Elliot M. Antman

Prognostic value of N-terminal pro-atrial and pro-brain natriuretic peptide in patients with acute coronary syndromes.

In summary, we have shown that circulating Nt-proANP and Nt-proBNP levels are associated with early death, but not with nonfatal recurrent AMI, in patients with non-ST-segment elevation acute coronary syndromes. This nested case-control study suggests that Nt-proBNP measurements provide complementary prognostic information to conventional risk indicators, including troponin I.

ACC/AHA guidelines for the evaluation and management of chronic heart failure in the adult: Executive summary: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines

Sharon A. Hunt, MD, FACC, Chair; David W. Baker, MD, MPH, FACP; Marshall H. Chin, MD, MPH; Michael P. Cinquegrani, MD, FACC; Arthur M. Feldman, MD, PhD, FACC; Gary S. Francis, MD, FACC; Theodore G. Ganiats, MD; Sidney Goldstein, MD, FACC; Gabriel Gregoratos, MD, FACC; Mariell L. Jessup, MD, FACC; R. Joseph Noble, MD, FACC; Milton Packer, MD, FACC; Marc A. Silver, MD, FACC, FACP, FCCP, FCGC; Lynne Warner Stevenson, MD, FACC

Prasugrel Versus Clopidogrel in Patients With ST-Segment Elevation Myocardial Infarction According to Timing of Percutaneous Coronary Intervention : A TRITON–TIMI 38 Subgroup Analysis (Trial to Assess Improvement in Therapeutic Outcomes by Optimizing Platelet Inhibition with Prasugrel–Thrombolysis In Myocardial Infarction 38)

OBJECTIVES This study sought to evaluate the efficacy of prasugrel versus clopidogrel in ST-segment elevation myocardial infarction (STEMI) by the timing of percutaneous coronary intervention (PCI). BACKGROUND Treatment strategies and outcomes for patients with STEMI may differ when treated with primary compared with secondary PCI. METHODS STEMI patients in the TRITON-TIMI 38 (Trial to Assess Improvement in Therapeutic Outcomes by Optimizing Platelet Inhibition with Prasugrel-Thrombolysis In Myocardial Infarction 38) were randomized to prasugrel or clopidogrel on presentation if primary PCI was intended or later during secondary PCI. Primary PCI was defined as within 12 h of symptom onset. The primary endpoint was cardiovascular death, myocardial infarction (MI), or stroke. Because periprocedural MI is difficult to assess in the setting of STEMI, we performed analyses excluding these events. RESULTS Reductions in the primary endpoint with prasugrel versus clopidogrel (hazard ratio [HR]: 0.79; 95% confidence interval [CI]: 0.65 to 0.97; p = 0.022) were consistent between primary and secondary PCI patients at 15 months (HR: 0.89; 95% CI: 0.69 to 1.13 vs. HR: 0.65; 95% CI: 0.46 to 0.93; p interaction = 0.15). However, a tendency toward a difference in treatment effect at 30 days (HR: 0.68; 95% CI: 0.54 to 0.87; p = 0.002) was observed between primary and secondary PCI patients (HR: 0.81; 95% CI: 0.60 to 1.09 vs. HR: 0.51; 95% CI: 0.34 to 0.76; p interaction = 0.06). When periprocedural MI was excluded, the efficacy of prasugrel remained consistent among primary and secondary PCI patients at 30 days (HR: 0.53; 95% CI: 0.34 to 0.81 vs. HR: 0.44; 95% CI: 0.22 to 0.88; p interaction = 0.68) and 15 months (HR: 0.76; 95% CI: 0.56 to 1.03 vs. HR: 0.75; 95% CI: 0.46 to 1.21; p interaction = 0.96). CONCLUSIONS The efficacy of prasugrel versus clopidogrel was consistent irrespective of the timing of PCI, particularly in preventing nonprocedural events. (Trial to Assess Improvement in Therapeutic Outcomes by Optimizing Platelet Inhibition with Prasugrel-Thrombolysis in Myocardial Infarction 38; NCT00097591).

Addition of nifedipine to maximal beta-blocker-nitrate therapy: Effects on exercise capacity and global left ventricular performance at rest and during exercise

Nifedipine is a potent coronary vasodilator in the resting state and an effective afterload-reducing agent. This study was undertaken because of the concern that the addition of nifedipine to beta-blocker therapy could produce serious untoward hemodynamic consequences. Although this combination is usually well tolerated, occasional reports suggest that the combination of nifedipine and beta-blocking agents may increase the likelihood of congestive heart failure, severe hypotension or exacerbation of angina. Further, there is a need to know if the addition of nifedipine to therapy with maximally tolerated doses of long-acting nitrates and beta blockers would provide further symptomatic relief without excessive adverse effects. Finally, the effect of adjunctive nifedipine on global left ventricular performance at rest and during exercise was examined. Sixteen patients, all of whom had 3 or more episodes per week of angina pectoris despite therapy with long-acting nitrates and beta blockers, were selected. Radionuclide ventriculography was performed at rest and during exercise; global ejection fractions (EFs) were determined by manually tracing the left ventricular end-diastolic perimeter with an electronic cursor. In the first phase, beta blockers and nitrates were used; in the second phase nifedipine, 10 mg every 6 hours, was added and titrated to reduce systolic blood pressure at rest by at least 10 mm Hg or until intolerable adverse effects occurred. When nifedipine was added to therapy, the difference between global EF at rest and during exercise was reduced from - 0.15 to + 0.02 (p less than 0.00001); exercise duration was increased from 431 seconds to 532 (p less than 0.001), with only 8 patients limited by angina, compared with 16 during the initial therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Relation Between Time of Symptom Onset of ST-Segment Elevation Myocardial Infarction and Patient Baseline Characteristics: From the National Cardiovascular Data Registry: Timing of symptom onset of STEMI

The presence of a morning excess of ST‐segment elevation myocardial infarction (STEMI) has been observed. The relation between patient characteristics and timing of STEMI may provide insight into the biological processes responsible for this phenomenon.

Rationale for the Management of Coronary Syndromes With Low-Molecular-Weight Heparins

The well-documented disadvantages of unfractionated heparin in the management of coronary syndromes, such as unpredictable bioavailability and maintenance of therapeutic range, has prompted several studies into the benefits of low-molecular-weight heparins (LMWHs). The favorable pharmacologic properties of LMWHs include a binding affinity for antithrombin III, anti-factor IIa activity, excellent bioavailability, minimal protein binding, predictable anticoagulant response, and clinical tolerance by patients. LMWHs are also characterized by having a specific anti-factor Xa effect and inducing only a small prolongation in general clotting tests-i.e., activated partial thromboplastin time, prothrombin time, and antithrombin activity-when used in high doses. Several studies have recently demonstrated that LMWHs are superior to placebo and are at least equal or superior to standard heparin when added to aspirin for the treatment of unstable angina and following non-Q-wave myocardial infarction. These studies, which include Thrombolysis in Myocardial Infarction (TIMI) 11A and Efficacy and Safety of Subcutaneous Enoxaparin versus intravenous unfractionated heparin in Non-Q-wave Coronary Events (ESSENCE), will be reviewed and discussed.