Gary E. Sander

Abciximab and bleeding during coronary surgery: results from the EPILOG and EPISTENT trials ∗

BACKGROUNDnAbciximab during percutaneous coronary revascularization reduces ischemic complications, but concern exists regarding increased bleeding risk should emergency coronary surgical procedures be required.nnnMETHODSnOutcomes were assessed among 85 patients who required coronary artery bypass grafting operations after coronary intervention in two randomized placebo-controlled trials of abciximab. Comparisons were made between patients in the pooled placebo and abciximab groups.nnnRESULTSnThe incidence of coronary surgical procedures was 2.17% and 1.28% among patients randomized to placebo and abciximab, respectively (p = 0.021). Platelet transfusions were administered to 32% and 52% of patients in the placebo and abciximab groups, respectively (p = 0.059). Rates of major blood loss were 79% and 88% in the placebo and abciximab groups, respectively (p = 0.27); transfusions of packed red blood cells or whole blood were administered in 74% and 80% of patients, respectively (p = 0.53). Surgical reexploration for bleeding was required in 3% and 12% of patients, respectively. Death and myocardial infarction tended to occur less frequently among patients who had received abciximab.nnnCONCLUSIONSnUrgent coronary artery bypass grafting operations can be performed without an incremental increase in major hemorrhagic risk among patients on abciximab therapy.

Pathophysiologic, Diagnostic, and Therapeutic Aspects of the Metabolic Syndrome

The metabolic syndrome, characterized by increases in waist circumference, blood pressure, and triglyceride concentrations combined with reduced high‐density lipoprotein and evidence of glucose intolerance, results from the interaction of visceral or central obesity with insulin resistance. This syndrome presents a clinical situation of systemic inflammation and increased cardiovascular risk. Blood pressure, even if only in the “prehypertensive” range, plays an important role in increasing the risk of cardiovascular disease. Recognition and treatment of each individual component of the metabolic syndrome is critical in reducing cardiovascular risk. Treatment should begin with lifestyle changes, including diet, exercise, and weight reduction. Antihypertensive therapy should be directed toward reduction of blood pressure to levels as close to optimal (<120/80 mm Hg) as feasible, and treatment protocols that do not cause worsening of glucose intolerance should be selected. Therapy for dyslipidemia should be directed at reducing triglycerides and increasing high‐density lipoprotein. Glucose‐lowering agents may be indicated, and drugs such as metformin and thiazolidinediones, which reduce insulin resistance, should form the basis of therapy. Carefully chosen therapy will effectively improve cardiovascular outcomes.

Beyond the usual strategies for blood pressure reduction: therapeutic considerations and combination therapies.

Rapidly accumulating clinical data have repeatedly demonstrated not only the critical importance of even small increases in blood pressure as a pathophysiologic factor in the development of cardiovascular disease, particularly in individuals with diabetes mellitus, but also the therapeutic necessity of more aggressive blood pressure reduction and the achievement of progressively lower blood pressure targets in reducing cardiovascular event rates. JNC VI has defined optimal blood pressure as ≤120/80 mm Hg, and Stage 1 hypertension as ≥140/80 mm Hg. Target blood pressures are now ≤130/80 mm Hg in patients with diabetes and <125/75 mm Hg for patients with hypertensive renal disease with proteinuria of>1 gm/24 hours. Achieving such target pressures is increasingly difficult, particularly in diabetic patients with chronic renal disease, who require complex multidrug antihypertensive regimens. This review attempts to provide some suggestions for constructing such antihypertensive regimens, and provides considerations for the appropriate use of diuretics and the most effective drug combinations. Factors potentially contributing to drug resistant hypertension include such problems as failure to maximize drug dosing, suboptimal diuretic use, noncompliance, and possible confounding effects of such concomitant medications as nonsteroidal and anti‐inflammatory drugs or decongestants. The issues underlying drug‐resistant hypertension are listed, together with strategies for overcoming this problem.