Angela Palazzo

A new regimen for heparin use in acute coronary syndromes

BACKGROUND Recent trials have demonstrated an association between high activated partial thromboplastin time (aPTT) and bleeding, intracranial hemorrhage, reinfarction, and death in patients with acute coronary syndromes treated with heparin. Of all the factors that affect aPTT in patients treated with heparin, body weight is most strongly correlated. METHODS We compared the efficacy of 2 weight-adjusted heparin regimens (groups 2 and 3) and the standard (group 1) non-weight-adjusted 5000-U intravenous bolus/1000 U/hr infusion to achieve an aPTT between 45 and 70 seconds in a nonrandomized prospective cohort of 80 patients admitted with unstable angina and non-ST elevation myocardial infarction. RESULTS Patients treated with the lower dose of weight-adjusted heparin (60 U/kg intravenous bolus, maximum of 4000 U; 12 U/kg/hr, maximum 900 U/kg), group 3, were more often within the target range for aPTT at 6 hours (34% vs 5% vs 0%) and required fewer heparin infusion changes (1.0 +/- 1.0 vs 1.9 +/- 1.0 vs 2.0 +/- 0.9) within the first 24 hours compared with the other regimens. Patients in groups 1 and 2 were overwhelmingly above target range at 6 hours (95% and 84%, respectively, compared with 48% in group 3). CONCLUSIONS Traditional heparin dosing regimens result in marked initial overanticoagulation in patients with acute coronary syndromes, which may place these patients at higher risk of adverse outcomes. A lower dose weight-adjusted heparin regimen is superior in achieving early aPTTs within the target range and reducing the need for infusion changes over the ensuing 24 hours.

Relation between infarct artery patency at late angiography after acute myocardial infarction and signal-averaged electrocardiography

The angiograms of 89 patients were reviewed from the LATE Ancillary Study (randomized trial of recombinant tissue plasminogen activator vs placebo in patients with symptom onset after 6 hours of myocardial infarction) to determine patency of the infarct-related artery (IRA). In the occluded IRA group (n = 35), the incidence of signal-averaged electrocardiographic abnormality (fQRS > 120 ms) was significantly higher (p = 0.04), the filtered QRS duration was significantly longer (p = 0.007), and the V40 was significantly shorter (p = 0.02), compared with the patent IRA group (n = 54).

Blood pressure paradox in patients with non-ST-segment elevation acute coronary syndromes: results from 139,194 patients in the Can Rapid risk stratification of Unstable angina patients Suppress ADverse outcomes with Early implementation of the American College of Cardiology/American Heart Association Guidelines (CRUSADE) quality improvement initiative.

BACKGROUND The relationship between systolic blood pressure (BP) and the risk of cardiovascular events is complex. In patients with chronic coronary artery disease, a J-shaped relationship has been shown, such that there is an increased risk of events both at high and low BP. The current coronary artery disease risk prediction models, however, considers a linear relationship between presenting BP and outcomes in patients presenting with acute coronary syndromes. METHODS We evaluated 139,194 patients with non-ST-segment elevation acute coronary syndromes in the Can Rapid risk stratification of Unstable anigina patients Suppress ADverse outcomes with Early implementation of the ACC/AHA guidelines (CRUSADE) quality improvement initiative. The presenting systolic BP was summarized as 10-unit increments. Primary outcome was a composite of in-hospital events all-cause mortality, reinfarction, and stroke. Secondary outcomes were each of these outcomes considered separately. RESULTS From the cohort of 139,194 patients, 9,566 (6.87%) patients had a primary outcome (death/reinfarction or stroke) of which 5,910 (4.25%) patients died, 3,724 (2.68%) patients had reinfarction, and 1,079 (0.78%) patients had a stroke during hospitalization. There was an inverse association between presenting systolic BP and the risk of primary outcome, all-cause mortality, and reinfarction such that there was an exponential increase in the risk with lower presenting systolic BP even after controlling for baseline variables. However, there was no clear relationship between stroke and lower presenting systolic BP. CONCLUSIONS In contrast to longitudinal impacts, there is a BP paradox on acute outcomes such that a lower presenting BP is associated with increased risk of in-hospital cardiovascular events. These associations should be considered in acute coronary syndrome prognostic models.

Safety and feasibility of intra-arterial bivalirudin bolus administration during primary angioplasty.

AimWe investigated the feasibility and safety of intra-arterial bivalirudin bolus during primary angioplasty. BackgroundBivalirudin has been shown to be an effective and safe anticoagulant during angioplasty. However, in the Harmonizing Outcomes with Revascularization and Stents in Acute Myocardial Infarction trial, the bivalirudin group experienced higher acute stent thrombosis rate compared with the heparin and glycoprotein IIb/IIIa inhibitor group. One possible explanation is suboptimal systemic administration. MethodsTo prevent this possibility and to potentially prevent acute stent thrombosis, we administered intra-arterial bivalirudin bolus during primary angioplasty in 100 consecutive patients. ResultsOur observational study suggests safety with no bleeding episode and no observed acute stent thrombosis. ConclusionWe conclude that intra-arterial bivalirudin bolus during primary angioplasty is safe and could ensure effective systemic delivery of bivalirudin.

Diagnosis and Treatment of Cardiogenic Shock

Cardiogenic shock is the leading cause of death in patients hospitalized with acute myocardial infarction [1, 2]. Cardiogenic shock is characterized by a state of inadequate tissue perfusion due to cardiac dysfunction and is classically manifested by systemic hypotension and end-organ hypoperfusion in the setting of adequate or elevated left ventricular fi lling pressures. The hemodynamic defi nition includes sustained hypotension (systolic blood pressure 30 mm Hg or more in mean arterial pressure from baseline for at least 30 minutes) and a reduced cardiac index (<2.2 L min m) [3]. In the SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK (SHOCK) Trial [4], tissue hypoperfusion was defi ned as cold peripheries (extremities colder than core), oliguria (<30 mL/h), or both. Subjects requiring pharmacological or mechanical circulatory support to maintain blood pressure are also included in this category. In the setting of an acute myocardial infarction, hypotension, tachycardia, peripheral vasoconstriction, decreased urine output, and altered mentation are all manifestations of the syndrome, which can range from “preshock” to fully developed pump failure. It is important to recognize the preshock syndrome because early investigation of its etiology and early intervention may reduce the development of frank cardiogenic shock. In this state, systolic blood pressure may be normal to borderline without pressors, but this “stability” occurs at the expense of an elevated peripheral resistance and elevated heart rate that support a borderline stroke volume. The signs of peripheral hypoperfusion may be obvious or subtle. This is also known as nonhypotensive cardiogenic shock and is associated with ineffective tissue perfusion and a severely depressed cardiac index. The preshock syndrome is associated with a high in-hospital mortality (43%), which is lower than that in patients with classic cardiogenic shock (66%) [5]. This syndrome predominately occurs in the setting of a large anterior wall myocardial infarction (MI). Recognition of this “preshock state” is important to avoid potentially cardiodepressant medications and to identify patients who might benefi t from aggressive revascularization strategies.