Section on Medical Neuroendocrinology, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD, USA.
University of Santo Tomas Hospital, España Boulevard, Manila, Philippines.
Horm Metab Res. 2019 Jul;51(7):458-469. doi: 10.1055/a-0669-9556. Epub 2018 Sep 18.
Pheochromocytomas and paragangliomas (PHEOs) are rare neuroendocrine tumors. Clinical manifestations include different cardiovascular signs and symptoms, which are related to excessive secretion of catecholamines. Catecholamine-induced cardiomyopathy in PHEO (CICMPP) is a rare but dreaded complication of PHEO. Once patient is diagnosed with this condition, the prognosis is worse and a surgical risk is much higher than expected. This article focuses on how catecholamines affect the heart and the pathophysiologic mechanism of CICMPP. The cardiovascular responses to catecholamine depend mostly on which catecholamine is released as well as the amount of catecholamine that is released. The acute release of norepinephrine and epinephrine from PHEO increases heart rate, systemic vascular resistance, myocardial contractility, and reduces venous compliance. The excessive adrenergic stimulation by catecholamine results in severe vasoconstriction and coronary vasospasm, myocardial ischemia, and subsequently damage, and necrosis. Chronically elevated catecholamine levels lead to significant desensitization of cardiac β-adrenoceptors. The increased levels of the enzyme β-adrenoceptors kinase (βARK) in the heart seems to mediate these biochemical and physiological changes that are consistently correlated with attenuated responsiveness to catecholamine stimulation. Through these mechanisms different types of cardiomyopathy (CMP) can be formed. This review discusses extensively the 3 types of cardiomyopathies that can be present in a PHEO patient. It also provides the clinical presentation and diagnostic and therapeutic algorithm in managing patients with CICMPP.
嗜铬细胞瘤和副神经节瘤(PHEO)是罕见的神经内分泌肿瘤。临床表现包括不同的心血管体征和症状,这与儿茶酚胺的过度分泌有关。嗜铬细胞瘤引起的心肌病变(CICMPP)是 PHEO 的一种罕见但可怕的并发症。一旦患者被诊断出患有这种疾病,预后就会更差,手术风险也比预期的高得多。本文重点介绍儿茶酚胺如何影响心脏以及 CICMPP 的病理生理机制。儿茶酚胺对心脏的心血管反应主要取决于释放的是哪种儿茶酚胺以及释放的儿茶酚胺的量。PHEO 中去甲肾上腺素和肾上腺素的急性释放会增加心率、全身血管阻力、心肌收缩力,并降低静脉顺应性。儿茶酚胺的过度肾上腺素能刺激会导致严重的血管收缩和冠状动脉痉挛、心肌缺血,随后导致损伤和坏死。慢性升高的儿茶酚胺水平导致心脏β-肾上腺素能受体显著脱敏。心脏中β-肾上腺素能受体激酶(βARK)的水平增加似乎介导了这些生化和生理变化,这些变化与对儿茶酚胺刺激的反应性减弱一致。通过这些机制,可以形成不同类型的心肌病(CMP)。本文详细讨论了可能出现在 PHEO 患者中的 3 种心肌病。它还提供了在管理 CICMPP 患者时的临床表现以及诊断和治疗算法。