Bonacchi Giacomo, Rossi Valentina Alice, Garofalo Manuel, Mollace Rocco, Uccello Giuseppe, Pieragnoli Paolo, Checchi Luca, Perrotta Laura, Voltolini Luca, Ricciardi Giuseppe, Beltrami Matteo
Cardiomyopathy Unit, Careggi University Hospital, 50134 Florence, Italy.
Department of Cardiology, University Hospital of Zurich, 8091 Zurich, Switzerland.
Biomedicines. 2024 Apr 30;12(5):981. doi: 10.3390/biomedicines12050981.
Heart failure with preserved ejection fraction (HFpEF) results from a complex interplay of age, genetic, cardiac remodeling, and concomitant comorbidities including hypertension, obesity, diabetes, and chronic kidney disease (CKD). Renal failure is an important comorbidity of HFpEF, as well as a major pathophysiological mechanism for those patients at risk of developing HFpEF. Heart failure (HF) and CKD are intertwined conditions sharing common disease pathways; the so-called "kidney tamponade", explained by an increase in intracapsular pressure caused by fluid retention, is only the latest model to explain renal injury in HF. Recognizing the different phenotypes of HFpEF remains a real challenge; the pathophysiological mechanisms of renal dysfunction may differ across the HF spectrum, as well as the prognostic role. A better understanding of the role of cardiorenal interactions in patients with HF in terms of symptom status, disease progression, and prognosis remains essential in HF management. Historically, patients with HF and CKD have been scarcely represented in clinical trial populations. Current concerns affect the practical approach to HF treatment, and, in this context, physicians are frequently hesitant to prescribe and titrate both new and old treatments. Therefore, the extensive application of HF drugs in diverse HF subtypes with numerous comorbidities and different renal dysfunction etiologies remains a controversial matter of discussion. Numerous recently introduced drugs, such as sodium-glucose-linked transporter 2 inhibitors (SGLT2i), constitute a new therapeutic option for patients with HF and CKD. Because of their protective vascular and hormonal actions, the use of these agents may be safely extended to patients with renal dysfunction in the long term. The present review delves into the phenotype of patients with HFpEF and CKD from a pathophysiological perspective, proposing a treatment approach that suggests a practical stepwise algorithm for the proper application of life-saving therapies in clinical practice.
射血分数保留的心力衰竭（HFpEF）是由年龄、遗传、心脏重塑以及包括高血压、肥胖、糖尿病和慢性肾脏病（CKD）在内的合并症之间复杂的相互作用所致。肾衰竭是HFpEF的一种重要合并症，也是那些有发生HFpEF风险患者的主要病理生理机制。心力衰竭（HF）和CKD是相互交织的病症，共享共同的疾病途径；所谓的“肾填塞”，是由液体潴留导致的囊内压升高所解释的，这只是解释HF中肾损伤的最新模型。认识HFpEF的不同表型仍然是一项真正的挑战；肾功能不全的病理生理机制在HF谱系中可能不同，其预后作用也不同。更好地理解心肾相互作用在HF患者的症状状态、疾病进展和预后方面的作用，在HF管理中仍然至关重要。从历史上看，HF和CKD患者在临床试验人群中很少有代表性。当前的担忧影响了HF治疗的实际方法，在这种情况下，医生在开具和调整新旧治疗药物时常常犹豫不决。因此，HF药物在具有多种合并症和不同肾功能不全病因的不同HF亚型中的广泛应用仍然是一个有争议的讨论问题。许多最近推出的药物，如钠-葡萄糖协同转运蛋白2抑制剂（SGLT2i），为HF和CKD患者构成了一种新的治疗选择。由于它们具有保护性的血管和激素作用，这些药物的使用从长期来看可以安全地扩展到肾功能不全患者。本综述从病理生理学角度深入探讨了HFpEF和CKD患者的表型，提出了一种治疗方法，该方法建议了一种实用的逐步算法，以便在临床实践中正确应用挽救生命的疗法。
