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Patient reported outcome measures in cardiovascular research and care: PRO(M)s and CONS.
IF 2.6 4区 医学 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2025-01-23 DOI: 10.1097/FJC.0000000000001669
Giuseppe Biondi-Zoccai, Giacomo Frati, Mariangela Peruzzi, Marco Bernardi, Luigi Spadafora, Elena Tremoli

Patient-reported outcome measures (PROMs) are vital tools in cardiovascular disease (CVD) research and care, providing insights that complement traditional clinical outcomes like mortality and morbidity. PROMs capture patient experiences with CVD, such as quality of life, functional capacity, and emotional well-being, allowing clinicians to assess how interventions impact daily life. PROMs are integral to cardiovascular investigations as well as management, especially in chronic conditions and rehabilitation, where they inform on the impact of personalized care plans by tracking symptom progression and patient adherence. Selecting and applying to cardiovascular research and practice effective PROMs involves evaluating their validity, reliability, and sensitivity to change, with instruments like the Kansas City Cardiomyopathy Questionnaire (KCCQ) and the Seattle Angina Questionnaire (SAQ) widely used for heart failure and coronary artery disease, respectively. Implementing PROMs in real-world practice requires addressing challenges related to workflow integration and patient adherence, emphasizing their value in patient-centered care. As digital health advances, remote PROM data collection through mobile applications and wearable devices will enhance access to and extent of PROMs, and AI-driven analytical tools will provide real-time, automated and plausible more poignant insights for personalized treatment. Future efforts should focus on culturally adapting PROMs for diverse populations to ensure global applicability. PROMs should also be established as essential components of innovative research and responsive, patient-centered cardiovascular care.

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引用次数: 0
Changes for 2025 at Journal of Cardiovascular Pharmacology: Introducing Our Junior Associate Editors, Podcasts, Feature, and New Board Members. 心血管药理学杂志2025年的变化:介绍我们的初级副编辑,播客,特写和新的董事会成员。
IF 2.6 4区 医学 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2025-01-21 DOI: 10.1097/FJC.0000000000001673
Antonio Abbate, Giuseppe Biondi-Zoccai, Raffaele Altara, George W Booz
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引用次数: 0
Activation of APJ Receptors by CMF-019, But Not Apelin, Causes Endothelium-Dependent Relaxation of Spontaneously Hypertensive Rat Coronary Arteries. CMF-019而非Apelin激活APJ受体,可引起自发性高血压大鼠冠状动脉内皮依赖性舒张
IF 2.6 4区 医学 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2025-01-21 DOI: 10.1097/FJC.0000000000001671
Santo Anto, Chengwen Sun, Stephen T O'Rourke

Receptors for the vasoactive adipokine apelin, termed APJ receptors, are G-protein-coupled receptors and are widely expressed throughout the cardiovascular system. APJ receptors can also signal via G-protein-independent pathways, including G-protein-coupled-receptor kinase 2 (GRK2), which inhibits nitric oxide synthase (eNOS) activity and nitric oxide (NO) production in endothelial cells. Apelin causes endothelium-dependent, NO-mediated relaxation of coronary arteries from normotensive animals, but the effects of activating APJ receptor signaling pathways in hypertensive coronary arteries are largely unknown. We hypothesized that apelin-induced relaxation is impaired in coronary arteries from spontaneously hypertensive rats (SHR). Western blot and mRNA analysis revealed increased GRK2 expression in cultured SHR coronary endothelial cells. Apelin failed to cause relaxation in isolated SHR coronary arteries but, in the presence of apelin, relaxations to acetylcholine (ACh) were impaired. Apelin had no effect on relaxation to DEA NONOate. The GRK2 inhibitor, CMPD101, increased apelin-induced phosphorylation of Akt and eNOS in SHR endothelial cells and restored relaxation to apelin in SHR arteries. CMPD101 also blocked the inhibitory effect of apelin on ACh-induced relaxation. Relaxations to the APJ receptor-biased agonist, CMF-019, which preferentially activates the G-protein-dependent pathway with minimal effect on GRK2, were similar in SHR and WKY coronary arteries. Immunoblot analysis in SHR coronary endothelial cells demonstrated that CMF-019 increased Akt and eNOS phosphorylation whereas apelin had no effect. Thus, APJ receptor signaling via GRK2 impairs NO production or release from SHR endothelial cells. APJ receptor-biased agonists, such as CMF-019, may be more effective than apelin in causing vasodilation of SHR coronary arteries.

血管活性脂肪因子APJ受体是一种g蛋白偶联受体,在整个心血管系统中广泛表达。APJ受体也可以通过g蛋白非依赖性途径发出信号,包括g蛋白偶联受体激酶2 (GRK2),其抑制内皮细胞中一氧化氮合酶(eNOS)活性和一氧化氮(NO)的产生。Apelin引起正常血压动物的内皮依赖性、no介导的冠状动脉松弛,但在高血压冠状动脉中激活APJ受体信号通路的作用在很大程度上是未知的。我们假设自发性高血压大鼠(SHR)冠状动脉中apelin诱导的舒张功能受损。Western blot和mRNA分析显示GRK2在培养的SHR冠状动脉内皮细胞中表达升高。Apelin不能引起离体SHR冠状动脉的松弛,但在Apelin存在时,乙酰胆碱(ACh)的松弛受到损害。Apelin对DEA NONOate的松弛无影响。GRK2抑制剂CMPD101增加了SHR内皮细胞中apelin诱导的Akt和eNOS的磷酸化,恢复了SHR动脉中apelin的松弛。CMPD101也阻断了apelin对乙酰胆碱诱导的松弛的抑制作用。APJ受体偏向激动剂CMF-019优先激活g蛋白依赖通路,对GRK2的影响最小,对SHR和WKY冠状动脉的松弛相似。SHR冠状动脉内皮细胞的免疫印迹分析显示,CMF-019增加了Akt和eNOS的磷酸化,而apelin没有影响。因此,通过GRK2传递APJ受体信号会损害SHR内皮细胞NO的产生或释放。APJ受体偏向性激动剂,如CMF-019,在引起SHR冠状动脉血管舒张方面可能比apf -019更有效。
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引用次数: 0
Transient Receptor Potential Canonical Channels in Cardiovascular Pathology and Their Modulators. 心血管病理中的典型瞬时受体电位(TRPC)通道及其调节剂。
IF 2.6 4区 医学 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2025-01-01 DOI: 10.1097/FJC.0000000000001643
Hussein N Rubaiy

Abstract: Ion channels play a crucial role in various aspects of cardiac function, such as regulating rhythm and contractility. As a result, they serve as key targets for therapeutic interventions in cardiovascular diseases. Cell function is substantially influenced by the concentration of free cytosolic calcium (Ca 2+ ) and the voltage across the plasma membrane. These characteristics are known to be regulated by Ca 2+ -permeable nonselective cationic channels, although our knowledge of these channels is still inadequate. The transient receptor potential (TRP) superfamily comprises of many nonselective cation channels with diverse Ca 2+ permeability. Canonical or classical TRP (TRPC) channels are a subgroup of the TRP superfamily that are expressed ubiquitously in mammalian cells. TRPC channels are multidimensional signaling protein complexes that play essential roles in a variety of physiological and pathological processes in humans, including cancer, neurological disorders, cardiovascular diseases, and others. The objective of this article was to focus on the role that TRPC channels play in the cardiovascular system. The role of TRPC channels will be deeply discussed in cardiovascular pathology. Together, a critical element in developing novel treatments that target TRPC channels is comprehending the molecular mechanisms and regulatory pathways of TRPC channels in related cardiovascular diseases and conditions.

离子通道在调节心律和收缩力等心脏功能的各个方面发挥着至关重要的作用。因此,它们是心血管疾病治疗干预的关键靶点。细胞功能在很大程度上受细胞膜游离钙(Ca2+)浓度和质膜电压的影响。众所周知,这些特性受 Ca2+ 渗透性非选择性阳离子通道的调节,尽管我们对这些通道的了解还很不够。瞬态受体电位(TRP)超家族由许多具有不同 Ca2+ 通透性的非选择性阳离子通道组成。典型或经典 TRP(TRPC)通道是 TRP 超家族的一个亚族,在哺乳动物细胞中普遍表达。TRPC 通道是一种多维信号蛋白复合物,在人类的各种生理和病理过程中发挥着重要作用,包括癌症、神经系统疾病、心血管疾病等。本文旨在重点介绍 TRPC 通道在心血管系统中发挥的作用。本文将深入讨论 TRPC 通道在心血管病学中的作用。此外,开发针对 TRPC 通道的新型疗法的一个关键因素是了解 TRPC 通道在相关心血管疾病和病症中的分子机制和调控途径。
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引用次数: 0
Investigating the Transfer of Lisinopril Into Human Milk: A Quantitative Analysis. 利辛普利向母乳转移的研究:定量分析
IF 2.6 4区 医学 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2025-01-01 DOI: 10.1097/FJC.0000000000001642
Julie Chugh, Jean Dai, Palika Datta, Kaytlin Krutsch

Abstract: Lisinopril is commonly prescribed to manage conditions such as hypertension and heart failure. Although concerns about fetal toxicity have traditionally limited the use of lisinopril in women of reproductive age, recent American College of Obstetricians and Gynecologists guidelines promote aggressive treatment of hypertension, which may require the use of pharmacologic agents not previously considered in the postpartum period. We aimed to estimate infant exposure to maternal lisinopril through breast milk and report the tolerance of the breastfed infant. Five volunteers taking lisinopril provided samples of their human milk and their associated health information for research through the InfantRisk Center Human Milk Biorepository. The milk pharmacokinetics of lisinopril were measured using liquid chromatography-mass spectrometry. The mean milk concentration of lisinopril was 0.49 ng/mL per 10 mg daily dose. The relative infant dose was 0.06% for lisinopril, more than 100 times lower than the standard 10% safety threshold. The minimal transfer of lisinopril into human milk in this study suggests the drug is unlikely to pose a clinically significant risk to healthy breastfed infants.

利辛普利通常用于治疗高血压和心力衰竭等疾病。尽管对胎儿毒性的担忧传统上限制了利辛普利在育龄妇女中的使用,但最近的美国妇产科协会指南提倡积极治疗高血压,这可能需要在产后使用以前未考虑过的药物。我们的目的是估计婴儿通过母乳接触母体利辛普利的情况,并报告母乳喂养婴儿的耐受性。五名正在服用赖诺普利的志愿者通过婴儿风险中心母乳生物储存库提供了母乳样本及其相关健康信息供研究使用。使用液相色谱-质谱法测量了利辛普利在乳汁中的药代动力学。每10毫克每日剂量的利辛普利平均乳汁浓度为0.49纳克/毫升。赖诺普利的相对婴儿剂量(RID)为 0.06%,比 10%的标准安全阈值低 100 多倍。在这项研究中,赖诺普利向母乳中的转移极少,这表明该药物不太可能对健康的母乳喂养婴儿造成临床重大风险。
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引用次数: 0
Role of Autophagy in Myocardial Remodeling After Myocardial Infarction. 自噬在心肌梗塞后心肌重塑中的作用
IF 2.6 4区 医学 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2025-01-01 DOI: 10.1097/FJC.0000000000001646
Run-Ze Tian, Dong-Lin Zhuang, Chi Teng Vong, Xuyu He, Qing Ouyang, Jing-Hua Liang, Yan-Ping Guo, Yu-Hong Wang, Shuang Zhao, Haiyun Yuan, Moussa Ide Nasser, Ge Li, Ping Zhu

Abstract: Autophagy is the process of reusing the body's senescent and damaged cell components, which can be regarded as the cellular circulatory system. There are 3 distinct forms of autophagy: macroautophagy, microautophagy, and chaperone-mediated autophagy. In the heart, autophagy is regulated mainly through mitophagy because of the metabolic changes of cardiomyocytes caused by ischemia and hypoxia. Myocardial remodeling is characterized by gradual heart enlargement, cardiac dysfunction, and extraordinary molecular changes. Cardiac remodeling after myocardial infarction is almost inevitable, which is the leading cause of heart failure. Autophagy has a protective effect on myocardial remodeling improvement. Autophagy can minimize cardiac remodeling by preventing misfolded protein accumulation and oxidative stress. This review summarizes the nestest molecular mechanisms of autophagy and myocardial remodeling, the protective effects, and the new target of autophagy medicine in cardiac remodeling. The future development and challenges of autophagy in heart disease are also summarized.

自噬是人体衰老和受损细胞成分的再利用过程,可视为细胞循环系统。自噬有三种不同的形式:大自噬、小自噬和伴侣介导的自噬。在心脏中,由于缺血和缺氧导致心肌细胞的新陈代谢发生变化,自噬主要通过有丝分裂来调节。心肌重塑的特点是心脏逐渐增大、心功能不全和异常的分子变化。心肌梗死后的心脏重塑几乎不可避免,这也是心力衰竭的主要原因。自噬对改善心肌重塑具有保护作用。自噬可以防止错误折叠蛋白的积累和氧化应激,从而最大限度地减少心脏重塑。本综述总结了自噬与心肌重塑的最巢分子机制、保护作用以及自噬医学在心脏重塑中的新靶点。此外,还总结了自噬在心脏病中的未来发展和挑战。
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引用次数: 0
Balancing the Interactions: Assessing Antiplatelet and Antiretroviral Therapy Drug-Drug Interactions in People Living With HIV. 平衡相互作用:评估 HIV 感染者体内抗血小板和抗逆转录病毒疗法药物之间的相互作用。
IF 2.6 4区 医学 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2025-01-01 DOI: 10.1097/FJC.0000000000001638
Athena Matsikas, Kassandra Marsh, Quy Huynh, Raymond Pashun, John Papadopoulos, Tania Ahuja

Abstract: The clinical effect of drug-drug interactions (DDIs) between antiplatelets and antiretroviral therapy (ART) on bleeding, thrombosis, and other major adverse cardiovascular events (MACE) is unknown. The objective of this retrospective study was to assess the incidence of DDI at P2Y12 inhibitor (P2Y12inh) initiation and the effect of DDI on patient outcomes. Adult people living with HIV (PLWH) receiving ART newly initiated on an oral P2Y12inh were included. The primary outcome was the incidence of DDI between ART and P2Y12inh at P2Y12inh initiation. Secondary outcomes included bleeding events, MACE, and switches in P2Y12inh. There were 149 PLWH included, of these, 119 (80%) were initiated on clopidogrel, 23 (15%) on ticagrelor, and 7 (5%) on prasugrel. Ninety-three PLWH (60%) had a DDI at time of P2Y12inh initiation, with highest incidence in the clopidogrel group (n = 84, 71%), followed by ticagrelor (n = 9, 39%) and none with prasugrel. Within 1 year, MACE occurred in 12 PLWH, with DDI present at the time of 4 events. There were 29 bleeding events occurring within 1 year, including 17 events with DDI at time of event. However, 88% of DDI in patients with bleeding events were expected to decrease the efficacy of P2Y12inh. Though we observed high incidence of DDI between P2Y12inh and ART in PLWH, MACE and bleeding events at 1 year did not correlate with DDI. It remains unknown whether DDI presence at P2Y12inh initiation with ART causes clinical outcomes of concern, or whether underlying platelet reactivity in PLWH is associated with these events.

抗血小板药物和抗逆转录病毒药物(ART)之间的药物相互作用(DDI)对出血、血栓形成和其他主要不良心血管事件(MACE)的临床影响尚不清楚。这项回顾性研究旨在评估 P2Y12 抑制剂(P2Y12inh)起始时 DDI 的发生率以及 DDI 对患者预后的影响。研究纳入了新开始接受口服 P2Y12inh 抗逆转录病毒疗法的成年人类免疫缺陷病毒感染者(PLWH;HIV)。主要结果是开始使用 P2Y12inh 时 ART 与 P2Y12inh 之间的 DDI 发生率。次要结果包括出血事件、MACE 和 P2Y12inh 的转换。共纳入了 149 名 PLWH,其中 119 人(80%)开始使用氯吡格雷,23 人(15%)使用替卡格雷,7 人(5%)使用普拉格雷。93 名 PLWH(60%)在开始使用 P2Y12inh 时出现了 DDI,其中氯吡格雷组的发生率最高(84 人,71%),其次是替卡格雷组(9 人,39%),普拉格雷组没有发生 DDI。在一年内,12 名 PLWH 发生了 MACE,其中 4 起事件发生时存在 DDI。1年内共发生29起出血事件,其中17起事件发生时存在DDI。然而,在发生出血事件的患者中,88% 的 DDI 预计会降低 P2Y12inh 的疗效。虽然我们在 PLWH 中观察到 P2Y12inh 和抗逆转录病毒疗法之间的 DDI 发生率很高,但 1 年后的 MACE 和出血事件与 DDI 无关。P2Y12inh与抗逆转录病毒疗法起始时的DDI是否会导致令人担忧的临床结果,或者 PLWH 潜在的血小板反应性是否与这些事件有关,目前仍不得而知。
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引用次数: 0
Drug Interaction of SGLT2Is and ARNI on Acute Kidney Injury: A Real-World Pharmacovigilance Analysis Through the FAERS. SGLT2Is和ARNI在急性肾损伤中的药物相互作用:通过FAERS进行现实世界药物警戒分析。
IF 2.6 4区 医学 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2025-01-01 DOI: 10.1097/FJC.0000000000001639
Subei Zhao, Ronghua He, Mei Mei, Meng Yu, Zheng Yang, Chunyan Tian, Ping Zhang, Rong Li

Abstract: Sodium-glucose cotransporter 2 inhibitors (SGLT2Is) and angiotensin receptor-neprilysin inhibitor (ARNI) may cause potential renal damage, the combined impact of SGLT2Is and ARNI on acute kidney injury (AKI) remains unclear. This pharmacovigilance study conducted a disproportionality analysis using reports from the FDA Adverse Event Reporting System database. The reporting odds ratio was used as an estimate for detecting AKI signal. A total of 659,573 reports on at least 1 glucose-lowering drug and/or ARNI were obtained. Of the 413 reports on cotherapy of SGLT2Is and ARNI, 99 (24.0%) reports mentioned AKI. Overall, the AKI reporting rate significantly increased in cotherapy (adjusted reporting odds ratio, 95% confidence interval: 8.04, 6.20-10.42, P < 0.001), with a stronger AKI signal in cotherapy of canagliflozin and ARNI (16.82, 3.75-75.57, P < 0.001). Specifically, no increased AKI signal was detected in patients with heart failure (HF) receiving cotherapy after adjustment for sex and age (HF: 1.27, 0.89-1.80, P = 0.189; HF plus diabetes: 2.08, 0.99-4.40, P = 0.055; or HF plus hypertension: 1.69, 0.53-5.35, P = 0.376), whereas enhanced AKI signals were detected in patients with diabetes (20.57, 11.93-35.46, P < 0.001), hypertension (4.30, 1.98-9.37, P < 0.001), or diabetes plus hypertension (5.44, 1.92-15.43, P = 0.001). This study reveals that superimposed renal impairment results from cotherapy with SGLT2Is and ARNI. It is necessary to be vigilant that the elderly patients with diabetes, hypertension, or chronic kidney disease are more susceptible to AKI, especially if they likewise receive diuretics. When cotherapy is unavoidable, early monitoring of renal function, blood volume, and blood pressure is excessively crucial. However, it is relatively safe in patients with HF.

钠-葡萄糖共转运蛋白2抑制剂(SGLT2Is)和血管紧张素受体-奈普利素抑制剂(ARNI)可能引起潜在的肾损害,SGLT2Is和ARNI对急性肾损伤(AKI)的联合影响尚不清楚。这项药物警戒研究使用FAERS数据库的报告进行了歧化分析。报告优势比(ROR)作为AKI信号检测的估计。共获得659,573份关于至少一种降糖药物和/或ARNI的报告。在413篇关于sglt2i和ARNI联合治疗的报道中,99篇(24.0%)报道提到AKI。总体而言,联合治疗的AKI报告率显著增加(校正ROR, 95%CI:8.04, 6.20-10.42, P
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引用次数: 0
The Potential Impact of Renin-Angiotensin System Inhibitors on Cancer Survival and Recurrence: A Systemic Review and Meta-Analysis. 肾素-血管紧张素系统抑制剂对癌症生存和复发的潜在影响:系统回顾与荟萃分析。
IF 2.6 4区 医学 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2025-01-01 DOI: 10.1097/FJC.0000000000001600
Kaneez Fatima, Aayat Ellahi, Mariam Adil, Haider Kashif, Muhammad Uzair, Naela Ashraf, Mehak Barolia, Mujtaba Hyder, Areeba Nakhuda, Michelle Ayub, Sofia Jamil Butt, Ahmed Mustafa Rashid

Abstract: Renin-angiotensin system inhibitors (RASis), specifically angiotensin-converting enzyme inhibitors (ACEis) and angiotensin II receptor blockers (ARBs), are widely used antihypertensives. Their impact on the prognostic outcomes among patients with cancer has been subject to scrutiny and debate. The aim of this study was to evaluate the effect of RASis on survival in patients with cancer.We systematically searched PubMed, Web of Science, Embase, and Cochrane Library for relevant studies published until April 1, 2022. All the studies, interventional or observational, which examined effects of ARBs and ACEis on cancer prognosis compared with a control group and reported the survival outcomes and hazard ratios were included in the analysis. From each study, pooled hazard ratios (HRs) with corresponding 95% confidence intervals (95% CIs) were identified and collected. Subgroup analysis was conducted to investigate heterogeneity.61 studies were included in this meta-analysis. Data of 343,283 participants were used in the study. It was found that RASis improved overall survival (HR = 0.88; 95% CI, 0.82-0.93; P < 0.0001), progression-free survival (HR = 0.72; 95% CI, 0.65-0.79; P < 0.00001), disease-specific survival (HR = 0.86; 95% CI, 0.71-1.04; P = 0.03), and recurrence-free survival (HR = 0.74; 95% CI, 0.58-0.93; P = 0.01) in patients with cancer. The effect of RASis on overall survival varied depending on the type of cancer or type of RASis (ACEis or ARBs), according to subgroup analysis.The usage of renin-angiotensin system inhibitors has a positive impact on survival outcomes and recurrence among patients with cancer.

肾素-血管紧张素系统抑制剂(RASi),特别是血管紧张素转换酶抑制剂(ACEi)和血管紧张素 II 受体阻滞剂(ARBs),是广泛使用的抗高血压药物。它们对癌症患者预后的影响一直备受关注和争议。本研究旨在评估 RASi 对癌症患者生存期的影响。我们系统地检索了 PubMed、Web of Science、Embase 和 Cochrane 图书馆中截至 2022 年 4 月 1 日发表的相关研究。所有研究,无论是干预性研究还是观察性研究,只要与对照组相比,考察了 ARB 和 ACEi 对癌症预后的影响,并报告了生存结果和危险比,均纳入分析。从每项研究中确定并收集了集合危险比(HR)及相应的 95% 置信区间(95% CI)。为研究异质性,还进行了分组分析。本次荟萃分析共纳入 61 项研究。研究使用了 343283 名参与者的数据。研究发现,RASi 可改善总生存期(OS)(HR=0.88;95% CI:0.82-0.93;P
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引用次数: 0
Modulating Sympathetic Nervous System With the Use of SGLT2 Inhibitors: Where There Is Smoke, There Is Fire? 使用 SGLT2 抑制剂调节交感神经系统:哪里有烟,哪里就有火?
IF 2.6 4区 医学 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2025-01-01 DOI: 10.1097/FJC.0000000000001644
Kyriakos Dimitriadis, Daphne Pitsiori, Polyxeni Alexiou, Nikolaos Pyrpyris, Athanasios Sakalidis, Eirini Beneki, Panagiotis Iliakis, Fotis Tatakis, Panagiotis Theofilis, Panagiotis Tsioufis, Dimitrios Konstantinidis, Konstantina Aggeli, Konstantinos Tsioufis

Heart failure (HF) has become even more prevalent in recent years, because of improved diagnostics and an increase in the risk factors predisposing to its pathology. Sodium-glucose cotransporter 2 inhibitors (SGLT2i) emerged as one of the key pharmacotherapy options for both reduced and preserved ejection fraction, providing cardio- and renoprotection and improving mortality and cardiovascular (CV) outcomes. The pleiotropism of SGLT2i has led to multiple efforts to understand their distinct pathophysiologic interactions with various pathways, including microcirculation, endothelial dysfunction, and inflammation. More recently, the role of SGLT2i on the sympathetic nervous system (SNS) is starting to be recognized, especially because observations of retained or reduced heart rate despite volume contraction have been noted by investigators in the large clinical trials testing the safety and efficacy of these agents. Both preclinical and clinical studies have been performed, with conflicting results. Interestingly, in both settings, although there are indications of SNS modulation by SGLT2i, other studies contradict such findings, without showing, however, worsening of the autonomic homeostasis. Given the importance of neuromodulation in HF, in both pharmacologic and interventional therapies, in this review, we aim to describe the role of SNS in CV disease, focusing on HF, analyze preclinical and clinical data regarding the efficacy of SGLT2i in modulating autonomic dysfunction by examining various markers of SNS activation, and provide the most plausible theoretical backgrounds on the mechanism of benefit of SNS from the inhibition of SGLT2 receptors.

近年来,心力衰竭(HF)的发病率越来越高,这是因为诊断方法的改进和导致其病理变化的风险因素的增加。钠-葡萄糖共转运体 2 抑制剂(SGLT2i)成为治疗射血分数降低和射血分数保留的主要药物疗法之一,它能保护心脏和肾脏,改善死亡率和心血管(CV)预后。SGLT2i 的多效性促使人们努力了解其与微循环、内皮功能障碍和炎症等各种途径之间不同的病理生理学相互作用。最近,人们开始认识到 SGLT2i 对交感神经系统(SNS)的作用,特别是在测试这些药物的安全性和有效性的大型临床试验中,研究人员发现,尽管有容量收缩,但心率(HR)仍然保持或降低。临床前研究和临床研究的结果相互矛盾。有趣的是,在这两种情况下,虽然有迹象表明 SGLT2i 对 SNS 有调节作用,但其他研究却与这些发现相矛盾,而且没有显示自律神经平衡的恶化。鉴于神经调节在高血压的药物治疗和介入治疗中的重要性,在本综述中,我们旨在描述 SNS 在心血管疾病中的作用,重点关注高血压,通过研究 SNS 激活的各种标志物,分析有关 SGLT2i 调节自律神经功能紊乱疗效的临床前和临床数据,并就抑制 SGLT2 受体对 SNS 的益处机制提供最合理的理论背景。
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引用次数: 0
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Journal of Cardiovascular Pharmacology
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