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Related Concept Videos

Antianginal Drugs: Calcium Channel Blockers and Ranolazine01:25

Antianginal Drugs: Calcium Channel Blockers and Ranolazine

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...
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,...
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...
Ischemic Heart Disease: Overview01:17

Ischemic Heart Disease: Overview

Ischemic heart disease occurs when the heart's blood supply dwindles, causing an ominous lack of oxygen and nutrients. This deficiency, stemming from reduced or obstructed blood flow, spells danger, leading to heart muscle damage and dysfunction.
Atherosclerosis, the primary malefactor, orchestrates this dangerous condition. It manifests as the accumulation of fatty deposits, akin to insidious plaques, within arterial walls. As time elapses, these plaques metamorphose, hardening and narrowing...
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 II Agents as β-Adrenergic Blockers01:24

Antiarrhythmic Drugs: Class II Agents as β-Adrenergic Blockers

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 indirectly block calcium...

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Related Experiment Video

Updated: May 8, 2026

Benefits of Cardiac Resynchronization Therapy in an Asynchronous Heart Failure Model Induced by Left Bundle Branch Ablation and Rapid Pacing
12:45

Benefits of Cardiac Resynchronization Therapy in an Asynchronous Heart Failure Model Induced by Left Bundle Branch Ablation and Rapid Pacing

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Ranolazine: effects on ischemic heart.

Andrea Rognoni, Lucia Barbieri, Chiara Cavallino

  • 1Coronary Care Unit and Catheterization Laboratory, "Maggiore della Carita" Hospital, Corso Mazzini 18, 28100 Novara, Italy. arognoni@hotmail.com.

Recent Patents on Cardiovascular Drug Discovery
|August 22, 2013
PubMed
Summary

Ranolazine, an antianginal drug, effectively treats chronic stable angina by improving exercise tolerance and reducing nitroglycerin use. It offers a safe therapeutic option for patients with persistent symptoms or intolerance to other treatments.

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Semi-Minimal Invasive Method to Induce Myocardial Infarction in Rats and the Assessment of Cardiac Function by an Isolated Working Heart System
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Semi-Minimal Invasive Method to Induce Myocardial Infarction in Rats and the Assessment of Cardiac Function by an Isolated Working Heart System

Published on: June 11, 2020

Related Experiment Videos

Last Updated: May 8, 2026

Benefits of Cardiac Resynchronization Therapy in an Asynchronous Heart Failure Model Induced by Left Bundle Branch Ablation and Rapid Pacing
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Benefits of Cardiac Resynchronization Therapy in an Asynchronous Heart Failure Model Induced by Left Bundle Branch Ablation and Rapid Pacing

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08:01

Semi-Minimal Invasive Method to Induce Myocardial Infarction in Rats and the Assessment of Cardiac Function by an Isolated Working Heart System

Published on: June 11, 2020

Area of Science:

  • Cardiology
  • Pharmacology

Background:

  • Coronary artery disease (CAD) is a leading cause of death globally, with angina pectoris being a primary symptom causing emergency visits.
  • Angina pectoris, characterized by chest discomfort, significantly impacts quality of life and functional capacity.
  • Current treatments aim to alleviate symptoms, improve function, and enhance prognosis for angina patients.

Purpose of the Study:

  • To evaluate the efficacy and safety of Ranolazine as an add-on therapy for symptomatic chronic stable angina.
  • To assess Ranolazine's impact on exercise duration, angina episodes, and nitroglycerin use.
  • To review Ranolazine's long-term effects on cardiovascular outcomes and arrhythmias.

Main Methods:

  • Review of short-term and long-term clinical trials and patent research on Ranolazine.
  • Analysis of Ranolazine's mechanism of action, specifically its inhibition of the late sodium current.
  • Assessment of patient-reported outcomes, exercise parameters, and cardiovascular event rates.

Main Results:

  • Ranolazine significantly improves exercise duration and time to angina, while reducing nitroglycerin consumption in chronic stable angina patients.
  • In non-ST segment elevation acute coronary syndromes, Ranolazine did not alter cardiovascular death or myocardial infarction rates but reduced recurrent ischemia.
  • Ranolazine is well-tolerated, with no increased risk of atrial or ventricular arrhythmias despite QTc interval prolongation.

Conclusions:

  • Ranolazine is a valuable therapeutic option for patients with chronic stable angina who remain symptomatic despite optimal therapy or are intolerant to traditional anti-ischemic drugs.
  • Its unique mechanism of action, targeting the late sodium current, provides antianginal benefits without affecting heart rate or blood pressure.
  • Ranolazine demonstrates a favorable safety profile, making it a suitable choice for managing persistent angina symptoms.