Thyroid Hormone Plays an Important Role in Cardiac Function: From Bench to Bedside

Thyroid hormones (THs) are synthesized in the thyroid gland, and they circulate in the blood to regulate cells, tissues, and organs in the body. In particular, they exert several effects on the cardiovascular system. It is well known that THs raise the heart rate and cardiac contractility, improve the systolic and diastolic function of the heart, and decrease systemic vascular resistance. In the past 30 years, some researchers have studied the molecular pathways that mediate the role of TH in the cardiovascular system, to better understand its mechanisms of action. Two types of mechanisms, which are genomic and non-genomic pathways, underlie the effects of THs on cardiomyocytes. In this review, we summarize the current knowledge of the action of THs in the cardiac function, the clinical manifestation and parameters of their hemodynamics, and treatment principles for patients with hyperthyroid- or hypothyroid-associated heart disease. We also describe the cardiovascular drugs that induce thyroid dysfunction and explain the mechanism underlying the thyroid toxicity of amiodarone, which is considered the most effective antiarrhythmic agent. Finally, we discuss the recent reports on the involvement of thyroid hormones in the regulation of myocardial regeneration and metabolism in the adult heart.

Lixarit — clinical and pharmaceutical aspects of efficacy and safety of flecainide acetate generic drug

The article considers the use of flecainide, an antiarrhythmic agent. The results of comparing the bioequivalence of Lixarit, flecainide acetate generic drug (flecainide acetate, 100 mg tablets, Laboratorios Normon SA, Spain), and Apocard®, flecainide acetate reference drug (Health Care Ltd, UK, 100 mg tablets), are presented.

Ivabradine is as effective as metoprolol in the prevention of ventricular arrhythmias in acute non-reperfused myocardial infarction in the rat

Ventricular arrhythmias are a major source of early mortality in acute myocardial infarction (MI) and remain a major therapeutic challenge. Thus we investigated effects of ivabradine, a presumably specific bradycardic agent versus metoprolol, a β-blocker, at doses offering the same heart rate (HR) reduction, on ventricular arrhythmias in the acute non-reperfused MI in the rat. Immediately after MI induction a single dose of ivabradine/ metoprolol was given. ECG was continuously recorded and ventricular arrhythmias were analyzed. After 6 h epicardial monophasic action potentials (MAPs) were recorded and cardiomyocyte Ca2+ handling was assessed. Both ivabradine and metoprolol reduced HR by 17% and arrhythmic mortality (14% and 19%, respectively, versus 33% in MI, p < 0.05) and ventricular arrhythmias in post-MI rats. Both drugs reduced QTc prolongation and decreased sensitivity of ryanodine receptors in isolated cardiomyocytes, but otherwise had no effect on Ca2+ handling, velocity of conduction or repolarization. We did not find any effects of potential IKr inhibition by ivabradine in this setting. Thus Ivabradine is an equally effective antiarrhythmic agent as metoprolol in early MI in the rat. It could be potentially tested as an alternative antiarrhythmic agent in acute MI when β-blockers are contraindicated.

Amiodarone-induced vortex keratopathy at a low maintenance dose

Vortex keratopathy is a common side effect of amiodarone, which is a class III antiarrhythmic agent. We describe a 50-year-old man who developed vortex keratopahy with amiodarone 200 mg BD for atrial fibrillation since two years. The daily (400 mg/day) and cumulative dose (100 g) combined with the length of therapy is associated with the toxicity. Toxic effects may also be observed at lower maintenance doses, as observed in this patient. This case indicates that multi-organ toxicity due to amiodarone may develop even with short-term use and a low maintenance dose. Having been off the medication for two months, it is expected that the deposition pattern will diminish, as is the case for the vast majority of patients.

Electrical Cardioversion of Supraventricular Arryhthmia Patient with Septic Shock

Supraventricular arrythmia (SVA) is a very common cardiac rhythm problem experienced by patients in intensive care unit (ICU), which both pharmacological and non-pharmacological treatment could treat. Recently, electrical cardioversion has been proven in improving haemodynamic and functional status. We report a case of 59 years old female patient with VA and septic shock with unstable haemodynamic that was immediately improved after electrical cardioversion. The electrical cardioversion (preferably biphasic) is identified in the patient with an absence of oppositions and is more suitable in combination with antiarrhythmic agent.

Amiodarone-induced diffuse alveolar haemorrhage: a rare but potentially life-threatening complication of a commonly prescribed medication

Amiodarone is an antiarrhythmic agent that is used commonly in clinical practice. It is associated with many side effects, the most common being pulmonary manifestations. Interstitial pneumonitis is one of the most common complications, however rarely amiodarone can cause diffuse alveolar haemorrhage (DAH) too. We describe the case of a 73-year-old woman who presented with shortness of breath and haemoptysis 4 days after starting amiodarone. She was diagnosed with amiodarone-induced DAH based on imaging and bronchoalveolar lavage. She was treated with intravenous and then oral steroids, and amiodarone was discontinued. The patient made a significant clinical and radiological recovery. She was discharged 10 days after her presentation. This case highlights a rare but potentially life-threatening complication of a commonly used medication.