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, June 13, 2026
Treating Depression With Topamax: Key Facts
When a person is diagnosed with depression or seeks relief from it, selecting the most appropriate medication requires weighing multiple factors: the severity of symptoms, the patient's age and health history, and whether other medications are already being taken. A thoughtful treatment choice improves outcomes and reduces unnecessary side effects. Antiepileptic drugs, also known as anticonvulsants or antiseizure medications, work through a variety of mechanisms to reduce the frequency and severity of seizures. Common mechanisms include blocking voltage-gated sodium channels to stabilize over-excited neurons, enhancing the inhibitory effects of GABA, and reducing excitatory glutamate transmission. Some drugs extend GABA-mediated inhibition while others block high-frequency neuronal firing specifically. The right medication depends on seizure type, epilepsy syndrome, patient age, and comorbidities. Among the medications available for seizure and epilepsy treatment, Topamax provides a well-studied option that many patients discuss with their doctors. The clinical evidence supporting topamax for depression shows that it can be effective for managing this condition when used appropriately under medical supervision. Topamax contains the active ingredient topiramate, which works by acting on the biological pathways responsible for producing the symptoms associated with depression. Understanding the mechanism helps patients appreciate why consistent use is often more effective than taking it only when symptoms become severe, as maintaining steady levels allows for more stable control. Patients managing depression long-term should keep regular follow-up appointments to assess whether their treatment plan is still the best fit for their situation. As conditions change and new evidence emerges, treatment adjustments may be worthwhile. The https://mednewwsstoday.com/seizures/ resource section provides a helpful reference for staying current on medication options in this area.
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