Search

There is a long latent period in the clinical course of aortic valve stenosis in adults. Symptoms ussually occur in the case of critical stenosis, when aortic orifice area is under 0.7cm² (0.4 cm²/m²). In this study 78 patients with critical aortic valve stenosis were investigated. The first manifestation of the disease was dyspnea (78.2%), angina (52.5%), less often a syncope (34.6%), while 17.9% of patients were asymptomatic. Left ventricular systolic function was preserved in 77% of patients, while left ventricular dyastolic dysfunction occured in almost all the patients. In 42 patients (53.4%) aortic valve replacement was performed. Left ventricular systolic function improved in 88.1% of patients postoperativelly, as well as in patients with preoperativelly preserved or poor systolic function. Recovery was fast particularly during the first 6 postoperative months. After the surgery the improvement of the left ventricular dyastolic function was slower then systolic, particularly in patients with extreme hypertrophy of myocardium in whom the process of recovery might last several years. [ABSTRACT FROM AUTHOR]

Background: The management of patients with acute pulmonary embolism (aPE) depends on the severity of aPE. The timing of death in various aPE risk subgroups is only partially known., Methods: 1618 patients with an objectively established aPE diagnosis with computed tomography pulmonary angiography enrolled in the regional PE registry were included in the study. According to ESC criteria, patients were stratified at admission to the hospital in four risk strata. The timing of PE-related and non-PE-related deaths was analyzed regarding mortality risk., Results: PE-related, and non-PE-related hospital death rates were 1.1 % and 1.5 % in low, 1.1 % and 4.8 % in intermediate-low, 8.1 % and 5.9 % in intermediate-high, and 27.7 % and 6.9 % in high-risk groups, respectively. The median time of PE-related and non-PE-related death across the PE mortality risk were: 4 (1.7-7.5) and 7.0 (4-14.7) days in low, 1.5 (1.0-9.5) and 11.5 (2.0-21.0) days in intermediate-low, 4.0 (2.0-9.0) and 9.0 (5.7-18.2) days in intermediate-high, 2.0 (1.0-4.75) and 7.0 (3.0-21.2) days in high-risk subgroups. 48.2 % and 17.1 % of patients who died in the high and intermediate-high risks died during the first hospital day. After the 6th hospitalization day, PE-related deaths were recorded in 43.9 % of deaths from intermediate-high and 17.9 % from high-risk subgroups., Conclusion: PE-related mortality is prominent on the first hospitalization day in high and intermediate-high-risk PE. A substantial proportion of intermediate-high and high-risk patient's PE deaths occurred after the first 6 days of hospitalization., Competing Interests: The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (© 2023 The Authors.)

Background: Electrocardiography (ECG) signs, typical or acute pulmonary embolism, and their changes can be used for the prediction of clinical and haemodynamic outcomes., Purpose: To study the predictive value of the resolution of admission ECG signs in higher risk pulmonary embolism patients for 30-day survival and for the decrease in right ventricular systolic pressure., Methods: We analysed the 12-lead ECGs at admission and daily for the first 5 days after hospitalisation in 110 intermediate-high and high-risk pulmonary embolism patients admitted to the intensive care unit of a single tertiary centre. The predictive value of the resolution of four ECG signs were analysed for 30-day survival and for the changes in right ventricular systolic pressure during hospitalisation: S-wave in the first standard lead, right bundle branch block pattern, S-wave in the aVL lead and negative T-waves in precordial leads., Results: ECG recordings showed the existence of S-wave in the I lead in 71 (64.5%), S-wave in the aVL in 77 (70%), right bundle branch block pattern in 30 (27.3%) and negative T-waves in 66 (60%) patients. All-cause 30-day in-hospital mortality was 13.6%. Among the ECG signs, only the presence of right bundle branch block at admission was significantly associated with 30-day all-cause mortality (hazard ratio (HR) adjusted for age, gender and right ventricular systolic pressure at admission was 7.7, 95% confidence interval (CI) 2.1-27.9; P =0.002). The resolution of three ECG signs during the first 5 days of hospitalisation, S-wave in the I lead (HR 26.4, 95% CI 3.1-226.6; P =0.003), S-wave in the aVL (HR 21.5, 95% CI 2.6-175.3; P =0.004) and right bundle branch block configuration (HR 5.2, 95% CI 1.3-20.8; P =0.020) were associated with 30-day survival. The intermediate-high and high-risk pulmonary embolism patients with S-wave resolution in lead aVL had 0.0% and 7.1% 30-day all-cause mortality, respectively. The patients with resolution of the S-wave in the first lead and in aVL as well as right bundle branch block had more pronounced changes in right ventricular systolic pressure at discharge (27±13 vs. 13±15 mmHg; P =0.011 for S-wave in I lead resolution, 27±12 vs. 15±17 mmHg; P =0.004 for S-wave in aVL resolution and 23±14 vs. 9±14 mmHg; P =0.040 for right bundle branch block resolution) than patients without resolution., Conclusion: Resolution of S-waves and right bundle branch block in ECG correlates with lower all-cause 30-day mortality in intermediate-high and high-risk pulmonary embolism patients. Resolution of S-waves in the first lead and in aVL and right bundle branch block correlates with a decrease of right ventricular systolic pressure.

Purpose: The purpose of this study is to investigate the effect of two of the most important functional CYP1A2 variations -3860G > A and -163C > A on carbamazepine pharmacokinetics in Serbian pediatric epileptic patients., Methods: The study involved 40 Serbian pediatric epileptic patients on steady-state carbamazepine treatment. Genotyping for -3860G > A and -163C > A was carried out using PCR-RFLP method, and carbamazepine plasma concentrations were determined by high pressure liquid chromatography (HPLC) method. For pharmacokinetic analysis, NONMEM software with implementation of ADVAN 1 subroutine was used., Results: CYP1A2 polymorphism -163C > A was found at the frequency of 65.0 %, while -3860G > A was not detected. The correlation between weight-adjusted carbamazepine dose and carbamazepine concentration after dose adjustment was significant only in carriers of -163C/C and C/A genotypes (r = 0.68, p = 0.0004). The equation that described population clearance (CL) was CL (l/h) = 0.176 + 0.0484 * SEX + 0.019 * CYP1A2 + 0.000156 * DD, where SEX has a value of 1 if male and 0 if female, CYP1A2 has a value of 1 if -163A/A and 0 if -163C/C or C/A, and DD is the total carbamazepine daily dose (mg/day)., Conclusions: CYP1A2 -163A/A genotype influence carbamazepine pharmacokinetics. In addition to sex and total carbamazepine daily dose, -163C > A CYP1A2 polymorphism should be considered as a predictor of carbamazepine clearance.

This study shows that the abrupt cessation of one-year clopidogrel treatment was not associated with thrombotic events in a prospective, multicentre study that enrolled 200 patients subjected to coronary stent implantation and treated with aspirin + clopidogrel 1 year after the stent placement. The aim of the study was to investigate the causes of a sustained increase of platelet aggregability, considering that the values of platelet aggregation stimulated with ADP + PGE1 (ADPHS values) significantly increased 10-90 days after the cessation of clopidogrel. Values of platelet aggregation induced by thrombin receptor activating peptide (TRAP values) and arachidonic acid (ASPI values) were divided into quartiles on the basis of ADPHS values 10 days after stopping clopidogrel (ADPHS10 ). There was a significant difference between TRAP values divided into quartiles according to ADPHS10 , 10, 45 and 90 days after stopping clopidogrel (P < 0.001, all), and ASPI values across the same quartiles 10 and 45 days after the cessation of clopidogrel (P = 0.028 and 0.003). The results of the study indicate that patients with early pronounced rebound phenomena to clopidogrel termination have a long-term (at least 90 days) increased platelet aggregation to other agonists such as thrombin-related activated protein and arachidonic acid, suggesting the complex mutual relationship of various factors/agonists influencing the function of platelets., (© 2016 John Wiley & Sons Australia, Ltd.)

We aimed to examine the rate of thrombotic events after discontinuation of one year clopidogrel therapy in patients with implanted coronary stent, and to determine platelet aggregability by multiple electrode analyzer after cessation of clopidogrel. This prospective, multicenter study enrolled 200 patients subjected to coronary stent implantation and treated with aspirin + clopidogrel one year after the stent placement. Platelet aggregation was measured using 3 agonists [adenosine diphosphate with PGE(1) (ADPHS), arachidonic-acid (ASPI), and thrombin receptor activating peptide (TRAP)] on the day of cessation of clopidogrel and at 10, 45, and 90 days after clopidogrel was stopped. Two thrombotic events were registered during the 6-months follow up (one ischemic stroke and one myocardial infarction; incidence of 1%). The mean values of ADP + PGE(1)- and ASPI-induced aggregation 10 - 90 days after the cessation of clopidogrel were significantly higher than values obtained before the termination of the drug (P < 0.001, all). Cessation of clopidogrel did not influence the TRAP-induced aggregation, which reached the plateau in all measurements. In conclusion, the incidence of thrombotic events after the cessation of one-year clopidogrel treatment might be lower than expected in patients with implanted coronary stent.

We report the case of 64-year-old female patient with pulmonary embolism and bilateral femoropopliteal deep vein thrombosis caused by heparin-induced thrombocytopenia type II (HIT II) resistant to danaparoid sodium and subsequently administered lepirudin in whom a single late plasmapheresis performed on day 6 of the initiation of treatment of HIT reversed the course of the disease, preventing its highly potential fatal outcome. Primarily administered lepirudin was not only ineffective but even led to further aggravation of the patient's clinical state and platelet count drop in the first stage of the HIT treatment. The improvement of the patient's clinical state was not achieved before therapeutic plasma exchange (TPE) had removed the greatest part of pathogenetic circulating substrate. Only after TPE, lepirudin, introduced again, led to the platelet count recovery. In the subsequent course of the treatment, lepirudin was combined with an overlapping oral anticoagulant. Previously positive heparin aggregation test and fast particle gel heparin-platelet factor 4 immunoassay were normalized as well as the patient's clinical status. Early plasmapheresis, administered within 4 days of the onset of thrombocytopenia in HIT, as a beneficial therapeutic measure in certain individual cases, is indisputable. However, our results do not concur with previously reported findings of the so far most comprehensive study on plasmapheresis performed in the management of HIT with thrombosis, discrediting late plasmapheresis administered 4 days after the onset of the disease not only as ineffective, but even as an aggravating factor. Our results suggest the possible beneficial impact of late plasmapheresis as a method that may reverse a prothrombotic process and lead to a fast improvement in the patient's platelet count, especially in cases initially resistant to thrombin inhibitors.