Order of magnitude smaller limit on the electric dipole moment of the electron.

The Standard Model of particle physics is known to be incomplete. Extensions to the Standard Model, such as weak-scale supersymmetry, posit the existence of new particles and interactions that are asymmetric under time reversal (T) and nearly always predict a small yet potentially measurable electron electric dipole moment (EDM), d(e), in the range of 10(-27) to 10(-30) e·cm. The EDM is an asymmetric charge distribution along the electron spin (S(→)) that is also asymmetric under T. Using the polar molecule thorium monoxide, we measured d(e) = (-2.1 ± 3.7stat ± 2.5syst) × 10(-29) e·cm. This corresponds to an upper limit of |d(e)| < 8.7 × 10(-29) e·cm with 90% confidence, an order of magnitude improvement in sensitivity relative to the previous best limit. Our result constrains T-violating physics at the TeV energy scale.

[Deviation of activated partial thromboplastin time from optimal level after 12 hours of intravenous infusion of unfractionated heparin -- an independent predictor of recurrence and unfavorable 30-day prognosis in patients with myocardial infarction].

Aim of the study was to assess significance of deviations of activated partial thromboplastin time (APTT) from optimal level (50-75 sec) after 48 hours of intravenous infusion of unfractionated heparin (UFH) in streptokinase treated patients with myocardial infarction (MI) for prognosis of nonfatal reinfarction and cumulative criterion comprising cardiac death, nonfatal MI and early postinfarction angina. Infusion of streptokinase (1,500,000 U in 30-60 min) was carried out after loading dose of aspirin (250 mg) and intravenous bolus (5,000 U) of UFH in 75 patients (age 34-76 years) admitted within 6 hours after onset of acute ST-elevation MI. UFH infusion was started prior to termination of administration of streptokinase and continued for 48 hours. During first 12 hours infusion rate was 1,000 or 800 U/hour in patients with body mass > or = 80 and < 80 kg, respectively. During initial 12 hours infusion rate was corrected if at 6 hours APTT was less than 40 or exceeded 150 sec. After 12 hours a nomogram was used for UFH dose adjustment according to APTT. Maximal number of optimal APTT values during UFH infusion just reached 50%. During first 12 hours prevailed values above 75 sec, after 24 and 36 hours -- values below 50 sec. Deviation of APTT from optimal level in 12 hours after onset of UFH infusion was the only independent predictor of nonfatal recurrent MI during following 30 days (relative risk [RR] 9.01, 95% confidence interval [CI]1.1 to 77.2; p=0.043). Independent predictors of cumulative criterion were level of risk of death according to TIMI scale (RR 1.47, 95% CI 1.-3 to 2.11; p=0.036) and deviation of APTT from optimal level in 12 hours after onset of UFH infusion (RR 3.24, 95%CI 1.05 to 10.5; p=0.046). It should be noted that rather than suboptimal excessive hypocoagulation by 12th hour of UFH infusion was associated with worse prognosis. APTT levels in 6, 24, and 36 hours of UFH infusion had no prognostic significance in relation to events assessed in the study.

[First experience of clopidogrel application in the treatment of acute myocardial infarction with ST-elevation]. / Pervyi opyt primeneniia klopidogrela pri lechenii ostrogo infarkta miokarda s pod''emom segmenta ST.

AIM: To examine efficacy of clopidogrel before thrombolytic therapy (TLT) in patients with acute myocardial infarction (AMI). MATERIAL AND METHODS: A total of 72 patients (48 males and 24 females) admitted to hospital within 6 hours since the onset of acute myocardial infarction (AMI) were divided into three groups. Group 1 and 2 patients (n = 38 and 20, respectively) were given a prehospital stress dose of aspirin (250-500 mg), group 3 patients (n = 14) received this dose at admission. TLT with streptokinase or actilise (1,500,000 IU and 100 mg, respectively) was given to all the patients. Before TLT group 2 received a stress dose of clopidogrel (300 mg), after TLT--75 mg/day. 12-Lead ECG, CFK activity and troponine content examinations were made. The patients were observed for 30 days. The recovery of coronary circulation (CC) was evaluated by dynamics of a total lowering of the elevated ST segment. RESULTS: CC completely recovered 60 min after TLT in 16, 10 and 7% patients of groups 1, 2 and 3, respectively. CC recovered partially in 24, 55 and 7% patients, respectively. In 90 min after TLT partial recovery of CC was observed in 21, 31 and 43%, respectively; in 180 min the effect was absent in 19, 15 and 38%, respectively. 30-Day lethality was 11.1% and was high in group 3. No lethal outcomes were seen in group 2. CONCLUSION: It is possible to achieve better myocardial reperfusion after TLT and improve 30-day outcomes in MI patients given combined antithrombocytic therapy.

[Comparison of eprosartan and captopril in left ventricular systolic dysfunction: relation of efficacy to myocardial viability]. / Eprosartan v sravnenii s kaptoprilom pri sistolicheskoi disfunktsii levogo zheludochka, obuslovlennoi infarktom miokarda: otsenka éffektivnosti v zavisimosti ot zhiznesposobnosti miokarda.

Patients with left ventricular ejection fraction below 45% (mean 39+/-3.7%) were randomized either to captopril (n=33) or eprosartan after miocardial infarction (n=33) on days 3-7 of myocardial infarction. All patients were subjected to echocardiography and 40 to perfusion myocardial scintigraphy with (99m)TC-Technetril. Myocardial viability was defined as presence of perfusion reserve in dysfunctional segments during test with nitroglycerin. Dysfunctional myocardium was found to be viable in 62.5% of patients. Fifty six patients completed 3 months follow up and were restudied. By the time of the second study 28 patients continued captopril (37.5-150 mg, average dose 72+/-34.2 mg/day) and 28 - eprosartan (300-600 mg, average dose 471+/-151 mg/day). Captopril was stopped or its dose corrected in 28% of patients. In eprosartan group there were no side effects which required withdrawal of the drug. Similar increases of ejection fraction occurred on both groups (from 38+/-2.1 to 49+/-6.7%, p<0.001 and from 39+/-4 to 51+/-6.5%, p<0.001, in eprosartan and captopril groups, respectively). Magnitude of left ventricular ejection fraction change did not depend on the presence of viable myocardium. However in both treatment groups improvement of myocardial perfusion and decrease of left atrial dimensions were found only in patients with viable myocardium at initial study.

[The use of a beta-blocker esmolol in patients with acute myocardial infarction treated with streptokinase]. / Opyt primeneniia beta-adrenoblokatora ésmolola u bol'nykh ostrym infarktom miokarda, poluchaiushchikh tromboliticheskuiu terapiiu streptokinazoi.

Infusion of esmolol (50-300 mcg/kg/min, mean 119-/+75.5 mcg/kg/min, average duration 3.2-/+1.22 h)) was carried out in 49 streptokinase treated patients within 6 hours of myocardial infarction. Infusion was associated with slowing of heart rate and lowering of mean dynamic systolic blood pressure (by 22%). No changes of stroke volume and index occurred. Complications requiring either cessation of infusion or decrease of its rate developed in 14.3% of patients (lowering of systolic blood pressure below 100 mm Hg in 5, complete atrio-ventricular block in 2) as a rule in the beginning of the infusion.