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Despite the advanced therapeutic arsenal in Heart Failure (HF), this progressive disease, symptomatic in many clinical aspects and potentially fatal when compared to oncologic diseases, remains a public health issue, involving both the patient, the clinician and also the health system. By the nature of its’ prolonged evolution, HF affects the quality of life more pronounced compared to other chronic diseases [1]...

Introduction Splenic abcess represents a rare complication of left-sided infective endocarditis. Unlike splenic infarction, which is a more benign condition, splenic abcess requires rapid diagnosis and treatment as its course can be fatal. We present the case of a 52- year old male, with diabetes and hypertension, admitted for shortness of breath and fever in the past two months. Clinical examination revealed respiratory distress, tachypnea, diastolic murmur on the left sternal border. Baseline laboratory investigations showed elevated inflammation markers, leukocytosis and thrombocytosis. Enterococcus faecalis was isolated from the hemocultures. Transthoracic echocardiography revealed a dilated left ventricle (LV), with preserved LV ejection fraction, with severe aortic regurgitation due to valve destruction. A large (11mm diameter) vegetation-like structure attached to the ventricular side of the right coronary cusp, protruding into the left ventricular outflow tract was identified. Further evaluation by transoesopahgeal echocardiography did not identify other lesions, except for secondary moderate mitral regurgitation, with intact mitral leaflets. Dual antibiotic therapy with Ampicilin and Gentamycin was initiated. Surgery was planned after infection control. The first three days were uneventful, with rapid resolution of fever and inflammatory markers, but on the fourth day, the patient developed severe abdominal pain, with its focal point in the left hypochondrium. Contrast abdominal CT was performed and large multiple subcapsular lesions were identified. These findings, correlated with the symptomatology, suggested embolic splenic abcess and infarction. The patient successfully underwent laparoscopic splenectomy, but soon after he developed sepsis with respiratory failure and neurological deterioration (with normal CT scan) and was admitted to the intensive care unit, where he was intubated and mechanically ventilated. Consensus after discussions between cardiology, cardiac surgery and neurology services was to immediately replace the aortic valve, given the inability to otherwise control the infection. Intraoperative images were consistent with perforation of the right coronary cusp. During hospitalization in the ICU following cardiac surgery, the patient was extubated and his neurological function markedly improved. Repeated TTE and TEE showed normal prosthetic valve function and resolution of mitral regurgitation. The patient continued to improve clinically until his discharge. Conclusions We presented a case of a rare pathogenic entity- splenic abscess and infarction- due to systemic embolization from infective aortic valve endocarditis. Multidisciplinary teamwork was required between cardiologist, intensive care specialist, neurologist, infectionist, general surgeon and cardiac surgeon. Splenectomy was performed before valve replacement, a treatment-course characteristic in the occurrence of these rare cases.

Background The presence of small mobile masses on the ventricular side of the aortic valves in the absence of valvular regurgitation and signs of systemic inflammation has been previously described as marantic endocarditis and is now referred to as nonbacterial thrombotic endocarditis (NBTE). It is thought to be associated with endothelial dysfunction and procoagulative status, as is the case of acute decompensated heart failure (HF). Case description We present a series of three male patients, with similar clinical characteristics, who were admitted for acute decompensated HF. All three patients had chronic HF, due to non-ischemic dilated cardiomyopathy with severe biventricular dysfunction, with resynchronization therapy, with elevated natriuretic peptides and previous HF hospitalizations in the past year requiring prolonged intravenous treatments. Other clinical, biological criteria for the definition of advanced HF were also met. All patients were under chronic anticoagulation treatment using a direct oral anticoagulant because of persistent atrial fibrillation. Thorough echocardiographic evaluation (both transthoracic and transoesophageal ultrasound) identified small mobile masses on the ventricular side of the aortic valves, centrally, on the line of cusp coaptation, with only minor central regurgitation. The lack of progression of valve lesion and the absence of gross signs of inflammation (no fever, normal hemoleucogram, normal CRP, repeated negative blood cultures) on serial examinations during several weeks follow-up allowed for the exclusion of infective endocarditis. In one case we also identified a left atrial appendage thrombus and presumably thrombotic masses attached to right side pacing leads. No clinically systemic embolic events were identified. Conclusion We consider this to be an incidental finding in the given subclinical prothrombotic and inflammatory predisposing milieu of advanced chronic HF and the increasing high quality echocardiography imaging. Its clinical significance is still unknown, while differential diagnosis from subacute or chronic endocarditis relies largely on clinical judgment.

Background Transcatheter valve replacement (TAVR ) is currently the optimal treatment for patients with severe aortic stenosis who are considered to have an intermediate to high operative risk for surgical intervention. Intramural hematoma secondary to balloon-expandable TAVR is a poorly reported complication with unknown outcome. Among the risk factors associated with this complication are advanced age, female gender, bulky calcifications, significant basal hypertrophy and severe prothesis oversizing. Case report We report the case of a 84 year old woman with a history of permanent atrial fibrillation, who was diagnosed with severe aortic stenosis symptomatic with heart failure NYHA class III. An important comorbidity was liver cirrhosis of viral etiology (hepatitis C virus) with secondary thrombocytopenia. Transthoracic and transoesophageal echocardiography (TEE) showed severe aortic stenosis with asymmetric calcifications, with preserved gradient (a peak velocity of 4.7 m/s, mean gradient of 63.3mmHg), mild left ventricular disfunction (ejection fraction 45%), and calculated aortic valve area of 0,9 cm2. As a frail, high risk patient, the heart team recommended transcatheter aortic valve implantation. After complete computer tomographic evaluation, a 26 mm Edwards Sapien 3 valve was implanted through a femoral approach. Intraprocedural transesophageal echocardiography showed the developement of an intramural hematoma in the aortic root (right coronary and noncoronary sinuses), associated with a small pericardial effusion. After administration of Protamine, betablockers and strict blood pressure control, no extension of the hematoma was noted. Serial TEE showed significant regression of the hematoma and of the pericardial effusion, with normal parametres of the prothesis, with a transprothetic gradient of 23 mmHg, no aortic leak, no other complications.The patient was discharged 12 days after the procedure, clinically stable. Conclusion Aortic intramural hematoma may occur during intra-TAVR procedure. Although it may have a benign course, timely recognition and adequate imaging follow-up are mandatory in order to limit the extent and prevent life-threatening complications.

Introduction Left ventricular non-compaction is a rare form of cardiomyopathy charactherized by the presence of a two layered ventricular wall- a thinner epicardial layer and an inner, non-compacted layer with prominent trabeculations associated with deep, intratrabecular recesses that communicate with left ventricle cavity. Clinical manifestations vary in severity, including symptoms of heart failure, thromboembolic events or arrhythmias. Left ventricular (LV) dysfunction leads to tethering of the mitral apparatus and is a cause for secondary significant mitral regurgitation. Case presentation We report the case of a 57 year-old female patient, diagnosed with severe mitral regurgitation one year before presentation, with severe heart failure (HF) symptoms, referred to our clinic for the surgical replacement of the mitral valve. Clinical examination revealed no signs of pulmonary or systemic congestion and systolic apical murmur. Blood tests were normal, except for the elevated BNP (552 pg/ml). Electrocardiogram showed sinus rhythm and left ventricular hypertrophy. Coronary angiogram did not identify any coronary artery lesions. Echocardiography revealed mildly dilated left ventricle, but wih proeminent trabeculations and two distinct myocardial layers with a non-compacted/compacted ratio of 2:1 in the anterior and lateral walls, diagnostic for left ventricular non-compaction cardiomyopathy. LV ejection fraction was 40% , with severe secondary mitral regurgitation due to significant antero-posterior dilation of the mitral ring, with intact mitral leaflets; mild pulmonary hypertension was present. Magnetic resonance imaging (MRI) identified a two layer antero-lateral myocardium and confirmed the echo diagnosis; there was no evidence of scarring as there was absent late gadolinium enhacement. In the absence of fibrosis on MRI or any arrhythmic events on repeated Holter ECG monitoring, the implantation of a cardiac defibrillator was deferred. Given the secondary cause for mitral regurgitation (LV dysfunction), specific HF medication with beta blocker and renin-angiotensin-aldosterone blockade was initiated and titrated to optimal doses. With medical treatment the evolution was favourable. Currently, 3 years after the initial diagnosis, 6 minutes walk test revealed good functional capacity (510 m), a BNP value of 104 pg/l, without any worsening of LV systolic function nor progression of pulmonary hypertension. Conclusion Left ventricular non-compaction cardiomyopathy is a rare cause of heart failure, but due to advances in imaging modalities and increasing awareness, its prevalence is growing. Its pathogenesis and prognosis largely remain unknown, but early and adequate initiation of neurohormonal medication may be just as essential in order to prevent complications and improve long term prognosis, as for other forms of cardiomiopathy, even in the presence of severe secondary mitral regurgitation.

SUMMARY Through the integration of high speed computer networks and interactive multimedia workstations, the IRI (Interactive Remote Instruction) system creates a geographically dispersed virtual classroom. Each student participates in a lesson using a personal workstation which can be used to view multimedia lectures, to make presentations, to take notes in a multimedia notebook and to interact via audio/video and shared computer tools. We compare this approach with other modes of instruction and describe lessons learned from the instructor, student and technical perspectives.

This paper discusses the important role of multicasting in designing, implementing, and managing interactive multimedia distance learning systems. This is achieved in the context of IRI, an Interactive Remote Instruction system for distance learning built at Old Dominion University. IRI is an Internet-based system which integrates continuous multimedia, shared applications and a variety of multi-user collaborative utilities. In this paper, we concentrate on the process architecture and dynamic multicast group handling as they pertain to managing multimedia resources, and show how they support robustness and short response time to user actions. IRI uses raw IP multicasting for audio and video streams and reliable multicasting for resource management and data sharing. The system is scalable (uses multicast for inter-process communication) and expandable(partitioned into a setof autonomousbutcooperating components).

Many distance learning systems claim to be interactive, but few can offer two-way video, on-the-fly interaction and application sharing. To address these limitations, our research group built the Interactive Remote Instruction (IRI) system, which links sites over a high-speed intranet, allowing students at geographically dispersed satellite campuses and community colleges to take a class together. Access from home PCs through a Windows NT port is planned but not yet available. IRI improves on the Old Dominion University's Teletechnet system in five areas: video resolution, asymmetrical video presence, interaction, teacher support and computer simulations.

Discusses the software architecture, interprocess communication and the reference implementation of the Interactive Remote Instruction (IRI) system for distance learning. IRI is an Internet-based system which integrates continuous multimedia, shared applications and a variety of multi-user collaborative utilities. Internet multicasting is used by IRI for group management and data sharing, UDP (Unix domain protocol) multicasting is used for audio and video streams, while a reliable multicasting protocol (RMP) is used by XTV, the data sharing engine of IRI. The system is both scalable and expandable. It is scalable through the use of multicasting for interprocess communication. It is expandable due to its partitioning into a set of autonomous but cooperating components. The interaction among components is specified by a set of messages and the functions needed to send and receive these messages.

The reactivity of the higher autonomic centers to hypoglycemia prior to and after the treatment with pyrithioxin or caffeine in patients with cerebral infarct was studied. Before treatment a hyporeact

SUMMARY 1 In 24 non-anaesthesized cats under the influence of curare studies were made of the effect of i.v.-administered quinidine on the cortical and thalamic post-discharges produced by focal electrical stimulation of the cortex and the thalamic nuclei, and on the discharges induced by local application of penicillin on the cerebral cortex. 2 Dosages lower than those which are necessary for the suppression of severe electro-convulsive crises, and which do not cause significant hypotensive effects (4–7 mg/kg) are sufficient for raising the threshold of the cortical and thalamic post-discharges up to 400%. These effects are long-lasting, persisting for several hours. 3 Dosages of 7–15 mg/kg suppress penicillin spikes during a short interval (5–10 minutes). Later on the spikes reappear and the development of general paroxysms cannot be avoided. Higher dosages (up to 30 mg/kg) lead to the disappearance of the electrical crises in the cortical leads. Only isolated spikes are observed, whereas the paroxysm continues to develop in the thalamic leads. RESUME 1 On a etudie sur 24 chats non-anesthesies et curarises l'effet de la quinidine administree par voie intraveineuse sur les post-decharges corticales et thalamiques, produites par la stimulation electrique focale du cortex et des noyaux thalamiques, ainsi que sur les decharges induites par l'application locale de la penicilline sur l'ecorce cerebrale. 2 Des doses plus faibles que celles necessaires pour la suppression des grandes crises electro-convulsives et qui n'entrainent pas des effets hypotensifs significatifs (4–7 mg/kg) sont efficientes pour elever le seuil des post-decharges corticales et thalamiques avec des valeurs qui vont jusqu'a 400%. Ces effets sont durables, persistant pour des heures. 3 Des doses de 7–15 mg/kg abolissent pour de courts intervalles (5–10 minutes) les pointes penicilliniques. Ulterieurement les pointes s'organisent de nouveau et ne peuvent pas etre empechees de determiner des paroxysmes generalises. Des plus fortes doses (allant jusqu'a 30 mg/kg) font disparaitre la crise electrique sur les derivations corticales et la remplacent par des pointes isoles, tandis que le paroxysme continue a se developper sur les derivations thalamiques.

SUMMARY 1 In 61 non-anaesthesized cats the action of a 1% quinidine sulphate solution was studied, observing the clinical and vasomotor aspect of crises induced by transcerebral electroshock. In curarized cats the cortical and thalamic electroencephalographical aspects of these crises were studied. 2 Intravenous administration of 10–17.5 mg/kg quinidine stops the electrical consulsive crises and, more frequently even, the transformation of its aspect from tonic to clonic (with the same parameters of stimulation as in the crisis test), and leads to the disappearance of the arterial hypertension, which accompanies the tonic epileptic crises. 3 The anticonvulsive action of quinidine sulphate is not due to the arterial hypotension produced by the drug, for the correction of the hypotension by means of adrenalin does not impede the anti-epileptic action of quinidine sulphate. Moreover, other experiments have shown that the clinical and vasomotor aspect of the epileptic crises is not a function of the arterial pressure. 4 A dosage of 7–10 mg/kg i.v., of quinidine results in a flattening of the curves in the EEG, immediately after the administration. Waves of 6 or 11 c/sec and with a large amplitude, which alternate with periods of no electrical phenomena are observed. This resembles more or less the preparation of the “isolated brain”. At these dosages the curves resume their normal aspect after 4–5 minutes. 5 Higher dosages of up to 30–40 mg/kg cause a considerable bradycardia and at the same time an almost complete disappearance of cortical and thalamic EEG-waves, on which the ECG is superposed. This aspect is reversible after 10–15 minutes, however. 6 Dosages of 10–12.5 mg/kg markedly reduce the electrical crisis, both in voltage and duration. Dosages of up to 30 mg/kg lead to the disappearance of the cortical crisis, whereas epileptic discharges are still present in the thalamic leads, though they are considerably reduced. 7 The neuraxial niveau of the action of quinidine is especially discussed. RESUME 1 On a etudie sur 61 chats non-anesthesies l'action du sulphate de quinidine (sol. 1%) en recherchant l'aspect clinique et vasomoteur des crises induites par electro-choc transcerebral, aussi bien que, chez le chat curarise, l'aspect electroencephalographique, cortical et thalamique, des memes crises. 2 L'administration par voie intraveineuse de 10–17.5 mg/kg de quinidine determine la suppression de la crise electroconvulsive, ou bien, plus frequemment, la transformation de son aspect tonique en clonique (aux memes parametres de stimulation que la crise test), ainsi que la disparition de l'hypertension arterielle qui accompagne les crises epileptiques toniques. 3 L'action anticonvulsivante du sulphate de quinidine n'est pas determinee par l'hypotension arterielle provoquee par le drogue, car sa correction avec l'adrenaline n'empeche pas son action antiepileptique; de meme, d'autres preuves experimentales ont montre que l'aspect clinique et vasomoteur de la crise epileptique n'est pas en concordance avec le niveau de la pression arterielle. 4 La quinidine (7–10 mg/kg, i.v.) agit sur l'EEG en determinant, immediatement apres l'administration, un aplatissement du trace, avec l'apparition des bouffees de 6 c/sec ou de 11 c/sec, de grande amplitude, alternant avec des periodes de silence electrique, ce qui rappelle dans une certaine mesure la preparation du „cerveau isole”. A ces doses, le trace revient a son aspect normal apres 4–5 minutes. 5 Des quantites plus grandes, allant jusqu'a 30–40 mg/kg, determinent une bradycardie importante et, parallelement, un silence electrique cortical et thalamique presque total, sur lequel se superpose l'ECG. Cet aspect est quand meme reversible apres 10–15 minutes. 6 Les doses de 10–12.5 mg/kg reduisent beaucoup la crise electrique, en tant que voltage et duree. Des doses allant jusqu'a 30 mg/kg font disparaitre la crise corticale, tandis que les derivations thalamiques continuent a presenter des decharges epileptiques, quoique beaucoup plus reduites. 7 On discute surtout le niveau nevraxiel d'action quinidinique.

A method of treatment consisting in administration of a neurodynamic drug, pyrithioxin, combined with a short period of hyperventilation (HV) was applied in cerebral infarct patients with hemiplegia. The combination was superior to pyrithioxin alone for the motor recovery of these patients. In some cases, it induced immediately a partial restoration of motility. The combination constantly brought about an increase in urinary excretion of norepinephrine and vanilmandelic acid, which failed to occur after pyrithioxin or HV alone. HV appears to facilitate the neural effects of the drug by promoting its transfer into the CNS.

Urinary excretion of catecholamines under insulin hypoglycemia was studied in cerebral infarct patients as well as in patients with Parkinson’s disease and subjects with lumbar discopathy (control group). While in the last two categories of subjects a normal response to hypoglycemia, i.e., an increase in urinary excretion of epinephrine was noticed, no such increase was found in patients with cerebral infarction. The disorder is attributed to the unresponsiveness to hypoglycemia of the brain stem centers controlling epinephrine secretion.

The oral erythrodiapedesis was studied by estimating the number of erythrocytes in the sediment of oral washing fluid. The investigation was performed in the acute period of cerebrovascular accidents. Most of the patients with cerebral infarct (84%) displayed a low oral erythrodiapedesis similar to that noticed in controls. On the contrary more than half of the cerebral hemorrhage patients exhibited a high oral erythrodiapedesis. The authors assume that the cerebral hemorrhages associated with enhanced oral erythrodiapedesis are caused by some general humoral disturbances with repercussion both on cerebral and other capillaries. They feel that the investigation of oral erythrodiapedesis is a reliable test for differentiation between hemorrhagic and ischemic cerebral accidents.

The angiographic course in 13 cases with occlusive cerebral infarct treated with repeated epinephrine injections and in 10 cases with the same diagnosis treated with cerebral vasodilators and heparin was followed. In 8 out of 13 cases of the first group, repermeabilization of the occluded cerebral vessel took place; in the second group, the clearing of the occlusive process was less frequent (2 out of 10 cases). The favourable results obtained by epinephrine administration might be ascribed to the activation of the higher autonomic centres, which displayed in patients with occlusive cerebral infarct a manifest inertia. Thus, the administration of epinephrine appears to be a causal treatment of this affection.

The dynamics of blood coagulability and fibrinolysis (comparison of the initial values of the heparin clotting time, recalcified plasma clotting time and plasma fibrinolytic activity with those obtained 30 and 120 min after the application of an emotional stimulus) was studied in patients with cerebral vascular accidents one or several months after a stroke. Emotional stress induced a sustained hypercoagulability only in patients with occlusive cerebral softening (verified by angiography) and in those with peripheral atherosclerosis obliterans; concomitantly, in these patients an unresponsiveness of the fibrinolytic system to stress was observed. The prolonged hypercoagulability induced by emotion in patients with occlusive cerebral softening is interpreted as expressing an imbalance between the clotting and the anticlotting factors in favour of the former.