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Related Concept Videos

Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers01:22

Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers

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Class I antiarrhythmic drugs are used to treat various types of arrhythmias or irregular heart rhythms. These drugs block the sodium (Na+) channels in the cardiac cells, thereby affecting the movement of electrical impulses across the heart. Class I antiarrhythmic drugs are divided into three subgroups: Class IA, Class IB, and Class IC, each with distinct mechanisms of action and effects on the heart.
Class 1A Antiarrhythmic Drugs: These drugs work by moderately blocking sodium channels,...
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Antiarrhythmic Drugs: Class III Agents as Potassium Channel Blockers01:12

Antiarrhythmic Drugs: Class III Agents as Potassium Channel Blockers

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Class III antiarrhythmic drugs are a group of medications that can prolong action potentials in the heart. They achieve this by blocking potassium channels or enhancing inward currents from sodium channels. However, these drugs have a unique property of "reverse use-dependence," which is most pronounced at slower heart rates and can lead to torsades de pointes—a specific type of arrhythmia. However, it is essential to note that excessive QT interval prolongation—a measure of...
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Antiarrhythmic Drugs: Class II Agents as β-Adrenergic Blockers01:24

Antiarrhythmic Drugs: Class II Agents as β-Adrenergic Blockers

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Adrenergic stimulation generally impacts cardiac rate and rhythm. Specifically, stimulation of the β-adrenoceptors triggers an increase in intracellular calcium ion influx and pacemaker currents, which may cause arrhythmias. Catecholamines like adrenaline also demonstrate β2-adrenoceptor-mediated hypokalemia, impacting cardiac action potential and disrupting the normal cardiac rhythm. Class II antiarrhythmic drugs are β-adrenoceptor antagonists or β-blockers, which...
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Antiarrhythmic Drugs: Class IV Agents as Calcium Channel Blockers01:20

Antiarrhythmic Drugs: Class IV Agents as Calcium Channel Blockers

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Class IV antiarrhythmic drugs, such as verapamil and diltiazem, block calcium channels. They primarily affect the heart, slowing the conduction in calcium-dependent tissues like the SA and AV nodes. These drugs manage reentrant supraventricular tachycardia (SVT) and reduce ventricular rate in atrial flutter/fibrillation.
Verapamil, a calcium channel blocker, inhibits calcium movement across myocardial cell membranes and vascular smooth muscle. This results in the dilation of coronary and...
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Antianginal Drugs: Calcium Channel Blockers and Ranolazine01:25

Antianginal Drugs: Calcium Channel Blockers and Ranolazine

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Angina pectoris, a primary symptom of ischemic heart disease, requires careful pharmacological interventions. In this context, calcium channel blockers (CCBs) and ranolazine have emerged as crucial pharmacotherapeutic agents, providing deep insights into the complexities of angina management.
CCBs, a diverse class that includes dihydropyridines (nifedipine) and diphenylalkylamines (verapamil and diltiazem), exert their effect by blocking calcium channels in cardiac and smooth muscle cells. This...
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ECG Interpretation of Arrhythmias II: Atrial, Junctional and Ventricular Arrhythmias01:25

ECG Interpretation of Arrhythmias II: Atrial, Junctional and Ventricular Arrhythmias

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Arrhythmia is a condition characterized by an irregular heart rhythm, with ECG changes that differ based on its origin and nature. The types of arrhythmias discussed below include atrial, junctional, and ventricular arrhythmias.Atrial ArrhythmiasPremature Atrial Complexes (PACs): PACs are early atrial beats caused by stress, caffeine, alcohol, electrolyte imbalances, hypoxia, hyperthyroidism, or certain medications (e.g., bronchodilators and decongestants). The ECG shows early P waves with an...
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Related Experiment Video

Updated: May 5, 2026

The WATCHMAN Left Atrial Appendage Closure Device for Atrial Fibrillation
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Ibandronate and ventricular arrhythmia risk.

Ingrid M Bonilla1, Pedro Vargas-Pinto, Yoshinori Nishijima

  • 1College of Pharmacy.

Journal of Cardiovascular Electrophysiology
|November 22, 2013
PubMed
Summary
This summary is machine-generated.

Ibandronate, used for osteoporosis, may cause heart rhythm problems like ventricular ectopy. This drug-induced proarrhythmia is linked to reduced ion channel current (Ito) and abnormal calcium handling.

Keywords:
Torsade de Pointesbiophosphonatescalciumibandronateion channelslong-QTpharmacologypotassiumproarrhythmia

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Area of Science:

  • Cardiovascular pharmacology
  • Electrophysiology
  • Drug safety

Background:

  • Bisphosphonates, such as ibandronate, are widely prescribed for osteoporosis management.
  • Understanding potential adverse cardiac effects is crucial for patient safety.

Observation:

  • A case report detailed a 55-year-old female experiencing arrhythmia and QT/QTc prolongation after a single ibandronate dose.
  • In vitro and in vivo canine models demonstrated ibandronate-induced repolarization instability and action potential duration prolongation.

Findings:

  • Ibandronate reduced the Ito current and increased early afterdepolarizations (EADs) in myocytes, suggesting proarrhythmic potential.
  • Abnormal intracellular calcium cycling and sarcoplasmic reticulum calcium load were observed.
  • Computational modeling supported that reduced Ito and altered RyR kinetics contribute to ibandronate's proarrhythmic effects.

Implications:

  • Ibandronate may increase susceptibility to ventricular arrhythmias.
  • This suggests a novel mechanism of drug-induced proarrhythmia involving ion channel dysfunction and calcium handling abnormalities.
  • Further research is warranted to fully elucidate the cardiac risks associated with ibandronate.