Percutaneous retrieval of an embolized Watchman device on a papillary muscle in the left ventricle.

The use of left atrial appendage occlusion (LAAO) devices have gained prominence as an alternative to long-term anticoagulation therapy in patients with atrial fibrillation at risk of stroke and high risk of bleeding. While these devices have shown efficacy in reducing stroke risk, there have been reported cases of embolization of the Watchman device. There are very few cases of successful percutaneous retrieval of embolized Watchman devices from the left ventricle (LV), as many of these cases require open heart surgery for safe removal. We are presenting a case of an 80-year-old male whose Watchman device embolized to the LV and was entrapped on the LV papillary muscle that was then successfully retrieved via percutaneous methods, which shows the percutaneous options remain a viable strategy to retrieve LAAO devices from the LV.

Hemopericardium with subsequent cardiac tamponade secondary to rivaroxaban treatment: a case report.

BACKGROUND: The 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 SUMMARY: A 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. DISCUSSION: While 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.

Supraventricular Tachycardia and Postural Orthostatic Tachycardia Syndrome Overlap: A Retrospective Study.

Postural orthostatic tachycardia syndrome (POTS) and supraventricular tachycardia (SVT) are disease states with distinctive features but overlapping clinical manifestations. Currently, studies on the presence of underlying SVT in patients with POTS are lacking. This retrospective study analyzed 64 patients [mean age: 43 years; 41 (61%) women] who had a POTS diagnosis and were found to have concomitant SVT during rhythm monitoring from September 1, 2013 to September 30, 2019 at our Syncope and Autonomic Disorders Clinic. The outcomes assessed were changes in disease severity, frequency of symptoms, heart rate, and blood pressure between before and after SVT ablation. The most frequent types of SVT noted on the electrophysiologic study were atrioventricular nodal reentrant tachycardia (57.81%), atrial flutter (29.68%), atrioventricular reentrant tachycardia (9.37%), atrial tachycardia (1.56%), and junctional tachycardia (1.56%). After SVT ablation, all 64 patients experienced an improvement in symptoms. Palpitations and lightheadedness experienced the most improvement after the procedure (72% vs. 31%; p < 0.001 and 63% vs. 22%; p < 0.001, respectively). There was a significant improvement in the resting heart rate (81.1 ± 12.8 vs. 75.8 ± 15.6 bpm; p < 0.002), but the orthostatic tachycardia on standing persisted (93.6 ± 16.5 vs. 77.3 ± 19.8 bpm; p = 0.14). Underlying SVT in patients with POTS can be missed easily. A strong suspicion and long-term ambulatory cardiac rhythm monitoring can help in diagnosing the condition.

Myocardial Infarction in a 28-Year-Old Male With Neurofibromatosis Type 1.

Neurofibromatosis type 1 (NF1) is an autosomal dominant genetic disorder that affects multiple systems throughout the body. Although there are multiple documented vasculopathies that can be seen in NF1, there are very few documented cases of coronary artery aneurysms with complete thrombosis of the ectatic vessel resulting in myocardial infarction. This case report describes a 28-year-old male with a past medical history of NF1 who presented with an anterolateral ST-segment elevation myocardial infarction. He underwent urgent cardiac catheterization, which was significant for severe thrombotic occlusion of the mid-left anterior descending artery (LAD) with thrombolysis in myocardial infarction (TIMI) flow 0. The LAD was noted to be severely ectatic. Percutaneous coronary intervention (PCI) with thrombectomy was attempted and was unsuccessful, with TIMI flow 0 after the intervention attempt. An echocardiogram was performed, which showed left ventricular ejection fraction (LVEF) of 30%-35%. This case report is presented to familiarize physicians with the rare vasculopathies that can occur in patients with NF1. Occlusive or aneurysmal disease can occur almost anywhere in the body in patients with NF1 due to the proliferation of fusiform endothelial cells in the blood vessels.

Meta-Analysis Comparing Multiple Arterial Grafts Versus Single Arterial Graft for Coronary-Artery Bypass Grafting.

Observational studies and randomized controlled trials (RCTs) have shown conflicting outcomes for multiple arterial graft (MAG) coronary artery bypass graft surgery compared with single arterial grafts (SAGs). The predominant evidence supporting the use of MAGs is observational. The aim of this meta-analysis of RCTs is to compare outcomes following MAG and SAG. We searched multiple databases for RCTs comparing MAG versus SAG. The clinical outcomes studied were all-cause mortality, cardiac mortality, myocardial infarction (MI), revascularization, stroke, sternal wound complications, and major bleeding. We used hazard ratio (HR), relative risk (RR), and corresponding 95% confidence interval (CI) for measuring outcomes. Ten RCTs (6392 patients) were included. The average follow-up in the studies was 4.2 years. The average age of the patients in the studies ranged from 56.3 years to 74.6. No significant difference was seen between MAG and SAG groups for all-cause mortality (11.8% vs 12.7%, HR 0.94, 95% CI 0.81 to 1.09, p 0.36), cardiac mortality (4.1% vs 4.5%, HR 0.96 95% CI 0.74 to 1.26, p 0.77), MI (3.5% vs 5.1%, HR 0.87 95% CI 0.67 to 1.12, p 0.28), and major bleeding (3.3% vs 4.9%, RR 0.85 95% CI 0.64 to 1.13, p 0.26). Repeat revascularization in MAG showed a lower RR than SAG when one of the confounding studies was excluded (RR 0.63, 95% CI 0.4 to 0.99, p 0.04). The incidence of stroke was lower in MAG than SAG (2.9% vs 3.9%, RR 0.74 95% CI 0.56 to 0.98, p 0.03). MAG had higher incidence of sternal wound complications than SAG (2.9% vs 1.7%, RR 1.75 95% CI 1.19 to 2.55, p 0.004). In conclusion, MAG does not have a survival advantage compared with SAG but is better in revascularization and risk of stroke. This benefit may be set off by a higher incidence of sternal wound complications in MAG.

The role of autoantibodies in the syndromes of orthostatic intolerance: a systematic review.

Orthostatic intolerance is defined as the provocation of symptoms upon standing, commonly caused by neurogenic orthostatic hypotension (OH) and postural tachycardia syndrome (POTS), the etiology for which has not been fully uncovered yet. Many reports have described the occurrence of dysautonomia, orthostatic intolerance and POTS following febrile illness, presumably viral and post-vaccine. Furthermore, patients with dysautonomia have higher rates of autoimmune disorders such as Hashimoto thyroiditis and SLE. Recent evidence has shown the presence of adrenergic and cholinergic receptor antibodies in patients with POTS and orthostatic hypotension. In patients with cholinergic receptor antibodies, higher titers correlate with the disease severity. Few reports have shown that immunomodulation therapy resulted in significant improvement in symptoms. In this article, we review the available literature correlating autoimmunity with orthostatic intolerance syndromes. Future studies are warranted to evaluate the prevalence of such antibodies and examine different treatment modalities in this sub group of patients.

Divergent effects of Tlr9 deletion in experimental late venous thrombosis resolution and vein wall injury.

Deep-vein thrombosis (DVT) resolves via a sterile inflammatory response. Defining the inflammatory response of DVT may allow for new therapies that do not involve anticoagulation. Previously, we have shown that Toll-like receptor 9 (Tlr9) gene deleted mice had impaired venous thrombosis (VT) resolution. Here, we further characterise the role of Tlr9 signalling and sterile inflammation in chronic VT and vein wall responses. First, we found a human precedent exists with Tlr9+ cells present in chronic post thrombotic intraluminal tissue. Second, in a stasis VT mouse model, endogenous danger signal mediators of uric acid, HMGB-1, and neutrophil extracellular traps marker of citrullinated histone-3 (and extracellular DNA) were greater in Tlr9-/- thrombi as compared with wild-type (WT), corresponding with larger VT at 8 and 21 days. Fewer M1 type (CCR2+) monocyte/macrophages (MØ) were present in Tlr9-/- thrombi than WT controls at 8 days, suggesting an impaired inflammatory cell influx. Using bone marrow-derived monocyte (BMMØ) cell culture, we found decreased fibrinolytic gene expression with exposure to several endogenous danger signals. Next, adoptive transfer of cultured Tlr9+/+ BMMØ to Tlr9-/- mice normalised VT resolution at 8 days. Lastly, although the VT size was larger at 21 days in Tlr9-/- mice and correlated with decreased endothelial antigen markers, no difference in fibrosis was found. These data suggest that Tlr9 signalling in MØ is critical for later VT resolution, is associated with necrosis clearance, but does not affect later vein wall fibrosis. These findings provide insight into the Tlr9 MØ mechanisms of sterile inflammation in this disease process.

A histological and functional description of the tissue causing chronic postthrombotic venous obstruction.

BACKGROUND: Postthrombotic intraluminal tissue causing postthrombotic syndrome (PTS) has not been well described. This study defines its histological characteristics and assess whether tissue function evolves over time. METHODS: Specimens from 18 common femoral veins (CFV) from 16 patients obtained during CFV endovenectomy and iliocaval recanalization were examined. Phase 1 used hematoxylin and eosin and Masson's trichrome stains for collagen, immunohistochemical, and Von Kossa stains. Phase 2 examined young (≤ one year) and mature (≥10years from acute DVT) specimens to evaluate evolution of endothelial function. Antibodies to four biomarkers were used to examine specific functions of endothelial cells lining neovessels and recanalization channels (RC). RESULTS: Phase 1: Specimens demonstrated 80-90% of collagen type I, 10-20% of collagen type III, and dystrophic calcification. Neovessels and RC were in close proximity to each other. Thrombus and smooth muscle cells were absent, but white blood cells were present. Phase 2: VEGFR2 receptor uptake was more abundant in neovessels than RC and more prominent in younger specimens. Neovascular, nonchannel cells were observed more frequently in young specimens. CD-31 was similar in young and mature specimens. TIE-2 and von Willebrand factor antibodies had greater uptake in mature specimens. CONCLUSION: Tissue causing chronic postthrombotic venous obstruction is predominantly type I collagen. Neovascularization and recanalization occur in close proximity. The biomarker for neovascularization and angiogenesis (VEGFR2) was more prominent in young specimens whereas TIE-2, a stabilizing biomarker and vWF were more frequently observed in mature specimens.