[The evolution of myocardial infarction treatment over the past decades. The significance of E.I. Chazov works].

The review is a brief historical insight into the study of myocardial infarction, in which the main discoveries are analyzed that have played an important role in improving the diagnosis and treatment of the disease. A special place in the review is occupied by the work of the outstanding cardiologist and health care organizer E.I. Chazov. More than the half - age, E.I. Chazov investigated various aspects of myocardial infarction, organized a system of medical care for heart attack at all stages. Many studies E.I. Chazov are recognized worldwide.

[Myocardial Hypoenhancement on Multidetector Computed Tomography in Patients With Non-ST Elevation Acute Coronary Syndrome].

The purpose of our study was analysis of myocardial hypoenhancement areas (MHAs) found by multidetector computed tomography (MDCT) in patients with non-ST elevation acute coronary syndrome (NSTEACS) and comparison of these findings with results of standard methods of diagnostics of myocardial infarction and ischemia [electrocardiography (ECG) and echocardiography (ECHO)]. METHODS: MHAs were found in 18 of 21 patients with non-ST segment elevation myocardial infarction (NSTEMI) (85.7%) and only in 3 of 22 patients with unstable angina (UA) (13.6%, p.

[Carotid Plaque Instability in Patients With Acute Coronary Syndrome as Assessed by Ultrasound Duplex Scanning].

AIM: to study carotid plaques structure in patients with acute coronary syndrome by ultrasound duplex scanning. MATERIALS AND METHODS: We included in this study143 patients with acute coronary syndrome (ACS) aged 32-83 years and 28 patients with documented coronary heart disease (CHD) aged 46-83 years. Duplex scanning of carotid arteries was carried out with Philips iU22 ultrasound system and L9-3 linear array transducer. Atherosclerotic plaques in CCA, CCA bifurcation, and ICA from right and left side were investigated. Off-line analysis of B-mode images and plaque gray scale median (GSM) was performed with computer semiautomated workstation MultiVox. RESULTS: 378 plaques of ACS and 59 plaques of CHD patients were studied. We assessed traditional (heterogenous structure, hypoechogenic component, irregular plaque surface) as well as additional (positive remodeling, "layered" structure of plaque, local calcification) criteria of plaque instability. In ACS compared with CHD group there were more plaques with hypoechogenic component (43.4 and 28.8%, p=0.0459), heterogenous structure (77.8 and 64.4%, p=0.0327), irregular surface including irregularities more than 2.0 mm (22.5 and 6.8%, p=0.0048, respectively). There was significant difference in "layered" structure (55.7 and 35.8%, p=0.0011) and insignificant difference in positive remodeling (16.3 and 7.5%, p=0.06, respectively). There were no differences of GSM value (53.1 and 57.2, p=0.24) and local calcification (23.2 and 24.5%, p=0.23, respectively). CONCLUSION: In our study ultrasound duplex scanning revealed that signs of plaque instability in carotid arteries in patients with ACS were more frequent than in patients with stable CHD. The newly introduced parameter "layered" structure of atherosclerotic plaque was found to be most significant.

Safety and efficacy of a novel calcium sensitizer, levosimendan, in patients with left ventricular failure due to an acute myocardial infarction. A randomized, placebo-controlled, double-blind study (RUSSLAN).

AIMS: To evaluate the safety and efficacy of levosimendan in patients with left ventricular failure complicating acute myocardial infarction. METHODS AND RESULTS: Levosimendan at different doses (0.1-0.4 microg x kg(-1) x min(-1)) or placebo were administered intravenously for 6h to 504 patients in a randomised, placebo-controlled, double-blind study. The primary end-point was hypotension or myocardial ischaemia of clinical significance adjudicated by an independent Safety Committee. Secondary end-points included risk of death and worsening heart failure, symptoms of heart failure and all-cause mortality. The incidence of ischaemia and/or hypotension was similar in all treatment groups (P=0.319). A higher frequency of ischaemia and/or hypotension was only seen in the highest levosimendan dose group. Levosimendan-treated patients experienced lower risk of death and worsening heart failure than patients receiving placebo, during both the 6h infusion (2.0% vs 5.9%; P=0.033) and over 24h (4.0% vs 8.8%; P=0.044). Mortality was lower with levosimendan compared with placebo at 14 days (11.7% vs 19.6%; hazard ratio 0.56 [95% CI 0.33-0.95];P =0.031) and the reduction was maintained at the 180-day retrospective follow-up (22.6% vs 31.4%; 0.67 [0.45-1.00],P =0.053). CONCLUSION: s Levosimendan at doses 0.1-0.2 microg x kg(-1) x min(-1) did not induce hypotension or ischaemia and reduced the risk of worsening heart failure and death in patients with left ventricular failure complicating acute myocardial infarction.

Superiority of ibutilide (a new class III agent) over DL-sotalol in converting atrial flutter and atrial fibrillation. The Ibutilide/Sotalol Comparator Study Group.

OBJECTIVE: To compare the efficacy and safety of a single dose of ibutilide, a new class III antiarrhythmic drug, with that of DL-sotalol in terminating chronic atrial fibrillation or flutter in haemodynamically stable patients. DESIGN: Double blind, randomised study. SETTING: 43 European hospitals. PATIENTS: 308 patients (mean age 60 years, 70% men, 48% with heart disease) with sustained atrial fibrillation (n = 251) or atrial flutter (n = 57) (duration three hours to 45 days) were randomised to three groups to receive a 10 minute infusion of 1 mg ibutilide (n = 99), 2 mg ibutilide (n = 106), or 1.5 mg/kg DL-sotalol (n = 103). Infusion was discontinued at termination of the arrhythmia. MAIN OUTCOME MEASURE: Successful conversion of atrial fibrillation or flutter, defined as termination of arrhythmia within one hour of treatment. RESULTS: Both drugs were more effective against atrial flutter than against atrial fibrillation. Ibutilide was superior to DL-sotalol for treating atrial flutter (70% and 56% v 19%), while the high dose of ibutilide was more effective for treating atrial fibrillation than DL-sotalol (44% v 11%) and the lower dose of ibutilide (44% v 20%, p < 0.01). The mean (SD) time to arrhythmia termination was 13 (7) minutes with 2 mg ibutilide, 19 (15) minutes with 1 mg ibutilide, and 25 (17) minutes with DL-sotalol. In all patients, the duration of arrhythmia before treatment was a predictor of arrhythmia termination, although this was less obvious in the group that received 2 mg ibutilide. This dose converted almost 48% of atrial fibrillation that was present for more than 30 days. Concomitant use of digitalis or nifedipine and prolongation of the QTc interval were not predictive of arrhythmia termination. Bradycardia (6.5%) and hypotension (3.7%) were more common side effects with DL-sotalol. Of 211 patients given ibutilide, two (0.9%) who received the higher dose developed polymorphic ventricular tachycardia, one of whom required direct current cardioversion. CONCLUSION: Ibutilide (given in 1 or 2 mg doses over 10 minutes) is highly effective for rapidly terminating persistent atrial fibrillation or atrial flutter. This new class III drug, under monitored conditions, is a potential alternative to currently available cardioversion options.

Protection of ischemic myocardium by exogenous phosphocreatine (neoton): pharmacokinetics of phosphocreatine, reduction of infarct size, stabilization of sarcolemma of ischemic cardiomyocytes, and antithrombotic action.

The effect of exogenous phosphocreatine on ischemic myocardium was studied in experimental infarction in rabbits and in total ischemia of pig heart tissue (in vitro). It is shown that single dose administration of phosphocreatine is followed by its rapid clearance from blood plasma (with a half lifetime of 4-6 min), but constantly high plasma concentration of phosphocreatine can be maintained by its intravenous infusion. When administered by this method into rabbits during experimental myocardial infarction, phosphocreatine reduces by 40% the size of the necrotic zone. Morphological electron microscopic studies using a lanthanum tracer method showed significant protection of the sarcolemma of cardiomyocytes in the perinecrotic zone by phosphocreatine. In vitro studies on the model of total ischemia also showed significant protection of cardiac sarcolemma from irreversible ischemic injury and reduction in the rate of high-energy phosphate depletion in the presence of phosphocreatine in the extracellular space. Additionally, it is demonstrated that creatine kinase released during myocardial infarction into the blood flow and exogenous phosphocreatine administered intravenously may significantly inhibit platelet aggregation by rapid removal of ADP, and thus potentially improve microcirculation during myocardial infarction.