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X Bosch

Publications and source records attributed to X Bosch.

At least 127 records · Page 7Linked to original sources

[Variability in the management and prognosis at short- and medium-term of myocardial infarct in Spain: the PRIAMHO study. Registration Project of Hospital Acute Myocardial Infarct].

BACKGROUND AND PURPOSE: The paucity of data on myocardial infarction management and results in Spain lead to the design of the PRIAMHO study (Proyecto de Registro de Infarto Agudo de Miocardio Hospitalario [Acute Myocardial Infarction Hospital Registration Project]) which developed standard methods to collect information on the management of patients with such a condition and their characteristics. The variability results among hospitals in myocardial infarction management and in one-year mortality are presented. METHODS: A cohort study with a one-year follow-up was designed to register all patients diagnosed with acute myocardial infarction discharged from 24 Spanish hospitals that completed all the requisites to participate. The demographic and clinical characteristics of the patients, their management during the coronary care unit stage, and the outcome and complications were prospectively registered. Standard definitions for diagnosis were used. Confidentiality regarding patient identity and participating centers was guaranteed. RESULTS: 5,242 (77.6%) of the 6,756 patients with myocardial infarction admitted in the 24 participating hospitals were registered in the coronary care units. Half of the centers had an on-site hemodynamic laboratory and in seven coronary surgery. The delay between symptom-onset and emergency room admission was 2 hours. Acute pulmonary edema or cardiogenic shock was developed by 16.6% of patients and 41.8% received thrombolysis. Mean time delay between symptom-onset and thrombolysis was 3 hours. A large variability in the use of beta-blockers, thrombolysis, echocardiography, coronary catheterization angiography and invasive revascularization was observed among hospitals. Mortality in the coronary care unit was 10.9% and increased to 14.0% at 28 days and to 18.5% at one year with considerable variation among hospitals. Four hospitals showed higher mortality among their patients, independently from the proportion of diabetes, hypertension, women, anterior location of myocardial infarction, non-Q-wave infarction, age and severity. CONCLUSIONS: The results of this study show that early and mid-term mortality from myocardial infarction is still high in Spain in the reperfusion era, and that a considerable variability in management and outcome exists among Spanish hospitals, which is not explained by the different case-mix among them.

Cardiovascular Agents↗

Microscopic polyangiitis (microscopic polyarteritis) with late emergence of generalised Wegener's granulomatosis.

OBJECTIVES: Recent proposals for the nomenclature of systemic vasculitis have focused on a distinction between (classic) polyarteritis nodosa (PAN) and microscopic polyangiitis or polyarteritis (MPA). Thus, MPA may cause necrotising vasculitis of medium sized or small arteries but, unlike PAN, involvement of "microscopic" vessels must always be present in the former. This study aimed to show that the term "MPA" may represent a source of misinterpretation and to help illustrate difficulties of applying diagnostic criteria/definitions for conditions of unknown aetiology or variable clinical presentation and course. METHODS: Among 1250 consecutive patients screened for antineutrophil cytoplasmic antibodies (ANCA), 59 had been found to have idiopathic necrotising and crescentic glomerulonephritis plus ANCA while five had been found to have isolated pulmonary haemorrhage with biopsy verified necrotising alveolar capillaritis plus ANCA. None of these patients had clinical or histological evidence of Wegener's granulomatosis (WG) or evidence of biopsy verified vasculitis involving vessels other than glomerular or pulmonary capillaries at the time of presentation. RESULTS: Six of the 64 patients who met definition criteria for MPA at the time of initial diagnoses had entered into complete clinical remission upon appropriate corticosteroid and cyclophosphamide treatment between two weeks and three months, though subsequently (20 to 72 months; mean time: 42.3 months) developed characteristic clinical and histological features of overt WG. CONCLUSIONS: Microscopic polyangiitis/polyarteritis may be a dynamic condition with clinical and histopathological features evolving over time to other forms of small vessel vasculitis, mainly WG, thereby meaning that follow up would be necessary not only to control a given patient but also to make a final diagnosis. This follow up should be for a long time as there may be a long interval between initial presentation and subsequent development of WG lesions.

Adult↗

The pulmonary-renal syndrome: a poorly understood clinicopathologic condition.

The co-existence of pulmonary hemorrhage and glomerulonephritis delineates a severe syndrome, often underestimated, resulting from several diseases and frequently associated with serum positivity for antineutrophil cytoplasmic antibodies (ANCA) or antiglomerular basement membrane (GBM) antibodies. The most common illness presenting as pulmonary-renal syndrome is systemic vasculitis. Moreover, the idiopathic pulmonary-renal syndrome is a distinctive clinicopathologic entity with different pathogenetic mechanisms. Tissue immunofluorescence studies are fundamental in distinguishing anti-GBM antibody-mediated forms from immune-complex-mediated and ANCA-associated forms. The type of glomerular or alveolar immunologic injury is the main factor determining the outcome and thus the prognosis of the pulmonary-renal syndrome. Development and improvement of appropriate serologic detection techniques have given reliable and early guidance for diagnosing these cases.

Anti-Glomerular Basement Membrane Disease↗

[The role of inflammation in the pathogenesis and prognosis of unstable angina].

Unstable angina is a clinical syndrome which results from the unstabilization of the coronary atherosclerothic plaque, leading to its ulceration or rupture and to the formation of superimposed thrombus. The mechanism underlying plaque unstabilization is a subject of intense basic research. In the last few years, new knowledge has emerged that relates inflammation in the atherosclerothic lesion with its gradual growth and development, as well as with its sudden transformation into a complicated plaque causing unstable angina or myocardial infarction. In this article we will review the evidence that links inflammation with the pathogenesis of unstable angina and its prognosis.

Angina, Unstable↗