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Biomedical subjects

N A Gratsianskiĭ

Publications and source records attributed to N A Gratsianskiĭ.

At least 19 recordsLinked to original sources

[Levels of fatty acid binding protein before and after direct current cardioversion of atrial fibrillation or flutter in patients without acute coronary syndrome].

UNLABELLED: It is not known whether FABP suggested as an early marker of myocardial necrosis increases after direct current cardioversion (DCC). Moreover there are no data on FABP levels in patients with atrial fibrillation (AF) and flutter. AIM: To find out whether DCC induces acute changes of FABP levels in patients with AF or flutter without acute coronary syndrome. METHODS: Serum FABP and troponin I (TnI) were measured in 63 pts treated with DCC (monophasic shocks) because of AF (n=45, 71.4%) or atrial flutter (n=18, 28.6%). Initial energy was 50J for atrial flutter and 200J for AF. Median total energy was 200J, max 660J. Blood was sampled before DCC and in 30, 60 min, 3, 6 h after first shock. TnI and FABP were measured with single-step sandwich method ("Hytest" Finland). Upper limit of normal range (ULN) for TnI was 0.4 ng/ml (recommended by manufacturer). Serum FABP was measured in healthy volunteers and 95th percentile was used as ULN (4.67 ng/ml). RESULTS: Most pts (n=40, 63.5%) had baseline FABP > ULN (median for all pts--5.55 ng/ml). In 11 pts (17.4%) baseline FABP was > 2 ULN. No relationship was found between baseline FABP and age, sex, duration of arrhythmia, concomitant ECG changes, and presence of overt coronary heart disease or clinical signs of heart failure. Median FABP level increased after DCC (p for trend 0.00014). FABP levels after DCC correlated with total delivered energy. Delivery of > or = 2 shocks compared with 1 shock was associated with higher FABP (median 60 min--9.65 and 5.24 ng/ml, p=0.009; 3 h--12.41 and 5.84 ng/ml, p=0.01, respectively). Median TnI levels were below ULN at each study point. After DCC TnI did not exceed ULN in 61 pts and remained unchanged in 2 pts with baseline TnI above ULN. CONCLUSION: Unexpectedly most pts with AF and atrial flutter had elevated FABP at baseline. After DCC FABP increased in proportion with total delivered energy. Elevations of FABP levels were not associated with rapid increases of TnI so skeletal muscle damage can be a likely cause of elevated FABP. AF, atrial flutter and DCC for these arrhythmias should be considered as sources of false positive results when FABP is used for diagnosis of acute myocardial infarction.

Acute Disease↗

[Short term simvastatin use in patients with heart failure of ischemic origin. Changes of blood lipids, markers of inflammation and left ventricular function].

AIM: To study changes of left ventricular function and some markers of inflammation during use of simvastatin in patients with ischemic systolic heart failure. METHODS: Statin naive patients (n=70) with coronary heart disease (CHD), NYHA class II-IV HF and LV ejection fraction (EF) 35% or less after 1 month of stabilization were randomized to simvastatin 40 mg/day (n=36) or no statin (n=34). Lipids, tumor necrosis factor alpha (TNF), and C-reactive protein (CRP) were measured and echocardiography carried out at baseline and in 4 months. In patients with sinus rhythm (n=48) left ventricular diastolic function was assessed by Doppler echo. Seven patients were not restudied and analysis included data from 32 (statin) and 31 (control) patients. RESULTS: Groups were similar except baseline CRP which was significantly higher in controls. In statin treated patients reduction of low density lipoprotein (LDL) cholesterol (CH) was 42%, triglyceride levels also significantly decreased. High density lipoprotein CH rose by 14.4 and 12.9% in statin and control groups, respectively. Despite lower initial level decrease of CRP was significant only in statin group. No significant changes of TNF occurred in either group. Left ventricular EF rose equally in statin treated (+5.7+/-4.7%) and untreated (+4.1+/-4.6%) patients (p=ns). Significant increase of peak atrial filling velocity (A) and decrease of E/A in statin group were difficult to interpret in the presence of systolic dysfunction. CONCLUSION: Short term simvastatin use in patients with systolic heart failure due to CHD caused lowering of LDLCH and CRP however this was not associated with changes of left ventricular EF different from those in control group.

Aged↗

[Early use of gemfibrozil in patients with non ST Elevation acute coronary syndrome. Changes of markers of inflammation and von Willebrand factor].

UNLABELLED: It is not known whether PPAR-alpha agonist gemfibrozil is able to exert rapidly its lipid modulating, potential antiinflammatory and antithrombotic effects in patients with non-ST elevation acute coronary syndrome (NSTEACS), as some other lipid lowering drugs e.g. statins do. METHODS: We randomized 44 patients with NSTEACS to open gemfibrozil (n=22, 600 mg b.i.d for 90 days) or no gemfibrozil (controls, n=22) within 24 hours after pain onset. Semiquantitative C-reactive protein (CRP) latex test was used at baseline for exclusion of patients with overt inflammation. All patients received dalteparin or enoxaparin for >48 hours and oral aspirin (125 mg/day) and were treated noninvasively. Lipids, high sensitive CRP, soluble CD40 ligand (CD40L) and von Willebrand factor (vWF) activity were assessed on days 1 (baseline), 4, 7, 14, 30 and (except CD40L) 90. RESULTS: Gemfibrozil use was associated with significant lowering of triglycerides by day 30, however it did not prevent acute significant decline of high density lipoprotein cholesterol (HDL-C), which was similar in both groups. CD40L level significantly increased while CRP levels decreased by day 30 in both groups. Moreover, selection of a subgroup with baseline HDL-C <1.0 mmol/l did not reveal any difference in changes of CRP or CD40L between gemfibrosil treated and control patients. vWF activity did not change in controls and significantly increased in gemfibrozil group by days 7, 14, but from lower baseline level. CONCLUSION: In patients with NSTEACS early administration of gemfibrozil was not associated with positive changes of CRP and CD40L levels or vWF activity compared with control group.

Acute Disease↗

[Prognostic significance of heart fatty acid binding protein in patients with non-ST elevation acute coronary syndrome: results of follow-up for twelve months].

UNLABELLED: Value of heart fatty acid binding protein (FABP) for medium term prognosis in patients with non-ST elevation acute coronary syndrome (NSTEACS) is not well established. AIM: To compare prognostic value of FABP levels with those of troponin I (TnI) and creatine kinase MB (CK MB) activity in patients with NSTEACS. METHODS: Serum FABP and TnI levels (HyTest), CK MB activity (Biocon) were measured in 203 patients with NSTEACS (mean age 63.9+/-11.5 years, 52.2% male). Blood was sampled at admission within 12 (median 3.83) hours and in 6 and 12 hours after onset of pain. Upper limits of normal range (ULN) for TnI and CK MB were 0.4 ng/ml and 25 U/l, respectively. Serum FABP was measured in 53 healthy volunteers (mean age 44.3+/-13.3) and 95th percentile was used as ULN (4.67 ng/ml). Deaths and nonfatal MIs (events) were registered during one year follow-up. RESULTS: There were 47 events (23%, 23 deaths and 24 nonfatal MIs). Patients with events compared with those without events had significantly higher TnI and CK MB 12 hours after onset of pain and significantly higher FABP at all time points of blood sampling. Multivariate (step-up) analysis selected the following independent predictors of events: elevated FABP 6 hours after pain onset (OR 2.45, 95% CI 1.14-5.24; p=0.021), T-wave inversion on admission ECG, age >65 and regular use of nitrates before hospitalization. Sensitivity of elevated FABP 6 hours after pain onset was 78.4%, specificity -- 45.1%. After exclusion from analysis of all or just admission and 6 hours FABP data elevated TnI 12 hours after onset of pain became an independent predictor of events. CONCLUSION: In this group of patients with NSTEACS among markers of myocardial necrosis (FABP, TnI, MB CK) obtained serially during first 12 hours after pain onset elevated FABP was the best predictor of events during 1 year follow up for subjects in whom blood sample could be done 6 hours after pain onset.

Aged↗

[Indirect comparison of changes of parameters of hemostasis during short-term use of ticlopidine and clopidogrel in patients with non-ST elevation acute coronary syndrome].

UNLABELLED: Effects of thienopyridines ticlopidine (TIC) and clopidogrel (CL) on hemostasis in patients (pts) with non-ST-elevation acute coronary syndromes (NSTEACS) have not been compared. AIM: To compare changes of some markers of coagulation and platelet activation during short term use of TIC and CL in pts with NSTEACS. METHODS: Aspirin treated pts with NSTEACS (<48 hours from pain onset, Braunwald class IIIb) were included into 2 consecutive studies: 37 pts receiving unfractionated heparin (UFH) were randomized to open TIC (n=19, 500 mg BID for 2 days and 250 mg BID for subsequent 5 days) or no TIC (n=18); 19 pts receiving enoxaparin were randomized to CL (n=10, 300 mg on day 1 and 75 mg/day for subsequent 6 days) or no CL (n=9). At baseline, on days 1, 3, 7 and 14 (7 days after thienopyridines discontinuation) we measured ADP-induced and spontaneous platelet aggregation (PA), levels of prothrombin fragment 1+2 (F1+2), thrombin-antithrombin complex (TAT), von Willebrand factor (vWF), fibrinogen, tissue type plasminogen activator antigen (tPA), plasminogen activator inhibitor activity (PAI) and D-dimer (Dd), and counted platelet number. RESULTS: Maximal suppression of PA was obtained on 7-th and 3-rd days in TIC and CL groups, respectively. Compared with their controls TIC treated pts in 7 days after TIC discontinuation had lower levels of TAT (3.61 and 2.77 ng/ml, respectively, r<0.05) and fibrinogen (3.84 and 3.16 g/l, respectively, r<0.05). There were no significant differences between intervention and control groups in these parameters in study with CL. Level of vWF in TIC treated pts was lower than in controls on days 3 (163 and 186%, respectively, r<0.05) and 14 (144 and 173%, respectively, p<0.01). In CL treated pts vWF level was lower relative to controls on days 3 and 7 (152 and 185%, r<0.05, 141 and 166%, r<0.05, respectively). tPA levels in study with TIC did not differ between intervention and control groups. tPA in CL treated pts exceeded its level in controls on days 3, 7, and 14 (25.7 and 20.2 ng/ml, 26.5 and 12.9 ng/ml, 24.6 and 15.7 ng/ml, respectively). On the same days level of Dd in pts receiving CL was significantly higher than in control group (969 and 702 ng/ml, 970 and 575 ng/ml, 806 and 484 ng/ml on days 3, 7 and 14, respectively). Activity of PAI in TIC group was higher than in controls on day 7 (13.6 and 8.2 U/l, r<0.05), and at this moment level of Dd was lower in TIC treated patient (770 and 515 ng/ml in control and TIC groups, respectively, r<0.05). CL and control groups had similar PAI activity. Mean platelet volume rose relative to initial level and to control group only in CL treated patients (9.0 and 8.4 fl, 9.6 and 8.4 fl, 9.4 and 8.5 fl in CL and control groups on days 0, 7 and 14, respectively; r<0.05 for comparison between groups on days 7 and 14). CONCLUSION: In pts with NSTEACS both thienopyridines attenuated acute phase elevation of vWF. The use of TIC in UFH treated pts was associated with indirect signs of decreased thrombin activity and some inhibition of fibrinolysis while the use of CL in enoxaparin treated pts was associated with signs of activation of fibrinolysis.

Anticoagulants↗

[Register of Acute Coronary Syndromes in Russia: Management and Inhospital Outcomes in ST Elevation Acute Coronary Syndrome].

Data of about 50 consecutive patients with acute coronary syndromes aged at least 18 years admitted to 59 hospitals in different Russian cities were collected from November 2000 to July 2001. In 1412 patients included into registry presumably ischemic symptoms within previous 24 hours were associated with ST-segment elevation or left bundle branch block on ECG. Demographics, history, characteristics of acute coronary syndrome, management and outcomes during hospitalization as well as diagnoses at presentation and discharge were analyzed. Markers of myocardial necrosis were measured in 61% of patients. Rates of interventions that may improve outcome appeared to be low. In acute phase aspirin was used in 79% (contraindications were reported in 6.2%). Within 12 hours of symptoms onset thrombolysis was performed in 12.9%, coronary angioplasty in 1.2%. In patients hospitalized within 12 hours of symptoms onset these rates were 21.3 and 1.9%, respectively. Beta-blockers were prescribed no more than in 60% of cases (fist dose intravenously in 4.3%). Lipid lowering drugs were recommended at discharge to 12.3% of patients (to 21.1% of those with known hypercholesterolemia). ACE inhibitors during hospitalization were used in 68.1% of patients. After acute phase of the disease coronary angioplasty was performed in 5 patients, CABG in 1. However hospital mortality appeared to be not high (8.5% in general, 10.1% in patients with overt acute myocardial infarction at presentation). Reinfaction rate in this registry was impossible to assess, angina recurrences were registered in every fifth patient.

Acute Coronary Syndrome↗

[Enoxaparin for the Treatment of Unstable Angina and Non-ST Segment Elevation Myocardial Infarction: the ENO-INT Study].

UNLABELLED: AIM. To assess safety and efficacy of enoxaparin in patients with UA/NSTEMI in an open-label, multi-centre, non-comparative study and to compare the results with data from large-scale randomized trials ESSENCE and TIMI-11B. METHODS: Patients hospitalized with a diagnosis of recent UA/NSTEMI were treated with 1 mg/kg enoxaparin every 12 hours for 2-8 days. The composite endpoint of the study was death, myocardial infarction (MI) or recurrent angina at day 15 (or hospital discharge). Minor and major bleedings were recorded. RESULTS: A total of 1902 patients were enrolled in 109 centers across 24 countries, of which 1901 received at least one injection of enoxaparin and 1785 (93.8%) completed the study (follow-up). Throughout the study (day 180) 21.4% of patients underwent at least one revascularization, of which 4.4% were urgent. The incidence of the composite efficacy endpoint was 16.3% after 15 days and 27.9% on day 180, which was comparable with the enoxaparin arm of the ESSENCE/TIMI 11B studies, and lower than the incidence found in the UFH arm of those studies. At day 15 or hospital discharge the occurrence of major and minor haemorrhages was 1.1 and 6.6%, respectively, which was lower than in ESSENCE/TIMI 11B. More bleeding complications (major and minor) were noted in patients aged </= 75 years (11.2%) versus those of <75 years (7.1%). Independent predictors of 180-day adverse outcome (death, MI, recurrent angina) were: age (OR 1.02, 95% DI: 1.01-1.03), prior aspirin treatment (OR 1.33, 95% DI: 1.15-1.47) and previous PTCA (OR 1.4, 95% DI: 1.11-1.59). CONCLUSION: These results which are highly consistent with those previously reported from ESSENCE and TIMI 11B trials evidence for safety and effectiveness of enoxaparin in the treatment of UA and NSTEMI.

Angina, Unstable↗

[Relationship between heart rate changes during reflex tests and heart rate variability in patients with recent myocardial infarction].

BACKGROUND: Low heart rate variability (HRV) reflecting predominance of sympathetic tone is an independent predictor of sudden cardiac death after myocardial infarction (MI). We have previously shown that decreased heart rate (HR) response during reflex tests (breathing 6 per minute and Valsalva maneuver at the end of the first week after MI is also associated with elevated risk of sudden death during subsequent 2 years. AIM: To elucidate relationship between HR response to breathing 6 per minute and Valsalva maneuver, and HRV as standard non-invasive method of assessment of autonomic regulation of the heart. MATERIAL: Tests with breathing 6 per minute and Valsalva maneuver were performed on 4-11 (median 8) days of MI in 188 patients (68.1% males) aged 34-75 (median 62) years, 93.6% of whom received beta-blockers. Parameters studied were difference between maximal and minimal HR during 1(st) min of controlled breathing (DHR) and Valsalva ratio (VR). Standard time- and frequency-domain HRV measures were calculated from 15-min ECG strips at bed rest just before tests and from 24-hour ECG recordings after tests. RESULTS: In patients with low values of DHR (<3.36) and VR (<1,13) most of HRV parameters were also significantly decreased. Most close association was found between low DHR and low SDNNi and LF power calculated from 24-hour Holter recordings, between low VR and low LF power at bed rest. CONCLUSION: Direct correlation between HR response to reflex tests and parameters of HRV allows to suggest that decreased HR response to controlled breathing and Valsalva maneuver in patients with recent MI also reflects presence of marked sympathetic predominance.

Autonomic Nervous System↗

[Relationship Between Lipid Lowering and Changes of Hemostasis and Inflammation During Use of Statins in Non-ST Elevation Acute Coronary Syndrome].

AIM: To analyze relationship between changes of lipid levels and parameters of hemostasis and inflammation in a previously reported comparative study of some biological effects of pravastatin and atorvastatin in patients with non ST elevation acute coronary syndrome (NSTEACS). METHODS: Ninety aspirin and heparin treated patients with NSTEACS were randomized to open pravastatin 40 mg/day (n=31) and atorvastatin 10 (n=30) or 40 mg/day (n=29). At baseline, on days 7 and 14 we measured levels of thrombin-antithrombin complex (TAT), prothrombin fragments 1+2 (F1+2), D-dimer, von Willebrand factor (vWF) and C-reactive protein (CRP) and assessed platelet aggregation. Spearman correlation coefficients were calculated for mean deltas of all parameters {[(baseline - day 7) + (baseline - day 14)]/2} for all patients. The patients were divided into quartiles according to absolute LDL CH lowering by day 14. RESULTS: Levels of LDL and total CH significantly decreased in all groups (atorvastatin 40 mg/day >> atorvastatin 10 mg/day > pravastatin). Contrary to pravastatin the use of atorvastatin was associated with increases of F 1+2, TAT, and decrease of vWF. Platelet aggregation decreased only in atorvastatin 40 mg/day group (p<0.05) and CRP decreased in combined atorvastatin group (p<0.05). Most pronounced relationship existed between changes of lipid levels and vWF. Lowering of total and LDL CH correlated positively with decreases of vWF (r=0.25, p=0.018, and r=0.23, p=0.032, respectively) and quartile analysis showed that vWF decreased only in patients with marked LDL CH lowering (quartiles 3, 4). Negative correlation was found between changes of total CH and those of TAT (r=-0.22, p=0.039), and between changes of CRP and HDL CH (r=-0.24, p=0.03). TAT and F 1+2 levels significantly increased in those patients in whom LDL CH level <2.5 mmol/l was achieved by day 14 and tended to decrease in other patients. No relationship was found between changes of lipids and platelet aggregation. CONCLUSION: Rapid (in 14 days) changes of some parameters of hemostasis occurring during treatment of patients with NSTEACS with various statins were related to degree of lipid lowering possibly irrespective of a statin used. Most evident was relationship between changes of lipids and von Willebrand factor.

Acute Coronary Syndrome↗

[Comparison of various methods of assessment of heart rate variability including simple cardiovascular reflex tests as predictors of sudden cardiac death after myocardial infarction.].

UNLABELLED: Long term heart rate variability is used for prediction of sudden cardiac death (SD). There are simpler methods of assessment of autonomic cardiac control - registration of heart rate response to reflex tests and determination of heart rate variability (HRV) on short ECG recordins. Comparative value for prognosis of SD after myocardial infarction (MI) of these 3 techniques has not been studied yet. METHODS: Valsalva maneuver with calculation of Valsalva ratio (VR) and deep breath test with calculation of difference between average maximal and minimal HR during first minute of test (HR difference - HRD) were performed in 188 patients on days 4-11 of MI (68.1% men, age 34-75 years, 93.6% on beta-blockers, without heart failure NYHA IV on the day of tests). Time and frequency domain HRV measures were assessed during 15 min at bed rest and at Holter monitoring for median 24 h on the same day as reflex tests. RESULTS: During follow up for 2.1+/-0.8 years there were 9 sudden and 13 non-sudden cardiac deaths. ROC analysis was used to determine cut-off values of VR, HRD and HRV measures for dichotomization of patients into those with low- and high-risk of SD and these values were used in logistic regression analysis. The following parameters were univariate predictors of SD: obtained at reflex tests - VR <1.13 (OR 7.8, 95% CI 1.6-39.0; p=0.012), HRD <3.36 (OR 4.3, 95% CI 1.1-16.9; p=0.034); HRV parameters from 15 min ECG recordings - total frequency power <739 ms(2), VLF power <294 ms(2), LF power <197 ms(2) and LF/HF <1.5; HRV parameters from long term ECG recording - LF power <491 ms(2), LF/HF <1.4. At multivariate analysis only LF power for 15 min <197 ms(2) among HRV parameters remained independent predictor of SD (OR 24.2, 95% CI 2.4-245.5; p=0.007). Other predictors were clinical - VF during acute phase of MI (OR 94.7, 95% CI 4.2-2115.2; p=0.004) and history of MI (OR 8.4, 95% CI 1.4-48.5; p=0.017). CONCLUSION: In this population of patients without severe heart failure low LF power on 15 min resting ECG recordings on days 4-11 of MI was more powerful predictor of sudden cardiac death during subsequent 2 years than other HRV parameters including heart rate response to Valsalva maneuver and deep breath test.

Death, Sudden, Cardiac↗

[Simple cardiovascular reflex tests in prediction of sudden death after myocardial infarction: which method to prefer?].

BACKGROUND: Some evidence exists that heart rate response to simple provocative maneuvers may predict sudden cardiac death (SD) after myocardial infarction (MI). However optimal test has not been not established yet. Aim of this study was to compare prognostic value of different noninvasive reflex tests after MI. METHODS: Four reflex tests were consecutively performed in 188 patients on days 4-11 of MI (68% men, age 34-75 years, 93.6% on beta-blockers, without heart failure NYHA IV on the day of tests). Time- and frequency domain heart rate variability measures were obtained during 5 min at active standing and at bed rest with controlled breathing 6 and 15 per minute. In addition difference between average maximal and minimal heart rate at first minute of breathing 6 per minute (HRD) and Valsalva ratio (VR) were calculated. ROC analysis was used to determine cut-off values of studied measures for dichotomization of patients into those with low- and high-risk of SD and these values were used in logistic regression analysis. RESULTS: During follow up for 2.1+/-0.8 years there were 9 SD. Univariate predictors of SD were follows: HRD <3.36; VR <1.13; pNN 50 <2.5, total spectral power <1021 ms(2), LF power <229 ms(2) and HF power <65 ms(2) at active standing; pNN 50 <2.3, LF power <129 ms(2) and HF power <111 ms(2) during controlled breathing 15 per minute. HF power <65 ms(2) during active standing (OR 28.8, 95% CI 4.1-104.2; p=0.0001, positive predictive value 29.4%) and VR <1.13 (OR 6.0, 95% CI 1.02-34.3; p=0.04, positive predictive value 11.5%) were independent predictors of SD. For combination of these parameters OR increased to 34.9 (95% CI 6.7-181.6; p<0.001), positive predictive value to 50%. CONCLUSION: Among simple noninvasive reflex tests in this small group of patients with routine beta-blockers use and without severe heart failure active standing with calculation of HF power seems preferable method for prediction of SD after MI. Its predictive value may be enhanced by combination with Valsalva ratio.

Adult↗