Cardiac biomakers for the evaluation of acute coronary syndrome.

The traditional diagnosis of myocardial infarction relies primarily within the exhibited patient's clinical presentation, electrocardiographic changes, and elevation in cardiac markers. Since the clinical presentation can be highly variable and EKG changes are not readily present for all patients, the use of markers of cardiac injury to support the diagnosis of myocardial infarction has become a fundamental part of the evaluation of a patient with suspected acute coronary syndrome. In 2007 the Joint European Society of Cardiology/ American College of Cardiology Committee for the Redefinition of Myocardial Infarction concluded that the main criteria for myocardial infarction should be a rise or fall of cardiac biomarkers (namely cardiac troponins and CK-MB) along with: (1) ischemic symptoms, (2) ischemic changes in EKG, (3) Q waves in EKG, or (4) imaging evidence of loss of myocardial viability or (5) wall motion abnormalities. These changes have increased search interests for more sensitive and specific markers of acute myocardial injury; furthermore, dedicated research has commenced in order to specifically allocate markers that could even predict myocardial ischemia. Therefore this article will review traditional employment of cardiac markers, providing current insight, information and experimental data with respect to emerging markers of myocardial ischemia.

Hyperinsulinemic-euglycemic therapy for intoxication with calcium channel blockers.

Conventional therapy for intoxication with calcium channel blockers consists of crystalloid solutions, calcium gluconate, glucagon and vasopressor agents. These therapies often fail to improve hemodynamic function in intoxicated patients. The pathophysologic mechanism proposed for intoxication with these agents, suggest hypoinsulinemia as the determinant factor. We will describe the case of a 77 years old man treated for an overdose of nifedipine and atenolol who arrived at our institution with hypotension and bradycardia. After conventional therapy failed to improve the patient's hemodynamic status, hyperinsulinemia and euglycemia contributed to the improvement of the patient's neurologic and hemodynamic condition. Thus, hyperinsulinemic-euglycemic therapy was of benefit in this patient with hemodynamic compromise secondary to intoxication with calcium channel blocker not responding to conventional therapy. We will review the mechanism of action of calcium channel blocker drugs as well as the clinical presentation and treatment options for calcium channel blocker intoxication.