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Regadenoson is a selective Adenosine-2A receptor agonist and is used for myocardial perfusion imaging. Dipyridamole causes indirect vasodilation by inhibiting cellular reuptake of adenosine. The purpose of this study was to assess whether regadenoson is a better coronary vasodilator than dipyridamole in normal volunteers and in patients.

Many MRI perfusion protocols perform rest imaging a few minutes after stress imaging. Regadenoson is a new, selective Adenosine-2A receptor agonist used for myocardial perfusion imaging. The purpose of this study was to assess how well rest perfusion imaging 20 minutes after regadenoson stress reflects true baseline rest perfusion.

Objectives: To combine data from all randomized trials of abciximab versus placebo or open-label control in patients with STEMI treated with primary stenting to assess the short-term and long-term mortality, reinfarction, and bleeding complications. Background: Clinical trials of adjunctive abciximab therapy in patients with ST-segment elevation myocardial infarction (STEMI) undergoing primary stenting have produced conflicting results. Methods: Formal searches of electronic databases (Medline, Cochrane) from January 1990 to April 2009 were performed. Five trials randomizing 2,937 patients (1,475 in the abciximab group, 1,462 in the placebo group) were included in the analysis. Results: When compared with placebo, abciximab was not associated with a significant reduction in the odds of 30-day (OR 0.71, 95% CI: 0.45–1.14, P = 0.16) or long-term (OR 0.85, 95% CI: 0.48–1.50, P = 0.57) mortality. Similarly, the rate of reinfarction was not statistically different at 30 days (OR 0.59, 95% CI: 0.30–1.17, P = 0.13) or at long-term follow-up (OR 0.67; 95% CI: 0.39–1.16, P = 0.16). However, when trials with upstream use of thienopyridines were excluded, abciximab was associated with a significant reduction in the composite of death or reinfarction at 30 days (OR 0.45; 95% CI: 0.26–0.77, P = 0.004) but not at long-term follow-up (OR 0.59; 95% CI: 0.27–1.28, P = 0.18). Conclusion: Routine use of abciximab in patients with STEMI treated with primary stenting may reduce short-term rates of death or reinfarction in patients not administered preprocedural thienopyridine therapy, but does not appear to be beneficial in those who receive preprocedural thienopyridines. © 2009 Wiley-Liss, Inc.

Background: Both short- and long-term benefits of abciximab therapy in primary angioplasty for acute myocardial infarction (AMI) have been reported. However, primary stenting is the preferred treatment of AMI and conflicting data exists on the effect of abciximab therapy on outcomes following primary stent treatment of AMI. We therefore performed a meta-analysis of all randomized trials of abciximab in primary stenting for AMI for which there was short-term (30-day) and long-term (≥ 1 year) follow-up. Methods: We searched the MEDLINE and Cochrane databases using the following key words: stent, acute myocardial infarction, abciximab and randomized trial. Four studies (ISAR-2, ADMIRAL, CADILLAC and ACE) were included in this analysis. The incidence of the individual end points of death, reinfarction and target vessel revascularization (TVR) at 30 days and at long-term follow-up was extracted. Follow-up data was available at 1 year for ACE and CADILLAC, at 3 years for ADMIRAL and 5 years for ISAR-2. A random effects model was used to calculate the combined odds ratio (OR) of reinfarction, TVR and mortality associated with the use of abciximab. Results: The 4 trials enrolled 2137 patients of whom 1074 were randomized to abciximab and 1063 to placebo. Long-term follow up was available for 2107 patients, 1064 in the abciximab group and 1043 in the control group. At 30 days, abciximab resulted in a significant reduction in the odds of TVR (OR 0.45, 95% CI, 0.27–0.75, P=0.003) and a non-significant reduction in the odds of reinfarction (OR 0.43, 95% CI, 0.18–1.0, P=0.06) but no reduction in 30-day mortality (OR 0.78, 95% CI, 0.47–1.2, P=0.34). During long-term follow up, abciximab treatment resulted in a non-significant reduction in the risk of TVR (OR 0.77, 95% CI 0.58–1.0, P=0.06) but no reduction in reinfarction (OR 0.58, 95% CI, 0.3–1.1, P=0.12) or mortality (OR 0.90, 95% CI, 0.48–1.6, P=0.74). Conclusions: Abciximab resulted in a significant reduction in TVR at 30 days that diminished over time. We were unable to demonstrate a significant reduction in reinfarction or mortality at 30 days or at 1–5 years. These results suggest the need for an appropriately powered clinical trial to define the role of abciximab during primary stenting for AMI.

The results of the AFFIRM (Atrial Fibrillation Follow-up Investigation of Rhythm Management) trial indicate that the rate control strategy is preferred for the majority of patients with paroxysmal and persistent atrial fibrillation (AF). If the patient remains symptomatic despite adequate rate control or if rate control cannot be achieved, then rhythm control therapies are indicated. The most likely explanation for the disappointing results of the AFFIRM trial is the poor efficacy and excessive toxicity of rhythm control medications, because the presence of sinus rhythm was associated with a favorable prognosis in AFFIRM. As a result, there is currently great interest in nonpharmacologic therapies such as AF ablation and development of new drugs for AF with a more favorable efficacy and toxicity profile. AF ablation should be reserved for patients who fail an initial trial of a rhythm control medication until additional clinical trial information is available to justify the use of AF ablation as first-line therapy. When rhythm control therapy is indicated, the choice of antiarrhythmic medication should be dictated by the presence or absence of structural heart disease, congestive heart failure, renal dysfunction, or other comorbidities in order to maximize efficacy and minimize the chance of proarrhythmia or extracardiac toxicity.

Heart failure affects 5 million persons in the United States, with 400,000 new cases occurring every year. Paradoxically, although advances in coronary angioplasty and effective drugs have increased survival post infarction, the myocardial damage and subsequent neurohormonal activation-induced remodeling causes significant morbidity years later in the form of heart failure. Angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) together with beta blockers modify the neurohormonal activation associated with heart failure and are key treatments for improving cardiac function and survival. Anemia is a significant risk factor predicting morbidity and mortality in heart failure. This article describes the various etiologies of anemia in heart failure. Of particular importance is the fact that recent stem cell studies have shown that the drugs acting on the renin-angiotensin system inhibit erythropoiesis in vivo and may cause anemia in patients with both normal renal function and end-stage renal disease (ESRD). The role of angiotensin-II as an erythropoietic growth factor and ACE in facilitating erythropoiesis is described in this article. Anemia has been shown to be a modifiable risk factor and its treatment correlates with improvement in clinical outcomes. Thus, anemia, its etiology (especially the contribution of ACEIs and ARBs), physiologic and prognostic impact, and treatment in the setting of heart failure are critical areas for investigation.

Background Previously, we have shown that increased visceral adiposity was an independent predictor of thoracic aortic wall thickness in elderly individuals at risk for future cardiovascular (CV) events. In this study, we sought to assess the influence of obesity on rest and stress induced changes in aortic stiffness in older individuals with hypertension, diabetes or coronary artery disease at risk for future CV events.

Quantitative myocardial perfusion to assess impaired coronary vasoreactivity has been used to identify subclinical atherosclerosis. Impaired coronary vasodilation has been observed in patients with cardiac risk factors in the MESA cohort. The coronary vasodilator response in patients with angiographically normal coronary arteries/minimal stenosis is not known. The purpose of this study was to compare the stress myocardial blood flow (MBF) of patients with normal coronaries/minimal stenosis with normal volunteers.

Background In animals and human subjects, an increase in background signal intensity observed on late gadolinium enhanced (LGE-SI) images is associated with a decrement in left ventricular ejection fraction (LVEF) during receipt of anthracycline chemotherapy. Moran’ sIs tatistic is a measurement of spatial dispersion of hyperenhanced voxels relative to the mean myocardial LGE-SI, ranging from highly clustered (I=+1) to highly diffuse (I=-1) (Figure 1). We hypothesize that a change in the distribution of hyperenhanced voxels (due to the development of high signal “micro clusters”) is associated with a decrement in LVEF after cardiotoxic chemotherapy. Methods We performed a prospective, extramurally-funded longitudinal cohort study of 51 participants (43 women, 8 men; aged 52±2 years) scheduled to receive 3 to 4 months of potentially cardiotoxic chemotherapy (anthracycline or trastuzumab) for treatment of breast cancer or hematologic malignancy. Before and then 3 and 6 months after chemotherapy initiation, participants underwent cardiovascular magnetic resonance (CMR) assessments of LVEF, LGE-SI, and Moran’s I statistic determined by personnel blinded to participant identifiers and all other aspects of the analyses. Results were analyzed using paired Student’s t-tests to test for a difference between baseline and subsequent examinations, and one-way ANOVA to test for trending change. All values are reported as mean ± standard deviation with p-values

Adult cancer survivors can have elevated cardiovascular magnetic resonance (CMR) left ventricular (LV) native T1 and extracellular volume (ECV) assessments. It remains undetermined whether these measures are related to the presence of cancer alone or cancer treatment. We performed prospective