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1.
J Am Coll Cardiol ; 38(5): 1395-401, 2001 Nov 01.
Artículo en Inglés | MEDLINE | ID: mdl-11691514

RESUMEN

OBJECTIVES: The aim of this study was to assess the impact of gender on clinical course and in-hospital mortality in patients with cardiogenic shock (CS) complicating acute myocardial infarction (AMI). BACKGROUND: Previous studies have demonstrated higher mortality for women compared with men with ST elevation myocardial infarctions and higher rates of CS after AMI. The influence of gender and its interaction with various treatment strategies on clinical outcomes once CS develops is unclear. METHODS: Using the SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK? (SHOCK) Registry database of 1,190 patients with suspected CS in the setting of AMI, we examined shock etiologies by gender. Among the 884 patients with predominant left ventricular (LV) failure, we compared the patient demographics, angiographic and hemodynamic findings, treatment approaches as well as the clinical outcomes of women versus men. This study had a 97% power to detect a 10% absolute difference in mortality by gender. RESULTS: Left ventricular failure was the most frequent cause of CS for both gender groups. Women in the SHOCK Registry had a significantly higher incidence of mechanical complications including ventricular septal rupture and acute severe mitral regurgitation. Among patients with predominant LV failure, women were, on average, 4.6 years older, had a higher incidence of hypertension, diabetes and a lower cardiac index. The overall mortality rate for the entire cohort was high (61%). After adjustment for differences in patient demographics and treatment approaches, there was no significant difference in in-hospital mortality between the two gender groups (odds ratio = 1.03, 95% confidence interval of 0.73 to 1.43, p = 0.88). Mortality was also similar for women and men who were selected for revascularization (44% vs. 38%, p = 0.244). CONCLUSIONS: Women with CS complicating AMI had more frequent adverse clinical characteristics and mechanical complications. Women derived the same benefit as men from revascularization, and gender was not independently associated with in-hospital mortality in the SHOCK Registry.


Asunto(s)
Insuficiencia Cardíaca/etiología , Mortalidad Hospitalaria , Infarto del Miocardio/complicaciones , Infarto del Miocardio/terapia , Caracteres Sexuales , Choque Cardiogénico/etiología , Choque Cardiogénico/mortalidad , Disfunción Ventricular Izquierda/etiología , Anciano , Angioplastia Coronaria con Balón , Australia/epidemiología , Bélgica/epidemiología , Brasil/epidemiología , Canadá/epidemiología , Causas de Muerte , Angiografía Coronaria , Puente de Arteria Coronaria , Progresión de la Enfermedad , Femenino , Fibrinolíticos/uso terapéutico , Humanos , Incidencia , Masculino , Infarto del Miocardio/diagnóstico , Nueva Zelanda/epidemiología , Selección de Paciente , Vigilancia de la Población , Pronóstico , Estudios Prospectivos , Sistema de Registros , Distribución por Sexo , Resultado del Tratamiento , Estados Unidos/epidemiología
2.
J Pediatr ; 139(3): 385-90, 2001 Sep.
Artículo en Inglés | MEDLINE | ID: mdl-11562618

RESUMEN

OBJECTIVE: To determine whether children with homozygous sickle cell anemia (SCD) who have silent infarcts on magnetic resonance imaging (MRI) of the brain are at increased risk for overt stroke. METHODS: We selected patients with homozygous SCD who (1) enrolled in the Cooperative Study of Sickle Cell Disease (CSSCD) before age 6 months, (2) had at least 1 study-mandated brain MRI at age 6 years or older, and (3) had no overt stroke before a first MRI. MRI results and clinical and laboratory parameters were tested as predictors of stroke. RESULTS: Among 248 eligible patients, mean age at first MRI was 8.3 +/- 1.9 years, and mean follow-up after baseline MRI was 5.2 +/- 2.2 years. Five (8.1%) of 62 patients with silent infarct had strokes compared with 1 (0.5%) of 186 patients without prior silent infarct; incidence per 100 patient-years of follow-up was increased 14-fold (1.45 per 100 patient-years vs 0.11 per 100 patient-years, P =.006). Of several clinical and laboratory parameters examined, silent infarct was the strongest independent predictor of stroke (hazard ratio = 7.2, P =.027). CONCLUSIONS: Silent infarct identified at age 6 years or older is associated with increased stroke risk.


Asunto(s)
Anemia de Células Falciformes/complicaciones , Infarto del Miocardio/complicaciones , Accidente Cerebrovascular/etiología , Niño , Humanos , Lactante , Imagen por Resonancia Magnética , Infarto del Miocardio/diagnóstico , Factores de Riesgo
3.
J Pediatr ; 124(6): 896-902, 1994 Jun.
Artículo en Inglés | MEDLINE | ID: mdl-8201473

RESUMEN

As part of the Hemophilia Growth and Development Study, we investigated the impact of human immunodeficiency virus (HIV) infection on statural growth, weight gain, and skeletal and sexual maturity in more than 300 boys with moderate to severe hemophilia, of whom 62% were infected with HIV. Age-adjusted height and weight were reduced in the HIV-infected subjects (p < 0.001). However, mean weight for height and triceps skin-fold thickness of the infected-boys closely resembled those of the uninfected group. In HIV-infected boys, height for age was positively related to the CD4+ lymphocyte count when the count was < 200 cells/mm3. Age-adjusted serum testosterone levels did not differ by HIV status, but in the infected participants the mean age-adjusted bone age was significantly reduced (p = 0.038) and the distribution of Tanner stages, adjusted for age, differed significantly (p = 0.003). The probability of advancing one or more Tanner stages in the first study year was significantly slowed in HIV-infected boys more than 14 years of age (p = 0.0003). We conclude that linear growth was significantly impaired in boys with hemophilia and HIV infection, but the wasting of malnutrition was not found. The delays in bone age and pubertal maturation strongly suggest that part of the growth failure seen in acquired immunodeficiency syndrome can be attributed to pubertal delay. We speculate that the lack of demonstrable difference in age-adjusted testosterone concentrations might reflect subtle differences in the pattern of secretion of testosterone or in the concentration of sex-hormone binding globulin.


Asunto(s)
Infecciones por VIH/fisiopatología , Hemofilia A/fisiopatología , Pubertad Tardía/fisiopatología , Adolescente , Adulto , Estatura , Peso Corporal , Niño , Infecciones por VIH/sangre , Infecciones por VIH/complicaciones , Hemofilia A/sangre , Hemofilia A/complicaciones , Humanos , Estudios Longitudinales , Masculino , Maduración Sexual , Testosterona/sangre
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