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Article

Association of Inadequately Low Left Ventricular Mass with Enhanced Myocardial Contractility in Severe Degenerative Aortic Stenosis

by
Bernadeta Chyrchel
1,
Dorota Długosz
2,
Klaudiusz Bolt
2,
Olga Kruszelnicka
3,†,
Artur Dziewierz
1,
Jolanta Świerszcz
4,
Ewa Wieczorek-Surdacka
5,
Tomasz Hryniewiecki
6,† and
Andrzej Surdacki
1,*,†
1
Second Department of Cardiology, Jagiellonian University Medical College, 17 Kopernika Street, 31-501 Cracow, Poland
2
Students’ Scientific Group at the Second Department of Cardiology, Jagiellonian University Medical College, 17 Kopernika Street, 31-501 Cracow, Poland
3
Department of Coronary Artery Disease and Heart Failure; The John Paul II Memorial Specialist Hospital, 80 Prądnicka Street, 31-202 Cracow, Poland
4
Department of Medical Education, Jagiellonian University Medical College, 16 Św. Łazarza Street, 31-530 Cracow, Poland
5
Chair and Department of Nephrology, Jagiellonian University Medical College, 15C Kopernika Street, 31-501 Cracow, Poland
6
Department of Valvular Heart Defects, Institute of Cardiology,42 Alpejska Street, 04-628 Warsaw, Poland
*
Author to whom correspondence should be addressed.
†
Joint senior authors on this work.
J. Clin. Med. 2018, 7(12), 464; https://doi.org/10.3390/jcm7120464
Submission received: 27 October 2018 / Revised: 16 November 2018 / Accepted: 20 November 2018 / Published: 22 November 2018
(This article belongs to the Section Cardiology)
Versions Notes

Abstract

:
Background: Left ventricular hypertrophy (LVH), traditionally considered an adaptive mechanism that is aimed at the maintenance of LV systolic function, is absent in 10%–35% of patients with severe aortic stenosis (AS). Our aim was to estimate the clinical and hemodynamic characteristics in patients with severe AS and absent LVH, or inadequately low LV mass (i-lowLVM) relative to an individual hemodynamic load. Methods: We retrospectively analyzed in-hospital records of 100 patients with pure severe degenerative AS, preserved LV systolic function and without relevant coexistent diseases, except for well-controlled hypertension or diabetes. Results: Clinical characteristics were similar in patients with and without LVH, as well as those with and without i-lowLVM, except for slightly lower GFR at i-lowLVM. When compared to their counterparts, subjects without LVH or with i-lowLVM had smaller LV cavities, decreased LV wall thicknesses and higher EF. There were no significant differences in stenosis severity and indices of afterload (valvulo-arterial impedance and circumferential end-systolic LV wall stress), according to the presence or absence of either LVH or i-lowLVM. However, LV fractional shortening at the midwall level was elevated only in patients with i-lowLVM, but not in those without LVH, compared to the remainder (15.8 ± 3.3 vs. 12.9 ± 3.2%, p < 0.001 for those with and without i-lowLVM, respectively; 13.7 ± 3.7 vs. 13.8 ± 3.6% for LVH presence and absence, p = 0.9). Conclusions: Inadequately low LVM relative to the individual hemodynamic load could potentially reflect a different mode of the LV response to severe AS, associated with enhanced load-independent LV systolic performance, i.e., better LV contractility. If confirmed in a large series of patients, our small preliminary study may add to the possible mechanisms of a previously reported counterintuitive tendency of a lower, not higher, risk of adverse outcome in patients with low LV mass despite severe AS. Prospective studies are warranted, in order to determine a potential utility of LVM inadequacy in the risk stratification of patients with AS.

1. Introduction

Left ventricular hypertrophy (LVH), traditionally considered an adaptive mechanism that is aimed at the maintenance of LV systolic function, is absent in 10%−35% of patients with severe aortic stenosis (AS) [1,2,3,4], the second common cause of LV pressure overload. Additionally, a classical paradigm of a net benefit from LVH has been challenged by clinical and experimental data [5,6,7,8,9,10,11,12]. Importantly, the presence and magnitude of LVH is a well-recognized independent predictor of adverse cardiovascular (CV) outcome, including death and developing heart failure (HF), in population-based cohorts, hypertension, and AS [6,7,8,9,10,11,12]. This is compatible with reports of no excessive mortality [4], or even better early postoperative survival [2] and lower risk of adverse CV events [3] in patients with severe AS and absent LVH.
Moreover, patients with inadequately low LV mass (i-lowLVM), i.e., observed LV mass (LVM) in the lower part of the distribution of the value predicted from an individual hemodynamic load, had either a similar [13] or lower [3] risk of adverse CV events than their counterparts with an appropriate LVM in hypertension [13] and severe AS [3].
Notably, only a few studies have been focused on characteristics of patients with low LVM, despite severe AS [1,2,3,4]. Therefore, our aim was to estimate the clinical and hemodynamic characteristics in patients with severe AS and absent LVH or i-lowLVM.

2. Materials and Methods

2.1. Patients

We retrospectively analyzed in-hospital records of patients with pure severe degenerative AS (aortic valve area index [AVAI] <0.6 cm2/m2 or mean transvalvular pressure gradient >40 mmHg) without relevant coexistent diseases, except for well-controlled diabetes or hypertension, with preserved LV ejection fraction (≥50%) [14]. A complete list of exclusion criteria, including clinical or angiographic evidence of significant coronary artery disease (CAD) and estimated glomerular filtration rate (GFR) below 30 mL/min per 1.73 m2 (by the CKD-EPI formula), was reported earlier in detail [15]. Besides patients with severe AS out of the previously described AS subjects with moderate-to-severe AS [15], additional patients were also included into the final analysis (Bioethical Committee of Jagiellonian University, approval No. 122.6120.228.2016), provided that they fulfilled the inclusion and exclusion criteria.

2.2. Data Analysis

From routinely recorded parameters of LV structure and function, we calculated LV fractional shortening at the midwall level (mwFS), assuming a constant volume of the inner myocardial “shell” between the LV midwall and the endocardium, according to a simplified spherical LV model [16,17]. Additionally, estimated circumferential end-systolic LV wall stress (cESS) and valvulo-arterial impedance (Zva), indices of LV afterload, were computed. cESS was calculated from LV internal diameter and wall thickness at end-systole, averaged-in hospital systolic blood pressure (SBP), and maximal transvalvular aortic pressure gradient (APGmax) [16,18,19,20], while Zva was derived from the SBP, mean transvalvular aortic pressure gradient, and stroke volume index [21]. Then, we computed a difference between the measured LVM (by the modified Devereux equation [22]) and that predicted from the height, gender, and an individual’s hemodynamic load (computed from a product of stroke volume and the sum of SBP and APGmax) by a previously validated formula [20,23,24]. Accordingly, LVMmeasured (g) = 0.8 × (1.04 × (((LVd + IVSd + PWd)3 − LVd3))) + 0.6, where LVd is the LV internal diameter, IVSd is the interventricular septum thickness, and PWSd is the posterior wall thickness (all measurements in end-diastole from the parasternal approach and expressed in cm) [22], while LVpredicted (g) = 55.37 + (0.009216 × (stroke volume (mL)) × (SBP + APGmax (mmHg))) + (6.63 × (height (m))2.7) − (18.1 − n), with n = 1 for men and n = 2 for women [3,17,20,23,24]. The difference between the measured and predicted LVM was termed an excess of LVM (eLVM), and expressed as a percentage of the predicted LVM, assumed to be 100%: eLVM = ((LVMmeasured − LVMpredicted)/LVMpredicted) × 100% [17]. Because LVH, defined according to the classical mass criteria (i.e., LVMmeasured >95 g/m2 for women and >115 g/m2 for men), was absent in 23% of our patients, for consistency, we assumed i-lowLVM as an eLVM below the 23th percentile of its distribution (i.e., eLVM <13%) in the study population. In addition to the indexation of LVM for body-surface area, we also repeated the analysis after the LVM normalization for height to the power of 2.7, as previously proposed [3,13,20].

2.3. Statistical Analysis

Data are shown as means and SD, or medians and interquartile range, and numbers with percentages. The analyzed subjects were compared according to the LVH presence or the LVM inadequacy by a 2-tailed Student’s t-test or the Mann–Whitney U-test, and Fisher’s test for continuous and categorical data, respectively. A Bonferroni-corrected p-value <0.05 was inferred significant, which corresponds to a pre-adjusted p-value <0.002.

3. Results

Clinical characteristics were similar in patients with and without LVH by the classical mass criteria, as well as with and without i-lowLVM relative to the individual hemodynamic load, except for slightly lower GFR in those with i-lowLVM (Table 1).
When compared to their counterparts, subjects without LVH or with i-lowLVM had smaller LV cavities, decreased LV wall thicknesses, and higher EF (Table 2). There were no significant differences in AVAI or in indices of afterload (cESS and Zva), according to the presence or absence of either LVH or i-lowLVM. However, mwFS was elevated only in patients with i-lowLVM, but not in those without LVH, in comparison to the remainder (Table 2).
The results were virtually unchanged when the LVH definition was based on the indexation of LVM for height instead of for body surface area.

4. Discussion

Our salient observation was an association of LVM inadequacy, but not LVH absence, with better LV systolic performance at the midwall level in severe AS. In addition, cESS and Zva—indices of afterload—were similar, while LV diastolic diameter, a raw measure of preload, was lower in AS patients with i-lowLVM than in their counterparts. Accordingly, this constellation of findings suggests that a load-independent increase in LV function, i.e., improved LV contractility, may be specific for AS subjects with i-lowLVM, and not for those with absent LVH.
Patients without LVH had smaller LV cavity sizes and thinner LV walls, as well as higher EF when compared to those with LVH, in agreement with previous reports [1,2,4]. Barasch et al. [4] speculated that some mechanisms could offset the detrimental effects of afterload excess in patients with severe AS and absent LVH, thereby explaining a tendency for better CV outcomes in that subset of AS subjects. Nevertheless, in our hands, cESS appeared to be unchanged in patients without LVH, which was secondary to LV concentric remodeling in the majority of this subgroup (as in earlier reports [1,2]), thus keeping cESS relatively constant. In addition, mwFS was also similar in patients with and without LVH. This indicates that, despite the absence of LVH, LV afterload and myocardial systolic function are preserved, while a higher EF in AS patients free of LVH seems rather to be a consequence of concentric LV geometry and better LV chamber function, not improved myocardial performance.
In contrast, patients with i-lowLVM exhibited increased both EF and mwFS in comparison to their counterparts, with a ratio of measured to predicted LVM above the 23th percentile of its distribution in the study population. This appears to be partially analogous to an early report by De Simone et al. [13] who described a higher cESS-corrected mwFS in hypertensive patients with low LVM, defined as an eLVM below −32% (corresponding to the 2.5th percentile of eLVM distribution in a reference population) despite similar LV end-diastolic diameter, a raw index of preload. That observation [13] was indicative of better LV contractility, as in our patients with i-lowLVM, who exhibited increased mwFS, unchanged cESS, and even smaller LV diameter, compared to the remainder. Of note, in those hypertensive subjects with low LVM, mean RWT was as low as 0.28 [13], while in our AS subjects with i-lowLVM, RWT averaged 0.47, reflecting concentric LV remodeling in most of them. As cESS was not elevated in AS patients with i-lowLVM, it may be concluded that—unlike in hypertension—concentric remodeling appears to be necessary to preserve normal cESS in the majority of patients with severe AS and i-lowLVM. With regard to a potential mechanism of this observation, it can be speculated that severe AS results in a fixed and probably more potent LV pressure overload, in contrast to hypertension, frequently associated with fluctuating blood pressure.
Notably, excessive LVH, i.e., inappropriately high LVM out of proportion to LV afterload, is associated with depressed mwFS, despite a lower or unchanged cESS, indicating depressed LV myocardial performance in patients with mild-to-severe AS [3,19,20], which has also recently been confirmed by our group in moderate AS [17]. Therefore, our results could reflect a continuum of the relationship between LV contractility, wall stress, and LVH adequacy, in agreement with a concept that was previously proposed by Aurigemma et al. [18,25], De Simone et al. [13], and Palmieri et al. [26] for hypertension, and later by Mureddu et al. [19] and Cioffi et al. [3,20] for AS. On the basis of LV stress-shortening relations, they suggested that excessive LVH may be a compensatory, albeit largely ineffective compensatory mechanism triggered by primary myocardial dysfunction, and aimed at restoring LV systolic performance through lowering LV wall stress. Consequently, this mechanism would not be operational in subjects with enhanced LV contractility, thereby contributing to the association of apparently low LVM with increased cESS-corrected mwFS in patients with hypertension [13]. Hence, our report is the first to demonstrate a similar mechanism in AS, another common cause of LV pressure overload.
The enhanced LV contractile function might be protective against LV dysfunction in severe AS with i-lowLVM. In accordance with this hypothesis, Kupari et al. [2] observed an increased EF, a 3-fold lower prevalence of HF, and a better 3-month postoperative outcome in patients with a lack of LVH, despite critical AS. Additionally, in an early report, Seiler and Jenni [1] described a better ergometric working capacity in AS patients with severe AS and no LVH. Unfortunately, the cited authors [1,2] estimated only the LVH presence, and not the LVM adequacy, which limits more detailed comparisons with the present study. Nonetheless, apart from this limitation, the proposed hypothesis can explain a lower risk of adverse CV events (whose majority consisted of aortic valve replacement and HF hospitalizations) in patients with severe AS in the lower tertile of the measured-to-predicted LVM ratio (<108%, i.e., eLVM <8%) [3], close to the cut-off value for i-lowLVM assumed in the present study (eLVM <13%). Consequently, LVM “inadequacy” can represent not a lack of putatively “compensatory” LVH, but rather, a different mode of LV response to pressure overload, as proposed by Kupari et al. [2] on the basis of an absence of LVM regression after aortic valve replacement in patients without LVH.
Due to a paucity of studies, determinants of absent LVH and especially i-lowLVM still remain unexplored. In agreement with earlier observations [1,2], the percentage of men in AS subjects without LVH was insignificantly higher than in those with LVH. A similar, albeit weaker, tendency was observed in AS patients with i-lowLVM. To the best of our knowledge, sex-dependent differences in the prevalence of i-lowLVM in severe AS have not been reported so far [3]. However, as a higher proportion of men had been described in AS with inappropriately high LVM versus appropriate LVM [3,20], it may be suggested that the adequacy of the LV hypertrophic response to chronic LV overload in AS appears to be modulated by gender.

Limitations

First, a retrospective design and a relatively low number of patients are major limitations of our report. However, exclusively subjects without coexistent diseases, including CAD, were entered into the final analysis, in order to reduce the heterogeneity of the study group. Second, the individual hemodynamic load was estimated on the basis of in-hospital BP recordings and echocardiography, while averaged values over a long period of time would be more appropriate. Nevertheless, we analyzed only patients with well-controlled hypertension and stable BP, which suggests that the computed parameters could be, to some degree, representative for a given subject. Third, medical therapy, which is known to affect LVM, was not uniform. However, the proportions of patients treated with renin–angiotensin system inhibitors, drugs with a well-recognized ability to attenuate LVH, were similar, according to LVH presence or LVM inadequacy.

5. Conclusions

Keeping in mind the limitations of our small retrospective study, inadequately low LVM relative to the individual hemodynamic load could potentially reflect a different mode of LV adaptation to AS, associated with enhanced load-independent LV systolic performance, i.e., better LV contractility. If confirmed in a large series of patients, our preliminary report might add to the possible mechanisms of a previously reported counterintuitive tendency of a lower, not higher, risk of adverse outcome in patients with low LV mass, despite severe AS. Prospective studies are warranted in order to determine a potential utility of LVM inadequacy for the prediction of clinical outcomes and risk stratification of patients with AS.

Author Contributions

Conceptualization, Methodology, and Formal Analysis, B.C., O.K., E.W.-S., T.H. and A.S.; Data Curation, A.S.; Investigation, D.D., K.B., A.D. and J.Ś.; Resources, Supervision, and Project Administration, O.K., T.H. and A.S.; Visualization: B.C., D.D. and A.S.; Writing—Original Draft Preparation, B.C. and A.S.; Writing—Review and Editing: B.C., O.K., A.D., J.Ś., E.W.-S., D.D., K.B., T.H., and A.S. All authors approved the final version of the manuscript.

Funding

The APC was funded by the Jagiellonian University Medical College (Cracow, Poland), grant no. K/ZDS/006105.

Conflicts of Interest

The authors declare no conflict of interest.

References

  1. Seiler, C.; Jenni, R. Severe aortic stenosis without left ventricular hypertrophy: Prevalence, predictors, and short-term follow up after aortic valve replacement. Heart 1996, 76, 250–255. [Google Scholar] [CrossRef] [PubMed]
  2. Kupari, M.; Turto, H.; Lommi, J. Left ventricular hypertrophy in aortic valve stenosis: Preventive or promotive of systolic dysfunction and heart failure? Eur. Heart J. 2005, 26, 1790–1796. [Google Scholar] [CrossRef] [PubMed]
  3. Cioffi, G.; Faggiano, P.; Vizzardi, E.; Tarantini, L.; Cramariuc, D.; Gerdts, E.; de Simone, G. Prognostic effect of inappropriately high left ventricular mass in asymptomatic severe aortic stenosis. Heart 2011, 97, 301–307. [Google Scholar] [CrossRef] [PubMed]
  4. Barasch, E.; Kahn, J.; Petillo, F.; Pollack, S.; Rhee, P.D.; Reichek, N. Absence of left ventricular hypertrophy in severe isolated aortic stenosis and preserved left ventricular systolic function. J. Heart Valve Dis. 2014, 23, 1–8. [Google Scholar] [PubMed]
  5. Drazner, M.H. The progression of hypertensive heart disease. Circulation 2011, 123, 327–334. [Google Scholar] [CrossRef] [PubMed]
  6. Levy, D.; Garrison, R.J.; Savage, D.D.; Kannel, W.B.; Castelli, W.P. Prognostic implications of echocardiographically determined left ventricular mass in the Framingham Heart Study. N. Engl. J. Med. 1990, 322, 1561–1566. [Google Scholar] [CrossRef] [PubMed]
  7. Koren, M.J.; Devereux, R.B.; Casale, P.N.; Savage, D.D.; Laragh, J.H. Relation of left ventricular mass and geometry to morbidity and mortality in uncomplicated essential hypertension. Ann. Intern. Med. 1991, 114, 345–352. [Google Scholar] [CrossRef] [PubMed]
  8. Messerli, F.H.; Grodzicki, T. Hypertension, left ventricular hypertrophy, ventricular arrhythmias and sudden death. Eur. Heart J. 1992, 13, 66–69. [Google Scholar] [CrossRef] [PubMed]
  9. Gottdiener, J.S.; Arnold, A.M.; Aurigemma, G.P.; Polak, J.F.; Tracy, R.P.; Kitzman, D.W.; Gardin, J.M.; Rutledge, J.E.; Boineau, R.C. Predictors of congestive heart failure in the elderly: The Cardiovascular Health Study. J. Am. Coll. Cardiol. 2000, 35, 1628–1637. [Google Scholar] [CrossRef]
  10. De Simone, G.; Gottdiener, J.S.; Chinali, M.; Maurer, M.S. Left ventricular mass predicts heart failure not related to previous myocardial infarction: The Cardiovascular Health Study. Eur. Heart J. 2008, 29, 741–747. [Google Scholar] [CrossRef] [PubMed]
  11. Bang, C.N.; Gerdts, E.; Aurigemma, G.P.; Boman, K.; de Simone, G.; Dahlöf, B.; Køber, L.; Wachtell, K.; Devereux, R.B. Four-group classification of left ventricular hypertrophy based on ventricular concentricity and dilatation identifies a low-risk subset of eccentric hypertrophy in hypertensive patients. Circ. Cardiovasc. Imaging 2014, 7, 422–429. [Google Scholar] [CrossRef] [PubMed]
  12. Gerdts, E.; Rossebø, A.B.; Pedersen, T.R.; Cioffi, G.; Lønnebakken, M.T.; Cramariuc, D.; Rogge, B.P.; Devereux, R.B. Relation of left ventricular mass to prognosis in initially asymptomatic mild to moderate aortic valve stenosis. Circ. Cardiovasc. Imaging 2015, 8, e003644. [Google Scholar] [CrossRef] [PubMed]
  13. De Simone, G.; Palmieri, V.; Koren, M.J.; Mensah, G.A.; Roman, M.J.; Devereux, R.B. Prognostic implications of the compensatory nature of left ventricular mass in arterial hypertension. J. Hypertens. 2001, 19, 119–125. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  14. Baumgartner, H.; Falk, V.; Bax, J.J.; Bonis, M.; Hamm, C.; Holm, P.J.; Iung, B.; Lancellotti, P.; Lansac, E.; Munoz, D.R.; et al. 2017 ESC/EACTS Guidelines for the management of valvular heart disease. Kardiol. Pol. 2018, 76, 1–62. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  15. Kruszelnicka, O.; Chmiela, M.; Bobrowska, B.; Świerszcz, J.; Bhagavatula, S.; Bednarek, J.; Surdacki, A.; Nessler, J.; Hryniewiecki, T. Depressed systemic arterial compliance is associated with the severity of heart failure symptoms in moderate-to-severe aortic stenosis: A cross-sectional retrospective study. Int. J. Med. Sci. 2015, 12, 552–558. [Google Scholar] [CrossRef] [PubMed]
  16. De Simone, G.; Devereux, R.B.; Roman, M.J.; Ganau, A.; Saba, P.S.; Alderman, M.H.; Laragh, J.H. Assessment of left ventricular function by the midwall fractional shortening/end-systolic stress relation in human hypertension. J. Am. Coll. Cardiol. 1994, 23, 1444–1451. [Google Scholar] [CrossRef] [Green Version]
  17. Długosz, D.; Bolt, K.; Sam, W.S.; Nawara, T.; Kruszelnicka, O.; Chyrchel, B.; Surdacki, A. 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? Kardiol. Pol. 2018, 76, 1486–1488. [Google Scholar] [CrossRef] [PubMed]
  18. Aurigemma, G.P.; Silver, K.H.; Priest, M.A.; Gaasch, W.H. Geometric changes allow normal ejection fraction despite depressed myocardial shortening in hypertensive left ventricular hypertrophy. J. Am. Coll. Cardiol. 1995, 26, 195–202. [Google Scholar] [CrossRef]
  19. Mureddu, G.F.; Cioffi, G.; Stefenelli, C.; Boccanelli, A.; de Simone, G. Compensatory or inappropriate left ventricular mass in different models of left ventricular pressure overload: Comparison between patients with aortic stenosis and arterial hypertension. J. Hypertens. 2009, 27, 642–649. [Google Scholar] [CrossRef] [PubMed]
  20. Cioffi, G.; de Simone, G.; Cramariuc, D.; Mureddu, G.F.; Gerdts, E. Inappropriately high left-ventricular mass in asymptomatic mild-moderate aortic stenosis. J. Hypertens. 2012, 30, 421–428. [Google Scholar] [CrossRef] [PubMed]
  21. Briand, M.; Dumesnil, J.G.; Kadem, L.; Tongue, A.G.; Rieu, R.; Garcia, D.; Pibarot, P. Reduced systemic arterial compliance impacts significantly on left ventricular afterload and function in aortic stenosis: Implications for diagnosis and treatment. J. Am. Coll. Cardiol. 2005, 46, 291–298. [Google Scholar] [CrossRef] [PubMed]
  22. Lang, R.M.; Badano, L.P.; Mor-Avi, V.; Afilalo, J.; Armstrong, A.; Ernande, L.; Flachskampf, F.A.; Foster, E.; Goldstein, S.A.; Kuznetsova, T.; et al. Recommendations for cardiac chamber quantification by echocardiography in adults: An update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging. Eur. Heart J. Cardiovasc. Imaging 2015, 16, 233–270. [Google Scholar] [CrossRef] [PubMed]
  23. De Simone, G.; Devereux, R.B.; Kimball, T.R.; Mureddu, G.F.; Roman, M.J.; Contaldo, F.; Daniels, S.R. Interaction between body size and cardiac workload: Influence on left ventricular mass during body growth and adulthood. Hypertension 1998, 31, 1077–1082. [Google Scholar] [CrossRef] [PubMed]
  24. Palmieri, V.; de Simone, G.; Roman, M.J.; Schwartz, J.E.; Pickering, T.G.; Devereux, R.B. Ambulatory blood pressure and metabolic abnormalities in hypertensive subjects with inappropriately high left ventricular mass. Hypertension 1999, 34, 1032–1040. [Google Scholar] [CrossRef] [PubMed]
  25. Aurigemma, G.P.; Devereux, R.B.; de Simone, G.; Roman, M.J.; O’Grady, M.J.; Koren, M.; Alderman, M.; Laragh, J. Myocardial function and geometry in hypertensive subjects with low levels of afterload. Am. Heart J. 2002, 143, 546–551. [Google Scholar] [CrossRef] [PubMed]
  26. Palmieri, V.; Wachtell, K.; Gerdts, E.; Bella, J.N.; Papademetriou, V.; Tuxen, C.; Nieminen, M.S.; Dahlöf, B.; de Simone, G.; Devereux, R.B. Left ventricular function and hemodynamic features of inappropriate left ventricular hypertrophy in patients with systemic hypertension: The LIFE study. Am. Heart J. 2001, 141, 784–791. [Google Scholar] [CrossRef] [PubMed]
Table
Table 1. Demographic and clinical characteristics according to LVH absence or LVM inadequacy.
Table 1. Demographic and clinical characteristics according to LVH absence or LVM inadequacy.
CharacteristicLV Hypertrophy
(LVH)		 Inadequately Low LVM
(i-lowLVM)
No
n = 23		Yes
n = 77		pYes
n = 23		No
n = 77		p
Age, years69 ± 870 ± 10NS72 ± 669 ± 11NS
Men/women, n (%)14 (61%)34 (44%)NS13 (56%)35 (45%)NS
BSA, m21.9 ± 0.11.8 ± 0.2NS1.9 ± 0.11.8 ± 0.2NS
BMI, kg/m230.4 ± 4.429.0 ± 4.6NS29.3 ± 4.429.5 ± 4.6NS
Hypertension, n (%)20 (87%)64 (83%)NS21 (91%)63 (82%)NS
Diabetes, n (%)7 (30%)22 (29%)NS9 (39%)20 (26%)NS
GFR, mL/min/1.73 m270 ± 1677 ± 190.0967 ± 1578 ± 200.02
Symptoms, n (%)14 (61%)37 (48%)NS15 (65%)36 (47%)NS
Mean BP, mm Hg95 ± 1192 ± 9NS94 ± 1192 ± 9NS
Medications, n (%)
ACEI or ARB7 (30%)20 (26%)NS9 (39%)18 (23%)NS
Beta-blocker13 (57%)44 (57%)NS15 (65%)42 (55%)NS
Diuretics12 (52%)36 (47%)NS15 (65%)33 (43%)0.07
Data are shown as mean ± standard deviation or numbers (percentages). ACEI: angiotensin-converting enzyme inhibitor; ARB: angiotensin receptor blocker; BMI: body mass index; BP: blood pressure; BSA: body surface area; GFR: estimated glomerular filtration rate; n: number; NS: non-significant.
Table
Table 2. Echocardiographic characteristics and LV afterload according to the presence of LVH or LVM inadequacy.
Table 2. Echocardiographic characteristics and LV afterload according to the presence of LVH or LVM inadequacy.
CharacteristicLV Hypertrophy
(LVH)		 Inadequately Low LVM
(i-lowLVM)
No
n = 23		Yes
n = 77		pYes
n = 23		No
n = 77		p
AVAI, cm2/m20.5 ± 0.10.4 ± 0.1NS0.5 ± 0.10.4 ± 0.1NS
LVd, cm4.4 ± 0.45.0 ± 0.7<0.0014.6 ± 0.65.0 ± 0.80.03
PWd, cm1.1 ± 0.11.3 ± 0.2<0.0011.0 ± 0.11.3 ± 0.2<0.001
IVSd, cm1.1 ± 0.21.5 ± 0.3<0.0011.1 ± 0.21.5 ± 0.3<0.001
RWT0.50 ± 0.070.57 ± 0.160.070.47 ± 0.060.58 ± 0.150.001
EF, %63 ± 1158 ± 70.00464 ± 1057 ± 7<0.001
mwFS, %13.8 ± 3.613.7 ± 3.7NS15.8 ± 3.312.9 ± 3.2<0.001
cESS, hPa201 ± 81178 ± 92NS188 ± 72181 ± 97NS
Zva, mmHg / mL/m26.0 ± 1.55.4 ± 1.9NS5.5 ± 1.25.4 ± 2.0NS
eLVM, %8 [−2,24]56 [26,81]<0.0015 [−6,9]57 [29,81]<0.001
Data are shown as mean ± standard deviation or median ± interquartile range. Significant Bonferroni-corrected p-values are marked in bold. AVAI: aortic valve area index; cESS: circumferential end-systolic LV wall stress; EF: ejection fraction; eLVM: excess of LV mass; IVSd: interventricular septum thickness at end-diastole; LV: left ventricular; LVd: LV end-diastolic diameter; LVM: LV mass; mwFS: LV midwall fractional shortening; n: number; NS: non-significant; PWd: posterior wall thickness at end-diastole; RWT: relative LV wall thickness; Zva: valvulo-arterial impedance.

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MDPI and ACS Style

Chyrchel, B.; Długosz, D.; Bolt, K.; Kruszelnicka, O.; Dziewierz, A.; Świerszcz, J.; Wieczorek-Surdacka, E.; Hryniewiecki, T.; Surdacki, A. Association of Inadequately Low Left Ventricular Mass with Enhanced Myocardial Contractility in Severe Degenerative Aortic Stenosis. J. Clin. Med. 2018, 7, 464. https://doi.org/10.3390/jcm7120464

AMA Style

Chyrchel B, Długosz D, Bolt K, Kruszelnicka O, Dziewierz A, Świerszcz J, Wieczorek-Surdacka E, Hryniewiecki T, Surdacki A. Association of Inadequately Low Left Ventricular Mass with Enhanced Myocardial Contractility in Severe Degenerative Aortic Stenosis. Journal of Clinical Medicine. 2018; 7(12):464. https://doi.org/10.3390/jcm7120464

Chicago/Turabian Style

Chyrchel, Bernadeta, Dorota Długosz, Klaudiusz Bolt, Olga Kruszelnicka, Artur Dziewierz, Jolanta Świerszcz, Ewa Wieczorek-Surdacka, Tomasz Hryniewiecki, and Andrzej Surdacki. 2018. "Association of Inadequately Low Left Ventricular Mass with Enhanced Myocardial Contractility in Severe Degenerative Aortic Stenosis" Journal of Clinical Medicine 7, no. 12: 464. https://doi.org/10.3390/jcm7120464

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