Quantification of myocardial iron overload by cardiovascular magnetic resonance imaging T2* and review of the literature.

Heart failure due to myocardial iron overload remains the leading cause of death in patients with transfusion-dependent anemias. Iron overload-induced cardiomyopathy is reversible if intensive chelation therapy is instituted on time. Thus, early detection of myocardial iron deposition is imperative to prevent overt heart failure. Conventional cardiac monitoring, including physical examination, electrocardiography, echocardiography or serum ferritin levels fail to predict manifest or subclinical myocardial involvement resulting from iron overload. Cardiovascular magnetic resonance imaging T2* (cMRI-T2*, pronounced T2 star) times correlate well with myocardial iron levels. This timely review focuses on the utility of cMRI-T2*, for the preclinical detection of myocardial iron overload and monitoring of myocardial iron content during chelation therapy.

Implantable cardioverter defibrillators save lives from lightning-related electrocution too!

We report an unusual case of a 75-year-old male electrocuted by lightning strike rescued by implantable cardioverter defibrillator (ICD) shock coincidentally. Lightning strikes are an unusual cause of fatal cardiac arrhythmias. Depending on the amount of energy and the current vector affecting the heart, the arrhythmia burden ranges from asystole to ventricular fibrillation.

Improving death certificate completion: a trial of two training interventions.

The death certificate is an important medical document that impacts mortality statistics and health care policy. Resident physician accuracy in completing death certificates is poor. We assessed the impact of two educational interventions on the quality of death certificate completion by resident physicians. Two-hundred and nineteen internal medicine residents were asked to complete a cause of death statement using a sample case of in-hospital death. Participants were randomized into one of two educational interventions: either an interactive workshop (group I) or provided with printed instruction material (group II). A total of 200 residents completed the study, with 100 in each group. At baseline, competency in death certificate completion was poor. Only 19% of residents achieved an optimal test score. Sixty percent erroneously identified a cardiac cause of death. The death certificate score improved significantly in both group I (14+/-6 vs 24+/-5, p<0.001) and group II (14+/-5 vs 19+/-5, p<0.001) postintervention from baseline. Group I had a higher degree of improvement than group II (24+/-5 vs 19+/-5, p<0.001). Resident physicians' skills in death certificate completion can be improved with an educational intervention. An interactive workshop is a more effective intervention than a printed handout.

Cardiac troponin I release in non-ischemic reversible myocardial injury from acute diphtheric myocarditis.

Cardiac troponins are highly specific markers of myocardial injury. It has been suggested that, unlike other markers of myocardial injury, troponins could be released in reversible myocardial injury and the myocardial necrosis does not have to occur for troponins to be released from myocytes. Reversibly injury related changes in myocyte membrane are considered sufficient for the release of cardiac troponins from the free cytosolic pool, whereas in case of irreversible myocardial injury the source of troponin release is the structural damage of the myocytes. Diphtheria is a localized infection of skin and mucous membranes with multi-system involvement caused by gram-positive aerobic rod Corynebacterium diphtheriae. The cardiac involvement in diphtheria is characterized by severe impairment of cardiac contractility. The myocardial injury induced by diphtheric toxins could be completely reversible with successful treatment. We report a case of diphtheric myocarditis in a 20-year-old female who presented with complaints of dysphagia, dysphonia, fatigue, generalized malaise and severe dyspnea. She developed severe left ventricular systolic dysfunction (ejection fraction 10%) with markedly elevated serum levels of cardiac troponin I (peak 48.5 ng/ml). Within a few days on treatment, the cardiac function became completely normal (left ventricular ejection fraction 60%) and the elevation in serum level of cardiac troponin I resolved. This case supports the notion that cardiac troponin I could be released in reversible myocardial injury and that in such case the recovery of myocardial function is independent of serum levels of cardiac troponin I measured during the acute phase of illness.