Chyrchel Bernadeta, Długosz Dorota, Bolt Klaudiusz, Kruszelnicka Olga, Dziewierz Artur, Świerszcz Jolanta, Wieczorek-Surdacka Ewa, Hryniewiecki Tomasz, Surdacki Andrzej
Second Department of Cardiology, Jagiellonian University Medical College, 17 Kopernika Street, 31-501 Cracow, Poland.
Students' Scientific Group at the Second Department of Cardiology, Jagiellonian University Medical College, 17 Kopernika Street, 31-501 Cracow, Poland.
J Clin Med. 2018 Nov 22;7(12):464. doi: 10.3390/jcm7120464.
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.
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.
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%, < 0.001 for those with and without i-lowLVM, respectively; 13.7 ± 3.7 vs. 13.8 ± 3.6% for LVH presence and absence, = 0.9).
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.
左心室肥厚（LVH）传统上被认为是一种旨在维持左心室收缩功能的适应性机制，但在10% - 35%的严重主动脉瓣狭窄（AS）患者中并不存在。我们的目的是评估严重AS且无LVH或相对于个体血流动力学负荷左心室质量过低（i-lowLVM）患者的临床和血流动力学特征。
我们回顾性分析了100例单纯严重退行性AS、左心室收缩功能保留且无相关并存疾病（除血压或血糖控制良好的高血压或糖尿病外）患者的住院记录。
有LVH和无LVH的患者以及有i-lowLVM和无i-lowLVM的患者临床特征相似，只是i-lowLVM患者的肾小球滤过率略低。与有LVH的患者相比，无LVH或有i-lowLVM的患者左心室腔较小，左心室壁厚度降低，射血分数较高。根据是否存在LVH或i-lowLVM，狭窄严重程度和后负荷指标（瓣膜 - 动脉阻抗和圆周收缩末期左心室壁应力）无显著差异。然而，与其余患者相比，仅i-lowLVM患者的左心室中层水平缩短分数升高，无LVH患者则未升高（有和无i-lowLVM患者分别为15.8±3.3%对12.9±3.2%，<0.001；有和无LVH患者分别为13.7±3.7%对13.8±3.6%，=0.9）。
相对于个体血流动力学负荷，左心室质量过低可能潜在反映了左心室对严重AS的不同反应模式，与增强的不依赖负荷的左心室收缩性能相关，即更好的左心室收缩性。如果在大量患者中得到证实，我们的小型初步研究可能有助于解释先前报道的尽管严重AS但左心室质量低的患者不良结局风险较低而非较高这一违反直觉趋势的可能机制。有必要进行前瞻性研究，以确定左心室质量不足在AS患者风险分层中的潜在效用。
