The surface electrocardiogram (ECG) can provide many clues to a patient’s underlying medical condition or tendency for arrhythmogenesis. An 80-year-old man with severe aortic stenosis and an implantable cardioverter-defibrillator (ICD) for advanced heart block presented with burping, chest discomfort and intermittent pounding sensations. His ECG showed atrial fibrillation with intermittent ventricular pacing at 60 bpm characterized by irregularly irregular rhythm, absent P waves, narrow intrinsic QRS complexes alternating with wide-paced beats (left bundle branch block [LBBB] morphology, superior axis) and visible pacing spikes. Device interrogation revealed ventricular tachycardia (VT) storm with multiple appropriate ICD shocks explaining his pounding sensations. This report highlights two key teaching points: recognizing atrial fibrillation during ventricular pacing—a frequently missed diagnosis affecting nearly half of patients with pacemakers—and managing VT storm to reduce shock burden. After device reprogramming and antiarrhythmic adjustment, the patient became asymptomatic.

Human ; Male ; Aged: 65-79 Yrs Old ; Thorax ; Teaching ; Tachycardia, Ventricular ; Electrocardiography ; Atrial Fibrillation ; Bundle-branch Block ; Constriction, Pathologic

CLINICAL PRESENTATION: This report describes a case of a 24-year-old, acyanotic, female patient presenting with mild effort dyspnea, a right ventricular heave, a displaced cardiac apex, a loud single S2, a holosystolic murmur on the left parasternal area, and a continuous murmur at the left posterior chest. Transthoracic and transesophageal echocardiography demonstrated dilated left atrium and ventricle, hypertrophied right ventricle and a large ventricular septal defect with overriding of the aorta. However, both studies failed to visualize the pulmonic valve. The patient underwent cardiac catheterization which revealed the presence of pulmonary atresia. A descending aortogram showed the presence of a single large major aortopulmonary collateral artery (MAPCA) arising from the descending thoracic aor ta which supplies confluent left and right pulmonary arteries. The pulmonary arterial vasculature is enlarged and pruned in appearance. The main pulmonary artery is non-atretic. Mean proximal pulmonary artery pressure was 68 mmHg, indicating severe pulmonary hypertension. Patient wasstarted on digoxin and sildenafil.
SIGNIFICANCE: This case report emphasizes the importance of a well-developed central pulmonary circulation and an adequate but not excessive pulmonary blood supply from an aortopulmonary vascular connection in the survival of patients with pulmonary atresia into adulthood.

Human ; Female ; Adult ; Young Adult ; Aorta ; Cardiac Catheterization ; Dyspnea ; Heart Atria ; Heart Septal Defects, Ventricular ; Hypertension, Pulmonary ; Pulmonary Atresia ; Pulmonary Circulation ; Pulmonary Valve ; Tetralogy Of Fallot

RESEARCH DESIGN AND METHODS: A systematic literature search through March 20, 2009 was conducted to identify randomized, placebo-controlled trials of statins that report data on the incidence of new-onset diabetes mellitus. Incidence of new-onset DM was treated as a dichotomous variable. Weighted averages were reported as relative risks (RR) with associated 95% confidence intervals (CI). A random-effects model was used.

RESULTS: Six prospective, randomized, placebocontrolled trials (n=57,593) were identified. Upon metaanalysis, the use of statins did not significantly increase the risk nor prevent the development of new-onset DM (relative risk 1.06; 95% confidence interval 0.93-1.22). Moderate statistical heterogeneity was observed in this analysis (I2=58%, Q statistic p=0.04) arising from pravastatinÊs tendency towards a reduction in risk of developing diabetes and the other statins showing an increase in risk. There was also no significant impact on the incidence of new-onset DM with either high- or low-dose statin use (RR 1.13, 95% CI 0.95 to 1.35 for low-dose statin; RR 1.02, 95% CI 0.84 to 1.25 for high-dose statin).

CONCLUSIONS: Statins as a class did not demonstrate a statistically significant positive or negative impact on a patientÊs risk of developing new-onset DM. Randomized controlled trials of statin therapy with incidence of newonset DM as a primary outcome are required to definitely determine its impact on the development of DM. The mechanisms by which these statins affect glucose metabolism also need to be studied further. However, the beneficial effects of statins in decreasing major vascular events and vascular mortality far outweigh the risks of any adverse effects of statin therapy on glucose metabolism.

Gastroparesis ; Diabetes Insipidus ; Glucose Intolerance