Cardiogenic shock (CS) is a complex multifactorial clinical syndrome, developing as a continuum, and progressing from the initial insult (underlying cause) to the subsequent occurrence of organ failure and death. There is a large phenotypic variability in CS, as a result of the diverse aetiologies, pathogenetic mechanisms, haemodynamics, and stages of severity. Although early revascularization remains the most important intervention for CS in settings of acute myocardial infarction, the administration of timely and effective antithrombotic therapy is critical to improving outcomes in these patients. In addition, other clinical settings or non‐acute myocardial infarction aetiologies, associated with high thrombotic risk, may require specific regimens of short‐term or long‐term antithrombotic therapy. In CS, altered tissue perfusion, inflammation, and multi‐organ dysfunction induce unpredictable alterations to antithrombotic drugs' pharmacokinetics and pharmacodynamics. Other interventions used in the management of CS, such as mechanical circulatory support, renal replacement therapies, or targeted temperature management, influence both thrombotic and bleeding risks and may require specific antithrombotic strategies. In order to optimize safety and efficacy of these therapies in CS, antithrombotic management should be more adapted to CS clinical scenario or specific device, with individualized antithrombotic regimens in terms of type of treatment, dose, and duration. In addition, patients with CS require a close and appropriate monitoring of antithrombotic therapies to safely balance the increased risk of bleeding and thrombosis.
BackgroundPatient adherence is an essential factor in obtaining efficient oral anticoagulation using vitamin K antagonists (VKAs), a situation with a narrow therapeutic window. Therefore, patient education and awareness are crucial for good management. Auditing the current situation would help to identify the magnitude of the problem and to build tailored education programs for these patients.MethodsThis study included 68 hospitalized chronically anticoagulated patients (mean age 62.6±13.1 years; males, 46%) who responded to a 26-item questionnaire to assess their knowledge on VKA therapy management. Laboratory and clinical data were used to determine the international normalized ratio (INR) at admission, as well as to calculate CHA2DS2-VASC and HAS-BLED scores for patients with atrial fibrillation.ResultsThe majority of patients (62%) were receiving VKA for atrial fibrillation, the others for a mechanical prosthesis and previous thromboembolic disease or stroke. In the atrial fibrillation group, the mean CHA2DS2-VASC score was 3.1±1.5, while the average HAS-BLED score was 1.8±1.2. More than half of the patients (53%) had an INR outside of the therapeutic range at admission, with the majority (43%) having a low INR. A correct INR value was predicted by education level (higher education) and the diagnostic indication (patients with mechanical prosthesis being best managed). Patients presenting with a therapeutic INR had a trend toward longer treatment duration than those outside the therapeutic range (62±72 months versus 36±35 months, respectively, P=0.06). There was no correlation between INR at admission and the patient’s living conditions, INR monitoring frequency, and bleeding history.ConclusionIn a tertiary cardiology center, more than half of patients receiving VKAs are admitted with an INR falling outside the therapeutic range, irrespective of the bleeding or embolic risk. Patients with a mechanical prosthesis and complex antithrombotic regimens appear to be the most careful with INR monitoring, especially if they have a higher level of education. Identifying patient groups with the lowest time interval spent in the therapeutic range could help attending physicians educate patients focusing on specific awareness issues.
1 This rare condition is frequently associated with hypertension, mostly secondary to renal artery (RA) stenosis in younger patients.2 Vascular abnormalities such as stenoses and aneurysms are a main cause of death in NF1 patients. 3Associated RA stenosis can increase the mortality rate because of the greater risk of cardiovascular events. We present the case of a teenager with NF1 and discuss our treatment decisions. Case ReportIn November 2014, a 17-year-old girl was referred to our cardiology department for asymp to matic severe hypertension-blood pressure (BP) as high as 240/120 mmHgincidentally diagnosed 6 weeks earlier. The patient was screened for secondary causes of hypertension. The patient's family history was negative for hypertension and neurofibromatosis.Clinical evaluation revealed a short teenager (height, 150 cm; weight, 58.5 kg) with abdominal obesity. Pigmented skin lesions characteristic of NF1 were noted (Fig. 1). The patient's BP at presentation was 175/110 mmHg in both arms (heart rate, 98 beats/min). Her peripheral pulses were normal, and there were no detectable heart, abdominal, or vascular murmurs.An electrocardiogram showed sinus rhythm and left ventricular hypertrophy (Sokolow-Lyon index, 43 mm). A chest radiograph showed nothing unusual. Laboratory findings included mild anemia (hemoglobin, 11 g/dL) and elevated levels of plasma renin (264 pg/mL) and aldosterone (599 ng/dL). Renal and liver func-
Although doxorubicin (Dox) is an effective antitumor antibiotic in the anthracycline class, it often induces the undesirable side effect of cardiomyopathy leading to congestive heart failure, which limits its clinical use. The primary goal of this study is to evaluate a reliable translational method for Dox-induced cardiotoxicity (CTX) screening, aiming to identify a high-risk population and to discover new strategies to predict and investigate this phenomenon. Early identification of the presence of iron deposits and genetic and environmental triggers that predispose individuals to increased risk of Dox-induced CTX (e.g., overexpression of Toll-like receptor 4 (TLR4)) will enable the early implementation of countermeasure therapy, which will improve the patient’s chance of survival. Our cohort consisted of 25 consecutive patients with pathologically confirmed cancer undergoing Dox chemotherapy and 12 control patients. The following parameters were measured: serum TLR4 (baseline), serum transferrin (baseline and 6-week follow-up) and iron deposition (baseline and 6-week follow-up). The average number of gene expression units was 0.121 for TLR4 (range 0.051–0.801). We subsequently correlated serum TLR4 levels in our cohort with myocardial iron overload using the cardiac magnetic resonance (CMR) T2* technique, the ventricular function (% ejection fraction, %EF) and serum transferrin levels. There is a strong negative linear relationship between serum TLR4 and CMR T2* values (r = − 0.9106, ****P < 0.0001). There is also a linear correlation (either positive or negative) with EF and transferrin; no established relationship related to the sex of the patients was found. Patients with elevated serum TLR4 at baseline also exhibited an increase in serum transferrin levels and Dox-induced left ventricular dysfunction with a decreased EF (< 50%); this phenomenon was observed in 7 of 25 patients (28%) at the 6-week follow-up. There were no significant differences or correlations based on sex. We concluded that there is a direct relationship between Dox-induced CTX (indicated by elevated serum TLR4) and the times (ms) for T2* (decreases in which correspond to immediate and rapid iron overload).
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