Thrombotic Material Research Articles

Paget-von Schröetter Syndrome: upper extremity deep vein thrombosis after heavy exercise.

We present a 52-year-old man with swelling, tightness, heaviness, and redness in the right half of his neck, face, upper arm, and right precordial area after repetitive exercises. No etiological factors such as trauma, venous catheter, malignancy, hematologic disorder history, or any chronic disease were noted. A Doppler ultrasound of the upper extremities was performed, which showed a complete thrombotic occlusion in the right internal jugular vein, partial occlusion in the right brachiocephalic and subclavian veins with thrombosis, and chronic thrombosis occluding the left brachial vein. Complete blood cell count, coagulation profiles, and rheumatologic and tumor markers were normal. The patient reported that he had taken spinning classes for the last 18 months, and for the past 4 days he reported that he had done his spinning exercises harder and more frequently. The swelling and redness regressed partially on the 3rd day of therapy with enoxaparin sodium. In the first month follow-up visit we performed a control Doppler ultrasound and it showed partially thrombosed areas in the right brachiocephalic and internal jugular veins. Also, chronic thrombosis persisted in the left brachial and basilic veins. Computed tomography images showed no evidence for malignancy and some sections showed filling defects in the vena cava superior, which was attributed to thrombotic materials. The patient was successfully treated with anticoagulants for 6 months.

Immunosuppressive Treatments in Acute Myocardial Infarction and Stroke

Atherosclerosis is an inflammatory disease that involves formation of atherosclerotic lesions characterized by deposition of lipids and cell debris in the arterial wall, fibrosis and recruitment of various cell types including smooth muscle, endothelial, immune and foam cells. Progressive enlargement of the atherosclerotic plaques together with development of necrosis, intraplaque hemorrhage and ulceration results into rupture of the plaques, with subsequent exposure to thrombotic material and occlusion of the artery. These phenomena culminate in myocardial infarction when they occur in the coronary arteries or stroke when cerebral arteries are affected. Several lines of evidence indicated that innate and adaptive immunity tightly regulate atherogenesis. In particular, activated T cells influence the stability of the atherosclerotic plaque and promote disease progression. Experiments performed on suitable animal models allowed to identify CD4+ lymphocytes as the major T cell subpopulation involved in atherogenesis. Furthermore, immunophenotypic and functional analyses demonstrated that human and murine plaques contain predominantly CD4+ T Helper (TH)1 cells producing proinflammatory cytokines. Taken together, these observations have fostered the evaluation in preclinical models of whether or not immunosuppressive drugs may represent an efficacious therapeutic strategy for atherosclerosis-associated diseases. This review focuses on the role of innate and adaptive immunity in atherogenesis and atherosclerosis progression, and discusses the potential immunosuppressive approaches for the treatment of patients affected by acute myocardial infarction and stroke, with particular emphasis on the use of tacrolimus and stem cell transplantation.

Trombectomia adjunta em intervenção percutânea primária para infarto agudo do miocárdio

Primary percutaneous coronary intervention (PCI) has become the favored reperfusion strategy in acute ST-segment elevation myocardial infarction. Lower post-PCI myocardial perfusion grade, no-reflow and even drug-eluting stent thrombosis have been related to the presence of intracoronary thrombus. Adjunctive thrombectomy refers to procedures and devices that remove thrombotic material from the infarction-related artery, in theory, before distal embolization can occur. There is substantial variability between randomized controlled trials of thrombectomy in primary PCI with regards to tested devices, procedural characteristics, adjuvant medical regimen and examined outcomes. As a general statement, improvements in myocardial perfusion endpoints do not translate into reductions in clinical outcomes. Yet, an increasing number of trials with a longer follow-up reported benefits arising late after the index myocardial infarction. Simple aspiration catheters may also produce better outcomes than devices that fragment the thrombus before aspirating debris. Clinical or angiographic variables which best predict benefits from the use of thrombectomy remain to be defined. The aim of this review is to provide perspective on the conclusions of available trials and meta-analysis of adjunctive thrombectomy in acute myocardial infarction. Targets for future studies are discussed.

Diagnostic performance of state-of-the-art imaging techniques for morphological assessment of vascular abnormalities in patients with chronic thromboembolic pulmonary hypertension (CTEPH)

To determine the most comprehensive imaging technique for the assessment of pulmonary arteries in patients with chronic thromboembolic pulmonary hypertension (CTEPH). 24 patients with CTEPH were examined by ECG-gated multi-detector CT angiography (MD-CTA), contrast-enhanced MR angiography (ce-MRA) and selective digital subtraction angiography (DSA) within 3 days. Two readers in consensus separately evaluated each imaging technique (48 main, 144 lobar and 449 segmental arteries) for typical changes like complete obstructions, vessel cut-offs, intimal irregularities, incorporated thrombus formations, and bands and webs. A joint interpretation of all three techniques served as a reference standard. Based on image quality, there was no non-diagnostic examination by either imaging technique. DSA did not sufficiently display 1 main, 3 lobar and 4 segmental arteries. The pulmonary trunk was not assessable by DSA. One patient showed thrombotic material at this level only by MD-CTA and MRA. Sensitivity and specificity of MD-CTA regarding CTEPH-related changes at the main/lobar and at the segmental levels were 100%/100% and 100%/99%, of ce-MRA 83.1%/98.6% and 87.7%/98.1%, and of DSA 65.7%/100% and 75.8%/100%, respectively. ECG-gated MD-CTA proved the most adequate technique for assessment of the pulmonary arteries in the diagnostic work-up of CTEPH patients. • A prospective single-centre study evaluated ECG-gated MDCTA, ce-MRA and DSA in CTEPH patients. • ECG-gated MD-CT angiography outperformed DSA and ce-MRA. • Right heart catheterisation should be reserved only for assessment of pulmonary haemodynamics.

Improved endothelialization and reduced thrombosis by coating a synthetic vascular graft with fibronectin and stem cell homing factor SDF-1α

Failure of synthetic small-diameter vascular grafts is determined mainly by the lack of endothelial cells, as these cells inhibit thrombosis and intimal hyperplasia. Coating of graft material with homing factors for circulating stem cells has the potential to improve endogenous endothelialization of these grafts and to reduce graft failure. Synthetic knitted polyester grafts (6mm diameter) were coated with FN and SDF-1α before surgical interposition in the carotid artery of sheep. Similar uncoated vascular grafts were implanted in the contralateral side as internal controls. To study the early attraction of stem cells, grafts were implanted in a first series of nine sheep and explanted after 1 or 3days. In coated grafts, four times higher fractions of CD34+ and three to four times higher fractions of CD117+ cells adhering to the vessel walls were found than in control grafts (P<0.05). When such coated and non-coated grafts were implanted in 12 other sheep and explanted after 3months, all coated grafts were patent, while one control graft was occluded. EcNOS staining revealed that FN-SDF-1α coating significantly increased coverage with endothelial cells from 27±4% of the graft to 48±4% compared with the controls (P=0.001). This was associated with a significant reduction of intimal hyperplasia (average thickness 1.03±0.09mm in controls vs. 0.69±0.04mm in coated grafts; P=0.009) and significantly less adhesion of thrombotic material in the middle part of the graft (P=0.029). FN-SDF-1α coating of synthetic small-caliber vascular grafts stimulated the attraction of stem cells and was associated with improved endothelialization and reduced intimal hyperplasia and thrombosis.

Urokinase-Type Plasminogen Activator Deficiency in Bone Marrow–Derived Cells Augments Rupture of Angiotensin II–Induced Abdominal Aortic Aneurysms

Abdominal aortic aneurysms (AAAs) are associated with fragmentation of extracellular matrix during development of aortic dilation and rupture. Therefore, it is important to identify specific protease systems involved in extracellular matrix degradation during AAA formation. The present study determined the contribution of the urokinase system to AAA formation and rupture. Angiotensin II (Ang II)-induced AAAs were associated with increased aortic abundance of both urokinase-type plasminogen activator receptor (uPAR) and urokinase-type plasminogen activator (uPA) proteins. However, this increased presence was unrelated to AAA formation because deficiencies of either uPAR or uPA had no effect on either the incidence or size of Ang II-induced AAAs in both normolipidemic mice and low-density lipoprotein receptor-/- mice fed a saturated fat-enriched diet. Although uPA deficiency did not affect development of AAAs, there was an effect of increasing mortality rate from AAA rupture in hypercholesterolemic mice. Bone marrow transplantation demonstrated that enhanced aneurysmal rupture was attributable to deficiency of uPA in leukocytes. uPA deficiency led to an increased propensity for impaired resolution of the thrombotic material within the aneurysmal tissue. Neither uPAR nor uPA deficiency had any effect on Ang II-induced atherosclerosis in low-density lipoprotein receptor-/- mice. The uPA-uPAR axis has no effect on the formation of Ang II-induced AAAs, but uPA deficiency promotes aneurysmal rupture.

Early thrombolysis in an elderly patient: case report

Background Pulmonary thromboembolism (TEP) is related to the migration of thrombotic material from the systemic venous circulation to pulmonary vascular tree, with obstruction of the pulmonary arterial circulation. The mortality rate is 30% in non-identifiable forms, and 2-8% in those treated earlier. The early use of thrombolytics determines the success of the lysis. Thrombolysis is considered a proven treatment in the management of acute, massive forms of TEP that accompany a hemodynamic instability, but differences arise over time, the doses and which thrombolytic use, to minimize the adverse events in compromised patients. Adverse events are: major bleeding, strokes, severe hypotension, allergies, re-thrombosis and reperfusion syndrome. Contraindications are: absolute (internal bleeding in progress, recent spontaneous intracranial hemorrhage) and relative (interventions Chir. <10 days, stroke <2m., Gastric bleeding <10 days, Major trauma <15 days, Recent CPR, PTL <100,000, poorly controlled severe hypertension, pregnancy).

Routine aspiration method during filter-protected carotid stenting: histological evaluation of captured debris and predictors for debris amount

A routine aspiration method in filter-protected carotid artery stenting (CAS) has been reported recently in which the proximal internal carotid artery (ICA) blood column was aspirated using an aspiration catheter after postdilatation regardless of flow state on digital subtraction angiography. We examined the debris particles captured by this method. The routine aspiration method was used in 71 CAS procedures. In two procedures, captured debris particles were examined histologically. In the remaining 69 procedures, the size and number of debris particles were measured under a stereoscopic microscope, and then relationships between the amount of debris particles and clinical variables were evaluated using multivariate regression analysis. Histologically, the captured debris contained platelet-precipitating, thrombotic, lipid-rich fibrous and calcified material. The number of debris particles ≥1 mm was 19.6 ± 12.1 (mean ± SD) in 60 procedures with normal flow and 25.9 ± 17.2 (mean ± SD) in 9 procedures with slow/stop flow. Multivariate regression analysis demonstrated that extension of a proximal ICA angulation was an independent predictor of the amount of debris particles with a maximum diameter of either ≥1 mm or <1 mm but ≥0.5 mm (p < 0.05). The captured debris appeared to originate from atheromatous plaques. If the routine aspiration method had not been used in the present series, the debris might have migrated into intracerebral arteries. Restriction of the extension of a proximal ICA angulation might reduce the amount of debris associated with CAS, especially when the proximal ICA angulation is pronounced.

The routine intra-operative use of pulse oximetry for monitoring can prevent severe thromboembolic complications in anterior surgery

Anterior access to the lumbar spine is established for disc replacement surgery and anterior interbody fusion in the lumbar spine. The spine is accessed normally from the left side either by a transperitoneal or retroperitoneal approach through a midline or oblique skin incision. After reaching the retroperitoneum and depending on the level of exposure, the surgeon has to mobilise and retract the aorta or left common iliac artery, as well as the left common iliac vein or internal vena cava to the right lateral border to address the whole disc space. The left common iliac artery is especially stretched during intervertebral disc exposure putting it at a greater risk of adverse events. Not surprisingly, vascular adverse events like direct injuries, thrombosis and embolism are feared complications in anterior surgery. Permanent intra-operative left leg oxygen saturation surveillance via pulse oximetry can help detecting embolic situations thereby allowing immediate treatment minimising the leg ischemia or preventing limb loss. In the presented case, a 61-year-old male patient undergoing a two-level anterior interbody fusion lost oxygen saturation in the left leg after vessel retraction for exposure. After cage insertion and release of the retractor blades, the pulse oximetry signal did not return and no pulses were found during instant Doppler investigation below the femoral artery, indicating severe embolism in the left leg. The left common iliac artery was clamped and opened showing a ruptured calcified plaque with adherent fresh thrombotic material. An endovascular embolectomy in the superficial and deep femoral artery revealed several small thrombi. An artherectomy of the common iliac artery followed by patch closure was performed. Immediately after clamp release, pulse oximetry returned and Doppler signals were detectable at the tibialis posterior and dorsalis pedis artery. Post-operative recovery was uneventful and pulses were palpable at all times. Arterial adverse events in anterior access surgery are rare complications but none the less, it is of paramount importance to detect and treat these situations immediately. This case highlights the need of routine pulse monitoring during the whole anterior surgery to prevent embolic complications. Even manual pulse control might not be sufficient to rule out any distal embolic events creating severe leg ischemia.

Leriche’s syndrome and Löffler endocarditis in a 30-year-old patient presenting with hypereosinophilic syndrome

Dear Editor, Here, we report a severe complication of hypereosinophilic syndrome (HES), the onset of Leriche’s syndrome, in a 30year-old patient. A 30-year-old man was referred to our institution due to acute onset of severe pain and symmetric sensory neuropathy of both legs. Contrast enhanced computed tomography showed occlusion of aortic bifurcation (Leriche’s syndrome) (Fig. 1a). Immediate thrombectomy secured reperfusion of the lower limbs. Histopathologic workup confirmed the presence of thrombotic material. Three weeks prior to admission, the patient had been diagnosed with a hypereosinophilic syndrome and Loffler’s endocarditis. At that time, he had presented with nonspecific abdominal pain accompanied by diarrhea and progressive general weakness that he had observed for more than 2 months. Diagnostic workup showed an abnormal eosinophil count 7.5 (10/l) with a corresponding myeloproliferative bone marrow. Fluorescence in situ hybridization (FISH) analysis for rearrangements of the platelet-derived growth factor receptors alpha and beta (PDGFRα/β) were evaluated as negative (LSI 4q12 Tri-Color Rearrangement probe set; Poseidon Repeat Free, 5q33, Break probe). Echocardiography indicated the presence of Loffler endocarditis. Intracardial thrombotic formations had been detectable. Oral anticoagulation with phenprocoumone had been started, and an INR between 2 and 3 was targeted. When Leriche’s syndrome was diagnosed, the INR was 2.0. The patient had been treated with prednisolone (1 g) for 2 days with a temporary drop of eosinophilis to 1.8 (10/l). At admission, hematologic workup confirmed massive increase of eosinophils 3.6 (10/l). Screening for causes of reactive eosinophilia was negative with regard to an allergic reaction and autoimmune, parasitic, or helminthic diseases. Echocardiography confirmed Loffler’s endocarditis (Fig. 1b). Examination of the bone marrow showed a hypercellular marrow with marked increase of eosinophilic granulocytes and their progenitors (Fig. 1c). Standard cytogenetic characterization showed a normal karyotype. Using the FIP1L1Chic2-PDGFRα dual-color probe which is optimized to detect the Chic2 deletion at 4q12 FISH analysis found a deletion in chromosome 4, band q12 [del(4)(q12)] (Fig. 1d). Thomas Klag and Thomas Schnetzke have contributed equally to this work.

Acute Stroke, Catheter Related Venous Thrombosis, and Paradoxical Cerebral Embolism: Report of Two Cases

Patent foramen ovale (PFO) has been associated with cryptogenic stroke, particularly in young adults. However, the source of particles leading to cerebral embolism remains frequently unknown despite comprehensive evaluation. To report and comment on therapeutic options for 2 patients with acute ischemic strokes, PFO, and venous access related thrombosis, sources of paradoxical embolism, from Boston Medical Center stroke database. Case 1. A 71-year-old man presented with brain magnetic resonance imaging (MRI) confirmed acute cerebellar infarction. Echocardiography showed a PFO and thrombotic material at the tip of a peripherally inserted central catheter (PICC) line in the superior vena cava (SVC) prolapsing into the right atrium (RA). Case 2. A 64-year-old woman with end-stage renal disease and PFO presented with brain MRI confirmed acute parietal lobe infarction. Three days prior to her stroke, she had thrombectomy and venoplasty of an arterio-venous (AV) dialysis graft followed by a post-thrombectomy fistulogram that showed persistent thrombotic material at the venous site. PFO associated with large venous access site thrombosis was the most likely mechanism of stroke in both cases. Local thrombosis at sites of large venous access may be an overlooked source of paradoxical embolism in patients with PFO as well as a preventable cause of stroke in critically ill patients.

Auf dem schmalen Grat zwischen Thrombosen und Verbluten

A 67-year-old lady was admitted with a myocardial infarction. Coronarography revealed thrombotic material within coronary arteries. The underlying disease was paroxysmal nocturnal hemoglobinuria (PNH), a stem cell defect characterized by episodes of complement-induced hemolysis and thromboembolic events. Anticoagulation and antiaggregation were initiated. Subsequently, massive cerebral bleeding developed, to which the patient finally succumbed despite neurosurgical craniectomy. This tragic case illustrates that an antithrombotic treatment is always a balancing act with an unsecure outcome.

Paradoxical renal embolism in a patient with congenital cardiac malformation

Paradoxical embolism is a rare phenomenon in which thrombotic material passes through a right–left shunt to the systemic circulation. This most often occurs across a patent foramen ovale.1 Usual sites of embolism are the brain and the extremities, paradoxical embolism into the kidney is much less common.2 A 35-year-old man was admitted with sudden new-onset pain in his right flank. He had been born with a complex cardiac malformation consisting of double outlet right ventricle with malposition of the great arteries, straddling of the tricuspid valve and large atrial and ventricular septal defects. During the newborn period, pulmonary artery banding was conducted. Three years later corrective surgery was attempted; however, de-banding of the pulmonary artery resulted in pulmonary congestion. Thus, pulmonary artery banding was restored and a palliative Mustard procedure was performed to achieve an increase in systemic arterial oxygen saturation by changing streaming and reducing the amount of venous blood that reaches the aorta (Figure 1). After this surgery, the patient developed relatively normal with only minor physical limitations. At the age of 33 years, cardiac function progressively deteriorated resulting in repetitive cardiac decompensation. Two months before the current admission, the patient presented with numbness and tingling of his left arm and leg, which was interpreted as a transient ischemic attack. Thromboembolism due to intermittent atrial fibrillation was assumed to be the most likely source, because the patient reported palpitations, and atrial tachycardia is a common late arrhythmia after the Mustard procedure.3 Figure 1. ( A ) Computed tomography demonstrating the enlarged right ventricle (RV) as well as …

Acute myocardial infarction caused by coronary embolization of a papillary fibroelastoma of the thoracic ascending aorta☆

Papillary fibroelastomas (PFE) are benign endocardial masses and generally originate from the cardiac valves, while PFE arising from the ascending thoracic aorta are an uncommon clinical finding. We report the case of a 78-year-old female who presented to the emergency department with an acute ST segment elevation myocardial infarction. Urgent coronary angiography showed no significant coronary artery obstructive disease but left ventriculography revealed the presence of a highly mobile mass located in the proximal portion of the ascending thoracic aorta. We postulated that the clinical symptoms were caused by embolization from the aortic mass and surgical excision of the peduncle was performed. Histopathological examination revealed a PFE with thrombotic material. Nowadays, surgical excision of PFE remains, the treatment of choice for symptomatic patients with excellent short- and long-term results but recurrence of PFE following surgical excision has not been reported.

Low Cardiac Output Due to Left Main Coronary Embolism During Mitral Valve Replacement

A 55-year-old woman underwent elective mitral valve replacement due to severe rheumatic mitral valve stenosis. After valve replacement with a mechanical prosthesis, the patient failed to wean from the cardiopulmonary bypass. An aortotomy was performed and thrombotic embolic material was removed from the left coronary ostia with a Fogarty catheter allowing for successful discontinuation from cardiopulmonary bypass. Peripheral emboli are a known complication in patients undergoing mitral valve surgery for rheumatic mitral stenosis. In this report, we describe the case of a patient who sustained an intraoperative coronary embolus during a mitral valve replacement for rheumatic mitral stenosis.

Blood-born tissue factor in cardiovascular disease: where are we now?

Over the last decade, many clinical, pathological and laboratory data have been obtained indicating that, in the majority of cases, acute coronary thrombosis occurs upon rupture of the thin fibrous cap of a vulnerable atherosclerotic plaques, a result of a series of immuno-inflammatory processes. The inner content of the plaque becomes then exposed to the circulating blood leading to the deposition of thrombotic material into the lumen [1]. Our data, as well as that acquired by others, demonstrate that one of the major determinants of the thrombogenicity of the disrupted atheroma is tissue factor (TF),which triggers the activation of coagulation by binding to factor VII/VIIa. TF is particularly abundant in the lipid-rich necrotic core of the lesion, which is therefore the most thrombogenic component of atherosclerotic plaque [2]. The binding of TF to factor VIIa causes thrombin generation, which in turn induces platelet activation and fibrin formation leading to a partial or total thrombotic occlusion of the artery, and to the occurrence of an acute coronary syndrome (ACS) [1]. We also have demonstrated that the activation of the coagulation cascade within the coronary vessel at sites of atherosclerotic plaque rupture is largely TF-dependent, since a significant reduction in both platelet and fibrin deposition can be obtained by local pretreatment of atherosclerotic lesions with the recombinant analog of the physiologic tissue factor pathway inhibitor (rTFPI) or with a specific anti-TF antibody [3]. Instabilization and rupture of the plaque are mainly due to inflammatory processes that take place in the vessel wall. Experimental studies demonstrate that inflammatory cells such as macrophages, macrophage-derived lipid laden ‘foam cells’, and T lymphocytes are major constituents of plaques, and infiltrate areas of superficial erosion and the shoulder region of the coronary lesions where the fibrous cap usually breaks [4]. Macrophages and ‘foam cells’ are also the major source of TF within the lesions, and therefore this protein can be considered a product of the inflammatory processes of the atheroma [1]. The interplay between these cells results in the production and local secretion of several inflammatory cytokines and chemokines like interleukin (IL)-1, interferon-c and TNF-a, which, in turn, lead to the release of metalloproteinases (MMPs), particularly of MMP-9, which degrade extracellular matrix and particularly collagen, thus inducing plaque weakening and fracture[1, 5, 6].

Contrast Enhanced Ultrasonography for the Evaluation of Coil Embolization of Splenic Artery Aneurysm

A 65-year-old woman with compensated liver cirrhosis secondary to hepatitis C virus infection was under surveillance for early detection of hepatocellular carcinoma with ultrasonography and, due to suboptimal ultrasound feasability, at longer intervals with computed tomography (CT). During follow-up, a splenic artery aneurysm appeared and progressively increased from 18 mm to ≈30 mm in diameter over a 9-month interval. The patient had severe splenomegaly secondary to portal hypertension and hypersplenism with a low platelet count (≈30.000/mL). Percutaneous arterial embolization was proposed to the patient1 because severe portal hypertension was considered a contraindication to surgical splenectomy. Embolization was carried out, preceded by platelet infusion, using “fibered” coils and interlocking detachable coils without complications. Eight weeks later, the patient underwent abdominal CT as part of the surveillance program for hepatocellular carcinoma; no nodule with pattern of hepatocellular carcinoma was identified; at the splenic level, frank metallic artifacts were evident and prevented assessment of treatment efficacy (Figure 1) as described in previous reports from the literature with this technique.2 Figure 1. CT scan of the upper abdomen at a level passing through the treated splenic aneurysm. Arrows, metallic artifacts (similar to rays departing from the coils) don’t allow adequate assessment of treatment efficacy. To investigate the splenic aneurysm status, an attempt was made with conventional ultrasound (Figure 2) and color duplex-doppler ultrasonography, which failed to provide definitive and unquestionable information about the success of the embolization. Doppler ultrasound …

Impact of primitive cells in intracoronary thrombi on lesion prognosis: temporal analysis of cellular constituents of thrombotic material obtained from patients with acute coronary syndrome

BackgroundClinical evidence suggests that intracoronary thrombus formation is associated with a high incidence of late restenosis after successful coronary intervention in patients with myocardial infarction (MI). However, little is known...

Architecture of the thrombi removed from coronary artery bypass grafts in a patient with acute myocardial infarction

Using scanning electron microscopy we analyzed thrombotic material removed from coronary bypass grafts in a 57-year-old woman with multilevel atherosclerosis presenting with acute myocardial infarction (AMI). A white thrombotic material removed from the marginal branch bypass that contained large amounts of activated platelets displaying pseudopodia clearly visible at a higher magnification with a relatively low amount of fibrin. The other thrombus obtained from the right posterior descendent branch (RPD) bypass showed a highly organized fibrin structure composed of thicker fibers with low amounts of cellular components. Our findings indicate that the thrombus structure is different in AMI patients in whom the infarct-related vessel is vein anastomosis compared to those with a native coronary artery occluded. These findings help explain resistance of such thrombi to fibrinolysis and faster plaque growth related to fibrin accumulation.

Ung kvinne med hjertestans

A 20-year-old woman presented with dyspnoea in the Emergency department and subsequently suffered a cardiac arrest. The initial rhythm was PEA (pulseless electrical activity). She had intermittent return of spontaneous circulation. Transthoracic echocardiography showed a dilated hypokinetic right ventricle and a collapsed left ventricle. The tentative diagnosis was pulmonary embolism, but she remained hemodynamically unstable despite thrombolysis. 90 min after the collapse she was put on cardiopulmonary bypass and surgical embolectomy was performed. Large masses of thrombotic material were collected from central parts of the right and left pulmonary artery. Therapeutic hypothermia was applied for 24 hours postoperatively. The remaining hospital stay was uneventful and ten days after the presentation she was transferred to her local hospital. At this point she was without neurological sequelae. The patient had used oral contraceptives (ethinyl estradiol/ drospirenone).