Sani Cyrus M, Pogue Elahn P L, Hrabia Joanna B, Zayachkowski Alexander G, Zawadka Magdaline M, Poniatowski Adrian G, Długosz Dorota, Leśniak Wiktoria, Kruszelnicka Olga, Chyrchel Bernadeta, Surdacki Andrzej
Students' Scientific Group at the Second Department of Cardiology, Jagiellonian University Medical College Kraków, Poland.
Second Chair of Internal Medicine, Jagiellonian University Medical College, Kraków, Poland.
Folia Med Cracov. 2018;58(2):45-55. doi: 10.24425/fmc.2018.124657.
A novel paradigm of diastolic heart failure with preserved ejection fraction (HFpEF) proposed the induction of coronary microvascular dysfunction by HFpEF comorbidities via a systemic pro-inflammatory state and associated oxidative stress. The consequent nitric oxide deficiency would increase diastolic tension and favor fibrosis of adjacent myocardium, which implies not only left ventricular (LV), but all-chamber myocardial stiffening. Our aim was to assess relations between low-grade chronic systemic inflammation and left atrial (LA) pressure-volume relations in real-world HFpEF patients.
We retrospectively analyzed medical records of 60 clinically stable HpEFF patients in sinus rhythm with assayed high-sensitive C-reactive protein (CRP) during the index hospitalization. Subjects with CRP >10 mg/L or coexistent diseases, including coronary artery disease, were excluded. LV and LA diameters and mitral E/E' ratio (an index of LA pressure) were extracted from routine echocardiographic records. A surrogate measure of LA stiffness was computed as the averaged mitral E/e' ratio divided by LA diameter.
With ascending CRP tertiles, we observed trends for elevated mitral E/e' ratio (p <0.001), increased relative LV wall thickness (p = 0.01) and higher NYHA functional class (p = 0.02). The LA stiffness estimate and log-transformed CRP levels (log-CRP) were interrelated (r = 0.38, p = 0.003). On multi- variate analysis, the LA stiffness index was independently associated with log-CRP (β ± SEM: 0.21 ± 0.07, p = 0.007) and age (β ± SEM: 0.16 ± 0.07, p = 0.03), which was maintained upon adjustment for LV mass index and relative LV wall thickness.
Low-grade chronic inflammation may contribute to LA stiffening additively to age and regardless of the magnitude of associated LV hypertrophy and concentricity. LA stiffening can exacerbate symptoms of congestion in HFpEF jointly with LV remodeling.
一种射血分数保留的舒张性心力衰竭（HFpEF）的新范式提出，HFpEF合并症通过全身促炎状态和相关的氧化应激诱导冠状动脉微血管功能障碍。随之而来的一氧化氮缺乏会增加舒张期张力，并有利于相邻心肌的纤维化，这不仅意味着左心室（LV），而且全腔心肌僵硬。我们的目的是评估真实世界中HFpEF患者低度慢性全身炎症与左心房（LA）压力-容积关系之间的关系。
我们回顾性分析了60例在窦性心律下临床稳定的HFpEF患者在指数住院期间的病历，这些患者检测了高敏C反应蛋白（CRP）。排除CRP>10 mg/L的受试者或并存疾病，包括冠状动脉疾病。从常规超声心动图记录中提取左心室和左心房直径以及二尖瓣E/E'比值（左心房压力指标）。左心房僵硬度的替代指标计算为平均二尖瓣E/e'比值除以左心房直径。
随着CRP三分位数的升高，我们观察到二尖瓣E/e'比值升高（p<0.001）、相对左心室壁厚度增加（p = 0.01）和纽约心脏协会功能分级升高（p = 0.02）的趋势。左心房僵硬度估计值与对数转换后的CRP水平（log-CRP）相关（r = 0.38，p = 0.003）。在多变量分析中，左心房僵硬度指数与log-CRP（β±SEM：0.21±0.07，p = 0.007）和年龄（β±SEM：0.16±0.07，p = 0.03）独立相关，在调整左心室质量指数和相对左心室壁厚度后仍保持这种关系。
低度慢性炎症可能与年龄相加，且与相关左心室肥厚和同心度的程度无关，共同导致左心房僵硬。左心房僵硬可与左心室重塑一起加剧HFpEF的充血症状。
