by Mark | 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...
by Mark | Mar 14, 2020 | Uncategorized
Due to the severe disruptions to medical student classroom learning as a result of the COVID pandemic, we will be offering the McCauley ECG course free online at YouTube for the next month. Each week, we will post a new series of lectures until all lectures are available online by the end of the month. Stay healthy and enjoy the videos...
by Mark | 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 !...
by Mark | 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...
by Mark | 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....
by Mark | Aug 28, 2019 | Cardiac Electrophysiology, Cardiology, General Public, Science
I am excited to announce that work from our laboratory was recently published in Circulation: Arrhythmia and Electrophysiology, as an Editor’s Choice Article. In this work, we show for the first time that the native electrical signal in the heart can be transferred from one region to another with a surgical suture made from carbon nanotube fibers (CNTf). The CNTf sutures have remarkable electrical conductivity, strength, and flexibility and are the first to be used in surgical applications to restore electrical conduction in the heart. The long-term impact of this work is that the reestablishment of cardiac conduction has the potential to revolutionize therapy for cardiac electrical disturbances, one of the most common causes of death in the United States. Link to the article can be found here: In Vivo Restoration of Myocardial Conduction with Carbon Nanotube Fibers. News media coverage can be found here: Physics World, Nanotechnology News, Phys.Org, Today’s Medical...
by Mark | 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...
by Mark | Dec 13, 2015 | Cardiac Electrophysiology, Cardiology, General Public
What is AVNRT? Rapid beating of the heart can cause the sensation of palpitations, which are often described as fluttering, pounding, and beating sensations in the chest. Sometimes these palpitations are rapid enough to affect other parts of the body, and people with palpitations may also describe feelings of lightheadedness, fatigue, and shortness of breath. Occasionally, these palpitations are rapid enough to cause people to pass out (syncope), though this is rare. Rapid palpitations may come from the heart’s upper chambers, the atria, and in most cases, are not generally considered life threatening (although rare exceptions do exist). Alternatively, palpitations may come from the heart’s lower chambers, the ventricles, which in some cases may be life-threatening. Also, the natural electrical “bridge” between the atria and ventricles, the atrio-ventricular (AV) node, can be a common site of arrhythmias causing palpitations. The best way to start the diagnosis of the cause of palpitations is to have an electrocardiogram (ECG) read by a physician experienced in heart rhythm disorders. Supraventricular tachycardia (SVT) is a category of arrhythmias that come from above the ventricles. The most common type of regular SVT is AtrioVentricular Nodal Reentrant Tachycardia (AVNRT), and is responsible for 50% of SVT cases (1). AVNRT is more common in women than men, and typically occurs in patients between 20 and 40 years old. This long, descriptive arrhythmia name details the biology of the abnormal electrical circuit within the heart that leads to the palpitations that are commonly described. In AVNRT, there is a small circular (Reentrant) electrical circuit that “spins” around in the AV node, the normal, natural electrical bridge between the atria and ventricles....
by Mark | Oct 1, 2015 | Cardiac Electrophysiology, Cardiology, Science
Indications for Pacemaker (Class I and IIa/b Recommendations) Sinus node dysfunction (SND) with symptomatic bradycardia Symptomatic chronotropic incompetence Required drug therapy causing symptomatic bradycardia SND with HR < 40 bpm; bradycardia and symptom connection unclear Unexplained syncope and EP study (+) for SND Conisder for minimal symptoms but HR < 40 bpm while awake Type II second-degree AV block, or complete third-degree AV block with: Bradycardia + symptoms Arrhythmias + required bradycardic meds Asymptomatic awake with pauses > 3 sec, Asymptomatic awake with v-rate < 40 bpm, Asymptomatic awake with infra-His conduction Asymptomatic awake with AF and > 5 sec pauses After catheter ablation of AV junction Post-operative AVB not expected to resolve Neuromuscular: myotonic dystrophy, Kearns-Sayre, Erb dystrophy, peroneal muscular atrophy Symptomatic bradycardia + second-degree AVB Asymptomatic bradycardia + type II second-degree AVB (narrow or wide QRS) Asymptomatic second-degree AVB at intra or infra His level on EP study Asymptomatic complete third-degree AVB with: V-rate < 40 bpm LV dysfunction Site of block below AV node Reasonable in V-rate > 40 and persistent First or Second Degree AVB with: Pacemaker syndrome Hemodynamic compromise Muscular dystrophy of any AV block, with or without symptoms Recurrence of AVB is expected after offending drug is withdrawn Advanced second-degree AVB or third-degree AVB Type II 2nd degree AVB Alternating Bundle Branch Block Syncope of unknown type after exclusion of other causes including VT HV > 100 msec, even if asymptomatic EP study with infra-Hisian block, even if non-physiological After STEMI with: persistent 2nd/3rd DAVB regardless of symptoms, transient infranodal AVB Carotid sensitivity causing syncope and ventricular asystole > 3 sec Hypersensitive cardioinhibition >...
by Mark | Sep 29, 2015 | Cardiology, Science
Constrictive Pericarditis Pathology of constriction: Thick scarred pericardium equalizes 4 chamber pressure, limits ventricular filling, reduces cardiac volume. JV pressure wave form in constriction: rapid ventricular (RV) filling causes rapid Y-descent Then, diastolic filling stops abruptly, causing a dip and plateau diastolic RV waveform Causes of constriction: Mediastinal radiation Chronic idiopathic pericarditis Cardiac surgery Tuberculous pericarditis Signs & Symptoms of Constriction: R-sided heart failure: JVD, hepatic congestion, ascites, peripheral edema Clear lungs Exercise intolerance, muscle wasting, cardiac cachexia Jugular veins with prominent X and Y descent Y descent may look like JV pulse is “falling away” from you Respiratory increase in jugular venous pressure (Kussmaul’s sign) Pericardial knock (high-pitched early diastolic sound) Imaging of Pericardial Constriction: CT with thickening +/- calcification of the pericardium CT/MRI preferred modalities to evaluate pericardial thickening Echo may show systolic discordance of LV/RV pressures, ventricular interdependence In constriction, cath of LV and RV will show discordance of LV and RV pressures Differential Diagnosis of Pericardial Constriction: Restrictive cardiomyopathy RCM and Constriction both have Kussmaul’s sign, RV cath “dip and plateau” sign in early diastole Whereas RCM has no significant respiratory mitral variation, Constriction has marked variation of mitral inflow (>25%) and hepatic flow Whereas RCM has early reduced diastolic mitral annular velocity (Ea), Constriction has normal Ea velocities Whereas RCM is associated with pulmonary congestion, Constriction usually has clear lungs Whereas RCM has a reduced mitral annular diastolic velocity < 8 cm/s, Constriction has mitral annular diastolic velocity > 8 cm/s Whereas RCM shows ventricular concordance on simultaneous LV/RV cath, Constriction has ventricular discordance on simultaneous LV/RV cath Cardiac Tamponade Constriction and Tamponade both have elevated JVP, Kussmaul’s sign, pulsus...
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