Background
Chronic kidney disease (CKD) is a major global public health problem, being closely connected to cardiovascular disease. CKD involves an elevated thromboembolic risk and requires anticoagulation, but the high rates of hemorrhage render it quite challenging.
Hypothesis
There are no consensus recommendations regarding anticoagulation in CKD. Due to the currently limited data, clinicians need practical clues for monitoring and optimizing the treatment.
Methods
Based on the available data, this review outlines the benefit‐risk ratio of all types of anticoagulants in each stage of CKD and provides practical recommendations for accurate dosage adjustment, reversal of antithrombotic effect, and monitoring of renal function on a regular basis.
Results
Evidence from randomized controlled trials supports the efficient and safe use of warfarin and direct oral anticoagulants (DOACs) in mild and moderate CKD. On the contrary, the data are poor and controversial for advanced stages. DOACs are preferred in CKD stages 1 to 3. In patients with stage 4 CKD, the choice of warfarin vs DOACs will take into consideration the pharmacokinetics of the drugs and patient characteristics. Warfarin remains the first‐line treatment in end‐stage renal disease, although in this case the decision to use or not to use anticoagulation is strictly individualized. Anticoagulation with heparins is safe in nondialysis‐dependent CKD, but remains a challenge in the hemodialysis patients.
Conclusions
Although there is a need for cardiorenal consensus regarding anticoagulation in CKD, adequate selection of the anticoagulant type and careful monitoring are some extremely useful indications for overcoming management challenges.
A persistent left superior vena cava (PLSVC) is the most frequent anomaly of the venous drainage system. While both a right and left superior vena cava (SVC) are usually present, a unique, left-sided SVC, also known as an isolated PLSVC, accounts for only 10–20% of cases. It is frequently associated with arrhythmias and other congenital cardiac anomalies. Though it is usually an asymptomatic condition, it may pose significant problems whenever central venous access is needed. We report a case of an isolated PLSVC that was diagnosed incidentally during pacemaker implantation for sinus node dysfunction. The venous anomaly was associated with subvalvular aortic stenosis determined by a subaortic membrane; this particular association of congenital cardiovascular anomalies is a rare finding, with only a few cases reported in the literature. We aim to highlight the clinical and practical implications of this condition, as well as to discuss the embryonic development and diagnostic methods of this congenital defect.
Myocardial infarction (MI) is the leading cause of death and morbidity worldwide, with an incidence relatively high in developed countries and rapidly growing in developing countries. The most common cause of MI is the rupture of an atherosclerotic plaque with subsequent thrombotic occlusion in the coronary circulation. This causes cardiomyocyte death and myocardial necrosis, with subsequent inflammation and fibrosis. Current therapies aim to restore coronary flow by thrombus dissolution with pharmaceutical treatment and/or intravascular stent implantation and to counteract neurohormonal activation. Despite these therapies, the injury caused by myocardial ischemia leads to left ventricular remodeling; this process involves changes in cardiac geometry, dimension and function and eventually progression to heart failure (HF). This review describes the pathophysiological mechanism that leads to cardiac remodeling and the therapeutic strategies with a role in slowing the progression of remodeling and improving cardiac structure and function.
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