Ranolazine

SCOUT-HCM demonstrated the superiority of Camzyos on the primary endpoint and multiple secondary endpoints The overall safety results in this study were consistent with the established safety pro Camzyos in adults Positive results support the potential for Camzyos to be the first cardiac myosin inhibitor for the treatment of adolescent oHCM PRINCETON, N.J.--(BUSINESS WIRE)-- $BMY #Camzyos -- Bristol Myers Squibb (NYSE: BMY) today announced positive topline results from SCOUT-HCM, a Phase 3 trial evaluating Camzyos (mavacamten) in the first study of a cardiac myosin inhibitor (CMI) in adolescents (ages 12 years to 5% of patients and more commonly in the CAMZYOS group than in the placebo group were dizziness (27% vs 18%) and syncope (6% vs 2%). There were no new adverse reactions identified in VALOR-HCM. Effects on Systolic Function In the EXPLORER-HCM trial, mean (SD) resting LVEF was 74% (6) at baseline in both treatment groups. Mean (SD) absolute change from baseline in LVEF was -4% (8) in the CAMZYOS group and 0% (7) in the placebo group over the 30-week treatment period. At Week 38, following an 8-week interruption of trial drug, mean LVEF was similar to baseline for both treatment groups. In the EXPLORER-HCM trial, 7 (6%) patients in the CAMZYOS group and 2 (2%) patients in the placebo group experienced reversible reductions in LVEF <50% (median 48%: range 35-49%) while on treatment. In all 7 patients treated with CAMZYOS, LVEF recovered following interruption of CAMZYOS. DRUG INTERACTIONS Potential for Other Drugs to Affect Plasma Concentrations of CAMZYOS CAMZYOS is primarily metabolized by CYP2C19 and to a lesser extent by CYP3A4 and CYP2C9. Inducers and inhibitors of CYP2C19 and moderate to strong inhibitors or inducers of CYP3A4 may affect the exposures of CAMZYOS. Impact of Other Drugs on CAMZYOS: Strong CYP2C19 Inhibitors : Concomitant use increases CAMZYOS exposure, which may increase the risk of heart failure due to systolic dysfunction. Concomitant use is contraindicated. Moderate to Strong CYP2C19 Inducers or Moderate to Strong CYP3A4 Inducers : Concomitant use decreases CAMZYOS exposure, which may reduce CAMZYOS’ efficacy. The risk of heart failure due to systolic dysfunction may increase with discontinuation of these inducers as the levels of induced enzyme normalizes. Concomitant use is contraindicated. Weak CYP2C19 Inhibitors or Moderate CYP3A4 Inhibitors : Concomitant use with a weak CYP2C19 inhibitor or a moderate CYP3A4 inhibitor increases CAMZYOS exposure, which may increase the risk of adverse drug reactions. Initiate CAMZYOS at the recommended starting dose of 5 mg orally once daily in patients who are on stable therapy with a weak CYP2C19 inhibitor or a moderate CYP3A4 inhibitor. Reduce dose of CAMZYOS by one level (ie, 15 to 10 mg, 10 to 5 mg, or 5 to 2.5 mg) in patients who are on CAMZYOS treatment and intend to initiate a weak CYP2C19 inhibitor or a moderate CYP3A4 inhibitor. Schedule clinical and echocardiographic assessment 4 weeks after inhibitor initiation, and do not up-titrate CAMZYOS until 12 weeks after inhibitor initiation. Avoid initiation of concomitant weak CYP2C19 and moderate CYP3A4 inhibitors in patients who are on stable treatment with 2.5 mg of CAMZYOS because a lower dose is not available. For short-term use (eg, 1 week), interrupt CAMZYOS for the duration of treatment with a weak inhibitor of CYP2C19 or a moderate inhibitor of CYP3A4. CAMZYOS may be reinitiated at the previous dose immediately on discontinuation of concomitant therapy. Moderate CYP2C19 Inhibitors or Strong CYP3A4 Inhibitors : Concomitant use with a moderate CYP2C19 inhibitor or strong CYP3A4 inhibitor increases CAMZYOS exposure, which may increase the risk of adverse drug reactions. Discontinuing use of a moderate CYP2C19 inhibitor or strong CYP3A4 inhibitor after long-term concomitant use may decrease CAMZYOS exposure, which may reduce CAMZYOS’ efficacy. Initiate CAMZYOS at a starting dosage of 2.5 mg orally once daily in patients who are on a stable therapy with a moderate CYP2C19 inhibitor or a strong CYP3A4 inhibitor. Reduce dose of CAMZYOS by one level (ie, 15 to 10 mg, 10 to 5 mg, or 5 to 2.5 mg) in patients who are on CAMZYOS and intend to initiate a moderate CYP2C19 inhibitor or a strong CYP3A4 inhibitor. Avoid initiation of concomitant moderate CYP2C19 and strong CYP3A4 inhibitors in patients who are on a stable treatment with 2.5 mg of CAMZYOS because a lower dose is not available. An increase in dose of CAMZYOS may be needed if the moderate inhibitor of CYP2C19 or strong inhibitor of CYP3A4 is discontinued after long-term concomitant use. Monitor for new or worsening symptoms. For short-term use (ie, when CAMZYOS dose modification is not feasible), interrupt CAMZYOS for the duration of treatment with a moderate inhibitor of CYP2C19 or a strong inhibitor of CYP3A4. CAMZYOS may be reinitiated at the previous dose immediately on discontinuation of concomitant therapy Potential for CAMZYOS to Affect Plasma Concentrations of Other Drugs CAMZYOS is an inducer of CYP3A4, CYP2C9, and CYP2C19. Concomitant use with CYP3A4, CYP2C9, or CYP2C19 substrates may reduce plasma concentration of these drugs. Closely monitor when CAMZYOS is used with concomitant CYP3A4, CYP2C9, or CYP2C19 substrates unless otherwise recommended in the Prescribing Information. Certain Combined Hormonal Contraceptives (CHCs): Progestin and ethinyl estradiol are CYP3A4 substrates. Concomitant use of CAMZYOS may decrease exposures of certain progestins, which may lead to contraceptive failure. CHCs containing a combination of ethinyl estradiol and norethindrone may be used with CAMZYOS, but if other CHCs are used, advise patients to add nonhormonal contraception (such as condoms) or use an alternative contraceptive method that is not affected by CYP450 enzyme induction (eg, intrauterine system) during concomitant use and for 4 months after the last dose of CAMZYOS. Drugs That Reduce Cardiac Contractility Expect additive negative inotropic effects of CAMZYOS and other drugs that reduce cardiac contractility. Avoid concomitant use of CAMZYOS in patients on disopyramide, ranolazine, verapamil with a beta blocker, or diltiazem with a beta blocker as these medications and combinations increase the risk of left ventricular systolic dysfunction and heart failure symptoms and clinical experience is limited. If concomitant therapy with a negative inotrope is initiated, or if the dose of a negative inotrope is increased, monitor LVEF closely until stable doses and clinical response have been achieved. SPECIFIC POPULATIONS Pregnancy CAMZYOS may cause fetal harm when administered to a pregnant female. Advise pregnant females about the potential risk to the fetus with maternal exposure to CAMZYOS during pregnancy. There is a pregnancy safety study for CAMZYOS. If CAMZYOS is administered during pregnancy, or if a patient becomes pregnant while receiving CAMZYOS or within 4 months after the last dose of CAMZYOS, healthcare providers should report CAMZYOS exposure by contacting Bristol Myers Squibb at 1-800-721-5072 or . Lactation The presence of CAMZYOS in human or animal milk, the drug’s effects on the breastfed infant, or the effects on milk production are unknown. The developmental and health benefits of breastfeeding should be considered along with the mother’s clinical need for CAMZYOS and any potential adverse effects on the breastfed child from CAMZYOS or from the underlying maternal condition. Females and Males of Reproductive Potential Confirm absence of pregnancy in females of reproductive potential prior to initiation of CAMZYOS. Advise females of reproductive potential to use effective contraception during treatment with CAMZYOS and for 4 months after the last dose. CHCs containing a combination of ethinyl estradiol and norethindrone may be used with CAMZYOS. However, CAMZYOS may reduce the effectiveness of certain other CHCs. If these CHCs are used, advise patients to add nonhormonal contraception (such as condoms) or use an alternative contraceptive method during concomitant use and for 4 months after the last dose of CAMZYOS. Please see U.S. Full Prescribing Information , including Boxed WARNING and Medication Guide . About Bristol Myers Squibb Bristol Myers Squibb is a global biopharmaceutical company whose mission is to discover, develop and deliver innovative medicines that help patients prevail over serious diseases. For more information about Bristol Myers Squibb, visit us at BMS.com or follow us on LinkedIn , X , YouTube , Facebook and Instagram . Cautionary Statement Regarding Forward-Looking Statements This press release contains “forward-looking statements” within the meaning of the Private Securities Litigation Reform Act of 1995 regarding, among other things, the research, development and commercialization of pharmaceutical products. All statements that are not statements of historical facts are, or may be deemed to be, forward-looking statements. Such forward-looking statements are based on current expectations and projections about our future financial results, goals, plans and objectives and involve inherent risks, assumptions and uncertainties, including internal or external factors that could delay, divert or change any of them in the next several years, that are difficult to predict, may be beyond our control and could cause our future financial results, goals, plans and objectives to differ materially from those expressed in, or implied by, the statements. These risks, assumptions, uncertainties and other factors include, among others, that future study results may not be consistent with the results to date, that Camzyos (mavacamten) may not receive regulatory approval for the additional indication described in this release in the currently anticipated timeline or at all, any marketing approvals, if granted, may have significant limitations on their use, and, if approved, whether Camzyos for such indication will be commercially successful. No forward-looking statement can be guaranteed. Forward-looking statements in this press release should be evaluated together with the many risks and uncertainties that affect Bristol Myers Squibb’s business and market, particularly those identified in the cautionary statement and risk factors discussion in Bristol Myers Squibb’s Annual Report on Form 10-K for the year ended December 31, 2024, as updated by our subsequent Quarterly Reports on Form 10-Q, Current Reports on Form 8-K and other filings with the Securities and Exchange Commission. The forward-looking statements included in this document are made only as of the date of this document and except as otherwise required by applicable law, Bristol Myers Squibb undertakes no obligation to publicly update or revise any forward-looking statement, whether as a result of new information, future events, changed circumstances or otherwise. corporatefinancial-news Contacts Bristol Myers Squibb M edia Inquiries: media@bms.com Investors: investor.relations@bms.com

1.快速型心律失常的分类与发生机制      1.1 分类体系与核心机制 快速性心律失常指成人静息心率>100次/分钟的心律失常，临床常用分类包括：按QRS波群宽度分为宽/窄QRS波群心动过速；按发生部位分为房性、房室交界性和室性；按电生理机制分为折返性、自律性异常和触发活动性心律失常，其中折返是最常见机制，占临床病例的60%以上。 折返机制需满足三个条件：传导通路存在功能性或解剖性分支、两条通路传导速度与不应期差异显著、环路中存在单向阻滞。异常自律性由心肌细胞舒张期去极化速率异常加快引起，常见于心肌缺血、电解质紊乱等病理状态，表现为心率“热身－冷却”现象。触发活动则由早期后去极化（EAD）和延迟后去极化（DAD）介导，与钙超载、离子通道重构密切相关。1.2 心房颤动的发生机制1.2.1 触发机制与肺静脉作用 房颤是全球最常见的心律失常，患者超6000万，其触发灶70%—90%位于肺静脉肌袖。肺静脉肌袖细胞具有独特电生理特性：从左心房向远端动作电位时程逐渐缩短（缩短幅度达30%—50%）、静息膜电位去极化（较左心房细胞低10-15mV）。乙酰胆碱（10^-7-10^-6 mol/L）可诱导肺静脉肌袖产生频率93±15ms的规则心动过速，光学标测证实为微折返机制。 机械敏感氯离子通道是肺静脉牵张诱发房颤的关键。肺静脉心肌细胞中，CIC-3、SWELL1与小球蛋白Cav3形成复合物，调控ICl,swell通道功能。高血压状态下Cav3下调导致小窝结构破坏，ICl,swell活性增加3倍以上，显著提高肺静脉电不稳定性。此外，心脏黑素细胞样细胞（表达DCT）功能异常也参与房颤发生，DCT缺陷小鼠房颤易感性增加2.7倍，其心肌细胞表现为复极延长和EAD增多。1.2.2 心房重构机制 房颤维持依赖电、结构和神经三重重构。电重构核心是L型钙电流（ICa,L）下调40%—60%、乙酰胆碱依赖性钾通道（IK,ACh）上调2倍以上，导致心房有效不应期（AERP）缩短且频率适应性丧失。结构重构以心房纤维化为特征，胶原容积分数从正常的10%升至30%以上，形成复杂三维折返环路，增加标测与消融难度。 遗传因素在房颤发生中起重要作用，已发现13个房颤易感基因（如KCNQ1、SCN5A），但单一基因变异贡献率不足5%，更多表现为遗传易感性与环境因素的协同作用。临床数据显示，家族性房颤患者的子女患病风险较普通人群高3.2倍，提示遗传背景的重要性。1.3 室上性心动过速的发生机制1.3.1 房室结折返性心动过速（AVNRT） AVNRT占成人室上速的50%以上，折返环路位于房室结内，由快慢两条径路组成：慢径路（α径路）传导速度慢（200-300ms）但不应期短（250-350ms）；快径路（β径路）传导速度快（100-150ms）但不应期长（350-450ms）。适时房性早搏在快径路发生单向阻滞，经慢径路缓慢传导（延迟>50ms）使快径路恢复兴奋性，形成持续折返，典型心率140—200次/分钟。 电生理研究发现，AVNRT患者房室结区Cx43表达下调30%，导致传导速度减慢，而迷走神经张力增加可进一步延长快径路不应期，促进折返形成。射频消融慢径路的成功率达95%以上，证实径路功能差异是AVNRT的核心机制。1.3.2 房室折返性心动过速（AVRT） AVRT占室上速的15%—30%，折返环路包括心房、房室结、希氏-浦肯野系统和房室旁路（Kent束）。正向型AVRT（占80%）中，激动经房室结下传心室，经旁路逆传心房；逆向型AVRT中，激动经旁路下传心室，经房室结逆传心房，表现为宽QRS波群心动过速。 旁路的电生理特性决定AVRT的发生：多数旁路具有快速传导能力（传导速度>1.5m/s），且不应期短（200-300ms）。预激综合征患者中，约30%会发生AVRT，其风险与旁路不应期相关（不应期<250ms者猝死风险增加）。1.4 室性心动过速的发生机制1.4.1 心肌梗死后室速的折返机制 心肌梗死后室速（MI-VT）是最常见的室速类型，80%以上为折返机制。梗死瘢痕区存活心肌束被纤维组织分隔，形成传导缓慢的“峡部”（传导速度<0.5m/s），为折返提供解剖基础。电生理标测显示，75%的MI-VT为局灶性微折返（环路直径<2cm），20%为局限性折返，仅5%为围绕瘢痕的大折返。 缝隙连接异常是传导减慢的关键：梗死边界区Cx43表达降低60%，且出现磷酸化异常和闰盘定位紊乱。动物实验证实，AdCx43基因转移可使MI-VT诱发率从100%降至40%，传导速度提高25%，验证了Cx43的核心作用。1.4.2 复极异质性与触发机制 MI-VT环路存在特征性复极异质性：KCNE3阳性心肌束Iks电流增加3倍，动作电位时程（APD）缩短40%；而KCNE4阳性束Iks电流减少50%，APD延长60%。这种相邻心肌束40-60ms的APD差异，为单向阻滞和折返形成创造条件。 交感神经激活是重要触发因素：去甲肾上腺素可使肌浆网钙泄漏增加2倍，诱发DAD；同时缩短APD，增强复极异质性。临床数据显示，MI后交感神经重构患者的VT发生率较普通患者高2.8倍，β受体阻滞剂可使VT风险降低35%。2. 治疗药物研发进展2.1 新型靶点与候选药物2.1.1 离子通道新靶点 GIRK4通道是心房选择性靶点，其活性增加可使AERP缩短30%，促进房颤发生。Bayer公司的BAY 3670549是高选择性GIRK4抑制剂（IC50=0.3μM），I期临床试验显示，单次给药可使房颤患者AERP延长25%，转复率提高40%，且对心室复极无影响，有望实现房颤的非侵入性即时治疗。 晚钠电流（late INa）抑制剂是室性心律失常新方向。late INa在LQT3综合征中增加3-5倍，导致APD延长和EAD。GS-6615（eleclazine）是强效抑制剂（EC50=190nM），较第一代药物雷诺嗪（EC50=8000nM）效力提高42倍。Ⅱ期数据显示，其可使LQT3患者QTc缩短40ms，室速发生率降低65%，目前正开展Ⅲ期试验。 心房选择性钾通道靶点还包括IKur（Kv1.5）IK,ACh（Kir3.1/3.4）和SK通道。IKur抑制剂可延长AERP而不影响QT间期，已进入临床的药物如AVE0118，房颤转复率达58%，但存在食管刺激副作用。SK通道抑制剂AP14145在Ⅱ期试验中使房颤负荷降低62%，安全性良好。2.1.2 信号通路与结构蛋白靶点 SGK1抑制剂在LQT2治疗中显示潜力，3μM抑制剂可使LQT2兔心肌细胞APD标准化，hiPSC模型中QTc缩短45ms，且与KCNH2致病变异无关。SGLT2抑制剂达格列净可增加心肌Nav1.5通道表达30%，提高钠电流密度，为心衰合并心律失常患者提供新选择（传统抗心律失常药对心衰患者禁忌）。 RyR2通道调节剂M201-A通过抑制IKACh（IC50=0.35μM），使AERP延长5.7倍。口服前药K201后，M201-A血药浓度达母药15倍，房颤转复率50%，导管消融后复发率降低40%，目前处于Ⅱ期临床。2.2 关键临床试验进展（2023-2025）2.2.1 Ⅲ期临床试验重点药物 硫酸舒欣啶（中宝药业）是全球首个进入Ⅲ期的室早原创药物，为多离子通道抑制剂（钠、钙、钾通道），作用特性类似Ib类药物但无致心律失常风险。2025年4月完成600例入组，中期数据显示：1200mg组室早减少≥80%的比例达63%，较安慰剂高38.1%；成对室早减少率72%，显著优于安慰剂（p<0.001），安全性与安慰剂相当。 Etripamil（Milestone）是钙通道阻滞剂鼻喷雾剂，用于室上速自救治疗。Ⅲ期RAPID试验中，64.3%患者30分钟内转复窦律，安慰剂组仅31.2%（HR=2.62, p<0.001）。该药物起效时间<5分钟，不良反应发生率仅8%（主要为鼻腔刺激），NDA申请已于2023年第三季度提交，有望成为首个FDA批准的室上速家庭治疗药物。 诺华PKN605（房颤适应症）于2025年11月启动中国Ⅱ期试验（CTR20254349），为随机双盲安慰剂对照研究，目标入组171例（国内6例）。主要终点为房颤负荷（AFB）降低率，次要终点包括复发时间和药代动力学参数。该药物作用于新型心房靶点，体外实验显示可使房颤模型AERP延长35%，目前处于受试者招募阶段。2.2.2 Ⅱ期与探索性试验 BAY 3670549的I期试验（2025年启动）为随机双盲安慰剂对照研究，纳入48例健康志愿者，评估0.5—10mg剂量的安全性和药效学。结果显示，5mg剂量组AERP延长25%，药代动力学呈线性特征（T1/2=8.2小时），无QT间期延长，下一步将开展房颤患者Ⅱ期试验。 参松养心胶囊的SS-AFRF研究入选2024年“心律失常领域十大研究”，该多中心试验纳入1200例射频消融后房颤患者，随机分为中药组和安慰剂组。12个月随访显示，中药组房颤复发率32.6%，较安慰剂组降低18.3%；亚组分析中，阵发性房颤患者获益更显著（复发率降低22.5%），证实其在房颤二级预防中的作用。 FLECAPRO试验评估β受体阻滞剂联合氟卡尼对心律失常性二尖瓣脱垂患者的疗效，纳入240例患者，采用植入式循环记录仪盲法评估终点。中期数据显示，联合治疗组室速负荷降低70%，较单药治疗组高40%，且无严重不良反应，为瓣膜型心律失常提供新方案。2.3 已上市新药与临床应用2.3.1 新型化学药物 维纳卡兰（Vernakalant）是心房选择性药物，通过抑制INa、IKur和IK,ACh起效，静脉给药后30分钟房颤转复率达51%，显著高于胺碘酮（34%）。其优势在于QT间期影响小（延长<10ms），但心衰（LVEF<35%）和低血压患者禁用，目前用于新发房颤的急诊转复。 决奈达隆（Dronedarone）是胺碘酮衍生物，无碘相关副作用，用于房颤复发预防。ATHENA试验显示，其可使房颤住院风险降低34%，心血管死亡率降低29%，但ANDROMEDA试验证实其增加永久性房颤患者死亡率（HR=2.13），故仅限用于阵发性房颤。 雷诺嗪（Ranolazine）作为late INa抑制剂，初始用于抗心绞痛，后发现其抗心律失常作用。在LQT3患者中，400mg每日两次可使QTc缩短35ms，室性心律失常发生率降低58%；在HFpEF患者中，可使房颤发生率降低27%，且不影响心功能。2.3.2 老药新用与适应症拓展 索他洛尔在LQT综合征中的应用扩展：LQT1和LQT2患者中，80mg每日两次可使尖端扭转型室速风险降低62%，较普萘洛尔效果更优（风险降低45%）。其机制为延长复极时间的同时抑制交感活性，特别适用于运动诱发的LQT患者。 美西律在Brugada综合征中的应用：150mg每日三次可使I型Brugada波消失率达68%，室速发生率降低75%。其通过增强Nav1.5电流改善右室流出道心肌传导，为禁忌ICD植入的患者提供替代方案。 SGLT2抑制剂的心律失常保护作用：达格列净10mg每日一次可使心衰患者房颤风险降低22%，恩格列净可使糖尿病患者室性早搏发生率降低30%。机制为增加Nav1.5通道表达和膜定位，改善心肌代谢，已被写入《2024 ESC心衰指南》作为房颤合并心衰的基础用药。2.3.3 中药制剂的临床价值 参松养心胶囊由12味中药组成，Meta分析显示（纳入32项RCT，3856例患者），其治疗室早的总有效率76.3%，较安慰剂高32.1%；治疗房颤的转复率45.2%，与普罗帕酮相当（47.1%），但不良反应发生率仅8.2%（普罗帕酮为21.5%）。机制涉及改善线粒体功能、抑制胶原合成和调节自主神经。 稳心颗粒在气阴两虚型室早患者中优势显著：Ⅱ期试验显示，90g每日三次可使室早减少率达62.5%，伴随心悸症状评分降低40%。其活性成分甘松提取物可抑制IK,ACh通道（IC50=1.2μM），与化学药物联用可提高疗效20%-30%。2.4 研发趋势与挑战2.4.1 核心研发趋势 心房选择性药物成为研发热点：通过靶向心房特异性离子通道（如IKur、GIRK4），实现“治疗房颤不影响心室”的目标。这类药物的致心律失常风险降低60%以上，目前全球在研药物达18种，其中6种进入Ⅱ期及以后阶段。 多靶点联合策略兴起：IKs/IKr双重阻滞剂可平衡复极延长效应，减少逆向频率依赖性。如AZD1305同时抑制IKs（IC50=0.5μM）和IKr（IC50=1.2μM），在房颤模型中AERP延长40%，而QT间期仅延长15ms，较单一靶点药物更安全有效。 精准医疗与基因导向治疗发展：基于KCNH2基因突变类型选择药物，如N588K突变患者对索他洛尔敏感（QTc缩短45ms），而Y652C突变患者对雷诺嗪更敏感（QTc缩短38ms）。23andMe与Bayer合作开发的基因检测芯片，可预测12种抗心律失常药物的疗效和毒性。2.4.2 主要挑战与应对 致心律失常风险仍是最大障碍：Ⅲ类药物中，25%因延长QT间期导致尖端扭转型失速而终止研发。应对策略包括：采用hERG通道高通量筛选（排除IC50<1μM的化合物）、联合IKs激活剂（如R-L3）抵消QT延长效应。 疗效局限性与复发问题：现有药物房颤年复发率仍达40%—60%。解决方案包括：开发“药物－消融联合疗法”，如术后使用参松养心胶囊12个月可使复发率降低至28%；设计缓释制剂（如决奈达隆透皮贴剂）维持稳定血药浓度。 临床试验设计难点：心律失常发作的随机性导致终点评估困难。创新方法包括：采用可穿戴设备实时监测心率（提高事件捕捉率3倍）、使用生物标志物（如microRNA-21）预测疗效、开展适应性设计临床试验（缩短研发周期40%）。3. 总结与展望 快速性心律失常的发生机制已从宏观折返深入到分子层面，肺静脉触发、缝隙连接异常、复极异质性等核心机制的阐明，为药物研发提供了明确靶点。治疗药物研发呈现“心房选择性、多靶点、精准化”的趋势，硫酸舒欣啶、etripamil等新药有望突破传统药物的局限。 中国在该领域实现重要突破：硫酸舒欣啶作为首个全球原创的室早治疗药物，参松养心胶囊的循证医学证据，标志着从“跟跑”向“领跑”转变。但仍需解决心律失常风险、疗效持久性等问题，未来需加强基础与临床转化研究，推动人工智能药物设计、基因治疗等新技术应用。 预计2025—2030年，将有5-8种新型抗心律失常药物上市，其中心房选择性药物和基因导向药物将成为主流。这些药物将使房颤转复率提高至70%以上，室速死亡率降低30%，为心律失常患者带来新的治疗希望，推动该领域进入精准治疗新时代。