulo-arterial impedance (3.8 ± 1.1 vs. 2.2 ± 0.5 mmHg per mL/m2, p < 0.001) and diminished systemic arterial compliance (0.45 ± 0.11 vs. 0.76 ± 0.23 mL/m2 per mmHg, p < 0.001), while circumferential end-systolic LV midwall stress (cESS), an estimate of afterload at the LV level, was similar in P-LFLG-AS and NFHG-AS (175 ± 83 vs. 198 ± 69 hPa, p = 0.3). LV midwall fractional shortening (mwFS) was depressed in P-LFLG-AS vs. NFHG-AS (12.3 ± 3.5 vs. 14.7 ± 2.9%, p = 0.006) despite similar EF (61 ± 6 vs. 59 ± 8%, p = 0.4). By multiple regression, the presence of P-LFLG-AS remained a significant predictor of lower mwFS compared to NFHG-AS upon adjustment for cESS (β ± SEM: −2.35 ± 0.67, p < 0.001); however, the significance was lost after further correction for LVd (β = −1.10 ± 0.85, p = 0.21). In conclusion, the association of P-LFLG-AS with a lower cESS-adjusted mwFS, an index of afterload-corrected LV circumferential systolic function at the midwall level, appears secondary to a smaller LV end-diastolic cavity size according to the Frank–Starling law. Thus, low LV preload, not intrinsic contractile dysfunction or excessive afterload, may account for impaired LV circumferential midwall systolic performance in P-LFLG-AS.

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“…Additionally, from echocardiography and mean in-hospital blood pressure (computed from all in-hospital blood pressure measurements), we calculated valvulo-arterial impedance (Zva)—an index of the sum of valvular and arterial components of LV afterload, and systemic arterial compliance, as previously proposed [24]. Zva was derived from systolic blood pressure, mean aortic pressure gradient and stroke volume index, whereas systemic arterial compliance from stroke volume index and pulse pressure [24], as in our earlier reports [25, 26].…”

Section: Methodsmentioning

confidence: 99%

Depressed systemic arterial compliance and impaired left ventricular midwall performance in aortic stenosis with concomitant type 2 diabetes: a retrospective cross-sectional study

Czestkowska

Rożanowska

Długosz

et al. 2019

Cardiovasc Diabetol

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Background: Degenerative aortic stenosis (AS), a disease of the elderly, frequently coexists with concomitant diseases, including type 2 diabetes (T2DM) which amplifies the cardiovascular (CV) risk. T2DM affects left ventricular (LV) structure and function via hemodynamic and metabolic factors. In concentric LV geometry, typical for AS, indices of LV midwall mechanics are better estimates of LV function than ejection fraction (EF). Effects of T2DM coexisting with AS on circumferential LV midwall systolic function and large artery properties have not been reported so far. Our aim was to compare characteristics of AS patients with and without T2DM, with a focus on LV midwall systolic function and arterial compliance.Methods: Medical records of 130 electively hospitalized patients with moderate or severe isolated degenerative AS were retrospectively analyzed. Exclusion criteria included clinical instability, atrial fibrillation, coronary artery disease and relevant non-cardiac diseases. From in-hospital echocardiography and blood pressure, we calculated LV midwall fractional shortening (mwFS), circumferential end-systolic LV wall stress (cESS) and valvulo-arterial impedance (Zva), estimates of LV afterload, as well as systemic arterial compliance. Results:Patients with (n = 50) and without T2DM (n = 80) did not differ in age, AS severity, LV mass and LV diastolic diameter. T2DM patients exhibited elevated cESS (247 ± 105 vs. 209 ± 84 hPa, p = 0.025) and Zva (5.8 ± 2.2 vs. 5.1 ± 1.8 mmHg per mL/m 2 , p = 0.04), and lower stroke volume index (33 ± 10 vs. 38 ± 12 mL/m 2 , p = 0.01) and systemic arterial compliance (0.53 ± 0.16 vs. 0.62 ± 0.22 mL/m 2 per mmHg, p = 0.01). mwFS (11.9 ± 3.9 vs. 14.1 ± 3.7%, p = 0.001), but not EF (51 ± 14 vs. 54 ± 13%, p = n.s.), was reduced in T2DM. mwFS and cESS were inversely interrelated in patients both with (r = − 0.59, p < 0.001) and without T2DM (r = − 0.53, p < 0.001) By multiple regression, higher cESS (p < 0.001) and T2DM (p = 0.02) were independent predictors of depressed mwFS. © The Author(s) 2019. This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creat iveco mmons .org/licen ses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver Conclusions:In AS, coexistent T2DM appears associated with reduced systemic arterial compliance and LV dysfunction at the midwall level, corresponding to slightly depressed myocardial contractility.

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Excessive left ventricular hypertrophy in moderate degenerative aortic stenosis: an ineffective compensatory mechanism triggered by primary myocardial dysfunction and enhanced by concomitant mild renal impairment?

Cited by 9 publications

References 12 publications

Is left ventricular hypertrophy a friend or foe of patients with aortic stenosis?

Is left ventricular hypertrophy a friend or foe of patients with aortic stenosis?

Impaired Left Ventricular Circumferential Midwall Systolic Performance Appears Linked to Depressed Preload, but Not Intrinsic Contractile Dysfunction or Excessive Afterload, in Paradoxical Low-Flow/Low-Gradient Severe Aortic Stenosis

Depressed systemic arterial compliance and impaired left ventricular midwall performance in aortic stenosis with concomitant type 2 diabetes: a retrospective cross-sectional study

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