Oral direct inhibitors of thrombin and activated factor Xa are approved as new anticoagulant drugs. In contrast to vitamin K antagonists (VKA) and heparins, the new agents have single targets in the coagulation cascade and more predictable pharmacokinetics, but they lack validated and available antidotes. Unlike VKA, they do not require routine monitoring of coagulation. However, the measurement of their pharmacologic effects might be of value in selected patients. They interfere with the routine coagulation tests, which should be interpreted with caution. Specific tests exist and can be used in case of emergencies. Adequate supportive care and temporary removal of all antithrombotic agents constitute the basis for management of serious bleeding complications. The administration of coagulation factors, such as fresh frozen plasma, prothrombin complex concentrates or recombinant activated FVII, can benefit in life-threatening bleeding or emergency surgery. Specific antidotes for non-vitamin K oral anticoagulants are in clinical development.This review aims at answering in a brief and simplified manner some clinical questions.
Coronary artery aneurysm (CAA) is generally defined as coronary dilatation that exceeds the diameter of normal adjacent segments or the diameter of the patient’s largest coronary vessel by 1.5 times. The prime cause of CAAs is atherosclerosis, and the most commonly affected artery is the right coronary artery. CAAs are quite commonly detected during X-ray coronary angiography. However, Coronary artery aneurysm (CAA) is generally defined as coronary dilatation that exceeds the diameter of normal adjacent segments or the diameter of the patient’s largest coronary vessel by 1.5 times. The prime cause of CAAs is atherosclerosis, and the most commonly affected artery is the right coronary artery. CAAs are quite commonly detected during X-ray coronary angiography. However, giant CAAs, especially with the diameter exceeding 100 mm, are extremely rare. The treatment method of choice of giant CAAs is the excision of aneurysm with coronary artery bypass grafting. We present a case of a 41-year-old apparently healthy woman with a giant right CAA. This was detected by noninvasive methods, including magnetic resonance coronary angiography, and its maximum diameter exceeded 100 mm. In emergency, the aneurysmal sac was excised and the aortocoronary saphenous vein graft was performed. We also present a review of the published studies of giant CAAs with the diameter exceeding 100 mm.
Niewydolność serca jest poważnym i częstym problemem klinicznym; w krajach uprzemysłowionych występuje u 1-2% dorosłej populacji. Częstość jej występowania zwiększa się z wiekiem i u osób powyżej 70. roku życia dotyczy co dziesiątego seniora [1]. Mimo postępów w diagnostyce i leczeniu niewydolności serca rokowanie w tej jednostce chorobowej wciąż pozostaje niekorzystne; czas przeżycia od pierwszej hospitalizacji do zgonu jest porównywalny z rokowaniem w chorobie nowotworowej [2, 3]. W patofizjologii niewydolności serca z obniżoną frakcją wyrzutową (HFREF, heart failure with reduced ejection fraction) podstawową rolę odgrywają szlaki neurohormonalne, głównie aktywacja układu współczulnego i układu renina-angiotensyna-aldosteron (RAA), oraz układ peptydów natriuretycznych [4]. Potwierdzeniem kluczowego znaczenia układu RAA jest korzystny wpływ blokerów tego układu (inhibitory konwertazy angiotensyny [ACE, angiotensin-converting enzyme], antagoniści receptora AT 1 dla angiotensyny II [ARB, angiotensin II type 1 receptor blocker(s)], antagoniści receptora mineralokortykoidowego dla aldosteronu [MRA, mineralocorticoid receptor antagonist]) w leczeniu niewydolności serca [5]. Podobnie korzystne działanie udokumentowano w odniesieniu do hamowania układu współczulnego beta-adrenolitykami [6]. W przypadku nietolerancji lub nieosiągnięcia docelowych wartości częstości rytmu serca za pomocą beta-andrenolityku w grupie pacjentów z obniżoną frakcją wyrzutową nie większą niż 35% Europejskie Towarzystwo Kardiologiczne (ESC, European Society of Cardiology) zaleca farmakoterapię iwabradyną, czyli wybiórczym blokerem kanału potasowego I f w węźle zatokowym [1]. W tabeli 1 zaprezentowano kluczowe badania kliniczne leków będących obecnie podstawą w farmakoterapii niewydolności serca [7-13]. Mimo istotnego postępu w farmakoterapii w ciągu ostatnich 20 lat dalsze badania są niezbędne w celu poszukiwania leków poprawiających wciąż niekorzystne rokowanie w niewydolności serca. Największe nadzieje pokłada się w molekułach modulujących szlaki neurohormonalne.
IntroductionAortic stenosis (AS) is the most common acquired valvular heart disease. The early identification of patients with severe AS is crucial. NT-proBNP is a well-known biomarker of pressure overload, and its role in patients with AS has been demonstrated in previous studies. Another, less well-known biomarker of pressure overload is sST2 protein, and its role in AS is unclear.AimTo evaluate the utility of sST2 protein, NT-proBNP and selected clinical parameters in the assessment of degenerative AS severity in a population with preserved left ventricular ejection fraction (LVEF).Material and methodsSixty-nine consecutive patients (mean age: 68.42 ±12.58 years, 55.07% male) with symptomatic degenerative AS and preserved LVEF ≥ 45% were prospectively included. At enrollment complete transthoracic echocardiographic examination, ECG analysis, and standard laboratory tests including NT-proBNP were performed and blood samples for sST2 were obtained.ResultsThere were 43 (62.32%) patients with severe AS. The multivariate stepwise linear regression models revealed that only systolic blood pressure (SBP), Sokolow-Lyon index and left ventricular end-diastolic diameter (LVEDD) were independently associated with severe AS. Spearman correlation coefficients analysis showed no correlations between sST2 levels and a mild to moderate correlation between NT-proBNP concentration and parameters of AS severity. However, levels of NT-proBNP (p = 0.1857) and sST2 (p = 0.7851) did not differentiate patients according to severity of AS.ConclusionsIn the study population with degenerative AS and preserved LVEF neither the NT-proBNP nor sST2 concentrations can be used to differentiate patients according to the severity of AS.
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