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Related Concept Videos

Mechanism of Cardiac Arrhythmias01:28

Mechanism of Cardiac Arrhythmias

Arrhythmias are irregular heart rhythms occurring when the heart's electrical impulses become abnormal. These disturbances can lead to various symptoms, depending on their severity and the underlying cause. Some common factors contributing to arrhythmias include hypoxia, ischemia, electrolyte imbalances, excessive catecholamine exposure, drug toxicity, and muscle overstretching. Arrhythmias can be classified into two main types based on the rate and site of origin of abnormal heart rhythms.
Antihypertensive Drugs: Action of Calcium Channel Blockers01:18

Antihypertensive Drugs: Action of Calcium Channel Blockers

Calcium ions are essential to contract smooth muscle cells in blood vessels. They enter these cells through voltage-dependent calcium channels, specifically L-type calcium channels in the cell membrane. These L-type calcium channels are integral to the excitation-contraction coupling process in smooth muscle. When a stimulus is received by smooth muscle cells, their membrane depolarizes. This alteration in membrane potential instigates the opening of L-type calcium channels. As a result,...
Antiarrhythmic Drugs: Class IV Agents as Calcium Channel Blockers01:20

Antiarrhythmic Drugs: Class IV Agents as Calcium Channel Blockers

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

Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers

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,...
G-Protein Gated Ion Channels01:21

G-Protein Gated Ion Channels

GPCRs are primarily responsible for our sense of smell, taste, and vision.  The binding of a sensory stimulus activates GPCR to stimulate effector proteins, many of which are ion channels in the sensory organs. GPCRs modulate the opening and closing of the target ion channels either directly by binding them, or by releasing second messengers that activate these channels. As ions move across the membrane, the membrane potential is altered, which induces an appropriate response.
Sensory organs,...
Antiarrhythmic Drugs: Class III Agents as Potassium Channel Blockers01:12

Antiarrhythmic Drugs: Class III Agents as Potassium Channel Blockers

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 the heart's...

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Assessment of Myofilament Ca2+ Sensitivity Underlying Cardiac Excitation-contraction Coupling
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Modifying L-type calcium current kinetics: consequences for cardiac excitation and arrhythmia dynamics.

Aman Mahajan1, Daisuke Sato, Yohannes Shiferaw

  • 1UCLA Cardiovascular Research Laboratory, Division of Molecular Medicine, Department of Anesthesiology, David Geffen School of Medicine at UCLA, Los Angeles, California, USA.

Biophysical Journal
|December 28, 2007
PubMed
Summary

Modifying the L-type calcium current (I(Ca,L)) shape, rather than blocking it, can prevent ventricular fibrillation. This strategy enhances dynamic wave stability without reducing cardiac contractility, offering a promising antifibrillatory approach.

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Area of Science:

  • Cardiovascular Physiology
  • Cardiac Electrophysiology
  • Computational Biology

Background:

  • The L-type calcium current (I(Ca,L)) is crucial for cardiac function but also implicated in ventricular fibrillation.
  • Current strategies to prevent ventricular fibrillation by blocking I(Ca,L) often depress cardiac contractility.

Purpose of the Study:

  • To investigate whether modifying the kinetic properties of I(Ca,L) can yield antifibrillatory effects without compromising contractility.
  • To explore a novel therapeutic strategy for preventing ventricular fibrillation.

Main Methods:

  • Overexpression of a mutant Ca-insensitive calmodulin (CaM(1234)) in rabbit ventricular myocytes to alter I(Ca,L) inactivation.
  • Pharmacological interventions (pinacidil or verapamil) to modulate action potential duration (APD).
  • Development and application of a new action potential model for cellular and tissue simulations.

Main Results:

  • Experimental manipulation of I(Ca,L) kinetics prevented APD alternans and flattened the APD restitution slope.
  • Simulations showed that altered I(Ca,L) prevented spatially discordant alternans and spiral wave breakup in cardiac tissue.
  • Contractility was preserved in myocytes with modified I(Ca,L) kinetics, unlike with traditional blockers.

Conclusions:

  • Targeting I(Ca,L) kinetics offers a potential antifibrillatory strategy that avoids the negative inotropic effects of direct blockade.
  • This approach may enhance dynamic wave stability in cardiac tissue, providing a promising avenue for treating cardiac arrhythmias.