Lack of sphygmomanometer calibration causes over- and under-detection of hypertension: a computer simulation study.

OBJECTIVE: To estimate the contribution of inadequate sphygmomanometer calibration to over- and under-detection of hypertension. DESIGN: Monte Carlo simulation of the measurement of blood pressure (BP) of a population with calibrated and uncalibrated sphygmomanometers. Simulated BP measurements included systematic sphygmomanometer error and random variability. MAIN OUTCOME MEASURES: The percentage of hypertensive adults (BP > 140/90 mmHg) not detected and the percentage of adults incorrectly classified hypertensive due to sphygmomanometer error. The percentage of the false positives and false negatives attributable to sphygmomanometer error. The number of additional visits patients need to make to obtain the same improvement in hypertension detection as is obtained by sphygmomanometer calibration. RESULTS: After three visits, uncalibrated sphygmomanometer error causes 20 and 28% of all undetected adult systolic and diastolic hypertension, respectively, and 15 and 31% of all falsely detected adult systolic and diastolic hypertension. In some groups, under-detection is worse; for example, sphygmomanometer error causes 27% of all missed systolic hypertension in 35-44-year-old females. In some age groups, over-detection is worse; for example, after three visits, sphygmomanometer error causes 63 and 50% of falsely detected systolic and diastolic hypertension in 18-24-year-old females, respectively. In-service sphygmomanometer calibration achieves the same or greater improvement in hypertension detection as an additional two visits. CONCLUSIONS: Uncalibrated sphygmomanometers are a preventable cause of clinically significant over- and under-detection of hypertension. Sphygmomanometers should be calibrated regularly by accredited organizations or technicians. Standards and guidelines governing sphygmomanometers in service should be revised. Sphygmomanometer calibration is a cost-effective way of improving hypertension detection.

Long-term effectiveness of extended-release nitrate for the treatment of systolic hypertension.

Isosorbide mononitrate (ISMN) is effective in the short-term for decreasing systolic blood pressure, pulse pressure, and pulse wave reflection in patients with systolic hypertension. To determine whether tolerance negates the efficacy of this nitrate in the long-term, a placebo-controlled study was performed in which ISMN was withdrawn briefly in a group of patients (n=16) who had received extended-release ISMN 60 to 120 mg once daily for 16 to 109 months. Blood pressure and wave reflection were determined by 24-hour ambulatory recorder and tonometer, respectively. During a 4-hour delay of the regular morning dose of ISMN, mean systolic blood pressure was higher than with the regular ISMN dosing schedule (P<0.0001). The maximum placebo-active difference was 16+/-4 mm Hg. The corresponding difference in augmentation index (a measure of pulse wave reflection) corrected for heart rate was 25+/-4% (P<0.001). The difference in pulse pressure was 13+/-3 mm Hg (P<0.001). There was no significant difference in diastolic blood pressure. For a subgroup (n=12) in which the effects of a single ISMN dose had been determined at the initiation of regular ISMN therapy, the mean change in augmentation index was of similar magnitude to that observed in their initial study. Thus, tolerance does not seriously diminish the antihypertensive efficacy of ISMN used as adjunct therapy in the chronic treatment of systolic hypertension. This agent lowers systolic blood pressure sufficiently to achieve therapeutic goal in some patients refractory to conventional treatment regimens.

Continuous positive airway pressure treatment improves pulmonary hemodynamics in patients with obstructive sleep apnea.

Daytime pulmonary hypertension (PH) is relatively common in obstructive sleep apnea (OSA) and is thought to be associated with pulmonary vascular remodeling (PRm). The extent to which PH is reversible with treatment is uncertain. To study this, we measured pulmonary hemodynamics (Doppler echocardiography) in 20 patients with OSA (apnea-hypopnea index [AHI] 48.6 +/- 5.2/h, mean +/- SEM) before and after 1 and 4 mo of CPAP treatment (compliance 4.7 +/- 0.5 h/night). Patients had normal lung function, and no cardiac disease or systemic hypertension. Doppler studies were performed at three levels of inspired oxygen concentration (11%, 21%, and 50%) and during incremental increases in pulmonary blood flow (10, 20, and 30 microg/kg/min dobutamine infusions). Treatment resulted in a decrease in pulmonary artery pressure (Ppa, 16.8 +/- 1.2 mm Hg before CPAP versus 13.9 +/- 0.6 mm Hg after 4 mo CPAP, p < 0.05) and total pulmonary vascular resistance (231.1 +/- 19.6 versus 186.4 +/- 12.3 dyn. s. cm(-)(5), p < 0.05). The greatest treatment effects occurred in the five patients who were pulmonary hypertensive at baseline. The pulmonary vascular response to hypoxia decreased after CPAP (DeltaPpa/DeltaSa(O(2)) 10.0 +/- 1.6 mm Hg before versus 6.3 +/- 0.8 mm Hg after 4 mo CPAP, p < 0.05). The curve of Ppa versus cardiac output (Q), derived from the incremental dobutamine infusion, shifted downward in a parallel fashion during treatment. Systemic diastolic blood pressure also fell significantly. Improvements in pulmonary hemodynamics were not attributable to changes in left ventricular diastolic function or Pa (O(2)). We conclude that CPAP treatment reduces Ppa and hypoxic pulmonary vascular reactivity in OSA and speculate that this may be due to improved pulmonary endothelial function.