Observations on haemodynamic effects of mexiletine

British Heart Journal
|February 1, 1979
PubMed

Insights

Intravenous mexiletine, an antiarrhythmic drug, showed no significant adverse hemodynamic effects in patients with valvular heart disease. Studies indicate mexiletine is safe for patients without heart failure, with only minor pulmonary artery pressure changes observed.

Area of Science:

  • Cardiology
  • Pharmacology

Background:

  • Valvular heart disease can affect cardiovascular hemodynamics.
  • Mexiletine is an antiarrhythmic medication.
  • Understanding the hemodynamic effects of mexiletine in specific patient populations is crucial.

Purpose of the Study:

  • To investigate the hemodynamic effects of intravenous mexiletine.
  • To assess the safety and efficacy of mexiletine in patients with valvular heart disease without heart failure.

Main Methods:

  • A study involving 16 patients with valvular heart disease.
  • Administration of a 150 mg bolus injection of mexiletine to 6 patients.
  • A double-blind trial comparing intravenous mexiletine with intravenous saline in 10 patients.

Main Results:

  • A bolus injection of mexiletine led to plasma concentrations above the therapeutic range for at least 5 minutes.
  • A small but significant increase in mean pulmonary artery pressure was observed.
  • No significant difference in hemodynamic effects was found between mexiletine and saline, with both causing a minor rise in pulmonary artery pressure.

Conclusions:

  • Intravenous mexiletine, at clinically effective doses, does not produce significant adverse hemodynamic effects in patients with valvular heart disease and no heart failure.
  • Mexiletine appears to be hemodynamically well-tolerated in this specific patient group.
  • Further research may explore mexiletine's role in managing arrhythmias in valvular heart disease patients without heart failure.

Related Concept Videos

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 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...
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...
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...
Pharmacodynamics in Geriatric Patients: Effects of Age01:27

Pharmacodynamics in Geriatric Patients: Effects of Age

Age-related pharmacokinetic changes are extensively documented, but understanding age-related pharmacodynamic alterations is relatively limited. This knowledge gap can be partly attributed to the complexity of developing appropriate measures of drug responses compared to bioanalytical methods for determining drug concentrations.Most information regarding age-related differences in human pharmacodynamics originates from cross-sectional studies. However, these studies assume that observed mean...
Pharmacodynamic Models: Linear Concentration–Effect Model01:15

Pharmacodynamic Models: Linear Concentration–Effect Model

The linear concentration–effect model, underpinned by the principle that pharmacological effect (E) is directly proportional to plasma drug concentration (C), emerges as a pivotal simplification of the Emax model for conditions where C is significantly less than EC50. This model portrays a linear trajectory of the concentration–effect relationship when drug levels are markedly below the EC50 threshold.Despite its inherent assumption of continuous effect augmentation with increasing drug...