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Cardiovascular Drugs during Pregnancy
Published in “Bert” Bertis Britt Little, Drugs and Pregnancy, 2022
Moricizine is used to treat ventricular tachycardia. According to the manufacturer, the drug is not associated with an increased frequency of birth defects in rodents exposed to the drug during organogenesis. Moricizine is an FDA category B drug.
Cardiovascular Drugs
Published in Radhwan Nidal Al-Zidan, Drugs in Pregnancy, 2020
Risk Summary: Although Moricizine has been assigned with the letter (B), according to the FDA categorization, but it should be used with caution because no human data is available and the reproduction studies in animals have shown low risk.
Pharmacokinetic-Pharmacodynamic Relationships of Cardiovascular Drugs
Published in Hartmut Derendorf, Günther Hochhaus, Handbook of Pharmacokinetic/Pharmacodynamic Correlation, 2019
There may be more information on the pharmacokinetic-pharmacodynamic relationships of cardiovascular drugs such as digoxin, beta-blockers, and antiarrhythmic agents than any other group of drugs. Over the past 25 years, the development of sensitive analytical methods to measure the small amounts of drugs in plasma and other biological fluids has provided a tremendous stimulus to the study of pharmacokinetics. However, our ability to measure pharmacologic response of drugs has not progressed nearly as fast. While it is possible to readily measure several different cardiovascular effects (e.g., heart rate, blood pressure, electrocardiographic parameters, etc.), they are often only surrogate effects which may or may not be good predictors of the ultimate therapeutic response that is sought. The best example is measuring the suppression of premature ventricular depolarizations (PVDs) on the electrocardiogram to predict the long-term efficacy of antiarrhythmic agents in patients with ischemic heart disease. Based on the increased mortality in patients with PVD suppression produced by encainide, flecainide, and moricizine, compared to placebo, the results of the Cardiac Arrhythmia Suppression Trial (CAST) have dramatically demonstrated the limitation of this particular surrogate measure to predict sudden cardiac death.3,4
Precision medicine in cardiac electrophysiology: where we are and where we need to go
Published in Expert Review of Precision Medicine and Drug Development, 2020
Ashish Correa, Syed Waqas Haider, Wilbert S. Aronow
From the 1960s through the 1980s, arrhythmia management rested on anti-arrhythmic drugs. However, over time, there was gradual recognition that any putative benefits brought on by these drugs were counterbalanced by various adverse effects, particularly pro-arrhythmic effects. The first major trial to demonstrate this was the Cardiac Arrhythmia Suppression Trial I (CAST I) in 1989 which randomized post-myocardial infarction patients to either antiarrhythmic therapy (with Class I agents flecainide, encainide, and/or moricizine) or placebo to analyze reduction sudden cardiac death (SCD) by malignant arrhythmias [1]. The trial had to be stopped early, because while the drugs did reduce premature ventricular contractions (PVCs) and non-sustained ventricular tachycardias (NSVT), they demonstrated a significant increase in mortality, primarily by pro-arrhythmic effects. This trial was followed by several other trials assessing anti-arrhythmics for the primary prevention of SCD, particularly in heart failure (HF) and post-myocardial infarction patients. These largely demonstrated no benefit, and sometimes even harm [2–4]. For atrial fibrillation (AF) and atrial flutter, apart from beta-blockers, calcium channel blockers, and the Class III agent amiodarone, very few anti-arrhythmic agents have shown long-term benefits. One notable exception is dofetilide, which was shown to be effective in cardioverting patients, both with and without concomitant HF, to sinus rhythm and in maintaining sinus rhythm [5,6].
Current pharmacotherapeutic strategies for cardiac arrhythmias in heart failure
Published in Expert Opinion on Pharmacotherapy, 2020
Ashish Correa, Yogita Rochlani, Wilbert S. Aronow
In the past, there was a great interest in the use of pharmacotherapy for the prevention of SCD from malignant arrhythmias, and antiarrhythmics were frequently used for this purpose. However, over the years, antiarrhythmics fell out of favor due to their proarrhythmic adverse effects. To a large extent, this began with CAST I which assessed the post-myocardial infarction (MI) population and randomized post-MI patients to either antiarrhythmic therapy (flecainide, encainide, and/or moricizine) or placebo for the suppressions of PVCs and NSVT to prevent SCD by malignant arrhythmias [61]. Most unexpectedly, while these agents indeed suppressed these arrhythmias, they significantly increased mortality, primarily by their proarrhythmic effects. In fact, the trial was stopped early for this reason. The conclusions of this trial can be extrapolated to the HF population. Additionally, Class I antiarrhythmics are avoided in HF due to their effects of blood pressure [66,67]. In subsequent years, many other trials were conducted to evaluate Class III antiarrhythmics for arrhythmia suppression in post-MI or in HF, and the trials either showed no benefit or actual harm [59,69,70].