Automated Office Blood Pressure Measurement

Manual blood pressure (BP) recorded in routine clinical practice is relatively inaccurate and associated with higher readings compared to BP measured in research studies in accordance with standardized measurement guidelines. The increase in routine office BP is the result of several factors, especially the presence of office staff, which tends to make patients nervous and also allows for conversation to occur. With the disappearance of the mercury sphygmomanometer because of environmental concerns, there is greater use of oscillometric BP recorders, both in the office setting and elsewhere. Although oscillometric devices may reduce some aspects of observer BP measurement error in the clinical setting, they are still associated with higher BP readings, known as white coat hypertension (for diagnosis) or white coat effect (with treated hypertension). Now that fully automated sphygmomanometers are available which are capable of recording several readings with the patient resting quietly, there is no longer any need to have office staff present when BP is being recorded. Such readings are called automated office blood pressure (AOBP) and they are both more accurate than conventional manual office BP and not associated with the white coat phenomena. AOBP readings are also similar to the awake ambulatory BP and home BP, both of which are relatively good predictors of cardiovascular risk. The available evidence suggests that AOBP should now replace manual or electronic office BP readings when screening patients for hypertension and also after antihypertensive drug therapy is initiated.

Automated Office Blood Pressure Measurement

Manual blood pressure (BP) recorded in routine clinical practice is relatively inaccurate and associated with higher readings compared to BP measured in research studies in accordance with standardized measurement guidelines. The increase in routine office BP is the result of several factors, especially the presence of office staff, which tends to make patients nervous and also allows for conversation to occur. With the disappearance of the mercury sphygmomanometer because of environmental concerns, there is greater use of oscillometric BP recorders, both in the office setting and elsewhere. Although oscillometric devices may reduce some aspects of observer BP measurement error in the clinical setting, they are still associated with higher BP readings, known as white coat hypertension (for diagnosis) or white coat effect (with treated hypertension). Now that fully automated sphygmomanometers are available which are capable of recording several readings with the patient resting quietly, there is no longer any need to have office staff present when BP is being recorded. Such readings are called automated office blood pressure (AOBP) and they are both more accurate than conventional manual office BP and not associated with the white coat phenomena. AOBP readings are also similar to the awake ambulatory BP and home BP, both of which are relatively good predictors of cardiovascular risk. The available evidence suggests that AOBP should now replace manual or electronic office BP readings when screening patients for hypertension and also after antihypertensive drug therapy is initiated.

How Leptin Controls the Drive to Eat

A complex set of brain based systems modulate feeding to maintain constant body weight. The adipose derived-hormone, leptin, plays a crucial role in this control by acting on diverse leptin receptor (LepRb)-expressing neurons in the hypothalamus and brainstem to modify behavior and metabolism. In addition to controlling energy expenditure and satiety, leptin controls motivation and the reward value of food by regulating two interconnected systems: hypocretin (HCRT) neurons and the mesolimbic dopamine (MLDA) system. Modest/acute decreases in leptin levels, as associated with mild caloric restriction, increase MLDA activity and overall food-seeking behavior; in contrast, severe starvation or complete leptin deficiency blunt MLDA activity, along with motivation and associated behaviors. Lateral hypothalamic (LHA) LepRb neurons project to dopamine (DA) neurons in the ventral tegmental area, where neurotensin (NT) release augments MLDA function; these LepRb(NT) cells also innervate HCRT neurons to control Hcrt expression and inhibit HCRT neurons. Ablation of LepRb in these cells abrogates the control of HCRT cells by leptin and decreases activity and MLDA function. We propose that this neural pathway regulates the MLDA, activity, and motivation in response to leptin and nutritional status.