No abstract

Cardiac hemochromatosis or primary iron-overload cardiomyopathy is an important and potentially preventable cause of heart failure. This is initially characterized by diastolic dysfunction and arrhythmias and in later stages by dilated cardiomyopathy. Diagnosis of iron overload is established by elevated transferrin saturation (>55%) and elevated serum ferritin (>300 ng/mL). Genetic testing for mutations in the HFE (high iron) gene and other proteins, such as hemojuvelin, transferrin receptor, and ferroportin, should be performed if secondary causes of iron overload are ruled out. Patients should undergo comprehensive 2D and Doppler echocardiography to evaluate their systolic and diastolic function. Newer modalities like strain imaging and speckle-tracking echocardiography hold promise for earlier detection of cardiac involvement. Cardiac magnetic resonance imaging with measurement of T2* relaxation times can help quantify myocardial iron overload. In addition to its value in diagnosis of cardiac iron overload, response to iron reduction therapy can be assessed by serial imaging. Therapeutic phlebotomy and iron chelation are the cornerstones of therapy. The average survival is less than a year in untreated patients with severe cardiac impairment. However, if treated early and aggressively, the survival rate approaches that of the regular heart failure population.

BackgroundPrior studies have found that smokers undergoing thrombolytic therapy for ST‐segment elevation myocardial infarction have lower in‐hospital mortality than nonsmokers, a phenomenon called the “smoker's paradox.” Evidence, however, has been conflicting regarding whether this paradoxical association persists in the era of primary percutaneous coronary intervention.Methods and ResultsWe used the 2003–2012 National Inpatient Sample databases to identify all patients aged ≥18 years who underwent primary percutaneous coronary intervention for ST‐segment elevation myocardial infarction. Multivariable logistic regression was used to compare in‐hospital mortality between smokers (current and former) and nonsmokers. Of the 985 174 patients with ST‐segment elevation myocardial infarction undergoing primary percutaneous coronary intervention, 438 954 (44.6%) were smokers. Smokers were younger, were more often men, and were less likely to have traditional vascular risk factors than nonsmokers. Smokers had lower observed in‐hospital mortality compared with nonsmokers (2.0% versus 5.9%; unadjusted odds ratio 0.32, 95% CI 0.31–0.33, P<0.001). Although the association between smoking and lower in‐hospital mortality was partly attenuated after baseline risk adjustment, a significant residual association remained (adjusted odds ratio 0.60, 95% CI 0.58–0.62, P<0.001). This association largely persisted in age‐stratified analyses. Smoking status was also associated with shorter average length of stay (3.5 versus 4.5 days, P<0.001) and lower incidence of postprocedure hemorrhage (4.2% versus 6.1%; adjusted odds ratio 0.81, 95% CI 0.80–0.83, P<0.001) and in‐hospital cardiac arrest (1.3% versus 2.1%; adjusted OR 0.78, 95% CI 0.76–0.81, P<0.001).ConclusionsIn this nationwide cohort of patients undergoing primary percutaneous coronary intervention for ST‐segment elevation myocardial infarction, we observed significantly lower risk‐adjusted in‐hospital mortality in smokers, suggesting that the smoker's paradox also applies to ST‐segment elevation myocardial infarction patients undergoing primary percutaneous coronary intervention.