Glucose fluctuations increase the incidence of atrial fibrillation in diabetic rats
Diabetes mellitus (DM) is a major risk factor for cardiovascular diseases such as ischaemic heart disease, heart failure, and arrhythmias. For decades, risk of cardiovascular complications in DM has been believed to correlate with elevated glycated haemoglobin (HbA1c) and fasting glucose levels.1,2 However, several large-scale clinical trials have recently proposed adverse effects caused by intensive glycaemic control. The Action to Control Cardiovascular Risk in Diabetes (ACCORD) trial revealed that intensive glycaemic control targeting a level of glycated haemoglobin <6.0% increased all-cause mortality more than standard therapy targeting 7.0–7.9%, and the study was terminated prematurely.3 The Normoglycemia in Intensive Care Evaluation and Survival Using Glucose Algorithm Regulation (NICE-SUGAR) study also demonstrated that intensive glycaemic control caused high mortality in patients hospitalized in an intensive care unit.4 These results have raised concerns that hypoglycaemic episode could aggravate patient prognosis. Furthermore, a basic research showed that recurrent hypoglycaemic episodes increased mitochondrial free radical release and exacerbated cerebral ischaemic damage.5 In addition, intermittent high glucose exposure exacerbated oxidative stress and apoptosis in endothelial cells.6 On the basis of these observations, we hypothesized that glucose fluctuations may directly affect cardiomyocytes by increasing reactive oxygen species (ROS) levels and predispose to cardiac complications.
Atrial fibrillation (AF) is a common but critical arrhythmia because of the high risk of cerebral thrombosis associated with it. Hypertension, heart failure, hyperthyroidism, and DM are the known major risk factors for AF.7,8 Structural remodelling due to increased cardiac fibrosis by DM was associated with greater atrial arrhythmogenicity in rats.9 Increased fibrosis in myocardium also has been reported in human diabetic hearts.10,11 Because ROS facilitate apoptosis and cardiac fibrosis, glucose fluctuations may aggravate AF in accordance with ROS increase.12,13 In the present study, we investigated whether glucose fluctuations induced by repeated starvation increase the incidence of AF by facilitating atrial fibrosis more than persistent hyperglycaemia. We also explored the mechanisms involved in the observed effects.
Methods
All experimental procedures were performed in accordance with the guidelines of the Physiological Society of Oita University, Japan, for the care and use of laboratory animals, which follow the guidelines established by the U.S. National Institutes of Health.
Haemodynamic parameters and echocardiography
Systolic blood pressure and heart rate were measured using the tail-cuff method. Transthoracic echocardiography (Hitachi Aloka Medical, Ltd, Tokyo, Japan) was then performed at the end of the sequential pattern of glucose fluctuations under anaesthesia by an intraperitoneal injection of a mixture of ketamine (60 mg/kg) and xylazine (10 mg/kg) which was confirmed not to decrease the blood pressure. Measurements included left atrial dimension (LAD), left ventricular (LV) end-diastolic dimension, LV end-systolic dimension, LV fractional shortening (FS), LV ejection fraction (LVEF), and LV end-diastolic posterior wall thickness (LVPWth). We also measured peak early (E) and late (A) transmitral flow velocities. The deceleration time of the mitral E-wave (DcT) was measured from its peak to the time when the descent of the wave intercepted the baseline.
Source: https://academic.oup.com/cardiovascres/article/104/1/5/317328/Glucose-fluctuations-increase-the-incidence-of
Saturday, May 16, 2026
Amantadine: Side Effects, Drug Interactions, And Precautions
Every medication carries the potential for side effects, and Amantadine (amantadine) is no exception. Understanding what side effects are possible, which are common versus rare, and what warning signs warrant medical attention allows patients to use the medication safely and confidently. Most people who take Amantadine as directed tolerate it without major problems, but individual responses vary. Antivirals typically work by interrupting one of several stages in the viral life cycle: preventing the virus from entering host cells, inhibiting the enzymes needed for viral replication, or blocking the assembly and release of new viral particles. Most antivirals are most effective when taken early in the course of infection, before the virus has had time to replicate extensively. For chronic viral infections, long-term antiviral therapy can suppress the virus to undetectable levels and prevent disease progression. The most frequently reported side effects of amantadine are typically mild and often resolve within days to weeks as the body adjusts. Serious side effects occur less frequently but are documented in prescribing information and patient safety guides. Complete side effect information and precautions are listed at https://mednewwsstoday.com/antivirals/amantadine/, which serves as a reliable reference for anyone beginning therapy with Amantadine or monitoring an ongoing treatment. Drug interactions are an important safety consideration for any medication. Amantadine may interact with other prescription drugs, over-the-counter medications, supplements, or certain foods, affecting how it is metabolized or how effective it is. A pharmacist or doctor can review a patient's full medication list to identify any clinically significant interactions before starting Amantadine. Patients should also avoid making changes to their medication regimen without first consulting a healthcare professional. More information on medications used in antiviral medications and how they compare in terms of safety and efficacy is available through the resource at https://mednewwsstoday.com/antivirals/. Staying informed helps patients participate actively in decisions about their care.
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