Search Results (9)

Background/Objectives: Left ventricular (LV) pseudoaneurysm is a rare but life-threatening complication after acute myocardial infarction, often resulting from inadequate excision of damaged myocardium and use of only a xenopericardial patch during primary LV free wall rupture repair. Methods: A 62-year-old female developed a giant LV pseudoaneurysm one year after initial surgical repair of a free wall rupture with a xenopericardial patch. Imaging confirmed a large pseudoaneurysm with a broad neck and mural thrombus. She underwent pseudoaneurysmectomy, LV reconstruction with a Dacron patch overlaid by a xenopericardial patch, and concomitant mitral and tricuspid valve repair. Results: Surgical exploration revealed a broad-necked pseudoaneurysm and dehisced patch material. The aneurysm was resected, and the LV was reconstructed, resulting in the exclusion of the pseudoaneurysm and improvement of the shape and function. The patient recovered uneventfully and was discharged in good clinical condition with restored LV function. Conclusions: Pseudoaneurysm formation after LV free wall rupture repair is often due to insufficient resection and the use of only a xenopericardial patch. Surgical management with complete excision, Dacron patch reconstruction, and xenopericardial reinforcement facilitates the favorable remodeling of LV geometry and function, and reduces the risk of recurrence. Full article

In the present case report, we describe the clinical course and postmortem findings of a 12-year-old Labrador retriever dog with a third-degree atrio-ventricular block that developed a chronic cough, and later dyspnea and weakness as a result of massive pulmonary thromboembolism 3 years after implantation of a transvenous permanent pacemaker. A large soft tissue mass was seen in the right ventricular chamber around the pacing lead with echocardiography. Initially, this was thought to be caused by mural bacterial endocarditis based on hyperthermia, severe leukocytosis and the appearance of runs of ventricular tachycardia, the latter suggesting myocardial damage. While blood culture results were pending, antibiotics were administered without a positive effect. Due to clinical deterioration, the owner elected for euthanasia and a post-mortem examination confirmed a right ventricular thrombus and surrounding myocarditis, without signs of bacterial infection, and a massive pulmonary thromboembolism. We conclude that pulmonary thromboembolism should be considered in dogs with a cough that have an endocardial pacing lead implanted. Serial screening for proteinuria before and after implantation of an endocardial pacing lead would allow timely initiation of prophylactic antiplatelet therapy. Local myocarditis can develop secondary to an intracavitary thrombus, which can subsequently lead to runs of ventricular tachycardia. Full article

Congenital absence of an internal carotid artery (ICA) is a rare vascular anomaly and occurs in less than 0.01% of the population. We report a case of aplastic internal carotid artery in a 34-year-old female. The patient presented to the emergency department with complaints of new-onset involuntary swaying-like movement of her right arm. Brain magnetic resonance imaging showed multifocal tiny areas of acute infarcts in the bilateral frontal, parietal, and left occipital lobes in the watershed distribution. There was no visualization of the flow of the intracranial left internal carotid artery. Follow-up CTA of the head and neck showed a congenital absence of the left internal carotid artery with no evidence of arterial dissection, occlusion, or aneurysm. Obstruction of the internal carotid artery has significant consequences for patients. This effect is amplified if the disruption occurs in the sole anterior blood supply to the parenchyma of the brain, as in this case. In our patient care, imaging was vital to the detection and subsequent treatment with anticoagulation to avoid further cerebral complications, and the patient will now have a better understanding of the increased lifetime risk of further events. Full article

Introduction. Spinal cord ischemia (SCI) accounts for less than 1% of all strokes, and mostly affects the anterior cord. The ascending aorta (AA) is the rarest site of localization for aortic thrombi (5%). We report a singular case of posterior SCI due to a floating thrombus in the AA. Case presentation. A 75-year-old male with acute left hemiparesis and left tactile and proprioceptive sensory loss below the C5 dermatome (NIHSS 3) is presented. Spinal cord MRI showed a C4–C6 ischemic lesion, involving the left lateral posterior hemi-cord. CT angiography showed a 6 mm floating thrombus in the AA. According to cardiovascular surgeons, dual antiplatelet therapy and high-dose statin were started. After seven days, the patient was discharged with mild left distal hemiparesis and an unchanged sensory deficit. Conclusions. Posterior SCI is rarer than anterior ischemia and potentially unilateral. Its clinical presentation is mainly sensory with possible, but not systematic, weakness of the homolateral limbs. SCI is often caused by aortic pathologies in the elderly, but the incidence rate of non-aneurysmal aortic mural thrombus is about 0.45% and the AA represents a very rare location. In similar cases, conservative medical treatment is preferred despite the high-risk rates of embolic recurrences. Full article

Background: Mural aortic thrombosis associated with chronic peripheral obstruction of the lower limbs is an unusual event. Repeated embolism of instability aortic mural thrombosis caused acute limb ischemia (Rutherford 2 classification) in patients with peripheral arterial disease (PAD). We report a single-center experience for patients with transmural aortic thrombosis and peripheral artery disease. Methods: We retrospectively analyzed data of 54 patients with aortic mural thrombus disease with PAD presentation, treated at our center between 2013 and 2022. Results: Thirty patients (six with proven SARS-CoV-2 infection) underwent hybrid or staged treatment for an aortic lesion and for lower limb ischemia, by the placement of an endovascular aortic stent graft and a femoro-distal or a popliteal-distal bypass graft. The remaining 24 cases were only subjected to an intravascular treatment of the thoracic or abdominal aorta. Transient renal failure occurred in three patients. No embolic events were detected during the procedures. Aortic-related mortality was reported in just one patient who died from multiple organ failure. There was an embolic stroke in one patient with proven SARS-CoV-2 infection, three major amputations in patients with proven SARS-CoV-2 infection and no aortic-related mortality. Conclusions: Stent coverage of complex aortic lesions, alone or in association with a distal bypass graft, supports this approach in a variety of settings. The COVID-19 pandemic caused an increased mortality and amputation rate. Full article

(1) Aim: The primary endpoint of this study was to evaluate the impact of frozen elephant trunk (FET) and conventional elephant trunk (CET) on aortic mural thrombus. The secondary endpoint was to investigate the incidence of persistent inflammatory response (IR) in the form of post-implantation syndrome (PIS) or persistent fever without infection focus after FET and CET, respectively, as well as the risk factors associated with its occurrence. (2) Methods: A single-center, retrospective, observational study of 57 consecutive patients treated with FET and CET between April 2015 and June 2020 was performed. Demographics, procedural data, perioperative laboratory exams as well as vital parameters were recorded. Pre- and postoperative computer tomography angiography (CTA) scans were analyzed with a dedicated software. IR was defined as the presence of continuous fever (>38°, lasting > 24 h) and leukocytosis (white blood cell count > 12 × 1000/µL) developing after surgery in the absence of an infection focus. (3) Results: Fifty-seven consecutive patients (mean age 58.4 ± 12.6 years, 36.8% females) treated with FET (66.6%) or CET (33.3%) for acute aortic dissection (56.1%), post-dissection-aneurysm (19.2%) or aortic aneurysm (24.5%) were included. The median thrombus volume on CTA preoperatively was 10.1 cm³ (range 2–408 cm³). After surgery, the median new-onset mural thrombus was 9.7 cm³ (range 0.2–376 cm³). Nineteen (33.3%) patients developed IR; patients with IR were significantly younger (p = 0.027), less frequently of female gender (p = 0.003) and more frequently affected from acute dissection (p = 0.002) and stayed in the intensive care unit (ICU) significantly longer (p = 0.033) than those without IR. Postoperatively, the volume of new-onset thrombus was significantly greater in the IR group (84.4 vs. 3.2 cm³, p < 0.001). (4) Conclusions: In the context of CET and FET, the persistent inflammatory response occurred in 33.3% of the patients with persistent fever without infection focus. IR was associated with a higher volume of new-onset thrombus and significantly prolonged ICU stay. Further studies to investigate these observations are needed. Full article

The patient presenting with stroke often has cardiac-related risk factors which may be involved in the mechanism of the stroke. The diagnostic assessment is predicated on recognition of this potential relationship. Naturally, an accurate history is of utmost importance in discerning a possible cause and effect relationship. The EKG is obviously an important clue as well as it allows immediate assessment for possible cardiac arrhythmia, such as atrial fibrillation, for possible acute ischemic changes reflective of myocardial ischemia, or there may be indirect factors such as the presence of left ventricular hypertrophy, typically seen with longstanding hypertension, which could be indicative of a hypertensive mechanism for a patient presenting with intracerebral hemorrhage. For all presentations in the emergency room, the vital signs are important. An elevated body temperature in a patient presenting with acute stroke raises concern about possible infective endocarditis. An irregular–irregular pulse is an indicator of atrial fibrillation. A markedly elevated blood pressure is not uncommon in both the acute ischemic and acute hemorrhagic stroke setting. One tends to focus on possible cardioembolic stroke if there is the sudden onset of maximum neurological deficit versus the stepwise progression more characteristic of thrombotic stroke. Because of the more sudden loss of vascular supply with embolic occlusion, seizure or syncope at onset tends to be supportive of this mechanism. Different vascular territory involvement on neuroimaging is also a potential indicator of cardioembolic stroke. Identification of a cardiogenic source of embolus in such a setting certainly elevates this mechanism in the differential. There have been major advances in management of acute cerebrovascular disease in recent decades, such as thrombolytic therapy and endovascular thrombectomy, which have somewhat paralleled the advances made in cardiovascular disease. Unfortunately, the successful limitation of myocardial damage in acute coronary syndrome, with intervention, does not necessarily mirror a similar salutary effect on functional outcome with cerebral infarction. The heart can also affect the brain from a cerebral perfusion standpoint. Transient arrhythmias can result in syncope, while cardiac arrest can result in hypoxic–ischemic encephalopathy. Cardiogenic dementia has been identified as a mechanism of cognitive impairment associated with severe cardiac failure. Structural cardiac abnormalities can also play a role in brain insult, and this can include tumors, such as atrial myxoma, patent foramen ovale, with the potential for paradoxical cerebral embolism, and cardiomyopathies, such as Takotsubo, can be associated with precipitous cardioembolic events. Full article

Selatogrel, a potent and reversible antagonist of the P2Y12 receptor, inhibited FeCl₃-induced thrombosis in rats. Here, we report the anti-thrombotic effect of selatogrel after subcutaneous applications in guinea pigs and mice. Selatogrel inhibited platelet function only 10 min after subcutaneous application in mice. In addition, in a modified Folts thrombosis model in guinea pigs, selatogrel prevented a decrease in blood-flow, indicative of the inhibition of ongoing thrombosis, approximately 10 min after subcutaneous injection. Selatogrel fully normalised blood flow; therefore, we speculate that it may not only prevent, but also dissolve, platelet thrombi. Thrombus dissolution was investigated using real-time intravital microscopy in mice. The infusion of selatogrel during ongoing platelet thrombus formation stopped growth and induced the dissolution of the preformed platelet thrombus. In addition, platelet-rich thrombi were given 30 min to consolidate in vivo. The infusion of selatogrel dissolved the preformed and consolidated platelet thrombi. Dissolution was limited to the disintegration of the occluding part of the platelet thrombi, leaving small mural platelet aggregates to seal the blood vessel. Therefore, our experiments uncovered a novel advantage of selatogrel: the dissolution of pre-formed thrombi without the disintegration of haemostatic seals, suggesting a bipartite benefit of the early application of selatogrel in patients with acute thrombosis. Full article

Background: Biological processes that lead to aneurysm formation, growth and rupture are insufficiently understood. Vessel wall inflammation and degeneration are suggested to be the driving factors. In this study, we aimed to investigate the natural course of vital (non-decellularized) and decellularized aneurysms in a rabbit sidewall and bifurcation model. Methods: Arterial pouches were sutured end-to-side on the carotid artery of New Zealand White rabbits (vital [n = 6] or decellularized [n = 6]), and into an end-to-side common carotid artery bifurcation (vital [n = 6] and decellularized [n = 6]). Patency was confirmed by fluorescence angiography. After 28 days, all animals underwent magnetic resonance and fluorescence angiography followed by aneurysm harvesting for macroscopic and histological evaluation. Results: None of the aneurysms ruptured during follow-up. All sidewall aneurysms thrombosed with histological inferior thrombus organization observed in decellularized compared to vital aneurysms. In the bifurcation model, half of all decellularized aneurysms thrombosed whereas the non-decellularized aneurysms remained patent with relevant increase in size compared to baseline. Conclusions: Poor thrombus organization in decellularized sidewall aneurysms confirmed the important role of mural cells in aneurysm healing after thrombus formation. Several factors such as restriction by neck tissue, small dimensions and hemodynamics may have prevented aneurysm growth despite pronounced inflammation in decellularized aneurysms. In the bifurcation model, rarefication of mural cells did not increase the risk of aneurysm growth but tendency to spontaneous thrombosis. Full article