Rationale: Heart failure (HF) following heart damage leads to a decreased blood flow due to a reduced pump efficiency of the heart muscle. A consequence can be insufficient oxygen supply to the organism including the brain. While HF clearly shows neurological symptoms, such as fatigue, nausea and dizziness, the implications for brain structure are not well understood. Few studies show regional gray matter decrease related to HF, however, the underlying mechanisms leading to the observed brain changes remain unclear.Objective: To study the relationship between impaired heart function, hampered blood circulation and structural brain change in a case-control study. Methods and Results: Within a group of 80 patients of the Leipzig Heart Center, we investigated a potential correlation between HF biomarkers and the brain's gray matter density (GMD) obtained by magnetic resonance imaging. We observed a significant positive correlation between cardiac ejection fraction and GMD across the whole frontal and parietal medial cortex reflecting the consequence of HF onto the brain's gray matter. Moreover, we also obtained a relationship between GMD and the N-terminal prohormone of brain natriuretic peptide (NT-proBNP) - a biomarker that is used for screening, diagnosis and prognosis of HF. Here we found a significant negative correlation between NT-proBNP and GMD in the medial and posterior cingulate cortex but also in precuneus and hippocampus, which are key regions implicated in structural brain changes in dementia. Conclusions: We obtained significant correlations between brain structure and markers of heart failure including EF and NT-proBNP. A diminished GMD was found with decreased EF and increased NT-proBNP in wide brain regions including the whole frontomedian cortex as well as hippocampus and precuneus. Our observations might reflect structural brain damage in areas that are related to cognition, however, whether these structural changes facilitate the development of cognitive alterations has to be proven by further longitudinal studies.

中文翻译：

---

心力衰竭导致的脑损伤：心脏生物标志物改变和灰色物质下降。

理由：心脏受损后的心力衰竭（HF）由于心肌泵效率降低而导致血流量减少。结果可能是无法为包括大脑在内的生物体提供足够的氧气。尽管HF清楚地显示出神经系统症状，例如疲劳，恶心和头昏眼花，但对脑结构的影响尚不清楚。很少有研究表明区域性灰质减少与心力衰竭有关，但导致观察到的脑部改变的潜在机制仍不清楚。目的：在病例对照研究中，研究心功能受损，血液循环受阻与脑部结构改变之间的关系。方法和结果：在莱比锡心脏中心的80名患者中，我们调查了HF生物标志物与大脑的潜在关系。通过磁共振成像获得的灰质密度（GMD）。我们观察到整个额叶和顶叶内侧皮质的心脏射血分数与GMD之间存在显着的正相关，这反映了HF对大脑灰质的影响。此外，我们还获得了GMD与脑利钠肽（NT-proBNP）N端激素（一种用于HF的筛查，诊断和预后的生物标志物）之间的关系。在这里，我们发现内侧扣带回和后扣带回皮质中的NT-proBNP与GMD之间存在显着的负相关性，而在早突神经和海马体中，NT-proBNP与GMD之间存在显着的负相关，这是与痴呆症的结构性脑部变化有关的关键区域。结论：我们获得了大脑结构与心力衰竭指标（包括EF和NT-proBNP）之间的显着相关性。发现GMD降低，EF降低，NT-proBNP升高，出现在整个大脑区域，包括整个额额皮质，海马和前突。我们的观察结果可能反映了与认知相关的区域中的结构性脑损伤，但是，这些结构性变化是否有助于认知改变的发展必须通过进一步的纵向研究来证明。