RESUMEN
Due to the discrepancy between higher symptom burden and lower disease prevalence, the diagnosis of coronary artery disease (CAD) in women is challenging. Cardiac CT can be particularly useful in CAD diagnosis and risk stratification in women. In this review, we explore cardiac CT in women with and without symptoms and for adjudication of functional tests. Novel CT technologies such as fractional flow reserve and stress perfusion imaging and their potential for usefulness in women are also examined.
Asunto(s)
Angiografía por Tomografía Computarizada/métodos , Angiografía Coronaria/métodos , Enfermedad de la Arteria Coronaria/diagnóstico por imagen , Prueba de Esfuerzo/métodos , Isquemia Miocárdica/diagnóstico por imagen , Imagen de Perfusión Miocárdica/métodos , Salud de la Mujer , Adolescente , Adulto , Anciano , Anciano de 80 o más Años , Enfermedad de la Arteria Coronaria/complicaciones , Medicina Basada en la Evidencia , Femenino , Humanos , Persona de Mediana Edad , Isquemia Miocárdica/etiología , Pronóstico , Intensificación de Imagen Radiográfica/métodos , Reproducibilidad de los Resultados , Sensibilidad y Especificidad , Vasodilatadores , Adulto JovenRESUMEN
Fibromuscular dysplasia (FMD) is a rare, nonatherosclerotic arterial disease for which the molecular basis is unknown. We comprehensively studied 47 subjects with FMD, including physical examination, spine magnetic resonance imaging, bone densitometry, and brain magnetic resonance angiography. Inflammatory biomarkers in plasma and transforming growth factor ß (TGF-ß) cytokines in patient-derived dermal fibroblasts were measured by ELISA. Arterial pathology other than medial fibrodysplasia with multifocal stenosis included cerebral aneurysm, found in 12.8% of subjects. Extra-arterial pathology included low bone density (P<0.001); early onset degenerative spine disease (95.7%); increased incidence of Chiari I malformation (6.4%) and dural ectasia (42.6%); and physical examination findings of a mild connective tissue dysplasia (95.7%). Screening for mutations causing known genetically mediated arteriopathies was unrevealing. We found elevated plasma TGF-ß1 (P=0.009), TGF-ß2 (P=0.004) and additional inflammatory markers, and increased TGF-ß1 (P=0.0009) and TGF-ß2 (P=0.0001) secretion in dermal fibroblast cell lines from subjects with FMD compared to age- and gender-matched controls. Detailed phenotyping of patients with FMD allowed us to demonstrate that FMD is a systemic disease with alterations in common with the spectrum of genetic syndromes that involve altered TGF-ß signaling and offers TGF-ß as a marker of FMD.
