Managing Thrombosis and Hemorrhage in a Man with Myocardial Infarction and Traumatic Hemopericardium with Cardiac Tamponade.
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ABSTRACT:
SUBMITTER: Bush AL
PROVIDER: S-EPMC8367290 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:BackgroundThe use and utility of novel oral anticoagulants has been increasing in clinical practice due to their relatively lower incidence of side effects such as intracranial haemorrhage, particularly in the elderly, when compared with vitamin K antagonists. Rivaroxaban is a factor Xa and prothrombinase inhibitor indicated for stroke and venous thromboembolism prophylaxis in non-valvular atrial fibrillation as well as treatment of venous thromboembolism.Case summaryA patient with history of paroxysmal atrial fibrillation on Rivaroxaban presented with generalized malaise, lightheadedness, and dizziness. The patient was found to be in profound cardiogenic shock despite unremarkable cardiac enzymes. Electrocardiogram revealed rate controlled atrial fibrillation and T-wave inversions in the inferolateral leads without associated electrical alternans. Bedside echocardiogram revealed a large pericardial effusion consistent with cardiac tamponade physiology. Following anticoagulation reversal, the patient underwent urgent pericardiocentesis yielding haemorrhagic fluid, with subsequent improvement in haemodynamic status. Despite the presence of retroperitoneal lymphadenopathy on previous computed tomography of the abdomen and concern for underlying malignant effusion secondary to lymphoma, cytology of the fluid revealed no evidence of malignant cells and follow-up flow cytometry and bone marrow biopsy were unremarkable.DiscussionWhile hemopericardium is not listed as a known side effect of Rivaroxaban, previous cases of hemopericardium secondary to Rivaroxaban have been described in the literature secondary to pre-disposing risk factors including CYP450 drug interactions or cardiac device implantations. In this case, the patient experienced a spontaneous hemopericardium on Rivaroxaban without any previously elucidated risk factors or evidence of malignancy.
| S-EPMC7898561 | biostudies-literature
Project description:We present the case of a patient with myocardial infarction and COVID-19 disease who developed hemorrhagic pericardial effusion and cardiac tamponade. The differential diagnosis included post-infarction pericarditis and mechanical complications, thrombolysis, Dressler syndrome, and viral pericarditis. The histopathologic examination of the pericardial tissue sample and electron microscopic examination established the diagnosis. (Level of Difficulty: Advanced.).
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Project description:Cardiac dysfunction (CD) importantly contributes to mortality in trauma patients, who survive their initial injuries following successful hemostatic resuscitation. This poor outcome has been correlated with elevated biomarkers of myocardial injury, but the pathophysiology triggering this CD remains unknown. We investigated the pathophysiology of acute CD after trauma using a mouse model of trauma hemorrhage shock (THS)-induced CD with echocardiographic guidance of fluid resuscitation, to assess the THS impact on myocardial integrity and function. Mice were subjected to trauma (soft tissue and bone fracture) and different degrees of hemorrhage severity (pressure controlled ~MABP < 35 mmHg or <65 mmHg) for 1 h, to characterize the acute impact on cardiac function. In a second study, mice were subjected to trauma and hemorrhage (MABP < 35 mmHg) for 1 h, then underwent two echocardiographic-guided resuscitations to baseline stroke volume at 60 and 120 min, and were monitored up to 180 min to study the longer impact of THS following resuscitation. Naïve and sham animals were used as controls. At 60 min post-THS injury, animals showed a lower cardiac output (CO) and stroke volume (SV) and an early rise of heart fatty acid-binding protein (H-FABP = 167 ± 38 ng/ml; 90% increase from shams, 3.54 ± 3.06 ng/ml), when subjected to severe hemorrhage and injury. Despite resuscitation, these animals maintained lower CO (6 ml/min vs. 23 ml/min), lower SV (10 μl vs. 46 μl; both ~75% decreased), and higher H-FABP (levels (340 ± 115 ng/ml vs. 10.3 ± 0.2 ng/ml; all THS vs. shams, P < 0.001) at 180 min post-THS injury. Histopathological and flow-cytometry analysis of the heart confirmed an influx of circulatory leukocytes, compared to non-injured hearts. Myocardial injury was supported by an increase of troponin I and h-FABP and the widespread ultrastructural disorganization of the morphology of sarcomeres and mitochondria. DNA fragmentation and chromatin condensation driven by leakage of apoptosis-inducing factor (AIF) may suggest a mitochondria-driven progressive cell death. THS modeling in the mouse results in cardiomyocyte damage and reduced myocardial function, which mimics the cardiac dysfunction seen in trauma patients. This CD model may, therefore, provide further understanding to the mechanisms underlying CD and act as a tool for developing cardioprotective therapeutics to improve survival after injury.
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Project description:In patients presenting with pericarditis or pericardial effusion without known malignancy, the likelihood of finding previously undiagnosed cancer in different publications typically ranges from 4% to 7%. Cardiac tamponade due to malignant pericardial effusion is thus a rare clinical entity and often acutely life threatening. The present report describes an unusual case of large pericardial bleeding causing tamponade in the setting of fondaparinux anticoagulation, heterozygous factor V Leiden mutation and eventual discovery of meta-static adenocarcinoma.
| S-EPMC2898533 | biostudies-other
Project description:Graphical abstract Highlights • Postoperative pericardial effusion may cause left-sided chamber compression.• Focal left-sided cardiac tamponade may present with atypical clinical or echo findings.• Focal tamponade can result in acute liver failure post–cardiac surgery.
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Project description:This study evaluated the safety and feasibility of transendocardial injections of VentriGel, a cardiac extracellular matrix hydrogel, in early and late post-myocardial infarction (MI) patients with left ventricular (LV) dysfunction. VentriGel was delivered in 15 patients with moderate LV dysfunction (25% ≤ LV ejection fraction ≤ 45%) who were between 60 days to 3 years post-MI and were revascularized by percutaneous coronary intervention. The primary endpoints were incidence of adverse events and abnormal clinical laboratory results. This first-in-man study established the safety and feasibility of delivering VentriGel in post-MI patients, thus warranting further evaluation in larger, randomized clinical trials.
| S-EPMC6834965 | biostudies-literature
Project description:Patients with cancer face a high short-term risk of arterial thromboembolism. One of the most fatal manifestations of arterial thromboembolism is myocardial infarction (MI), and patients with cancer face a 3-fold greater risk of MI than patients without cancer. The individual risk for arterial thrombotic events in patients with cancer is determined by the complex interaction of baseline cardiovascular risk factors, cancer type and stage, chemotherapeutic regimen, and other general contributing factors for thrombosis. Managing MI in patients with cancer is a clinical challenge, particularly due to cancer's unique pathophysiology, which makes it difficult to balance thrombotic and bleeding risks in this specific patient population. When patients with cancer present with MI, a limited proportion are treated with guideline-recommended therapy, such as antiplatelet therapy or invasive revascularization. Despite the limited evidence, existing reports consistently suggest similar clinical benefits of guideline-recommended therapy when administered to patients with cancer presenting with MI. In this review, we briefly summarize the available evidence, clinical challenges, and future perspectives on simultaneous management of MI and cancer, with a focus on invasive strategy.
| S-EPMC6533845 | biostudies-literature
Project description:ObjectivePost-partum hemorrhage (PPH) is the leading direct cause of maternal mortality in India. Uterine balloon tamponade (UBT) is recommended for atonic PPH cases not responding to uterotonics. This study assessed cost-effectiveness of three UBT devices used in Indian public health settings.MethodsA decision tree model was built to assess cost-effectiveness of Bakri-UBT and low-cost ESM-UBT alternatives as compared to the recommended standard of care i.e. condom-UBT intervention. A hypothetical annual cohort of women eligible for UBT intervention after experiencing atonic PPH in Indian public health facilities were evaluated for associated costs and outcomes over life-time horizon using a disaggregated societal perspective. Costs by undertaking primary costing and clinical parameters from published literature were used. Incremental cost per Disability Adjusted Life Years (DALY) averted, number of surgeries and maternal deaths with the interventions were estimated. An India specific willingness to pay threshold of INR 24,211 (USD 375) was used to evaluate cost-effectiveness. Detailed sensitivity analysis and expected value of information analysis was undertaken.ResultsESM-UBT at base-case Incremental Cost-Effectiveness Ratio (ICER) of INR -2,412 (USD 37) per DALY averted is a cost-saving intervention i.e. is less expensive and more effective as compared to condom-UBT. Probabilistic sensitivity analysis however shows an error probability of 0.36, indicating a degree of uncertainty around model results. Bakri-UBT at an ICER value of INR -126,219 (USD -1,957) per DALY averted incurs higher incremental societal costs and is less effective as compared to condom-UBT. Hence, Bakri-UBT is not cost-effective.ConclusionFor atonic PPH management in India, condom-UBT offers better value as compared to Bakri-UBT. Given the limited clinical effectiveness evidence and uncertainty in sensitivity analysis, cost-saving result for ESM-UBT must be considered with caution. Future research may focus on generating high quality comparative clinical evidence for UBT devices to facilitate policy decision making.
| S-EPMC8372914 | biostudies-literature
Project description:While human organoid systems have provided a powerful platform in modeling diseases caused by genetic disorders, non-genetic factors, such as lifestyle and environment, are the largest attributable factors to devastating diseases like cardiovascular disease (CVD), the leading cause of death worldwide. Specifically, myocardial infarction (MI) (i.e., heart attack) makes up ~8.5% of CVD and is a common cause of heart failure with a 40% five-year mortality after the first MI. This highlights an urgent need to develop relevant human heart failure models for drug development. This is further evidenced by the disappointing performance of heart failure drugs in clinical trials during the last decade, which has been partially attributed to the distinct differences between human patient hearts and animal heart failure models. Here, we combined major non-genetic causal factors of MI with our previously established cardiac organoids to create the first human organoid model of cardiac infarction. In particular, we leveraged the diffusion limitation in 3D microtissues to recreate the nutrient diffusion gradient across infarcted hearts (i.e., infarct-border-remote zones) in human cardiac organoids to induce cardiac organotypic response to infarction. This enabled the recapitulation of major MI hallmarks in human cardiac organoids at the transcriptomic, structural and functional level.
2020-04-14 | GSE113871 | GEO