(Circulation. 2004;110:241.)
© 2004 American Heart Association, Inc.
Issue Highlights |
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
HEART FAILURE AND SUDDEN DEATH IN PATIENTS WITH TACHYCARDIA-INDUCED CARDIOMYOPATHY AND RECURRENT TACHYCARDIA, by Nerheim et al.
Incessant tachycardia, most commonly from atrial fibrillation, is an important cause of potentially reversible heart failure. In animal models, structural changes occur suggesting that the recovered ventricle may not be normal. The observations of Nerheim and coworkers in 24 patients support this concern. After initial recovery of ventricular function, recurrent tachycardia produced precipitous deterioration in 5 patients. Three patients died suddenly after initial improvement. Prompt treatment of chronic, persistent tachycardia is prudent in the hope of preventing ventricular dysfunction. Those with tachycardia-induced cardiomyopathy warrant close long-term follow-up, even after recovery of ventricular function. See p 247.
CLINICAL AND ECONOMIC OUTCOMES OF PERCUTANEOUS CORONARY INTERVENTIONS IN THE ELDERLY: AN ANALYSIS OF MEDICARE CLAIMS DATA, by Clark et al.
The cost of percutaneous coronary revascularization is attracting increased attention, especially as costly new drug-eluting stents are introduced. The economic value of these new stents depends on the economic burden of restenosis. In the largest national study of its kind, investigators examined a national sample of Medicare beneficiaries and determined that 
17% of PCI patients required 1 or more repeat revascularization procedures during the subsequent year. Each repeat revascularization was associated with a $19 000 higher cost. The authors speculate that, if drug-eluting stents can reduce this rate by 70% to 75%, then they may produce cost offsets of as much as $2000 per patient. Owing to the current cost of stents and the number of stents placed per patients, however, they are unlikely to produce a net cost saving from the payer perspective. See p 259.
HEME OXYGENASE-1 INHIBITS ANGIOTENSIN II–INDUCED CARDIAC HYPERTROPHY IN VITRO AND VIVO, by Hu et al.
There is now appreciation that reactive oxygen species can act as intracellular signaling molecules to