526 : !TERATURE Hkl’!i~!’ ~

Barth C, Ojile M, Pearson AC, Labovitz AJ: Ultra short-acting intravenous P-adrenergic blockade as add-on therapy in acute unstable angina. Am Heart J 121:782-788,199l

After baseline Doppler echocardiographic examination, intrave- nous esmolol was titrated to reduce rate-pressure product by at least 20% in 21 patients with persistent angina despite conven- tional medical therapy. Esmolol dose at target response was 17 mgimin (range, 8 to 24). During therapy, heart rate and blood pressure decreased significantly. Chest pain was alleviated in 18 of 21 patients. Cardiac output was decreased secondary to heart rate reduction and stroke volume was unchanged. Left ventricular ejection fraction was unchanged. Early diastolic ventricular filling was improved indicating improvement in left ventricular diastolic function.

van der Linden J, Casimir-Ahn H: When do cere- bral emboli appear during open heart operations? A transcranial Doppler study. Ann Thorac Surg 51:237- 241,199l

A transcranial Doppler ultrasound velocimeter placed over the right middle cerebral artery was used to detect cerebral air emboli in 10 patients during valvular cardiac operations. Hypothermic cardiopulmonary bypass was used with membrane oxygenators without arterial filters. Scattered emboli were observed during aortic cannula insertion. initiation of cardiopulmonary bypass, and aortic unclamping with the heart beating while empty. Despite vigorous deairing maneuvers, a large number of emboli were recorded during the filling of the beating heart in all patients. The authors conclude that cerebral emboli in cardiac procedures are most likely during translocation of blood from the heart-lung machine to the patient when the heart is beginning to eject despite careful deairing procedures. The authors advocate use of a short period of filling of the beating heart before final closure of the aortic incision or vent to decrease the incidence of cerebral emboli.

Lu H, Soria C, Cramer EM, et al: Temperature dependence of plasmin-induced activation or inhibi- tion of human platelets. Blood 77:996-1005,199l

In an in vitro study of human platelets incubated with plasmin, the relationship of temperature- and plasmin-induced platelet changes was studied. At 37”C, platelets exposed to low-dose plasmin (0.2 CU/mL) underwent shape change but no release reaction. At 22”C, the same dose of plasmin caused platelet degranulation, increased expression of platelet surface fibrinogen receptors, and platelet aggregation. This study suggests that temperature-dependent plasmin-platelet interaction may contrib-

Nagaoka H, lnnami R, Murayama F, et al: Effects of aprotinin on prostaglandin metabolism and plate- let function in open heart surgery. J Cardiovasc Surg 32:31-37, 1991

The en%& of aprotinin were evaluated in a controlled study involving 23 patients undergoing cardiopulmonary bypass. In the treated patients. 2 x IO4 KIUikg of aprotinin was infused following induction of anesthesia and was also included in the pump prime. A continuous aprotinin infusion, 0.5 x 10’ KIU/kg/h, was adminis- tered during bypass. Platelet counts decreased similarly in both patient groups during bypass. Thromboxane B, and P-thrombo- globulin levels in the control group increased significantly during bypass, indicating platelet activation and release reaction. These increases were significantly suppressed in the aprotinin-treated patients. Platelet aggregability to adenosine diphosphate and collagen was decreased significantly during bypass in the control group. No reduction occurred in the treated patients.

Paradis NA, Martin GB, Rosenburg J, et al: The effect of standard and high-dose epinephrine on coronary perfusion pressure during prolonged car- diopulmonary resuscitation. JAMA 265:1139-1144, 1991

The effect of two epinephrine doses on coronary perfuslon pressure during cardiopulmonar)i resuscitation was studied in 32 patients with prolonged cardiac arrest refractory to advanced cardiac life support. Patients remaining in cardiac arrest after multiple 1-mg doses of epinephrine (average time elapsed from hospital arrival, 25 minutes: estimated time elapsed from collapse, 47 minutes) received a high dose. 0.2 mgikg. Coronary perfusion pressure was not significantly increased following standard epineph- rine dose. The increase in pressure after the high dose (11.3 mm Hg) was significant. High-dose epinephrine was more likely to elevate coronary perfusion pressure above the previously demon- strated critical value of 15 mm Hg. The authors conclude that high-dose epinephrine has the potential to improve rates ot resuscitation because coronary perfusion pressure is a strong predictor of outcome. The clinical implications to be derived from this report are discussed in an accompanying editorial.

ACKNOWLEDGMENT

The papers reviewed in this issue were selected from those published in the following journals: American Heart Journal, Ameti- can Journalof Cardiology. Annals of Thorucic Surgery, Blood, Journul of the American College of Cardiology, Journal of the American Medical Association, and Journal of Curdiovascular Surgery.