RESUMEN
Most current guidelines recommend tighter blood pressure (BP) control in hypertensive patients with comorbidities. These recommendations are based on epidemiologic data indicating that cardiovascular risk increases at lower BP levels in hypertensive patients with comorbidities than in those without comorbidities. Hypertension guidelines usually reflect outcomes from previous studies, but current recommendations for patients with comorbidities have preceded the evidence. We review recent studies investigating whether these new targets can be achieved, whether they are well tolerated, and whether they positively affect the outcomes. The results of the few current studies about outcomes in lower BP target groups are either negative or somewhat--but not decidedly--positive. There is a need for new trials designed to evaluate the validity of current recommendations for tighter BP control in hypertensive patients with comorbidities. Additionally, existing data from published trials could be reanalyzed to provide further clarification.
Asunto(s)
Presión Sanguínea/efectos de los fármacos , Diabetes Mellitus Tipo 2/epidemiología , Hipertensión , Enfermedades Renales/epidemiología , Accidente Cerebrovascular/prevención & control , Anciano , Comorbilidad , Medicina Basada en la Evidencia , Guías como Asunto , Humanos , Hipertensión/complicaciones , Hipertensión/epidemiología , Hipertensión/fisiopatología , Hipertensión/terapia , Estilo de Vida , Persona de Mediana Edad , Educación del Paciente como Asunto , Ensayos Clínicos Controlados Aleatorios como Asunto , Factores de Riesgo , Prevención Secundaria , Accidente Cerebrovascular/etiología , Resultado del TratamientoRESUMEN
There is ample evidence in the epidemiological and clinical literature that hypertension and overweight are closely and causally interrelated. Sympathetic nervous system (SNS) overactivity has been well documented in both hypertension and overweight, but it is not clear whether this is a coincidental finding or whether the association reflects a mechanistic role of SNS in these two interrelated clinical conditions. Whereas in this review we focus on the evidence for a primary role of SNS in the development of hypertension and overweight, it is clear that the process can be initiated from other starting points such as primary overeating or sleep apnea. After overweight evolves, hormones secreted by fat cells further accelerate SNS overactivity, weight gain, and blood pressure increase. The main thesis of this article is that regardless of where the process started, the same clinical picture of hypertension, overweight, and SNS overactivity will emerge. There is good evidence that in genetically prone individuals, prolonged SNS stimulation elicits a down regulation of beta-adrenergic receptors. This in turn decreases the ability to dissipate calories and diminishes the beta-adrenoceptor-mediated vasodilatation. We hypothesize that beta-adrenoceptor downregulation is the linchpin in the association of SNS with overweight and hypertension.