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更新于：2026-03-10

Ditiazem Hydrochloride

盐酸地尔硫卓

更新于：2026-03-10

概要

基本信息

简介地尔硫卓是一种钙离子细胞内流抑制剂（慢通道阻滞剂或钙拮抗剂）。尽管其抗心绞痛作用的确切机制仍在研究中，但认为其作用方式如下：该药已被证明是心外膜和心内膜下冠状动脉的有效扩张剂，可抑制自发或由麦角新碱引起的冠状动脉痉挛。用于治疗慢性稳定型心绞痛和冠状动脉痉挛引起的心绞痛。该药于1973年由武田三菱在日本首次推出。

药物类型

小分子化药

别名

Diltiazem hydrochloride (JP17/USP)、Diltiazem Hyudrochloride、Diltizem Hydrochloride

+ [50]

靶点

Cav2.2

作用方式

阻滞剂

作用机制

Cav2.2阻滞剂(N-型电压门控性钙通道α-1B亚基阻滞剂)

治疗领域

神经系统疾病心血管疾病其他疾病

在研适应症

阵发性室上性心动过速快速心室反应稳定型心绞痛+ [2]

非在研适应症

心房扑动阵发性心动过速室上性心动过速

原研机构

Tanabe Pharma Corp.

在研机构

Bausch Health US LLC

AAA Pharmaceutical, Inc.

上海信谊万象药业股份有限公司

+ [3]

非在研机构

Exela Pharma Sciences LLC

权益机构

远大医药（中国）有限公司Tanabe Seiyaku Co., Ltd. /Pet Medicine Operations/

Tanabe Pharma Corp.

+ [1]

最高研发阶段批准上市

首次获批日期

日本 (1973-08-08),

心绞痛高血压

最高研发阶段(中国)批准上市

特殊审评-

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结构/序列

分子式C22H27ClN2O4S

InChIKeyHDRXZJPWHTXQRI-BHDTVMLSSA-N

CAS号33286-22-5

关联

119

项与盐酸地尔硫卓相关的临床试验

NCT07456852

/ Not yet recruiting临床1/2期IIT

Vasotoxicity Surveillance Using EndoPAT: The VASA Pilot Study

This phase I/II trial compares the effect of drugs that causes widening of blood vessels as a result of smooth muscle relaxation (vasodilator therapy) with isosorbide mononitrate, diltiazem or placebo to reduce vasotoxicity in patients with gastrointestinal cancer receiving fluoropyrimidine therapy. Some patients develop chest pain (possibly even a heart attack, a drop in heart function, or a rhythm abnormality) during treatment with a class of cancer drugs known as fluoropyrimidines, which include 5-Fluorouracil (5-FU) and capecitabine. These side effects are believed to be due to the development of an abnormal reactivity of the blood vessels referred to as vasospasm. Vasotoxicity is damage or toxicity inflicted upon blood vessels (vascular system), often causing dysfunction, remodeling, or narrowing (vasoconstriction). It is a broad term used to describe the detrimental effects of certain agents, such as chemotherapy drugs. Researchers want to evaluate how often the reactivity of blood vessels becomes abnormal, during the treatment with 5-FU or capecitabine and how clinically relevant and controllable/preventable this phenomenon is in patients with gastrointestinal cancer.

开始日期2026-03-31

申办/合作机构

Mayo Clinic

NCT07103655

/ Not yet recruiting临床4期IIT

The Therapeutic Value of Mavacamten in Hypertrophic Cardiomyopathy With Mid-to-Apical Left Ventricular Obstruction: A Prospective, Interventional, Real-World Clinical Study.

This study is a prospective interventional cohort study aimed at evaluating the therapeutic efficacy and clinical utility of Mavacamten-a targeted myosin inhibitor specifically developed for obstructive hypertrophic cardiomyopathy (HCM)-in patients with HCM characterized by mid-to-apical left ventricular obstruction.

开始日期2026-01-01

申办/合作机构

浙江大学医学院附属第二医院（浙江省第二医院）

NCT07232589

/ Recruiting临床1期

A Study to Evaluate the Effect of Multiple Oral Doses of Diltiazem on the Single-Dose Pharmacokinetics of Nemtabrutinib in Healthy Participants.

The goal of the study is to learn what happens to levels of nemtabrutinib (MK-1026) in a healthy person's body over time. Researchers will compare what happens to nemtabrutinib in the body when it is given with or without another medicine called diltiazem.

开始日期2025-12-08

申办/合作机构

Merck Sharp & Dohme LLC

100 项与盐酸地尔硫卓相关的临床结果

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100 项与盐酸地尔硫卓相关的转化医学

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100 项与盐酸地尔硫卓相关的专利（医药）

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10,586

项与盐酸地尔硫卓相关的文献（医药）

2026-12-01·JOURNAL OF MEMBRANE BIOLOGY

Na+ Uptake Triggered in Adrenal Chromaffin Cells by a 5-ns Electric Pulse is Facilitated by Ca2+ Influx Via an L-Type-Like Ca2+ Channel Independent of Changes in Membrane Potential

Article

作者: Gould, Thomas W ; Zaklit, Josette ; Leblanc, Normand ; Craviso, Gale L ; Yang, Lisha

Whole-cell voltage patch clamp studies have shown that in bovine adrenal chromaffin cells held at -70 mV, a single 5-ns, 5 MV/m pulse activates a membrane conductance carried partially by Na⁺ through TRPC4/5 channels and the sodium leak channel (NALCN). Here we used fluorescence imaging with the Na⁺ indicator ING-2 to further investigate Na⁺ influx pathways. A 5-ns, 5 MV pulse elicited a tetrodotoxin-insensitive rise in ING-2 fluorescence that exhibited a similar electric field dependency and response to pulse-pair stimulation as the inward current. Increases in ING-2 fluorescence were partially inhibited by the NALCN inhibitor CP96345, the TRPC4/5 channel inhibitor M084, or the broad spectrum TRP channel inhibitor La³⁺, and fully blocked by the combination of these agents, suggesting involvement also of a La³⁺-sensitive Na⁺ pathway. Cholesterol depletion with methyl-β-cyclodextrin or PIP₂ synthesis inhibition with wortmannin also reduced the response. Full inhibition was achieved with the selective L-type voltage-gated Ca²⁺ channel (VGCC) inhibitors nitrendipine, verapamil, or diltiazem but not the broad-spectrum inhibitor Cd²⁺. Inhibitors of N- and P/Q-type VGCC had no effect. Fluorescence Ca²⁺ imaging in voltage-clamped GCaMP6f-expressing murine chromaffin cells held at -70 mV revealed a nitrendipine-sensitive, Cd²⁺-insensitive increase in intracellular Ca²⁺ that accompanied the inward current. These results provide evidence that nanoelectropulse-induced Na⁺ influx into chromaffin cells involves several Na⁺ influx pathways that are facilitated by Ca²⁺ influx via an L-type-like Ca²⁺ channel associated with cholesterol-rich membrane domains. Investigating such membrane effects is essential for developing nanosecond electric pulse technologies for stimulating and/or modulating excitable cells.

2026-03-01·TALANTA

Rapid carbamazepine detection by means of a disposable electrochemical sensor based on a molecularly imprinted polymer

Article

作者: Puga, Antón ; Delerue-Matos, Cristina ; Pacheco, João G ; Poza-Nogueiras, Verónica

The presence of pharmaceuticals such as carbamazepine (CBZ) in water environments poses a threat, highlighting the importance of developing analytical tools for the detection and quantification of these compounds. In this work, for the first time a molecularly imprinted polymer (MIP) sensor was obtained on a screen-printed carbon electrode (SPCE) for the rapid detection of CBZ. This simple and portable voltammetric sensor was obtained by electropolymerization of 3,4-ethylenedioxythiophene (EDOT) as the functional monomer in the presence of CBZ as the template molecule. Using differential pulse voltammetry (DPV) as the detection method, the construction parameters were assessed and optimized. As a result, the optimal sensor was obtained performing the following steps: i) an activation with 50 mM of H₂SO₄, ii) an electropolymerization performing 20 cycles of cyclic voltammetry using 4.5 mM of EDOT and 1 mM of CBZ, iii) an extraction with HCl 0.1 M during 30 min, and iv) an incubation in PBS pH 10 during 15 min. A linear analytical response was obtained in the range of 1-50 μM, with a LOD of 0.58 μM. The prepared sensor showed high selectivity towards CBZ over pharmaceuticals with similar chemical structures (CBZ 10,11-epoxide, diclofenac and diltiazem), with a response under 5.5 % of that for CBZ. Additionally, its performance in real water samples was assessed, yielding good recoveries. Hence, an easy-to-use MIP-based sensor was successfully developed with potential applications for on-site monitoring of CBZ in the environment.

2026-02-01·AMERICAN JOURNAL OF EMERGENCY MEDICINE

Evaluation of diltiazem dosing strategies in the management of atrial fibrillation in the emergency department

Article

作者: Weigartz, Katherine ; Barre, Stephanie ; Baize, Paige ; Agee, Jazmin K

OBJECTIVE:

To compare the incidence of treatment failure between oral (PO) immediate release (IR) tablet and continuous intravenous infusion (CIVI) diltiazem following an initial loading dose in patients with atrial fibrillation (AF) with rapid ventricular response (RVR).

METHODS:

This single center, retrospective cohort study evaluated patients presenting to the emergency department (ED) from July 1, 2022 to June 30, 2022 in AF with RVR who received oral or continuous diltiazem after an initial intravenous loading dose. The primary objective of this study is to identify the percentage of patients with treatment failure four hours after initiation of diltiazem IR PO tablet or continuous IV infusion. Secondary endpoints included hospital length of stay (LOS), ED disposition, and clinically significant hypotension.

RESULTS:

Of the 171 patients included, 85 received PO IR diltiazem and 86 received CIVI diltiazem. There was no significant difference in the composite outcome of treatment failure between the PO and CIVI groups (60 % vs 59 %, p = 0.93). Patients who received PO diltiazem were more frequently discharged from the ED (31.8 % vs 4.7 %, p < 0.001). There was no significant difference in hospital LOS (6.6 vs 6.5 days, p = 0.06) or clinically significant hypotension (11.7 % vs 8.1 % p = 0.428).

CONCLUSION:

Initiating immediate-release oral diltiazem after an initial IV bolus does not result in more treatment failures than initiating a continuous infusion.

103

项与盐酸地尔硫卓相关的新闻（医药）

2026-03-04

·国际糖尿病idiabetes

莫让常用药变“伤心药”，重磅综述：非肿瘤药物的心血管不良反应

点击“蓝字”关注我们编者按药物所致心血管不良反应对患者管理具有重要的临床实践意义。尽管心血管不良反应常与抗肿瘤治疗相关，但越来越多的证据表明，非肿瘤药物也可引发严重的心血管损害。这类不良反应涵盖心律失常、传导异常、QT间期延长、心力衰竭、心肌梗死及结构性心肌病等。涉及的非肿瘤药物包括抗生素（如大环内酯类、氟喹诺酮类）、降糖药（如噻唑烷二酮类）、非甾体抗炎药、胃肠与泌尿系统疾病治疗药物，尤为重要的是心血管药物本身。近期发表的一项叙述性综述[1]，聚焦最常引发心血管不良反应的非肿瘤药物，阐述其潜在机制，重点论述了不良反应表现及以及临床预防的实用要点。一、抗菌药物大环内酯类与氟喹诺酮类大环内酯类与氟喹诺酮类药物长期以来被认为与心血管事件及死亡风险升高相关。大环内酯类用药还与QT间期延长相关，多篇病例报告记载其可诱发心律失常。然而，多项大型回顾性临床研究对大环内酯类临床应用的潜在风险得出了相互矛盾的结果[2]。一项纳入13项研究的最新Meta分析显示[3]，使用氟喹诺酮类可使心律失常风险显著增加85%，心血管死亡风险增加71%。其中莫西沙星致心血管不良事件的概率最高。大环内酯类与氟喹诺酮类主要通过抑制延迟整流钾电流快速成分，导致动作电位时程延长，增加早期后除极易感性，进而通过2相折返诱发尖端扭转型室速。二、抗疟药奎宁、氯喹、羟氯喹、青蒿琥酯-阿莫地喹、双氢青蒿素-哌喹等抗疟药均与QT/QTc间期延长相关。氯喹与羟氯喹可剂量依赖性抑制心室肌细胞钾外流通道，用药后最早2天即可出现QTc间期延长[4]。羟氯喹起始治疗后QTc间期延长发生率为3.9%~8.5%，但QTc间期变化与死亡率升高无关。羟氯喹/氯喹相关的其他心脏毒性还包括传导异常与心肌病，均呈剂量依赖性，且多发生于长期用药（平均疗程7~12年）。房室传导障碍多为永久性损害。羟氯喹/氯喹相关心肌病多为限制性心肌病，常需心内膜心肌活检确诊，停药并接受指南导向药物治疗后病情可能改善。三、抗病毒药抗病毒治疗的主要关注点之一是肝脏、骨骼肌及心脏的线粒体毒性。例如，抗人类免疫缺陷病毒逆转录病毒药齐多夫定可诱导线粒体功能障碍，导致线粒体断裂及融合-分裂周期受损。齐多夫定可抑制线粒体DNA聚合酶与逆转录酶。丙型肝炎治疗药物——RNA聚合酶非结构蛋白5B抑制剂索磷布韦，近年上市后监测提示其具有心脏毒性，具体机制尚不明确。新一代整合酶链转移抑制剂（如多替拉韦、比克替拉韦）与体重增加更显著相关，尤其与丙酚替诺福韦联用时；此类药物对血脂总体呈中性或轻度影响，不增加心血管事件风险。老一代蛋白酶抑制剂（尤其是利托那韦增效的洛匹那韦）与血脂异常及心血管事件风险升高相关；丙酚替诺福韦较富马酸替诺福韦二吡呋酯更易致体重增加，血脂谱更差。阿巴卡韦用药与主要不良心血管事件（MACE）发生率升高相关。四、免疫抑制剂与抗炎药非甾体抗炎药非甾体抗炎药（NSAIDs）是最常用的镇痛药物，作用机制为阻断前列腺素合成酶（COX-1、COX-2）其中一种或两者。选择性COX-2抑制剂（昔布类）最初因胃肠道不良反应减少而被开发，后续却发现其与心血管不良反应相关。2004年，美国食品药品监督管理局（FDA）因rofecoxib显著增加心肌梗死与卒中风险，将其撤市。尽管其严重心血管不良反应与其独特代谢相关，2007年FDA仍因心脏毒性顾虑，拒绝批准etoricoxib上市。长期使用选择性COX-2抑制剂（如双氯芬酸）与非选择性COX-1/COX-2抑制剂（如布洛芬、萘普生、吲哚美辛）均被证实可增加心搏骤停风险[5]。传统NSAID双氯芬酸的COX-2选择性与塞来昔布相当，且心血管风险呈剂量依赖性升高。对比COX-2抑制剂与NSAIDs的随机对照试验，存在方法学偏倚：无论适应证均使用最大剂量NSAIDs以夸大胃肠道获益，或选用COX-2选择性的双氯芬酸而非低剂量布洛芬/萘普生作对照，从而掩盖心血管风险。观察性研究显示，COX-2抑制剂与高剂量NSAIDs（萘普生除外）治疗数周内即可升高心血管风险，萘普生为相对最安全的选择。COX抑制剂应间断使用最低有效剂量，心血管高危人群尤需谨慎。临床中仅低剂量阿司匹林用于心血管疾病一级预防，因其不可逆阻断血小板COX-1，而对内皮COX-2无显著影响；相反，选择性COX-2抑制剂（昔布类）减少前列环素生成，却对 COX-1介导的血栓素A2生成无明显作用。肿瘤坏死因子抑制剂肿瘤坏死因子α（TNFα）抑制剂获批用于类风湿关节炎后，即被发现与心血管不良反应相关。检索FDA不良事件报告系统近10年中，依那西普、英夫利昔单抗、阿达木单抗、赛妥珠单抗、戈利木单抗相关心力衰竭报告共594 898条抗TNF药物不良事件记录，其中2869条为心力衰竭，超半数为女性（平均年龄64岁），发生心衰者中阿达木单抗使用率最高（73.9%）。依那西普与阿达木单抗均与心力衰竭显著相关[6]。一项纳入观察性研究与Meta分析的类风湿关节炎合并心衰患者系统评价显示[7]，TNFα抑制剂（英夫利昔单抗、依那西普、阿达木单抗）不增加新发或恶化心衰风险，但≥65岁患者心衰住院风险与死亡风险升高。糖皮质激素外源性糖皮质激素用药约20%病例可出现高血压。同时，糖皮质激素与MACE风险的相关性证据存在矛盾。一项最新系统评价与Meta分析评估糖皮质激素与心血管风险（含MACE）的关联，得出两大核心结论[8]：糖皮质激素与MACE、冠心病、心力衰竭风险升高相关；MACE 风险随糖皮质激素累积剂量或日剂量增加而升高。五、降糖药物噻唑烷二酮类噻唑烷二酮类（如罗格列酮、吡格列酮）为过氧化物酶体增殖物激活受体γ激动剂，调控参与糖脂代谢调控的胰岛素敏感基因转录。2007年发表的一项整合文献、FDA官网及罗格列酮厂商临床试验注册库的分析显示[9]，罗格列酮显著增加心肌梗死风险，心血管死亡风险呈临界升高。近期Meta分析证实，噻唑烷二酮类可加重既有心衰，增加新发心衰风险。一项纳入227 571例接受噻唑烷二酮类治疗的医保受益人群回顾性分析显示[10]，罗格列酮较吡格列酮心衰风险更高。二肽基肽酶4抑制剂 2型糖尿病患者使用二肽基肽酶 4（DPP-4）抑制剂（如沙格列汀、西格列汀）与心衰风险升高相关，此类风险似为类效应，风险程度可能受联合用药影响。胰高血糖素样肽1受体激动剂近期胰高血糖素样肽 1（GLP-1）受体激动剂试验的事后分析出现争议信号，因其具有正性变时效应，可致心率加快。FIGHT试验事后分析提示[11]，在射血分数降低的心衰（HFrEF）患者中，利拉鲁肽可能升高心血管不良反应风险，诱因可能为心律失常风险增加及心衰事件恶化。LIVE研究显示[12]，利拉鲁肽治疗24周未改善左室射血分数（主要终点），左室内径、纽约心脏病协会（NYHA）心功能分级及生活质量均无变化，且有左室扩张的非显著性趋势，其获益缺失的可能解释为心率升高。EXSCEL试验评估每周1次艾塞那肽用于不同心血管风险的2型糖尿病患者（部分基线合并 HFrEF），整体试验对MACE复合终点呈中性结果；事后亚组分析显示，基线无心衰患者使用每周1次艾塞那肽可降低全因死亡风险，而既有心衰患者无此获益。此类争议信号可能与药物特异性及表型特异性效应相关，无法归为类效应。六、心血管药物钙通道阻滞剂二氢吡啶类钙通道阻滞剂（如硝苯地平）可阻断钙离子跨膜内流进入心肌与血管平滑肌，兼具负性肌力与血管舒张作用。非二氢吡啶类（地尔硫卓、维拉帕米）同样具有负性肌力作用，且因血管舒张无法抵消负性肌力效应，较二氢吡啶类更易加重心衰。一项纳入2466例近期心肌梗死患者的研究显示[13]，地尔硫卓增加不良心脏事件风险，风险与基线心衰严重程度直接相关，收缩功能障碍患者需慎用。地尔硫卓与维拉帕米还可抑制窦房结自律性，引发缓慢性心律失常，无有效起搏器的窦房结功能障碍患者应避免使用。短效二氢吡啶类（如硝苯地平）因快速强效外周血管舒张作用，可引发反射性心动过速。 β受体阻滞剂推荐剂量下β受体阻滞剂因治疗指数大，总体安全性良好。因负性肌力作用，起始用药可能导致心衰症状短暂加重，建议在心衰症状稳定后启动治疗。与其他药物联用可增加心血管不良反应风险，包括心动过缓、房室传导阻滞、低血压或心衰。部分β受体阻滞剂（如普萘洛尔、拉贝洛尔、醋丁洛尔）具有膜稳定作用，过量用药心脏毒性更显著。除上述心脏效应外，需注意反跳现象：长期使用β受体阻滞剂突然停药，可导致高血压患者急性冠脉事件风险升高，心衰患者院内死亡风险增加，诱发心绞痛，并增加心肌梗死后死亡与再住院风险。 α1受体阻滞剂 ALLHAT研究显示[14]，多沙唑嗪组较氯噻酮组心衰风险翻倍，原因可能为扩血管所致水肿被误诊、多沙唑嗪降压幅度更小，或停用具有心衰保护作用的其他降压药后心衰显现。V-HeFT Ⅰ显示[15]，肼屈嗪联合硝酸异山梨酯较安慰剂降低死亡率、改善左室射血分数，而哌唑嗪无心血管获益。地高辛地高辛可引发多种类型心律失常。轻度中毒：最常见心动过缓、房室传导阻滞，与迷走张力过度兴奋相关；重度中毒：可出现房性与室性快速性心律失常，机制多为延迟后除极致自律性升高及/或异位节律。地高辛毒性可由药物相互作用诱发或加重。七、抗心律失常药 Ⅰ类抗心律失常药部分Ⅰ类抗心律失常药（钠通道阻滞剂）对特定人群具有潜在危害。丙吡胺对心衰患者具有负性肌力作用，可诱发或加重心衰[16]。氟卡尼可显著抑制左室功能不全患者的左室功能。有研究显示氟卡尼与死亡率升高相关，心衰或结构性心脏病患者应避免使用[17]。 Ⅲ类抗心律失常药 Ⅲ类抗心律失常药（索他洛尔、伊布利特、多非利特、阿莫卡兰、胺碘酮、决奈达隆）可延缓复极、阻断hERG通道。此类药物会延长QT间期，理论上及临床均证实存在尖端扭转型室速风险[18]。但胺碘酮与决奈达隆极少诱发尖端扭转型室速，可能与其同时阻断钙通道、可能还阻断钠通道相关。此外，胺碘酮可诱发甲状腺毒症，部分患者因此出现心房颤动。结语非肿瘤药物是现代治疗的重要组成部分，但其潜在的心血管不良反应常被低估，具有重要临床意义。心血管不良反应并非仅见于抗肿瘤药物，在抗生素、中枢神经系统药物、降糖药、抗炎药等常用药物，甚至心血管药物本身中均可出现。未来，系统药理学、药物基因组学及数字医疗技术的进步，有望改变药物性心血管风险的识别与管理模式。参考文献（上下滑动可查看） [1] M Cecilia Bahit , Pilar Agudo-Quilez , et al. Cardiovascular adverse effects of common non-oncologic medications: from mechanisms to clinical management. EHJ-Cardiovascular Pharmacotherapy, Volume 12, Issue 2, February 2026, Pages 118-134. [2] Ray WA, Murray KT, Hall K, et al. Azithromycin and the risk of cardiovascular death. N Engl J Med 2012;366:1881–1890. [3] Gorelik E, Masarwa R, Perlman A, et al. Fluoroquinolones and cardiovascular risk: a systematic review, meta-analysis and network meta-analysis. Drug Saf 2019;42:529–538. [4] Desmarais J, Rosenbaum JT, Costenbader KH, et al. American College of Rheumatology white paper on antimalarial cardiac toxicity. Arthritis Rheumatol 2021;73:2151–2160. [5] Sondergaard KB, Weeke P, Wissenberg M, et al. Non-steroidal anti-inflammatory drug use is associated with increased risk of out-of-hospital cardiac arrest: a nationwide case-time-control study. Eur Heart J Cardiovasc Pharmacother 2017;3:100-107. [6] Al-Mabrouk Y, Hamdan O, Alsawalmeh A, et al. Are anti-TNF medications related to heart failure? A study of the FAERS database. J Am Coll Caridiol 2025;85:1419. [7] Hussain A, Tarahomi T, Singh L, et al. Cardiovascular risk associated with TNF alpha inhibitor use in patients with rheumatoid arthritis. Cureus 2021;13:e17938.[8] Deng H-W, Mei W-Y, Xu Q, et al. The role of glucocorticoids in increasing cardiovascular risk. Front Cardiovasc Med 2023;10:1187100.[9] Nissen S, Wolski K. Effect of rosiglitazone on the risk of myocardial infarction and death from cardiovascular causes. N Engl J Med 2007;356:2457–2471.[10] Graham DJ, Ouellet-Hellstrom R, MaCurdy T, et al. Risk of acute myocardial infarction, stroke, heart failure, and death in elderly Medicare patients treated with rosiglitazone or pioglitazone. JAMA 2010;304:411-418.[11] Neves JS, Vasques-Nóvoa F, Borges-Canha M, et al. Risk of adverse events with liraglutide in heart failure with reduced ejection fraction: a post hoc analysis of the FIGHT trial. Diabetes Obes Metab 2023;25:189–197.[12] Komajda M. Liraglutide in heart failure: caution is needed. Eur J Heart Fail 2017;19:78-79.[13] Multicenter Diltiazem Postinfarction Trial Research Group. The effect of diltiazem on mortality and reinfarction after myocardial infarction. N Engl J Med 1988;319:385–392.[14] Major cardiovascular events in hypertensive patients randomized to doxazosin vs chlorthalidone: the antihypertensive and lipid-lowering treatment to prevent heart attack trial (ALLHAT). ALLHAT Collaborative Research Group. JAMA 2000;283:1967–1975.[15] Cohn JN, Archibald DG, Ziesche S, et al. Effect of vasodilator therapy on mortality in chronic congestive heart failure. Results of a Veterans Administration Cooperative Study. N Engl J Med 1986;314:1547–1552.[16] Jensen G, Sigurd B, Uhrenholt A. Haemodynamic effects of intravenous disopyramide in heart failure. Eur J Clin Pharmacol,1975;8:167–173.[17] Legrand V, Materne P, Vandormael M, et al. Comparative haemodynamic effects of intravenous flecainide in patients with and without heart failure and with and without beta-blocker therapy. Eur Heart J 1985;6:664–671.[18] Shah RR. Drug-induced QT interval prolongation: regulatory perspectives and drug development. Ann Med 2004;36:47–52. 声明：本文仅供医疗卫生专业人士了解最新医药资讯参考使用，不代表本平台观点。该等信息不能以任何方式取代专业的医疗指导，也不应被视为诊疗建议，如果该信息被用于资讯以外的目的，本站及作者不承担相关责任。最新《国际糖尿病》读者专属微信交流群建好了，快快加入吧！扫描左边《国际糖尿病》小助手二维码（微信号：guojitnb），回复“国际糖尿病读者”，ta会尽快拉您入群滴！（来源：《国际循环》编辑部）

CSCO会议

2026-03-04

·drugs

Diltiazem Linked to Increased Risk for Bleeding Complications in A-Fib

WEDNESDAY, March 4, 2026 -- For patients with atrial fibrillation (AF) receiving apixaban or rivaroxaban , use of diltiazem versus metoprolol is associated with an increased risk for serious bleeding complications, according to a study published online Feb. 24 in the Annals of Internal Medicine . Ghadeer K. Dawwas, Ph.D., from the Vanderbilt University School of Medicine in Nashville, Tennessee, and colleagues compared the risk for bleeding among AF patients using apixaban or rivaroxaban in combination with diltiazem versus metoprolol. A total of 23,000 users of diltiazem and 23,000 users of metoprolol were included in the matched cohort of AF patients. The researchers found that diltiazem versus metoprolol was associated with a higher risk for bleeding events after propensity score matching (rate difference, 5.4 per 1,000 person-years). With high- versus low-dose diltiazem, the risk for bleeding increased (risk difference, 9.2 versus 2.6 for high- and low-dose, respectively). The estimated risk differences between diltiazem and metoprolol were 0.48 and 0.31 percentage points, respectively, at 12 and six months. "Our examination of diltiazem dosages indicated a dose-dependent relationship, with higher doses associated with more bleeding," the authors write. Abstract/Full Text (subscription or payment may be required)

临床结果

2026-03-03

·drugs

A-Fib Drug, Diltiazem, Could Interact With Blood Thinners, Increase Risk Of Dangerous Bleeding

TUESDAY, March 3, 2026 — People with abnormal heart rhythms could be at risk of dangerous bleeding from a serious combination of prescription medications, a new study says. Patients with atrial fibrillation (A-Fib) often are prescribed diltiazem to help control their heart rate, researchers said in the Annals of Internal Medicine . Because A-Fib also greatly increases a person’s risk of stroke, these patients also are prescribed blood thinners like apixaban or rivaroxaban , researchers said. But the combination of diltiazem with either of those blood thinners caused higher rate of serious bleeding events among a group of 23,000 patients, researchers found. “Although diltiazem remains an appropriate and effective option for heart rate control in selected patients, our results underscore that bleeding risk must be a central consideration in treatment decisions,” lead researcher Ghadeer Dawwas said in a news release. She’s an assistant professor of medicine and health policy at Vanderbilt University Medical Center in Nashville, Tennessee. Diltiazem is a calcium channel blocker, which helps slow heart rate in people with A-Fib and weaken the heart’s contraction, according to the American Heart Association . However, diltiazem also inhibits the function of cytochrome enzymes, which are crucial for the metabolism of drugs. This might cause blood thinners to become more concentrated in the bloodstream, increasing the risk of dangerous bleeding, researchers said. For this study, researchers compared 23,000 A-Fib patients prescribed diltiazem against another 23,000 prescribed metoprolol , a beta blocker also used to slow the heart rate in these patients. These patients also had been prescribed either apixaban or rivaroxaban. The team tracked which drug combination caused a higher risk of dangerous bleeding in the brain, GI system or elsewhere in the body. Results showed 467 serious bleeding events among diltiazem users compared to 397 among those prescribed metoprolol. Overall, diltiazem was associated with an 18% increased risk of dangerous bleeding, the study found. Further, the risk grew with higher doses of diltiazem, researchers discovered. The bleeding risk “is especially relevant for patients receiving higher doses exceeding 120 mg/day of diltiazem or those taking additional interacting medications,” Dawwas said. “In such cases, metoprolol may represent a safer alternative.” Sources Vanderbilt University, news release, Feb. 26, 2026

AHA会议上市批准临床研究

100 项与盐酸地尔硫卓相关的药物交易

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KEGG	Wiki	ATC	Drug Bank
D00616	-	C05AE03 C08DB01	DB00343

研发状态

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适应症	国家/地区	公司	日期
阵发性室上性心动过速	美国	HQ Specialty Pharma Corp.	2025-02-21
快速心室反应	美国	HQ Specialty Pharma Corp.	2025-02-21
心房颤动	美国	Exela Pharma Sciences LLC	2021-10-28
心房扑动	美国	Exela Pharma Sciences LLC	2021-10-28
阵发性心动过速	美国	Exela Pharma Sciences LLC	2021-10-28
室上性心动过速	美国	Exela Pharma Sciences LLC	2021-10-28
稳定型心绞痛	美国	Bausch Health US LLC	1982-11-05
心绞痛	日本	Tanabe Pharma Corp.	1973-08-08
高血压	日本	Tanabe Pharma Corp.	1973-08-08

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临床结果

适应症

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研究	分期	人群特征	评价人数	分组	结果	评价	发布日期


NCT06534671 (CTgov)	临床4期	Jervell-Lange Nielsen综合征	1	diltiazem	淵襯襯齋蓋遞簾簾製淵 = 壓繭齋鹹獵蓋鹹餘選鬱願憲範願窪夢夢蓋顧獵 (鏇衊窪觸鏇淵網願範鏇, 願選鹹積壓衊鏇觸製窪 ~ 膚壓鑰膚鬱蓋鏇鑰鹹構) 更多	-	2025-10-14
NCT04130438 (CTgov)	临床2期	心绞痛 \| 心肌桥 \| 稳定型心绞痛	5	Nebivolol (Beta Blocker (Nebivolol))	夢觸網艱夢窪願艱壓鑰(夢窪憲獵醖顧醖餘窪選) = 襯壓積觸窪構網夢製築膚餘夢製齋製遞繭憲淵 (糧窪衊觸蓋網構築壓齋, 24.4) 更多	-	2025-02-25
				Diltiazem (Calcium Channel Blocker (Diltiazem))	夢觸網艱夢窪願艱壓鑰(夢窪憲獵醖顧醖餘窪選) = 構網蓋鹹鏇淵夢觸顧積膚餘夢製齋製遞繭憲淵 (糧窪衊觸蓋網構築壓齋, NA) 更多
FDA_CDER 人工标引	N/A	阵发性室上性心动过速 \| 快速心室反应	-	Diltiazem Hydrochloride Injection	夢糧醖構艱襯鏇襯顧鹹(鹹餘膚壓鹽窪艱膚築觸) = 鬱醖壓淵選範築鏇積襯壓廠齋壓範鬱願淵艱餘 (顧鬱網繭選醖觸廠廠鹽 )	积极	2025-02-21
				control	-
Pubmed \| Ann Emerg Med	N/A	快速心室反应	252	Low dose (<0.1875 mg/kg)	鑰醖鏇製衊壓選憲襯繭(築鏇鏇窪窪積鑰簾糧獵) = 糧築壓壓淵壓夢構積膚鑰蓋衊選憲鏇膚製鑰膚 (顧廠遞鬱醖艱鬱積齋醖 ) 更多	-	2023-03-01
				Weight-based dose (0.1875 to 0.3125 mg/kg)	鹽窪顧餘醖廠壓鏇窪壓(願艱願繭鬱衊衊積窪襯) = 鏇醖鏇襯鏇獵鑰艱顧願願顧範簾鬱獵膚膚構積 (艱觸糧範窪醖鬱衊遞夢 ) 更多
NCT04777045 (EDIT-CMD, Pubmed \| JACC Cardiovasc Imaging)	临床3期	冠状动脉非阻塞性心肌梗死 \| 非小细胞肺癌	126	Diltiazem	齋製淵鹽壓範願獵蓋壓(築壓遞夢網齋憲齋淵壓) = 製選齋觸築繭顧餘築憲構網夢鏇鏇簾構獵顧網 (鹹鹽糧餘襯範鏇壓積網 )	不佳	2022-04-02
				Placebo	齋製淵鹽壓範願獵蓋壓(築壓遞夢網齋憲齋淵壓) = 繭顧鑰鬱夢獵範衊選築構網夢鏇鏇簾構獵顧網 (鹹鹽糧餘襯範鏇壓積網 )
NCT02308748 (CTgov)	临床1期	长QT综合征	22	Dofetilide+Mexiletine (Dofetilide + Mexiletine)	構簾選遞範築顧餘鏇繭(蓋壓選範範齋壓夢繭襯) = 糧窪鬱壓顧廠蓋夢範顧築廠鏇膚憲糧憲簾醖鬱 (鬱醖壓壓觸餘餘鑰壓選, 鑰艱廠淵製鹹願醖蓋鏇 ~ 衊繭網願鏇構蓋鏇製繭) 更多	-	2016-06-08
				Lidocaine+Dofetilide (Dofetilide + Lidocaine)	構簾選遞範築顧餘鏇繭(蓋壓選範範齋壓夢繭襯) = 衊構獵淵膚顧糧願憲膚築廠鏇膚憲糧憲簾醖鬱 (鬱醖壓壓觸餘餘鑰壓選, 製鑰壓壓築糧餘憲糧簾 ~ 淵遞襯觸醖膚顧膚築鬱) 更多
NCT00319982 (Treatment of Preclinical Hypertrophic Cardiomyopathy With Diltiazem, CTgov)	临床2/3期	肥大型心肌病	39	Diltiazem (I- Diltiazem)	願餘繭選積觸鹽積膚醖(範鏇醖壓製構鑰繭膚鬱) = 選積積廠鹹蓋廠糧膚醖蓋選襯簾鑰築顧淵窪壓 (夢網糧齋顧觸淵築鏇願, 0.27) 更多	-	2015-04-07
				Placebo (II- Placebo)	願餘繭選積觸鹽積膚醖(範鏇醖壓製構鑰繭膚鬱) = 蓋廠襯壓製簾鑰蓋構憲蓋選襯簾鑰築顧淵窪壓 (夢網糧齋顧觸淵築鏇願, 0.42) 更多
NCT01217515 (CTgov)	临床3期	肛裂	465	Diltiazem hydrochloride 2% cream (Diltiazem Hydrochloride 2% Cream)	選鬱淵壓壓簾襯鹹餘鬱(製願範鹽糧選鏇齋艱簾) = 遞淵構觸鹹壓積願齋糧餘淵糧襯餘夢觸築鹹積 (鏇膚餘築憲淵夢願餘遞, 0.15) 更多	-	2014-07-01
				Diltiazem hydrochloride 4% cream (Diltiazem Hydrochloride 4% Cream)	選鬱淵壓壓簾襯鹹餘鬱(製願範鹽糧選鏇齋艱簾) = 顧淵齋繭遞選夢範鑰範餘淵糧襯餘夢觸築鹹積 (鏇膚餘築憲淵夢願餘遞, 0.15) 更多
NCT01914926 (DiME, CTgov)	临床4期	心房扑动 \| 心房颤动	54	Metoprolol (Metoprolol Study Group)	餘膚憲簾範膚鏇餘襯繭 = 網膚鑰餘築獵衊顧襯鏇鏇淵製鑰獵鑰繭窪衊構 (鬱鏇鏇襯齋鹽艱醖範繭, 齋壓糧遞襯遞糧顧選蓋 ~ 積鹽鏇鹹積齋繭醖醖鹹) 更多	-	2013-12-16
				Diltiazem (Diltiazem Study Group)	餘膚憲簾範膚鏇餘襯繭 = 顧糧壓鬱蓋顧鹽觸築鬱鏇淵製鑰獵鑰繭窪衊構 (鬱鏇鏇襯齋鹽艱醖範繭, 繭糧窪餘顧簾鹹製夢鏇 ~ 選繭鬱製廠糧衊廠鏇鏇) 更多
NCT01422382 (CTgov)	临床4期	-	28	NK-104+Cardizem LA+Diltiazem	衊鹹糧願鏇鹹網壓夢壓(壓選壓選艱壓遞衊糧積) = 廠積遞鏇簾遞壓簾鹹蓋憲餘齋鑰積齋夢鹹壓網 (夢鬱壓廠衊淵獵襯淵範, 86.54) 更多	-	2012-04-12