Obesity, Metabolism, and Atrial Fibrillation

by | Aug 22, 2020 | Uncategorized

Congratulations to members of the McCauley and Darbar labs for publishing this important work in Circulation Arrhythmia and Electrophysiology linking metabolism to ion channel function in atrial fibrillation.  These results will help inform which anti-arrhythmic drugs may be of best use in patients with metabolic syndrome.  See the abstract, graphic, and link below. Ion Channel and Structural Remodeling in Obesity-Mediated Atrial Fibrillation   Mark D. McCauley, Liang Hong, Arvind Sridhar, Ambili Menon, Srikanth Perike, Meihong Zhang, Ivson Bezerra , da Silva, JiaJie Yan, Marcelo G. Bonini, Xun Ai, Jalees Rehman, Dawood Darbar   Background: Epidemiological studies have established obesity as an independent risk factor for atrial fibrillation (AF), but the underlying pathophysiological mechanisms remain unclear. Reduced cardiac sodium channel expression is a known causal mechanism in AF. We hypothesized that obesity decreases Nav1.5 expression via enhanced oxidative stress, thus reducing INa, and enhancing susceptibility to AF. Methods: To elucidate the underlying electrophysiological mechanisms a diet-induced obese mouse model was used. Weight, blood pressure, glucose, F2-isoprostanes, NOX2 (NADPH oxidase 2), and PKC (protein kinase C) were measured in obese mice and compared with lean controls. Invasive electrophysiological, immunohistochemistry, Western blotting, and patch clamping of membrane potentials was performed to evaluate the molecular and electrophysiological phenotype of atrial myocytes. Results: Pacing-induced AF in 100% of diet-induced obese mice versus 25% in controls (P<0.01) with increased AF burden. Cardiac sodium channel expression, INa and atrial action potential duration were reduced and potassium channel expression (Kv1.5) and current (IKur) and F2-isoprostanes, NOX2, and PKC-α/δ expression and atrial fibrosis were significantly increased in diet-induced obese mice as compared with controls. A mitochondrial antioxidant reduced AF burden, restored INa, ICa,L, IKur, action potential duration, and reversed atrial fibrosis...

Amy Writes for the Hinsdalean and Life in the Woodlands

by | Oct 3, 2019 | Uncategorized

Congratulations to my wife Amy for her first newspaper article in the Hinsdalean ! She is writing for the Hinsdale newspaper and also for a local magazine Life in the Woodlands.   A link to her first article is here:  There’s No Taste Like Home    Also, here’s a link to her blog: Maison McCauley Congrats and much love !...

Scientific Work Linking Obesity and Atrial Fibrillation

by | Oct 1, 2019 | Uncategorized

I am pleased to share that our work linking obesity and atrial fibrillation won the Paul D. White Award for the Best Abstract in the United States at the American Heart Association Basic Cardiovascular Sciences Session in Boston, MA. Congrats to the entire team for a job well done...

News: The McCauley ECG Course Launches Online

by | Aug 29, 2019 | Uncategorized

I am pleased to announce that the McCauley ECG Course has officially launched online.  This course is specifically geared towards the needs of students (medical, nursing, health professions, industry) in learning how to interpret electrocardiograms (ECG).  I created this course because I found no resources, either in books or online, that specifically targets the needs of students for board exams and clinical rotations.  What makes this course different is the organized top-to-bottom workflow for reading ECGs, highlighted real-time frames showing which parts of the ECG to focus on, and clinical case correlations, which bring the clinical relevance of each ECG into focus.  This course is what I was looking for as a medical student, but could never find.  In short, if you’re wondering which ECG resource to use for your basic science and clinical rotations, this is it  !  Click on the image below to get started....

Device Guidelines for Patients with Genetic Heart Disease: Pacemakers

by | Dec 20, 2016 | Uncategorized

Device Guidelines for Patients with Genetic Heart Disease:  Pacemakers   Permanent Pacemaker (2008 guidelines)   Long QT Syndrome (LQTS) Class IIa Permanent pacing is reasonable for high-risk patients with congenital long-QT syndrome.  Class III Permanent pacing is not indicated for frequent or complex ventricular ectopic activity without sustained VT in the absence of the long-QT syndrome.   Hypertrophic Obstructive Cardiomyopathy (HoCM) Class I Permanent pacing is indicated for SND or AV block in patients with HCM as described previously. Class IIb Permanent pacing may be considered in medically refractory symptomatic patients with HCM and significant resting or provoked LV outflow tract obstruction. As for Class I indications, when risk factors for SCD are present, consider a DDD ICD Class III Permanent pacemaker implantation is not indicated for patients who are asymptomatic or whose symptoms are medically controlled. Permanent pacemaker implantation is not indicated for symptomatic patients without evidence of LV outflow tract obstruction.     HOCM Guidelines (2011) Class IIa In patients with HCM who have had a dual-chamber device implanted for non-HCM indications, it is reasonable to consider a trial of dual-chamber atrial-ventricular pacing (from the right ventricular apex) for the relief of symptoms attributable to LVOT obstruction. Class IIb Permanent pacing may be considered in medically refractory symptomatic patients with obstructive HCM who are suboptimal candidates for septal reduction therapy. Class III: No Benefit Permanent pacemaker implantation for the purpose of reducing gradient should not be performed in patients with HCM who are asymptomatic or whose symptoms are medically controlled. Permanent pacemaker implantation should not be performed as a first-line therapy to relieve symptoms in medically refractory...