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Biomedical subjects

Michal Tendera

Publications and source records attributed to Michal Tendera.

33 records · Page 2Linked to original sources
PubMed2004

Efficacy of tenecteplase in combination with enoxaparin, abciximab, or unfractionated heparin: one-year follow-up results of the Assessment of the Safety of a New Thrombolytic-3 (ASSENT-3) randomized trial in acute myocardial infarction.

BACKGROUND: In the ASsessment of the Safety of a New Thrombolytic 3 (ASSENT-3) study, full-dose tenecteplase plus enoxaparin or half-dose tenecteplase plus abciximab reduced the frequency of ischemic complications of acute myocardial infarction, when compared to full-dose tenecteplase plus unfractionated heparin. The aim of the present study was to determine the effect of these fibrinolytic regimens on 1-year mortality. METHODS AND RESULTS: Vital status at 1 year was available for 5942 patients (97.5%) of the 6095 initially enrolled in the study. At 1 year, 515 patients (8.7%) had died. Elderly or female patients and patients with low body weight, previous myocardial infarction, anterior wall myocardial infarction, and diabetes were at increased risk for death at 1 year. Mortality at 1 year was 7.9 % (n = 161) in the heparin group, 8.1% (n = 166) in the enoxaparin group, and 9.3% (n = 188) in the abciximab group (P =.226). Overall, pairwise comparisons did not show a significant difference among treatment regimens: relative risk 1.03 (95% CI 0.82-1.30) for enoxaparin versus heparin (P =.794) and relative risk 1.18 (95% CI 0.95-1.47) for abciximab versus heparin (P =.144). However, 1-year outcome tended to be worse with abciximab in diabetic patients. CONCLUSION: Mortality at 1 year after acute myocardial infarction remains high. Despite a reduction in ischemic complications after acute myocardial infarction with the use of full-dose tenecteplase plus enoxaparin or half-dose tenecteplase plus abciximab, mortality at 1 year was similar in these treatment groups.

Abciximab↗
PubMed2004

The epidemiology of heart failure.

Heart failure is becoming increasingly common. More than 20 million people worldwide are estimated to have heart failure. Prevalence is rising because the population is ageing: in both men and women, the prevalence of heart failure in those aged 80-89 years is roughly 10 times the prevalence in those aged 50-59 years. Coronary artery disease is now the most common cause of heart failure. Better treatment of myocardial infarction means that more people survive with impaired myocardial function, and some of these will develop heart failure in time. Hypertension is also an important contributing factor. Valvular disease, once a major cause of heart failure, has become less prevalent. The median survival after diagnosis of heart failure was only 1.7 years for men and 3.2 years for women, according to Framingham data for the years 1948 to 1988. After five years, only 25% of men and 38% of women were still alive. Preventive and treatment measures have improved this picture somewhat: deaths from heart failure have decreased by about 12% per decade. However, heart failure continues to carry a grave prognosis.

Cardiac Output, Low↗
PubMed2004

The pro- and anti-inflammatory markers in patients with acute myocardial infarction and chronic stable angina.

The aim of this study was to assess the plasma levels of VEGF and interleukin-10 in patients with acute myocardial infarction (AMI) and stable chronic angina (SA) and correlate the values with traditional CHD risk factors, left ventricular ejection fraction (LVEF) and established inflammatory marker hsCRP. Fifty patients with AMI and 30 with SA were enrolled. IL-10 levels in AMI patients were lower than in SA patients (9.81 +/- 5.0 versus 22.63 +/- 8.38 pg/ml, p < 0.00001). IL-10 levels were lower in AMI and SA patients with multiple CHD risk factors than in patients < or = 2 risk factors (SA: 19.48 +/- 2.94 versus 23.77 +/- 2.94 pg/ml; p < 0.005; AMI: 8.64 +/- 4.43 versus 11.85 +/- 4.09 pg/ml; p < 0.05) and patients with AMI and single-vessel than with multi-vessel disease (8.45 +/- 3.86 versus 10.72 +/- 3.95 pg/ml; p < 0.05). VEGF levels in AMI patients were higher than in SA patients (312.0 +/- 67.0 versus 221.0 + /- 50 pg/ml; p < 0.005). VEGF levels were higher in AMI patients with multi-vessel disease than in patients with single-vessel disease (348.74 +/- 45.23 versus 252.05 +/- 21.12 pg/ml; p < 0.005), with LVEF <40% and Killip class III-IV than in patients with LVEF >40% and Killip class I-II (338.8 +/- 51.59 versus 271.8 +/- 50.51 pg/ml; p < 0.005 and 340.71 +/- 52.94 versus 275.45 +/- 49.48 pg/ml; p < 0.05, respectively) and with chest pain > 6 h versus < 6 h (330.03 +/- 58.58 versus 292 +/- 57.53 pg/ml; p < 0.05). HsCRP concentrations in AMI patients were higher than in SA (1.24 +/- 0.47 versus 0.42 +/- 0.14; p < 0.0001). HsCRP was correlated with IL-10 (r = -0.413; p < 0.05) and VEGF (r = 0.319; p < 0.05). Acute myocardial infarction is associated with elevated VEGF levels and decreased concentration of IL-10. There is a significant correlation between levels of inflamatory markers and CHD risk factors and the function of the left ventricle on admission.

Adult↗
PubMed2003

Role of antiplatelet drugs in the prevention of cardiovascular events.

Antiplatelet drugs have an established place in the prevention of vascular events in a variety of clinical conditions, such as myocardial infarction, stroke and cardiovascular death. Both European and American guidelines recommend the use of antiplatelet drugs in patients with established coronary heart disease and other atherosclerotic disease. In high-risk patients, such as those with post-acute myocardial infarction (AMI), ischaemic stroke or transient ischaemic attack, and in patients with stable or unstable angina, peripheral arterial occlusive disease or atrial fibrillation, antiplatelet treatment may reduce the risk of a serious cardiovascular event by approximately 25%, including reduction of non-fatal myocardial infarction by 1/6, non-fatal stroke by 1/4 and cardiovascular death by 1/6. Some data indicate that antiplatelet drugs may also have a role in primary prevention. In people who are aged over 65 years, or have hypertension, hypercholesterolaemia, diabetes, obesity or familial history of myocardial infarction at young age, aspirin may reduce both cardiovascular deaths and total cardiovascular events. Aspirin has been studied and used most extensively. It may exert its beneficial effect not only by acting on platelets, but also by other mechanisms, such as preventing thromboxane A2 (TXA2)-induced vasoconstriction or reducing inflammation. Indeed, experimental data show that low-dose aspirin may suppress vascular inflammation and thereby increase the stability of atherosclerotic plaque. Moreover, in human studies, aspirin seems to be most effective in those with elevated C-reactive protein levels. Vascular events, however, do occur despite aspirin administration. This may be due to platelet activation by pathways not blocked by aspirin, intake of drugs that interfere with aspirin effect or aspirin resistance. In the CAPRIE (Clopidogrel vs. Aspirin in Patients at Risk of Ischaemic Events) study, long-term clopidogrel administered to patients with atherosclerotic vascular disease was more effective than aspirin in reducing the combined risk of ischaemic stroke, myocardial infarction or vascular death. In the setting of coronary stenting, a double regimen including aspirin and ticlopidine or clopidogrel has proved more effective in the prevention of in-stent thrombosis than aspirin alone. Chronic oral administration of the inhibitors of platelet membrane receptor GP IIb/IIIa has been largely disappointing.

Aspirin↗
PubMed2003

Effects of initiating carvedilol in patients with severe chronic heart failure: results from the COPERNICUS Study.

CONTEXT: Beta-blockers remain underused despite their established utility for improving outcome in heart failure. Concerns that initiation of treatment produces few immediate benefits and may have important risks may be deterring widespread use. OBJECTIVE: To evaluate the early effects of the beta-blocker carvedilol in patients with severe heart failure. DESIGN, SETTING, AND PATIENTS: Randomized, double-blind, placebo-controlled trial conducted from October 28, 1997, to March 20, 2000, at 334 hospital centers in 21 countries among 2289 patients with symptoms of heart failure at rest or with minimal exertion who were clinically euvolemic and had a left ventricular ejection fraction of less than 25%. INTERVENTION: Patients were randomly assigned to receive carvedilol, with start dosage of at 3.125 mg twice daily with uptitration to a target dosage of 25 mg twice daily (n = 1156), or placebo (n = 1133), in addition to their usual medications for heart failure. MAIN OUTCOME MEASURES: Death, hospitalization, or permanent withdrawal from study drug, as well as adverse events during the first 8 weeks of treatment. RESULTS: The carvedilol group experienced no increase in cardiovascular risk but instead had fewer patients who died (19 vs 25; hazard ratio [HR], 0.75; 95% confidence interval [CI], 0.41-1.35); who died or were hospitalized (134 vs 153; HR, 0.85; 95% CI, 0.67-1.07); or who died, were hospitalized, or were permanently withdrawn from treatment (162 vs 188; HR, 0.83; 95% CI, 0.68-1.03). These effects were similar in direction and magnitude to those observed during the entire study, and were apparent particularly in the 624 patients with recent or recurrent decompensation or a very depressed left ventricular ejection fraction. Differences in favor of carvedilol became apparent as early as 14 to 21 days following initiation of treatment. Worsening heart failure was the only serious adverse event with a frequency greater than 2% and was reported with similar frequency in the placebo and carvedilol groups (6.4% vs 5.1%). CONCLUSIONS: These data suggest that, in clinically euvolemic patients, the relation of benefit to risk during initiation of treatment with carvedilol is similar to that seen during long-term therapy with the drug. Our findings should provide the reassurance needed to encourage the high levels of use that are warranted by the results of long-term clinical trials.

Adrenergic beta-Antagonists↗
PubMed2002

Effect of carvedilol on the morbidity of patients with severe chronic heart failure: results of the carvedilol prospective randomized cumulative survival (COPERNICUS) study.

BACKGROUND: Beta-blocking agents improve functional status and reduce morbidity in mild-to-moderate heart failure, but it is not known whether they produce such benefits in severe heart failure. METHODS AND RESULTS: We randomly assigned 2289 patients with symptoms of heart failure at rest or on minimal exertion and with an ejection fraction <25% (but not volume-overloaded) to double-blind treatment with either placebo (n=1133) or carvedilol (n=1156) for an average of 10.4 months. Carvedilol reduced the combined risk of death or hospitalization for a cardiovascular reason by 27% (P=0.00002) and the combined risk of death or hospitalization for heart failure by 31% (P=0.000004). Patients in the carvedilol group also spent 27% fewer days in the hospital for any reason (P=0.0005) and 40% fewer days in the hospital for heart failure (P<0.0001). These differences were as a result of both a decrease in the number of hospitalizations and a shorter duration of each admission. More patients felt improved and fewer patients felt worse in the carvedilol group than in the placebo group after 6 months of maintenance therapy (P=0.0009). Carvedilol-treated patients were also less likely than placebo-treated patients to experience a serious adverse event (P=0.002), especially worsening heart failure, sudden death, cardiogenic shock, or ventricular tachycardia. CONCLUSION: In euvolemic patients with symptoms at rest or on minimal exertion, the addition of carvedilol to conventional therapy ameliorates the severity of heart failure and reduces the risk of clinical deterioration, hospitalization, and other serious adverse clinical events.

Adrenergic beta-Antagonists↗
PubMed2002

Age-adjustment of HRV measures and its prognostic value for risk assessment in patients late after myocardial infarction.

THE AIMS OF OUR STUDY WERE: (1) to establish the normal limit of the heart rate variability (HRV) indices in a healthy population and in its four age-related subgroups, including a new HRV index, HRV fraction; and (2) to analyse the frequency and predictive value of abnormally low HRV in a population of post-infarction patients in respect to the cut-points chosen (raw or age-adjusted). METHODS: Normal population of 296 healthy subjects (81 f, 215 m, aged 47+/-10 years) and post-infarction population of 298 patients (>3 months after acute MI, 65 f, 233 m, aged 56+/-10) were examined. The normal population was divided into 4 subsets based on age at entry: <35, 35-44, 45-54 and >54 years. Based on a 24 h ECG the standard HRV analysis was performed to obtain the following indices: mean RR interval, SDNN and SDANN. A new index of HRV, HRV fraction (HRVF, %) was calculated based on a numerical processing of the RR intervals return map. All patients were followed for 24 months. The endpoints of the study were death (of any reason) and cardiac death. RESULTS: Means and normal limits for SDNN, SDANN and HRVF were: 147+/-36 ms [95% CI 89-220], 136+/-36 ms [79-212] and 53+/-9% [35-68]. The HRV values below the lower normal limit (LNL) were observed in 20-25% of post-MI patients. During a 2 year follow-up there were 36 deaths (total mortality 12.1%), while cardiac mortality was 9.1% (27 cases). The prognostic value of the analysed indices was similar (sens approximately 53-61%, spec approximately 79-84%, PPV 22-26%, NPV 93-94%) irrespective of the cut-points chosen (calculated either for the entire population or age-related). Multivariate Cox regression analysis showed that a decrease of any index below the LNL was associated with a approximately 2.5 and approximately 4-6 times greater risk for death and cardiac death, irrespective of the cut-points chosen. CONCLUSIONS: The age-dependence of the HRV indices does not seem to significantly influence their prognostic value. Thus, a single cut-point of a particular HRV index, based on the entire population, is sufficient to be treated as a risk predictor. In the late phase of myocardial infarction the value of any global HRV index lying below the lower normal limit indicates independently an increased risk of death, especially cardiac death. The new index (HRV fraction) seems to be a promising substitute for currently used standard indices.

Adult↗
PubMed2002

Time and frequency analysis of beat-to-beat R-T interval variability in patients with ischaemic left ventricular dysfunction providing evidence for non-neural control of ventricular repolarisation.

BACKGROUND: Determinants of temporal lability in ventricular repolarisation are not fully recognised. We aimed to analyse the sources of RT variability by comparing normal subjects and patients after myocardial infarction (MI) with either depressed or preserved left ventricular (LV) function. METHODS: One hundred and nine patients (27 women, 82 men, aged 51 +/- 9 years) were divided into three groups: 24 patients (pts) with an uncomplicated angiographically proven coronary heart disease (CHD-group), 59 post-MI pts with preserved LV function (LVEF > 40%, PMI-N-group) and 26 post-MI pts with depressed LV function (LVEF < 40%, PMI-L-group). An ECG signal of low-noise 512 heartbeats was recorded using a computer-assisted amplifier (16 bit, 2 kHz). The onset and offset of the R-wave and T-wave were determined automatically. The magnitude of R-R and R-T variability was measured as the standard deviation of all intervals (SD-RR and SD-RT, ms, respectively). Their relationship was quantified by the correlation coefficient r(RT/RR). Power spectral density of RR or RT variability was estimated with the FFT (Welch's averaged periodogram, Hanning window) and frequency relation was quantified using a squared coherence spectrum (SCS). For all spectral and cross-spectral measurements two frequency ranges were considered: high (0.15-0.50 Hz, HF) and low (0.04-0.15 Hz, LF). Spectral power and SCS of RR and RT variability for both ranges (HF(RR), LF(RR), HF(RT), LF(RT), SCS(HF), SCS(LF)), and the ratios LF/HF(RR) and LF/HF(RT) were drawn for comparisons. The central frequency of HF(RR) was considered as the frequency of respiration (f(resp), Hz). RESULTS: In the PMI-L group the SD-RT was significantly greater compared to the remaining groups and accounted for almost 10% of the SDRR. Also, the coefficient r(RT/RR) was weakest in this group. The spectral indices of RR variability were similar in all groups, while the greatest value of the HFRT was observed in the PMI-L group. The SCS(LF) was insignificant in this group, contrary to the CHD and PMI-N groups. Additionally, there were significant negative relationships between f(resp) and spectral indices of RT variability in PMI-patients with depressed LV function. CONCLUSION: A greater beat-to-beat variation in RT interval duration along with increased power of its HF component indicates an important role of respiration in ventricular repolarisation control, while reduced time- and frequency RT-RR relationships seem to relate to an impaired process of ventricular duration adaptation.

Adult↗