Atrial fibrillation is a common manifestation seen in patients with hyperthyroidism and thyroid storm. The presence of excess thyroid hormone (TH) alters adrenergic receptors in the heart and blood vessels, thereby causing an increase in sympathetic function and atrial fibrillation as a sequela of this excess circulating hormone. Excess thyroid hormone (T3) shortens the action potential of cardiomyocytes in the pulmonary vein, which facilitates the generation of reentrant circuits causing atrial fibrillation. Thyroid hormone can regulate cardiac beta-adrenergic receptor expression leading to enhanced catecholamine sensitivity of betaadrenergic coupled cardiac response. We present a case of a 64-year-old female with a history of hypertension (HTN), nonobstructive coronary artery disease (CAD), congestive heart failure (CHF) [ejection fraction (EF) 35-40%], chronic obstructive pulmonary disease (COPD) on long-term oxygen therapy (LTO2), obstructive sleep apnea (OSA)/hypoventilation syndrome, atrial flutter/atrial fibrillation with a loop recorder on rivaroxaban, and obesity who presented to the emergency department (ED) with gastroenteritis symptoms precipitating difficulty breathing and atrial fibrillation with a rapid ventricular response (HR 140-150) requiring ICU admission for rate and rhythm control. During the course of hospitalization, she was treated with an amiodarone infusion, which induced thyrotoxicosis and increased the ectopic electrical activity in the atrium, worsening atrial fibrillation. On day 3, amiodarone was stopped, and IV esmolol and metoprolol tartrate PO were continued with no resolution of atrial fibrillation. The patient was transitioned to propranolol, which achieved adequate heart rate control prior to discharge. The aim of our review is to highlight that propranolol should be used over metoprolol in patients with hyperthyroidism-induced atrial fibrillation due to the effect of propranolol on blocking the activity of T4 conversion to active T3 and, as such, blocking its effect on cardiac myocytes, terminating reentrant atrial excitation.
Wellens' syndrome is well-known for its critical stenosis of the proximal left anterior descending artery (LAD) with characteristic electrocardiographic findings of biphasic or deeply inverted T waves in V2-V6 under specific diagnostic criteria. Although the syndrome is known as a high-grade LAD lesion, its sequence of events can also be seen with the right coronary artery (RCA) and the left circumflex artery (LCX). This systemic review attempts to expand on these findings while analyzing the prevalence of Wellens' syndrome with the RCA and/or the circumflex artery. This study also comparatively indicated that Wellens' syndrome is seen in RCA and circumflex artery stenoses when present; the indication of the same medical management is warranted for effective treatment and survival. We extracted and analyzed 24 case reports each with an atypical presentation of acute coronary syndrome (ACS) and specific Wellens' syndrome pattern of electrocardiogram (ECG) presentation with critical stenosis in the LAD, RCA, and left circumflex artery. The risk of bias assessment was undertaken using internal risk analysis by utilizing medical libraries and certain search phrases to find research articles with the involvement of the LAD as opposed to the RCA and LCX in Wellens' syndrome. Based on the number of respective primary research articles found, a bias calculation was done on the reported respective coronary artery involvement.The finding of our systemic review confirms that Wellens' syndrome is a precordial lead disease with T wave abnormalities that present with critical stenosis of not only the LAD but also the RCA and circumflex artery.The result of our systemic review affirmed that although most Wellens' syndrome cases reported involve the stenosis of the LAD, the critical occlusion of the RCA and/or the circumflex artery was found with Wellens' syndrome pattern of ECG presentation, meaning that the sequence of events is not limited to the proximal LAD.
Atrial fibrillation (AFib) is a common type of cardiac arrhythmia, characterized by disorganized atrial electrical activity with features of irregularly irregular heart rhythm and often with rapid ventricular response increasing the risk of stroke and heart failure due to tachyarrhythmia. The pathophysiology mechanism of AFib is either triggered by atrial distension, abnormality in conducting system, catecholamine excess, or increased atrial irritation or automaticity. Risk factors include uncontrolled diabetes, obesity, obstructive sleep apnea, hypothyroidism, and certain stimulants. Based on recent research, liver disease has recently been identified as a risk factor for AFib. Considering the progression of chronic liver disease, this literature review aims to investigate and summarize the relationship between liver disease and AFib and explore clinical interventions that can be utilized to prevent AFib aggravation.
Cardiomyopathy is a disease of the cardiomyocytes that affects their structural function, leading to heart failure (HF). Non-ischemic cardiomyopathy (NICM) includes a subtype of dilated cardiomyopathy (DCM), restrictive cardiomyopathy (RCM), and hypertrophic cardiomyopathy (HCM). These types of cardiomyopathies have no coronary artery vessel involvement. The most common cause of NICM is DCM. In the ischemic cardiomyopathy (ICM) subtype, the utilization of implantable cardioverter-defibrillators (ICDs) has been effective in the prevention of sudden cardiac death (SCD). However, the relevance of ICDs in patients with NICM having an ejection fraction (EF) ≤35%, who are also receiving effective quadruple therapy (i.e., angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARB), beta-blockers, mineralocorticoid receptor antagonists, and sodium-glucose cotransporter-2 (SGLT2) inhibitors) for HF has been a topic of debate. The purpose of this review is to analyze the benefits of preventive ICDs in NICM patients on adequate quadruple therapy for HF. The current guidelines recommend ICD implantation in patients with NICM who have a left ventricular ejection fraction of ≤35%, come under the New York Heart Association (NYHA) class II or III, and are in sinus rhythm with optimal medical therapy. The evidence supporting this recommendation is limited. Numerous clinical studies and meta-analyses have been conducted to look into this issue. While some have discovered a substantial decrease in mortality with the implantation of an ICD in patients with NICM, others have not found significant changes. Thereby, further investigations are required to define the function of ICDs in this population.
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