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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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Cardiac Action Potential01:30

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Cardiac action potentials are essential for proper heart function, enabling the rhythmic contractions needed for adequate blood circulation. Nodal cells and Purkinje fibers, specialized for electrical conduction, generate these action potentials.
The cardiac action potential process involves a series of phases characterized by the movement of ions across the cardiac cell membranes, leading to the depolarization and repolarization of the cardiac myocytes.
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Dysrhythmias VI: Management of Dysrhythmias01:25

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Dysrhythmia management involves a multifaceted approach, incorporating pharmacological treatments, medical procedures, surgical interventions, lifestyle modifications, and patient education.Pharmacological ManagementAntiarrhythmic Drugs:Class I (Sodium Channel Blockers): This class includes quinidine and procainamide, which reduce the speed of impulse conduction in the heart, stabilize the cardiac membrane, and control arrhythmias. Quinidine and procainamide are Class IA agents that prolong the...
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Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers01:22

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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 IV Agents as Calcium Channel Blockers01:20

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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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Antiarrhythmic Drugs: Class II Agents as β-Adrenergic Blockers01:24

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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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Defining Cardiomyocyte Repolarization Response to Pharmacotherapy in Long-QT Syndrome Type 3.

Ning Ge1,2, Rui Li3, Min Liu4

  • 1Regenerative Medicine Institute, School of Medicine University of Galway Galway Ireland.

Journal of the American Heart Association
|October 8, 2024
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Summary

This study developed patient-specific models of Long-QT syndrome type 3 (LQT3) using human induced pluripotent stem cell-derived cardiomyocytes. These models accurately replicate LQT3 characteristics and can be used for drug testing and personalized treatment strategies.

Keywords:
CRISPR/Cas9SCN5Ahuman induced pluripotent stem cellslong‐QT syndromemultielectrode array

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Area of Science:

  • Cardiovascular Medicine
  • Genetics
  • Stem Cell Biology

Background:

  • Long-QT syndrome (LQT3) is a cardiac ion channelopathy causing ventricular arrhythmias due to delayed repolarization.
  • Current disease modeling approaches have limitations in recapitulating patient-specific LQT3 characteristics.

Purpose of the Study:

  • To establish patient-specific human induced pluripotent stem cell (hiPSC)-derived cardiomyocyte models for LQT3.
  • To utilize these models for disease mechanism exploration and drug screening.

Main Methods:

  • Generated hiPSCs from an LQT3 patient with an SCN5A variant and a healthy control.
  • Used CRISPR/Cas9 gene editing to create an isogenic LQT3 model in healthy control hiPSCs.
  • Differentiated hiPSCs into cardiomyocytes for electrophysiological assessments.

Main Results:

  • Both patient-derived and genetically engineered LQT3 cardiomyocytes exhibited prolonged repolarization.
  • Mexiletine (NaV1.5 blocker) shortened repolarization in LQT3 models but not controls.
  • Calcium channel blockers (nifedipine, verapamil) rescued the LQT3 phenotype in a dose-dependent manner.

Conclusions:

  • Patient-derived and engineered LQT3 hiPSC-derived cardiomyocytes faithfully model LQT3.
  • This in vitro model aids in exploring novel therapies and stratifying drug risks.
  • Facilitates a personalized, targeted treatment approach for high-risk LQT3 patients.