17-year trends in incidence and prognosis of cardiogenic shock in patients with acute myocardial infarction in western Sweden.

BACKGROUND: Cardiogenic shock remains the leading cause of in hospital death in acute myocardial infarction (AMI) and is associated with a mortality rate of approximately 50%. Here we investigated the 17-year trends in incidence and prognosis of AMI-induced cardiogenic shock in Västra Götaland in western Sweden, an area with approximately 1.6 million inhabitants. The study period includes the transition from thrombolysis to primary percutaneous coronary intervention (PCI) as the region-wide therapy of choice for patients with ST-elevation myocardial infarction (STEMI). METHODS: Data on patients hospitalized in cardiac care units in Västra Götaland, Sweden between 1995 and 2013 were obtained from the Swedish Websystem for Enhancement of Evidence-based Care in Heart Disease Evaluated According to Recommended Therapies (SWEDEHEART). We determined the incidence of cardiogenic shock among patients diagnosed with AMI and the risk of death associated with developing cardiogenic shock. We fitted logistic regression models to study which factors predicted post-AMI cardiogenic shock. Analyses were performed on complete case data as well as after multiple imputation of missing data. RESULTS: Incidence of cardiogenic shock as a complication of AMI declined in western Sweden in the past decade, from 14% in 1995 to 4% in 2012. The risk of dying once cardiogenic shock had developed increased during the study period (p<0.01). Patients presenting with STEMI were more likely to develop cardiogenic shock than patients presenting with non STEMI (p<0.001). CONCLUSIONS: The incidence of cardiogenic shock has declined but cardiogenic shock carries a worse prognosis today than in 1995.

Potentiating and inhibiting effects of steroid hormones on the incidence of 90Sr induced osteosarcoma.

Eight hundred and twenty male CBA-mice, 75 +/- 3 days of age were divided into four main series. Three of these; A, B and C were further divided into three subgroups. To these 90Sr was given at three different dose levels alone (A) or in combination with either oestrogen (B) or prednisolone (C). In one series (D) all animals were given only oestrogen. The development of intramedullary oestrogen induced bone formation and the early events of bone tumour induction are reported. The 90Sr activities were selected in such a way that the lowest one would be below, the intermediate beyond and the highest well above the limit of bone tumour induction. Comparing the 90Sr injected animals with those given also oestrogen revealed that oestrogen had no promoting effect at the lowest and intermediate dose levels but increased the tumour incidence with a factor 4 at the highest dose level whereas prednisolone had an inhibitory effect. From the results obtained it was proposed that oestrogen may act only as a preparatory promoter and not assist in the initiating events. As has been reported elsewhere, the frequency of osteoblastic and osteoclastic osteosarcomas was higher in animals given oestrogen and 90Sr than 90Sr only. Mice given only oestrogen did not develop bone tumours.

Virulence of Staphylococcus aureus in a mouse mastitis model: studies of alpha hemolysin, coagulase, and protein A as possible virulence determinants with protoplast fusion and gene cloning.

Mutants of a genetically well-characterized strain of Staphylococcus aureus [SA113(83A)] were isolated after mutagenization. Alpha-hemolysin- (hla), coagulase- (coa), and protein A- (spa) negative mutants were characterized by more than 90 biochemical tests for production of extracellular proteins and biochemical profile to exclude pleiotropy. Protoplast fusion was then used to isolate double-defective (hla and coa) recombinants and recombinants with regained properties, i.e., production of alpha-hemolysin and coagulase. Studies of such mutants and recombinants in the mouse mastitis model showed that one alpha-hemolysin [SA113(83A) hla-5] and one coagulase-negative [SA113(83A) coa-147] mutant were lower in virulence compared with the wild-type strain SA113(83A). The double-negative mutant SA113(83A) hla-5 coa-147 showed a drastic decline in virulence and only induced very mild changes, as determined by microscopic examinations of infected mammary gland tissue. The recombinant with regained properties, however, was as virulent as the wild-type strain. This suggests that alpha-hemolysin and coagulase are virulence determinants of S. aureus. A high-level protein A-producing mutant (U300) showed the same virulence as the parent strain SA113(83A) in this model. One low virulence protein A-negative mutant (U320) did not markedly increase in virulence when a plasmid containing the cloned gene for protein A (pSPA15) was introduced into this mutant. By these and earlier observations, it seems likely that protein A is not an important virulence determinant in mastitis of mice. The reduced virulence of the protein A-negative mutant U320 compared with the wild-type SA113(83A) may be due to pleiotropic loss of some other unknown virulence determinant(s). Our data confirm earlier findings that pleiotropic changes are common in protein A-negative mutants.

Histopathology and pathogenesis of mouse mastitis induced with Staphylococcus aureus mutants.

Mammary glands of mice were inoculated with a well-defined strain of Staphylococcus aureus or with derived mutants lacking alpha-haemolysin, coagulase or protein A, in order to evaluate the pathogenicity of these factors. Alpha-haemolysin-negative and coagulase-negative mutants showed less virulence than the wild-type strain. Various protein A-negative mutants gave contradictory results. The lesions ranged from consistently non-reactive necrosis of the entire mammary gland to a limited inflammatory reaction. The necroses, especially when affecting the whole mammary gland, were mostly associated with vascular lesions. Because the necroses were non-reactive, the vascular lesions were considered to be primary, but they could not be linked exclusively with the effect of alpha-haemolysin and a multifactorial aetiology seemed most probable. After inoculation with coagulase-lacking bacteria the development of parenchymal lesions was delayed, hypothetically because of increased phagocytic activity. The investigation indicated that protein A could have influenced the pathogenesis of the lesions, since all but one of the mutants lacking protein A showed low virulence, whereas a high protein A-producing, haemolysin-negative mutant was as virulent as the wild-type strain. A connection between protein A, bacterial adherence and bacterial growth rate is therefore conceivable. The possibility cannot be excluded, however, that during mutagenesis some as yet unknown cell surface factors were affected.

Primary progressive muscular dystrophy in the dog.

A case of primary progressive muscular dystrophy in a labrador dog is described. The differential diagnosis with respect to certain muscular and nervous disorders is discussed. The possibility of the hereditary nature of the disease is indicated.

Induction of pituitary tumours by combination of oestrogenic hormones and 90Sr.

The present investigation was initiated to analyse the carcinogenic effect of combined treatment with 90Sr and oestrogenic hormones or corticosteroids in inbred CBA mice. Pituitary tumours appeared in a remarkably high incidence in mice treated with oestrogens + 90Sr in low doses--0.925 kBq/g body weight (44%) and 1.850 kBq/g body weight (37%)--as compared with mice treated with 90Sr only--1 and 3 per cent, respectively. The syncancerogenic effect is ascribed the oestrogen induced proliferation of pituitary cells and their increased sensitivity to radiation. The reverse relation found between number of pituitary tumours and dose of 90Sr in oestrogen treated mice is explained by the reduction of the survival time with increasing dose. Preneoplastic histologic changes of the pituitary are described and pituitary tumours which mainly appeared in pars distalis, are classified according to the growth and tinctorial characteristics.