sFlt-1, PlGF, sFlt-1/PlGF ratio and uterine artery Doppler for preeclampsia diagnostics.

BACKGROUND AND OBJECTIVE: Angiogenic factors such as soluble fms-like tyrosine kinase 1 (sFlt-1) and placental growth factor (PlGF) play a key role in the pathogenesis of preeclampsia. Uterine artery (UA) blood flow is important for preeclamptic pregnancy outcome, but small amount of evidence suggests UA dopplerometry for preeclampsia diagnostics and management. The aim of our study was to compare the value of angiogenic factors and UA dopplerometry in preeclampsia diagnosis and determine cut-off values to obtain the highest sensitivity and specificity of the parameter. MATERIALS AND METHODS: We performed a case controlled study of 72 pregnant women with preeclampsia and 72 healthy matched controls. SFlt-1 and PlGF were measured in serum samples, the sFlt-1/PlGF ratio was calculated and UA pulsatility (PI) and resistance (RI) indexes were registered. RESULTS: Significantly higher levels of sFlt-1, sFlt-1/PlGF ratio and mean UAPI and UARI and lower levels of PlGF were found in preeclampsia group when compared to controls. The highest sensitivity and specificity for preeclampsia had SFlt-1/PlGF and PlGF with the cut-off values of ≥35 (sensitivity of 95.8% and specificity of 96.2%, respectively) and ≤138.6pg/mL (sensitivity of 95.8% and specificity of 93.7%, respectively). For diagnostics of early-onset preeclampsia, all factors sFlt-1, PlGF and sFlt-1/PlGF had equal significance with the cut-off values of ≥7572pg/mL (specificity of 97.5%, sensitivity 92.3%), ≤100.5pg/mL (specificity 96.2%, sensitivity of 100%) and ≥54.6 (specificity 97.5%, sensitivity 97.5%) respectively. CONCLUSIONS: The sFlt-1/PlGF ratio and PlGF are superior to sFlt-1, UAPI and UARI for preeclampsia diagnosis. For early-onset preeclampsia diagnostics either sFlt-1 or PlGF is sufficient.

Strain value in the assessment of left ventricular function and prediction of heart failure markers in aortic regurgitation.

BACKGROUND: This study aimed to examine the relationship between biochemical heart failure markers and conventional left ventricular (LV) measurements and strain assessed by speckle-tracking echocardiography in chronic aortic regurgitation (AR) patients. METHODS AND RESULTS: LV strain, rotation assessed by speckle-tracking echocardiography, LV measurements, mitral annular plane excursion measured by M-mode, and systolic annular plane velocity measured by tissue Doppler echocardiography were analyzed in 64 controls and 65 chronic AR patients. Reduced LV longitudinal strain with increased apical rotation was seen in normal plasma NT-proBNP patients. Increased NT-proBNP (>400 pg/mL) was associated with reduced longitudinal and circumferential strain, diminished mitral annular plane excursions and systolic annular plane velocity. Global systolic longitudinal strain was an indepentent predictor of NT-proBNP level. Longitudinal strain less than 16.0% was the cutoff value for NT-proBNP>400 pg/mL (P<0.05). CONCLUSIONS: LV strain analysis in conjunction with NT-proBNP evaluation is a useful tool in assessing LV function in AR patients.

Tetramethylphenylenediamine protects the isolated heart against ischaemia-induced apoptosis and reperfusion-induced necrosis.

BACKGROUND AND PURPOSE: Cytochrome c when released from mitochondria into cytosol triggers assembly of the apoptosome resulting in caspase activation. Recent evidence suggests that reduced cytochrome c is unable to activate the caspase cascade. In this study, we investigated whether a chemical reductant of cytochrome c, N,N,N',N'-tetramethylphenylene-1,4-diamine (TMPD), which we have previously shown to block cytochrome c-induced caspase activation, could prevent ischaemia-induced apoptosis in the rat perfused heart. EXPERIMENTAL APPROACH: The Langendorff-perfused rat hearts were pretreated with TMPD and subjected to stop-flow ischaemia or ischaemia/reperfusion. The activation of caspases (measured as DEVD-p-nitroanilide-cleaving activity), nuclear apoptosis of cardiomyocytes (measured by dUTP nick end labelling assay), mitochondrial and cytosolic levels of cytochrome c (measured spectrophotometrically and by elisa), and reperfusion-induced necrosis (measured as the activity of creatine kinase released into perfusate) were assessed. KEY RESULTS: We found that perfusion of the hearts with TMPD strongly inhibited ischaemia- or ischaemia/reperfusion-induced activation of caspases and partially prevented nuclear apoptosis in cardiomyocytes. TMPD did not prevent ischaemia- or ischaemia/reperfusion-induced release of cytochrome c from mitochondria into cytosol. TMPD also inhibited ischaemia/reperfusion-induced necrosis. CONCLUSIONS AND IMPLICATIONS: These results suggest that TMPD or related molecules might be used to protect the heart against damage induced by ischaemia/reperfusion. The mechanism of this protective effect of TMPD probably involves electron reduction of cytochrome c (without decreasing its release) which then inhibits the activation of caspases.

[Evaluation of a chronic fatigue in patients with moderate-to-severe chronic heart failure]. / Serganciuju vidutinio sunkumo ir sunkiu letiniu sirdies nepakankamumu letinio nuovargio tyrimas.

THE AIM OF THE STUDY: To evaluate the chronic fatigue and its relation to the function of hypothalamus-pituitary-adrenal axis in patients with New York Heart Association (NYHA) functional class III-IV chronic heart failure. MATERIAL AND METHODS: A total of 170 patients with NYHA functional class III-IV chronic heart failure completed MFI-20L, DUFS, and DEFS questionnaires assessing chronic fatigue and underwent echocardiography. Blood cortisol concentration was assessed at 8:00 am and 3:00 pm, and plasma N-terminal brain natriuretic pro-peptide (NT-proBNP) concentration was measured at 8:00 am. Neurohumoral investigations were repeated before cardiopulmonary exercise test and after it. RESULTS: The results of all questionnaires showed that 100% of patients with NYHA functional class III-IV heart failure complained of chronic fatigue. The level of overall fatigue was 54.5+/-31.5 points; physical fatigue - 56.8+/-24.6 points. Blood cortisol concentration at 8:00 am was normal (410.1+/-175.1 mmol/L) in majority of patients. Decreased concentration was only in four patients (122.4+/-15.5 mmol/L); one of these patients underwent heart transplantation. In the afternoon, blood cortisol concentration was insufficiently decreased (355.6+/-160.3 mmol/L); reaction to a physical stress was attenuated (Delta 92.9 mmol/L). Plasma NT-proBNP concentration was 2188.9+/-1852.2 pg/L; reaction to a physical stress was diminished (Delta 490.3 pg/L). CONCLUSION: All patients with NYHA class III-IV heart failure complained of daily chronic fatigue. Insufficiently decreased blood cortisol concentration in the afternoon showed that in the presence of chronic fatigue in long-term cardiovascular organic disease, disorder of a hypothalamus-pituitary-adrenal axis is involved.

[Heart rate and systolic blood pressure response during the early exercise test and cardiovascular mortality after myocardial infarction]. / Kruvio sukelti sirdies susitraukimu daznio bei kraujospudzio svyravimai ir serganciuju miokardo infarktu mirstamumas.

UNLABELLED: Exercise cardiography still remains the cornerstone of noninvasive evaluation of functional status of cardiovascular system and is almost uniformly performed after myocardial infarction. The patients after myocardial infarction can be divided into relative high- and low-risk groups for subsequent cardiac events if all information available on the exercise test is used. OBJECTIVE: The aim of this study was to evaluate the prognostic significance of the shape of heart rate and systolic blood pressure curves (their dynamic characteristics) during the early exercise testing and after it and to design the prognostic system capable to recognize patients with a high risk of coronary death during 2 years after myocardial infarction. MATERIAL AND METHODS: The submaximal exercise testing within 3 weeks of acute myocardial infarction was performed on 894 patients. Cases of noncardiac deaths or patients subjected to coronary bypass surgery were excluded from the further analysis. At the end of 2 years after myocardial infarction, there were 426 survivors and 42 cases of cardiac death. At 2-year follow-up after infarction in the nonsurvivor group, there were only 42.2% of patients with exercise-induced ST segment depression. This shows that prognostic importance of ST depression is insufficient and demands research of more consistent signs. RESULTS: The cardiovascular response to exercise was interpreted as transiting process of self-regulation of cardiovascular system, and the new predictive signs were found based on the curves of heart rate and systolic blood pressure during the exercise and after it. The prognostic value of these signs was established. The combined use of both the new predictive signs and usual data of early exercise test shows the high predictive possibility of test - the early cardiac death was predicted in 80% of cases. CONCLUSION: The combined use of both, the widely accepted data of early exercise test after myocardial infarction and dynamic characteristics of heart rate and systolic blood pressure, increased the predictive power of the test.

Brain natriuretic peptide and other cardiac markers predicting left ventricular remodeling and function two years after myocardial infarction.

BACKGROUND: Left ventricular remodeling is a complex pathologic process of progressive left ventricular dilatation, leading to dysfunction and heart failure in patients after myocardial infarction. OBJECTIVE: To evaluate biochemical markers, reflecting cardiac remodeling process after first myocardial infarction and compare those markers with clinical characteristics of left ventricular remodeling. MATERIAL AND METHODS: Brain natriuretic peptide, troponin I, creatine kinase, creatine kinase MB mass, lactate dehydrogenase levels were measured in 30 patients with acute myocardial infarction on days 1, 2, 3-7 . Brain natriuretic peptide was measured at 3 months, 6 months, and 2 years after myocardial infarction. Echocardiographic parameters of left ventricular remodeling were determined in acute phase (day 1-3), at 3 months, 6 months, and 2 years after MI. RESULTS: In acute phase, brain natriuretic peptide level progressively increased according to worsening of left ventricular geometry: in normal left ventricle geometry group, brain natriuretic peptide level was 84.1 (58.7-121) pg/mL, in concentric remodeling group - 125 (69.2-165) pg/mL, in concentric hypertrophy group - 128 (74-368) pg/mL, and in eccentric hypertrophy group - 470 (459-494) pg/mL, P=0.02. Patients who had increased left ventricular end diastolic diameter index during 2-year period had higher brain natriuretic peptide level in the acute phase (584 (249-865) pg/mL vs. 120 (67-202) pg/mL, P=0.04) and also higher peak lactate dehydrogenase and troponin I levels. CONCLUSIONS: Brain natriuretic peptide level in acute phase of myocardial infarction is strongly associated with the markers of myocardial injury and related to left ventricular geometry changes and remodeling. Brain natriuretic peptide together with troponin I levels in acute phase of myocardial infarction might be useful in predicting subsequent cardiac function.

[Prevalence of cardiovascular risk factors in coronary heart disease patients with different low-density lipoprotein phenotypes]. / Serganciuju isemine sirdies liga rizikos veiksniu daznumas esant skirtingam mazo tankio lipoproteinu fenotipui.

UNLABELLED: Low-density lipoprotein (LDL) heterogeneity is now well recognized as an important factor reflecting differences in lipoprotein composition, size, metabolism and genetic influences. There is an abundant evidence of data supporting the clinical importance of small, dense LDL particles in the development of coronary heart disease. The aim of the study was to determine the prevalence of LDL phenotypes A and B in coronary artery disease patients and to assess the incidence of cardiovascular risk factors in groups with different phenotype. MATERIAL AND METHODS: Demographic, anamnestic and clinical data as well as complete lipid profile--total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein (HDL) cholesterol and triglycerides--were collected on 1,220 patients (63.7% male and 36.3% female, mean age 61.3+/-11.0 years) with coronary artery disease. Triglycerides/HDL cholesterol ratio was calculated. By value of triglycerides/HDL cholesterol ratio, proposed V. Hanak and authors, the patients were identified as having LDL phenotype A when the ratio was < or =1.64 (a value of 3.8 as expressed in milligrams per deciliter) and phenotype B when the ratio was >1.64. RESULTS: LDL profile in 60.5% of patients was identified as phenotype A and in 39.5%--as phenotype B. The incidence of coronary heart disease risk factors was higher in phenotype B patients as compared to phenotype A subjects (hypertension - 85.1% vs. 75.2%, p<0.001, diabetes mellitus--13.9% vs. 5.5%, p<0.001, obesity--46.7% vs. 28.0%, p<0.001, reduced physical activity--64.5% vs. 57.0%, p<0.001). Metabolic syndrome was present in 85.1% of phenotype B patients, while this cluster of metabolic disorders was detected only in 36.8% of phenotype A subjects. The incidence of myocardial infarction, presence of multiple high-grade coronary lesions were also higher in phenotype B patients as compared to their counterparts with phenotype A (22.2% vs. 17.2%, p<0.05 and 13.7% vs. 8.7%, p<0.05). CONCLUSION: LDL phenotype B was determined in 39.5% of coronary heart disease patients. Atherogenic LDL subclass pattern B correlated with higher incidence of major coronary heart disease risk factors.

Brain natriuretic peptide and other cardiac markers in predicting left ventricular remodeling in patients with the first myocardial infarction.

UNLABELLED: Left ventricular remodeling is a complex pathologic process of progressive dilatation, leading to dysfunction and heart failure in patients with acute myocardial infarction. The aim of our study was to determine and evaluate biochemical markers, reflecting cardiac remodeling process in the patients with the first myocardial infarction and to compare those markers with clinical characteristics of left ventricular remodeling. MATERIAL AND METHODS: Concentrations of brain natriuretic peptide and markers of myocardial necrosis were measured on 1st , 2nd and 7th day after the onset of the first acute myocardial infarction, as well as after 3 and 6 months in 30 patients. Parameters of left ventricular remodeling were determined by echocardiographic investigation, which was performed in the acute phase and after 3 and 6 months. RESULTS: Brain natriuretic peptide concentration was found to be related to the left ventricular geometry in the acute phase: brain natriuretic peptide peak level was lower in the patients with the normal left ventricular geometry than in the patients with the changed left ventricular geometry (140.6+/-63.3 pg/ml vs. 385.7+/-283.9, p<0.05). Brain natriuretic peptide concentration in the acute phase was higher in the patients who had increased left ventricular end diastolic diameter through 6-month period (348.9+/-309.4 pg/ml vs. 145.1+/-109.6 pg/ml, p<0.05). Higher troponin I (58.8+/-33.6 ng/ml vs. 30.9+/-31.3 ng/ml, p<0.05) and troponin T (4.5+/-2.2 ng/ml vs. 1.9+/-2.0 ng/ml, p<0.05) levels were also associated with left ventricular dilatation through 6 months after myocardial infarction. CONCLUSIONS: Brain natriuretic peptide level in acute phase of myocardial infarction is related to the left ventricular geometry changes and remodeling. Brain natriuretic peptide together with other cardiac markers might be useful in predicting subsequent cardiac function.

[Comparison of clinical performance of troponin T and troponin I in diagnosing acute myocardial infarction]. / Troponino T ir troponino I informatyvumas diagnozuojant umini miokardo infarkta.

In this article we investigate clinical specificity and sensitivity of cardiac troponin T and cardiac troponin I tests in the patients who were admitted to the hospital with suspected acute coronary syndrome. We investigated 87 patients: the clinical investigation was performed, electrocardiogram was recorded and concentrations of cardiac troponin T and troponin I were estimated. According to the recommendations of the manufacturers of troponin T and troponin I tests, threshold diagnostic troponin T concentration for myocardial infarction was considered > or =0.1 ng/ml and troponin I > or =1.0 ng/ml. Troponin T concentration was analyzed in 60 patients; the sensitivity of troponin T test in diagnosing acute myocardial infarction was 85%, and the specificity was 87.2%. Troponin I test was performed in 46 patients; the sensitivity of the test was 76% and the specificity was 76.2%. In case when both troponin T and I tests were performed, the sensitivity of troponin T was 100% and specificity was 78% and of troponin I - respectively 86% and 78%. According to the receiver operator characteristic analysis there was no significant difference between the general accuracy of troponin T and troponin I in distinguishing patients with and without acute myocardial infarction. According to the results of receiver operator characteristic analysis, the biggest clinical sensitivity and specificity were achieved when threshold myocardial infraction diagnostic concentration of troponin T was considered >0.04 ng/ml and of troponin I >0.69 ng/ml.