INSIDE THIS ISSUE OF JACC
Inside This Issue of JACC
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Interventional Cardiology
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DES or BMS: Effect on Quality of Life.
Garg and colleagues designed a Markov model to explore the effects on quality-adjusted life expectancy of choosing drug-eluting stents (DES) versus bare-metal stents (BMS). The model attempts to answer the question: what excess risk of late stent thrombosis with DES would be an acceptable tradeoff for suppressing restenosis compared with BMS? Data regarding the relative and absolute risks of DES, BMS, and secondary procedures, and the effect of these outcomes on quality of life were compiled from a wide variety of published studies. The models indicate that if the excess risk of very late stent thrombosis is <0.14% per year over 4 years, most patients would prefer DES to BMS. This article may help physicians more effectively compare the risks and benefits of DES. See pages 1844 and
1854. See figure.
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Myocardial Infarction
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New ANP Biomarker Assay Helps Predict Acute MI Mortality.
While B-type natriuretic peptide (BNP) is well validated as a post-myocardial infarction (MI) risk stratifier, the initial studies with atrial natriuretic peptide (ANP) were less compelling. Khan and colleagues noted that the ends of ANP may be degraded by proteases, and therefore developed an assay that recognizes epitopes in the mid-region of the ANP prohormone (MR-proANP), an area that is less likely to degraded. Levels of MR-proANP and N-terminal (NT)-proBNP were analyzed 3 to 5 days after the onset of chest pain in almost 1,000 persons who suffered an MI and were then followed for up to 2 years. Levels of both assays were higher in patients who died than in those who survived; the highest risk was in patients in the upper quartile for both measurements. MR-proANP is a useful risk stratifier, especially in those with an elevated NT-proBNP. See page 1857. See figure.
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Heart Failure
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Measuring BNP Precursor Peptide May Improve Diagnostic Accuracy.
The initial translation and processing of the B-type natriuretic peptide (BNP) messenger ribonucleic acid results in an 108 amino acid peptide denoted as proBNP. ProBNP is then further cleaved into two fragments: BNP, a vasoactive 32 amino acid peptide, and the N-terminal peptide fragment (NT-proBNP). The currently available assays for BNP and NT-proBNP likely cross react with proBNP in the serum. This study by Waldo and colleagues used 3 different assays to measure proBNP, BNP, and NT-proBNP in patients with decompensated heart failure. The proBNP levels were not affected by body mass index (BMI), renal function, or age. All 3 peptides were significantly elevated in patients who died within 90 days. This preliminary comparison suggests that NT-proBNP has a slightly higher diagnostic yield for predicting death, but the apparent lack of interference with BMI, renal dysfunction, and age suggests that proBNP should be further studied. See page 1874. See figure.
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Heart Failure
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ET Does Not Cause Long-Term Changes in Myocardial Energy Metabolism.
Reductions in phosphocreatine and adenosine triphosphate have been implicated in the altered myocardial energy metabolism that contributes to contractile dysfunction. High energy phosphate metabolism can be measured by 31P-MR spectroscopy (MRS). Beer and colleagues performed MRS on patients with non-ischemic cardiomyopathies to study the effect of an intensive exercise training (ET) program for 2 months. The ET improved peak VO
2, left ventricular (LV) end-systolic volume, and LV ejection fraction. The improvement in cardiac function was not accompanied by changes in cardiac high-energy phosphate concentrations. This study demonstrates that ET can produce substantial improvements in exertional capacity without an effect on myocardial energy metabolism; this lack of effect may be beneficial, as other modalities that stimulate the myocardium may deplete myocardial energy stores and increase mortality. See pages 1883 and
1892. See figure.
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Hypertension
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Evidence that Cardiac Autonomic Dysfunction Precedes Hypertension.
This study by Wu and colleagues examined the hypothesis that cardiac autonomic function (CAF) is altered in pre-hypertensive subjects and those with a family history of hypertension (FHH). Nearly 1,500 subjects were classified as having normotension (<120/80 mm Hg), pre-hypertension (120 to 139/80 to 89 mm Hg), or hypertension ( 140/90 mm Hg). Cardiac autonomic function was determined by multiple methods, including standard deviation of RR interval, the heart rate variability with standing, and respiratory variation in the heart rate. There was a significant, graded difference in all CAF indexes along the spectrum of hypertension. This study provides evidence that CAF plays a role in pre-hypertension and that altered autonomic function is already present in subjects with FHH. See pages 1896 and
1902. See figure.
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Interpreting the Music of Drug-Eluting Stents: Halcyon Song or Albatross Dirge?
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Interventional Cardiology
Myocardial Infarction
