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INSIDE THIS ISSUE

Inside This Issue

	State-of-the-Art Paper

Top State-of-the-Art Paper Clinical Research News from the NHLBI

Wael Al Jaroudi, Ami E. Iskandrian

The Food and Drug Administration recently approved regadenoson for stress testing in conjunction with myocardial perfusion imaging. Regadenoson is a selective A_2A agonist. Activation of cardiac A_2A and A_2B adenosine receptors causes vasodilation in the coronary and peripheral arterial beds and increases myocardial blood flow. The side effects of adenosine, including negative chronotropism and bronchial constriction, are thought to be secondary to stimulation of the other adenosine receptors. Clinical trials have shown regadenoson to be noninferior to adenosine for detection of perfusion abnormalities with fewer side effects. This review by Al Jaroudi and Iskandrian summarizes the pre-clinical and clinical data on regadenoson regarding its use as a vasodilator stress agent.

	Clinical Research

Top State-of-the-Art Paper Clinical Research News from the NHLBI

 
Interventional Cardiology.   Incidence and Management of Restenosis After Left Main PCI
1131

Imad Sheiban, Dario Sillano, Giuseppe Biondi-Zoccai, Alaide Chieffo, Antonio Colombo, Sabine Vecchio, Massimo Margheri, Julian P. Gunn, Tushar Raina, Francesco Liistro, Leonardo Bolognese, Michael S. Lee, Jonathan Tobis, Claudio Moretti

Sheiban and colleagues studied the incidence and management of restenosis following drug-eluting stent (DES) implantation for unprotected left main (ULM) disease in over 700 subjects. Post-DES restenosis in the ULM occurred in 9.7% of patients, 84% of whom were treated percutaneously. A total of 10% of patients underwent coronary artery bypass grafting, and 6% were treated medically. There was only 1 in-hospital major adverse cardiac event (MACE) for repeat percutaneous coronary intervention (PCI) patients. During a median follow-up of more than 2 years, patients treated with medical, interventional, and surgical therapy had the following MACE rates: 50%, 25%, and 14%, respectively. DES restenosis in the ULM artery can often be managed percutaneously with favorable early and late results.

Coronary Artery Physiology.   The Predominant -1-Adrenergic Receptor Subtype in Human Coronary Arteries is 1D

1137

Brian C. Jensen, Philip M. Swigart, Marie-Eve Laden, Teresa DeMarco, Charles Hoopes, Paul C. Simpson

Jensen and colleagues used explanted human coronary arteries to determine which of the 3 1-adrenergic receptor (AR) subtypes was most prevalent in human coronary arteries. The 1D subtype was 85% of total coronary 1-AR messenger ribonucleic acid and 75% of total 1-AR protein. In contrast, there was a low prevalence of 1D in the left ventricular myocardium. Total coronary 1-AR levels were one-third of β-ARs, which were 99% of the β2 subtype. This distribution of 1-AR subtypes is similar to the mouse, where myocardial 1A- and 1B-ARs mediate vasodilation and coronary 1Ds mediate vasoconstriction. This suggests that a 1D-selective antagonist could stimulate coronary vasodilation.

Editorial Comment: Oscar Ö. Braun, Paul A. Insel, p. 1146

Antiplatelet Therapy.   Less Inhibition of Clopidogrel With Pantoprazole Than Omeprazole

1149

Thomas Cuisset, Corinne Frere, Jacques Quilici, Raphael Poyet, Bénédicte Gaborit, Laurent Bali, Olivier Brissy, Pierre-Emmanuel Morange, Marie-Christine Alessi, Jean-Louis Bonnet

Omeprazole has been reported to significantly decrease the efficacy of clopidogrel. Cuisset and colleagues randomized post-percutaneous coronary intervention patients to either omeprazole or pantoprazole to see if both proton pump inhibitors (PPIs) had a similar effect. After 1 month, patients receiving pantoprazole had a significantly better platelet reactivity index vasoactive stimulated phosphoprotein, but there was no significant difference in adenosine diphosphate-induced aggregation. These findings suggest that pantoprazole may have less interference with clopidogrel and should be used preferentially over omeprazole in patients who need treatment with a PPI.

Hypertension.   Benefit of Amlodipine Over Atenolol Not Affected by Baseline Heart Rate

1154

Neil R. Poulter, Joanna E. Dobson, Peter S. Sever, Björn Dahlöf, Hans Wedel, Norm R. C. Campbell, on behalf of the ASCOT Investigators

Some have postulated that patients with high baseline heart rates and hypertension, possibly caused by high adrenergic tone, may benefit more from a beta-blocker–based antihypertensive regimen. Poulter and colleagues reanalyzed data from ASCOT (Anglo-Scandinavian Cardiac Outcomes Trial), which randomized patients to either an atenolol- or an amlodipine-based antihypertensive regimen to determine if baseline heart rate affected the relative benefits. The relative risk reduction for total cardiovascular events and procedures with amlodipine was 0.81 and did not vary with baseline heart rate. Similar results were obtained for coronary and total stroke outcomes. These data suggest that a high baseline heart rate is not an indication for preferential use of beta-blocker–based therapy.

Editorial Comment: Carl J. Lavie, Franz H. Messerli, Richard V. Milani, p. 1162

Biomarkers.   Normal Plasma Levels of cTnI Measured by New High-Sensitivity Assay
1165

Per Venge, Nina Johnston, Bertil Lindahl, Stefan James

Studies on patients with acute coronary syndromes (ACS) have shown that even minor elevations of cardiac troponins are associated with increased risk of death. However, the normal plasma levels of cardiac troponins are not known. Venge and colleagues evaluated the analytical and clinical performance of a new hypersensitive cardiac troponin I assay in both healthy subjects and in randomly selected patients of the GUSTO IV (Global Utilization of Strategies To open Occluded arteries IV) trial. Cardiac troponin I (cTnI) levels were measurable in >95% of the healthy subjects. The median level in healthy subjects <60 years of age was 0.0032 µg/l, with the 99th percentile being 0.010 µg/l. This high-sensitive cTnI prototype assay shows that cTnI is detectable in low levels in almost all healthy subjects.

Editorial Comment: Judd E. Hollander, p. 1173

Peripheral Vascular Disease.   CKD Predisposes to Both High and Low ABI
1176

Joachim H. Ix, Ronit Katz, Ian H. De Boer, Brian R. Kestenbaum, Matthew A. Allison, David S. Siscovick, Anne B. Newman, Mark J. Sarnak, Michael G. Shlipak, Michael H. Criqui

A low ankle-brachial index (ABI) is sensitive and specific for atherosclerosis; alternatively, a high ABI reflects stiffening of the lower limb arteries and has high specificity for medial arterial calcification. Ix and colleagues studied the relationship between chronic kidney disease (CKD) and ABI in >4,000 elderly subjects. CKD was defined by an estimated glomerular filtration rate <60 ml/min/1.73 m². In multivariable models, CKD was associated with both low ABI (<0.9, relative risk [RR]: 2.0) and high ABI (>1.40, RR: 1.6). CKD is associated with both the high and low extremes of ABI and may be an important mechanism leading to cardiovascular disease in persons with CKD.

	News from the NHLBI

Top State-of-the-Art Paper Clinical Research News from the NHLBI

 
News from the NHLBI.   Cardiovascular Disease and HIV
1185

Cheryl L. McDonald, Jonathan R. Kaltman

The currently available evidence is that there is an excess risk of cardiovascular events in human immunodeficiency virus (HIV)-infected persons. Antiretroviral drugs may be associated with insulin resistance and dyslipidemia, but they are not the only factors likely involved in the increased cardiovascular disease risk. Traditional risk factors may be increased in these patients, such as increased rates of smoking; HIV itself may affect traditional risk factors, including lipid profiles; and/or there may be increased underlying inflammation. The National Heart, Lung, and Blood Institute encourages the continued partnership of basic and clinical cardiovascular and infectious diseases researchers in their efforts to tackle the still unanswered questions of cardiovascular disease in HIV/acquired immunodeficiency syndrome.

Related Articles

Regadenoson: A New Myocardial Stress Agent

Wael Al Jaroudi and Ami E. Iskandrian
J. Am. Coll. Cardiol. 2009 54: 1123-1130. [Abstract] [Full Text] [PDF]

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