Division of Cardiology, Department of Medicine, College of Medicine, University of Illinois at Chicago, 840 S. Wood St., 920S (MC 715), Chicago, IL, 60612, USA.
Jesse Brown VA Medical Center, Chicago, IL, USA.
Heart Fail Rev. 2024 Jan;29(1):79-93. doi: 10.1007/s10741-023-10352-z. Epub 2023 Oct 14.
Diastolic heart failure (DHF), in which impaired ventricular filling leads to typical heart failure symptoms, represents over 50% of all heart failure cases and is linked with risk factors, including metabolic syndrome, hypertension, diabetes, and aging. A substantial proportion of patients with this disorder maintain normal left ventricular systolic function, as assessed by ejection fraction. Despite the high prevalence of DHF, no effective therapeutic agents are available to treat this condition, partially because the molecular mechanisms of diastolic dysfunction remain poorly understood. As such, by focusing on the underlying molecular and cellular processes contributing to DHF can yield new insights that can represent an exciting new avenue and propose a novel therapeutic approach for DHF treatment. This review discusses new developments from basic and clinical/translational research to highlight current knowledge gaps, help define molecular determinants of diastolic dysfunction, and clarify new targets for treatment.
舒张性心力衰竭(DHF),其心室充盈受损导致典型心力衰竭症状,占所有心力衰竭病例的 50%以上,与代谢综合征、高血压、糖尿病和衰老等危险因素有关。该疾病的相当一部分患者通过射血分数评估,保持正常的左心室收缩功能。尽管 DHF 患病率很高,但目前尚无有效的治疗药物,部分原因是舒张功能障碍的分子机制仍知之甚少。因此,通过关注导致 DHF 的潜在分子和细胞过程,可以提供新的见解,为 DHF 的治疗开辟一条令人兴奋的新途径,并提出一种新的治疗方法。本文综述了基础和临床/转化研究的新进展,以突出目前的知识空白,帮助确定舒张功能障碍的分子决定因素,并阐明治疗的新靶点。