Ramirez Ariana Y, Doman Elizabeth R, Sanchez Kevin, Chilton Robert J
Department of Cardiology, Brooke Army Medical Center.
Department of Cardiology, University of Texas Health Sciences Center, San Antonio, Texas, USA.
Cardiovasc Endocrinol Metab. 2025 Apr 16;14(2):e00332. doi: 10.1097/XCE.0000000000000332. eCollection 2025 Jun.
Insulin resistance (IR) and microvascular ischemia together result in cardiovascular dysfunction by impairing the heart's energy balance. IR in cardiomyocytes disrupts glucose metabolism, leading to energy deficits that can drive cardiac hypertrophy and heart failure. Microvascular ischemia exacerbates these effects by limiting oxygen and nutrient delivery, intensifying oxidative stress, mitochondrial dysfunction, and cell death. IR also reduces the effectiveness of vasodilators like nitroglycerin and sodium nitroprusside, exacerbating endothelial dysfunction and oxidative stress, thus impairing oxygen delivery during ischemia. This combination of IR and microvascular ischemia heightens the risk of left ventricular dysfunction and heart failure. Understanding these interactions is critical for developing targeted therapies to improve outcomes in patients with IR and ischemic heart disease. This study examines the relationship between IR, microvascular ischemia, and myocardial metabolism, with a focus on clinical management and therapeutic strategies.
胰岛素抵抗（IR）和微血管缺血共同作用，通过损害心脏的能量平衡导致心血管功能障碍。心肌细胞中的IR会破坏葡萄糖代谢，导致能量不足，进而引发心肌肥大和心力衰竭。微血管缺血通过限制氧气和营养物质的输送、加剧氧化应激、线粒体功能障碍和细胞死亡，进一步加重这些影响。IR还会降低硝酸甘油和硝普钠等血管扩张剂的疗效，加剧内皮功能障碍和氧化应激，从而在缺血期间损害氧气输送。IR和微血管缺血的这种组合增加了左心室功能障碍和心力衰竭的风险。了解这些相互作用对于开发针对性疗法以改善IR和缺血性心脏病患者的预后至关重要。本研究探讨了IR、微血管缺血与心肌代谢之间的关系，重点关注临床管理和治疗策略。
