Ludwina Szczepaniak-Chicheł

Asymmetric dimethylarginine and vascular indices of atherosclerosis in patients after coarctation of aorta repair

OBJECTIVE Cardiovascular events are the main cause of premature death after successful repair of aortic coarctation (CoA). The aim of this study was to assess the selected biochemical markers of atherosclerosis in normotensive CoA repaired patients and to establish its relation to ultrasound indexes of vascular pathology. METHODS 62 patients after CoA repair (37 males, age: 34.1 ± 1.4 yrs) and 20 control individuals (10 males, age: 34.8 ± 2.2 yrs) were enrolled in the study. The serum markers: asymmetric dimethylarginine (ADMA), nitrites/nitrates (NOx), high-sensitivity C-reactive protein (hsCRP), and following vascular parameters: flow-mediated dilatation (FMD), intima-media thickness (IMT) and pulse wave velocity (PWV) were analyzed. RESULTS 33 CoA repaired patients were normotensive, and compared to controls, they presented higher serum ADMA concentrations (0.59 ± 0.04 umol/l vs. 0.46 ± 0.03 umol/l, p=0.035). An analysis of the vascular parameters revealed decreased FMD (4.75 ± 0.5%), NMD (11.86 ± 0.8%) and increased PWV (6.90 ± 0.2 m/s) values in the normotensive patients as compared with the control group (FMD: 8.6 ± 0.9%, p<0.001, NMD: 20.94 ± 1.7%, p<0.001; PWV: 5.49 ± 0.2, p=0.023). There were no differences in the serum levels of NOx, hsCRP as well as IMT values between normotensive patients and the control group. A multivariate regression analysis revealed that serum ADMA level was a factor independently associated with the FMD value (r=-0.334; p=0.031) in normotensive CoA repaired group. CONCLUSIONS Early biochemical and vascular indices of atherosclerosis such as increased serum ADMA concentration as well as impaired vasodilatation and increased arterial stiffness are observed in patients after CoA repair. Serum ADMA is a strong predictor of endothelial dysfunction in patients with CoA repair.

Assessment of coagulation profile by thromboelastometry in adult patients with cyanotic congenital heart disease

BACKGROUND Patients with cyanotic congenital heart disease (CCHD) have an increased risk of bleeding and thrombotic complications. Prolonged conventional coagulation screening parameters, such as activated partial thromboplastin time or prothrombin time, are reported in less than 20% of CCHD patients. METHODS The aim of this study was to determine the haemostatic abnormalities in 32 adult patients with CCHD by rotation thromboelastometry (ROTEM) with assessment of coagulation dynamic properties, as a guide for perioperative prophylaxis or haemostatic therapy. The control group consisted of 35 healthy subjects. RESULTS Our results suggest that CCHD patients, in comparison to healthy controls, had a tendency to hypocoagulate with delayed activation of haemostasis and clot formation, initiated by both intrinsic and extrinsic activators. The growth of the clot was slower and the clot firmness was decreased, which may additionally contribute to bleeding diathesis. Moreover, the clot lysis readings suggest higher clot stability in the CCHD group. All velocity parameters were markedly lower in the CCHD patients, indicating a decreased rate of clot formation. Although coagulation tests and platelet count were normal, the usefulness of rotation thromboelastometry in monitoring or guiding therapy in CCHD patients is demonstrated. CONCLUSION In conclusion, our results provide new insights into the data on hypocoagulation with impaired clot lysis in adult CCHD patients as determined by ROTEM. Our findings may assist in determining the optimal management of patients with CCHD undergoing surgery.

Arterial stiffness and arterial function in adult cyanotic patients with congenital heart disease

BACKGROUND Mortality in cyanotic patients with congenital heart diseases (CHD) is high, mainly due to cardiovascular complications. It is known that endothelial dysfunction, increased arterial stiffness, and impaired vascular function have negative influence on cardiovascular prognosis. The aim of the study was to assess parameters of arterial stiffness and vascular dysfunction in cyanotic patients with CHD as well as their potential relation to impaired blood oxygen saturation and polycythemia parameters typical for cyanosis. METHODS A total of 36 CHD cyanotic patients (17 males) (42.3±16.3 years) and 35 healthy individuals (16 males) (39.6±10.4 years) were enrolled. Assessed parameters were intima media thickness and flow-mediated dilatation (FMD). Assessed parameters using applanation tonometry methods were aortic systolic pressure, aortic pulse pressure (AoPP), augmentation pressure (AP), augmentation index (AI), pulse pressure amplification (PPampl), and pulse wave velocity (PWV). RESULTS AoPP (37.3±11.1mmHg vs. 29±6.5mmHg; p=0.002), AP (10.1±7.3mmHg vs. 1.1±3.9mmHg; p=0.00001), AI (24.7±13.5% vs. 3.0±13.6%; p=0.00001), and PWV (7.4±2.1m/s vs. 6.3±0.7m/s; p=0.003) were higher, and PPampl was lower (135.3±16.1% vs. 160.4±12.8%; p=0.00001) in the studied group compared to controls and proved the presence of the increased stiffness of arteries. Impairment of FMD was observed (9.0±5.6 vs. 10.9±4.7; p=0.04). No significant correlations were found between analyzed arterial parameters and biochemical ones characterizing cyanotic patients depicting rheological properties of blood. CONCLUSIONS Cyanotic patients with CHD are characterized by increased arterial stiffness estimated with pulse wave analysis parameters and by deteriorated arterial function expressed with worse vasodilatative response in comparison with healthy population. It may confirm relevance of those mechanisms in development of increased rate of cardiovascular events in this population. Association between oxygen saturation or polycythemia and arterial stiffening or vascular dysfunction was not found in these patients.

Difference between central and peripheral blood pressure in healthy and hypertension-complicated pregnancy.

ObjectiveHemodynamics of a pregnant woman differ and change over time depending on the age of gestation. In the general population, brachial–aortic systolic pressure (SBP–AoSP) difference is known and discussed, whereas in pregnancy, it is not established. On the basis of theoretical premises it is probably different and changes with time of gestation. As AoSP is more relevant for internal organs, also for placental perfusion, and still not widely available in clinical practice, knowledge of the average SBP–AoSP difference in a healthy and complicated pregnancy could be of additional value for the management of pregnancy hypertension. The aim of this study was to assess the SBP–AoSP difference in healthy and hypertensive pregnancies in comparison with nonpregnant controls. Participants and methodsAortic blood pressure with applanation tonometry and brachial blood pressure under standardized conditions were measured monthly and once postpartum in 36 normotensive pregnant women (age: 29.6±4.8 years) and compared with 25 hypertensive pregnancies (age: 30.5±5.4 years) before antihypertensive treatment implementation and with 25 nonpregnant controls (age: 30.2±5.5 years). ResultsIn hypertensive pregnancies, the SBP–AoSP difference was smaller throughout the entire pregnancy than in healthy pregnancies (in the second and third trimester: 14.44 vs. 15.7 mmHg, P=0.002, and 12.9 vs. 14 mmHg, P=0.02), and smaller than that in nonpregnant controls (14.88 mmHg, for third trimester, P=0.036). Comparison of healthy pregnancy and controls showed an insignificant increase in SBP–AoSP difference in the first and second trimester, whereas in the third trimester, because of a larger increase of AoSP, the SBP–AoSP difference was smaller than that in nonpregnant controls (14.66 mmHg, P>0.05). ConclusionA reduced SBP–AoSP difference was found in hypertensive pregnancies compared with healthy controls, which may signify a narrower safety margin for complications. Comparison of pregnant women with nonpregnant controls showed that a significant difference for the SBP–AoSP difference was present only for the postpartum period.

Nadciśnienie oporne a zespół obturacyjnego bezdechu sennego

Obturacyjny bezdech senny (OSA) jest obecnie uwazany za jedną z najczestszych przyczyn nadciśnienia tetniczego opornego. Związek miedzy OSA i nadciśnieniem tetniczym opornym byl opisywany w wielu badaniach. W przebiegu OSA nadciśnienie tetnicze stwierdza sie u 37–56% chorych, a wśrod pacjentow z nadciśnieniem tetniczym opornym OSA wystepuje az u 70–85%. Do rozwoju nadciśnienia tetniczego opornego u osob z obturacyjnymi zaburzeniami oddychania podczas snu dochodzi prawdopodobnie przez wspoldzialanie kilku mechanizmow. Kluczową role odgrywa hipoksja, ktora doprowadza do aktywacji ukladu wspolczulnego, pobudzenia ukladu RAA, zwiekszonego stresu oksydacyjnego i wzrostu wydzielania endoteliny. Pobudzenie ukladu RAA i związane z tym podwyzszone stezenie angiotensyny II i aldosteronu generuje wzrost oporu naczyniowego, co w konsekwencji zwieksza obciązenie nastepcze serca. Wspolistnienie OSA zmniejsza skutecznośc terapii hipotensyjnej. W celu uzyskania kontroli ciśnienia tetniczego w tej grupie chorych konieczne jest rownoczesne stosowanie kilku lekow hipotensyjnych o zroznicowanym mechanizmie dzialania, w tym leku moczopednego.