Ijaz A. Khan

Electrocardiographic features of hypothermia.

Accessible online at: www.karger.com/crd A 40-year-old homeless man presented on a cold winter night with unconsciousness, and was found to have a core body temperature of 85°F (26 °C). The initial electrocardiogram (ECG) showed sinus bradycardia and prolonged QTc interval (533 ms) as well as prolonged QRS complex which displayed the typical Osborn waves of hypothermia, most pronounced in leads II, III, aVF, and V3–V6 (fig. 1). Laboratory examination revealed normal values of serum electrolytes. After the patient was rewarmed by conventional means (warmed air and infusions) to 98°F (37 °C) an ECG obtained was normal and the Osborn waves had disappeared (fig. 2). No serious cardiac rhythm disturbances occurred during rewarming and the patient survived with no adverse consequences. Hypothermia is defined as a core body temperature ^95°F (35°C). Hypothermia can adversely affect the electrical system of the heart leading to cardiac arrhythmias, Osborn waves, and conduction abnormalities. In the initial stages, sinus tachycardia develops as a part of the stress reaction. As the temperature drops below 90 °F, sinus bradycardia supervenes. Characteristic ECG changes are due to decreased impulse conduction, which results in prolonged intervals, including RR, PR, QRS, and QT (table 1). In addition J point elevation can be seen causing a characteristic Osborne wave that represents distortion of the earliest phase of membrane repolarization. Around 86°F, atrial ectopic activity is often noted, which can progress to atrial fibrillation. With temperatures !86°F, a progressive widening of the QRS complex increases the risk of ventricular fibrillation and below 60 °F asystole supervenes.

Left bundle branch block in type 2 diabetes mellitus: A sign of advanced cardiovascular involvement

Objective:u2003To evaluate left bundle branch block (LBBB) as an indicator of advanced cardiovascular involvement in diabetic (DM) patients by examining left ventricular systolic function and proteinurea.

Brugada and long QT-3 syndromes: Two phenotypes of the sodium channel disease

Brugada and long QT‐3 syndromes are two allelic diseases caused by different mutations in SCN5A gene inherited by an autosomal dominant pattern with variable penetrance. Both of these syndromes are ion channel diseases of the heart manifest on surface electrocardiogram by ST‐segment elevation in the right precordial leads and prolonged QTc interval, respectively, with predilection for polymorphic ventricular tachycardia and sudden death, which may be the first manifestation of the disease. Brugada syndrome usually manifests during adulthood with male preponderance, whereas long QT3 syndrome usually manifests in teenage years, although it can also manifest in adulthood. Class IA and IC antiarrhythmic drugs increase ST‐segment elevation and predilection for polymorphic ventricular tachycardia and ventricular fibrillation in Brugada syndrome, whereas these agents shorten the repolarization and QTc interval, and thus may be beneficial in long QT‐3 syndrome. Beta‐blockade also increases the ST‐segment elevation in Brugada syndrome but decreases the dispersion of repolarization in long QT‐3 syndrome. Mexiletine, a class IB sodium channel blocker decreases QTc interval as well as dispersion of repolarization in long QT‐3 syndrome but has no effect on Brugada syndrome. The only effective treatment available at this time for Brugada syndrome is implantable cardioverter defibrillator, although repeated episodes of polymorphic ventricular tachycardia can be treated with isoproterenol. In symptomatic patients of long QT‐3 syndrome in whom the torsade de pointes is bradycardia‐dependent or pause‐dependent, a pacemaker could be used to avoid bradycardia and pauses and an implantable cardioverter defibrillator is indicated where arrhythmia is not controlled with pacemaker and beta‐blockade. However, the combination of new devices with pacemaker and cardioverter‐defibrillator capabilities appear promising in these patients warranting further study.

Atrial septal aneurysm with multiple atrial septal defects: cribriform atrial septal aneurysm.

septal defect with left-to-right shunt was demonstrated with color Doppler and saline contrast techniques ( fi g. 1, 2 ). No other cardiac abnormality was detected. Magnetic resonance imaging of the heart revealed no other abnormalities in the heart and great vessels except for the atrial septal aneurysm. He underwent a successful surgical repair of the atrial septal defect. Gross exA 28-year-old male presented with complaints of decreased exercise tolerance and palpitations for about a year. He denied light-headedness or syncope associated with his symptom. He smoked one pack a day of cigarettes but denied illegal drug use and alcohol addiction. He denied family history of heart disease and was not on any medication. On physical examination, he appeared mildly obese with no apparent distress. His blood pressure was 124/84 mm Hg with regular heart rate of 88 beats/min. His cardiovascular examination revealed fi xed split second heart sound and a soft ejection systolic murmur at upper left parasternal border. His respiratory examination was normal. There was no clubbing of fi ngers or cyanosis. Electrocardiography showed normal sinus rhythm with borderline fi rst-degree atrioventricular block and occasional premature atrial complexes. Transthoracic echocardiography was performed and showed normal right and left ventricular systolic function. Prominent atrial septal aneurysm was detected. He subsequently underwent transesophageal echocardiography. Atrial septal aneurysm was confi rmed and fenestrated ostium secundum atrial Received: November 11, 2004 Accepted: November 28, 2004 Published online: May 31, 2005