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1.
Ir Med J ; 108(7): 207-9, 2015.
Article in English | MEDLINE | ID: mdl-26349350

ABSTRACT

Heart failure (HF) is the most common cause for admission in patients over 65 and hospitalisations account for almost 1% of the health care budget in Ireland. A need to understand the epidemiological data in relation to hospitalisations for HF plays an important part in the planning and distribution of heart care services. The aim of this study was to analyse the temporal trends in hospitalisations for HF and look at potential areas for improvement. Cross sectional data was obtained from the Eurostat database. Data was extracted with the ICD 10 code for heart failure (1-50). The years 2002-2010 were analysed between the ages of 0-105. Between 2002 and 2010 there were 51369 admissions for HF in Irish hospitals. Of these, 54.7% were males and 87% were older than 65 years. The age standardised hospitalisation rates decreased from 157.5 per 100,000 to 127.2 per 100,000, a relative decrease of 19.2% (p = 0.02). There was an increase in HF hospitalizations for those aged > 85 from 17.9% to 26.7% (p = 0.001). There was no significant change in length of stay (12.0 days in 2002 and 12.4 days in 2010). This study of epidemiological surveillance data on Irish HF hospitalisations has shown a 19% reduction in hospitalisations between 2002 and 2010. Although this study shows an overall successful reduction in HF admission rates, the challenges remain in ensuring we manage the burden of those > 65 years, in particular those > 85 years.


Subject(s)
Disease Management , Heart Failure , Hospitalization , Patient Acceptance of Health Care/statistics & numerical data , Age Factors , Aged , Aged, 80 and over , Cross-Sectional Studies , Female , Health Care Rationing/methods , Health Care Rationing/statistics & numerical data , Heart Failure/epidemiology , Heart Failure/therapy , Hospitalization/statistics & numerical data , Hospitalization/trends , Humans , International Classification of Diseases , Ireland/epidemiology , Length of Stay , Male , Needs Assessment , Quality Improvement/trends , Sex Factors
3.
Br J Haematol ; 52(3): 495-502, 1982 Nov.
Article in English | MEDLINE | ID: mdl-6812616

ABSTRACT

Inhibition of activated human protein C was assessed in an amidolytic assay system using normal human plasma and samples from patients with hereditary coagulation abnormalities. In eight experiments normal plasma inhibited 63.5% (+/- 15.6%) protein C activity. Plasma from patients with haemophilia A or isolated factor V deficiency gave results which were not significantly different from normal. However, plasma from patients with combined factor V and factor VIII deficiencies inhibited an average of 24.5% (+/- 13.6%) of the amidolytic activity (P less than 0.01). Two of these plasma samples failed to inhibit any protein C activity. The relationship between the level of inhibitor and those of factor V and factor VII coagulant antigens (VCAg and VIIICAg) in the combined defect was investigated. There was no significant correlation between the level of inhibitor and any of the coagulation immunoassays on these stored samples but there was significant correlation between VCAg and VIIICAg in some assay systems. The levels of VCAg and VII CAg was low in most samples from patients with the combined defect which was in contrast to the results obtained when normal plasma was incubated with activated protein C in vitro. The findings are consistent with the presence of biochemical similarities between factors V and VIIIC molecules, but the role of activated protein C and its inhibitor in hereditary combined factor V/VIII deficiency remains to be firmly established.


Subject(s)
Antigens/analysis , Blood Coagulation Factors/antagonists & inhibitors , Blood Proteins/antagonists & inhibitors , Factor V Deficiency/immunology , Factor VIII/immunology , Factor V/immunology , Glycoproteins/antagonists & inhibitors , Hemophilia A/immunology , Factor V/analysis , Factor V Deficiency/blood , Factor V Deficiency/complications , Factor VIII/analysis , Hemophilia A/blood , Hemophilia A/complications , Humans , Protein C
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