ABSTRACT
Magnesium is an important co-factor that helps regulates the movement of ions through voltage-mediated channels within myocardial tissues by the membrane sodium-potassium pump, and its deficiency can reduce the pump's activity, leading to partial depolarization and changes in the activity of many potential-dependent membrane channels leading to arrhythmias. In this case report, we are looking to establish the direct relationship between hypomagnesemia caused by proton pump inhibitors (PPIs), which could lead to cardiac arrhythmias. Here, we present a 45-year-old Hispanic female, with a known past medical history of supraventricular tachycardia (SVT), hiatal hernia on proton pump inhibitor (PPI), and chronic smoking, who presented to the emergency department complaining of dizziness and palpitations that started two hours prior arrival to the hospital. At triage, the patient was found to have a heart rate of 190 beats per minute (bpm), and an electrocardiogram (EKG) revealed supraventricular tachycardia with a heart rate of 185 bpm. During the review of this case, no other confounding factors besides hypomagnesemia were noted, leaving this one to be the most likely cause of the arrhythmia. Patients on long-term PPI therapy are at higher risk of developing hypomagnesemia, which could lead to cardiac arrhythmia.
ABSTRACT
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.
ABSTRACT
Several prospective epidemiological studies have shown that there is a clear inverse relationship between serum high-density lipoprotein-cholesterol (HDL-C) concentrations and risk for coronary heart disease (CHD), even at low-density lipoprotein-cholesterol (LDL-C) levels below 70 mg/dL. However, more recent evidence from genetic studies and clinical research has come to challenge the long-standing notion that higher HDL-C levels are always beneficial, while lower HDL-C levels are always detrimental. Thus, it becomes apparent that HDL functionality plays a much more important role in atheroprotection than circulating HDL-C levels. HDL cholesterol efflux capacity (CEC) from macrophages is a key metric of HDL functionality and exhibits a strong inverse association with both carotid intima-media thickness and the likelihood of angiographic coronary artery disease (CAD), independent of the HDL-C level. Thus, extensive research is being conducted to identify new agents with a favorable side effect profile, which would be able to enhance CEC, improve HDL functionality and potentially decrease cardiovascular risk. This review aims to present and discuss the current clinical and scientific evidence pertaining to the significance of HDL functionality over the actual HDL-C concentration in mediating the favorable effects on the cardiovascular system. Thus, we conducted a PubMed search until December 2017 through the English literature using the search terms 'HDL function/functionality', 'HDL properties', 'cardiovascular risk' and 'cholesterol efflux capacity'. We also included references from the articles identified and publications available in the authors' libraries.
