Stepwise evaluation of unexplained syncope in a large ambulatory population.

BACKGROUND: Up to 60% of syncopal episodes remain unexplained. We report the results of a standardized, stepwise evaluation of patients referred to an ambulatory clinic for unexplained syncope. METHODS AND RESULTS: We studied 939 consecutive patients referred for unexplained syncope, who underwent a standardized evaluation, including history, physical examination, electrocardiogram, head-up tilt testing (HUTT), carotid sinus massage (CSM) and hyperventilation testing (HYV). Echocardiogram and stress test were performed when underlying heart disease was initially suspected. Electrophysiological study (EPS) and implantable loop recorder (ILR) were used only in patients with underlying structural heart disease or major unexplained syncope. We identified a cause of syncope in 66% of patients, including 27% vasovagal, 14% psychogenic, 6% arrhythmias, and 6% hypotension. Noninvasive testing identified 92% and invasive testing an additional 8% of the causes. HUTT yielded 38%, CSM 28%, HYV 49%, EPS 22%, and ILR 56% of diagnoses. On average, patients with arrhythmic causes were older, had a lower functional capacity, longer P-wave duration, and presented with fewer prodromes than patients with vasovagal or psychogenic syncope. CONCLUSIONS: A standardized stepwise evaluation emphasizing noninvasive tests yielded 2/3 of causes in patients referred to an ambulatory clinic for unexplained syncope. Neurally mediated and psychogenic mechanisms were behind >50% of episodes, while cardiac arrhythmias were uncommon. Sudden syncope, particularly in older patients with functional limitations or a prolonged P-wave, suggests an arrhythmic cause.

Obesity markers and blood pressure in a sample of Portuguese children and adolescents.

Little information exists regarding the effect of several obesity markers on blood pressure (BP) levels in youth. Transverse study including 2494 boys and 2589 girls. Height, weight and waist were measured according to the international criteria and body fat (BF) by bioimpedance. BP was measured by an automated device. Hypertension was defined using sex-specific, age-specific and height-specific observation-points. Body mass index (BMI) and waist were positively related with systolic blood pressure (SBP) and diastolic blood pressure (DBP) and heart rate in both sexes, whereas the relationships with BF were less consistent. Stepwise linear regression analysis showed that BMI was positively related with SBP and DBP in both sexes, whereas BF was negatively related with SBP in both sexes and with heart rate in boys only; finally, waist was positively related with SBP in boys and heart rate in girls. Age and heart rate-adjusted values of SBP and DBP increased with BMI: for SBP, 117+/-1, 123+/-1 and 124+/-1 mmHg in normal, overweight and obese boys, respectively; corresponding values for girls were 111+/-1, 114+/-1 and 116+/-2 mmHg (mean+/-SE, P<0.001). Overweight and obese boys had an odds ratio for being hypertensive of 2.26 (95% confidence interval: 1.79-2.86) and 3.36 (2.32-4.87), respectively; corresponding values for girls were 1.58 (confidence interval 1.25-1.99) and 2.31 (1.53-3.50). BMI, not BF or waist, is consistently and independently related to BP levels in children; overweight and obesity considerably increase the risk of hypertension.

Trazodone increases arousal threshold in obstructive sleep apnoea.

A low arousal threshold is believed to predispose to breathing instability during sleep. The present authors hypothesised that trazodone, a nonmyorelaxant sleep-promoting agent, would increase the effort-related arousal threshold in obstructive sleep apnoea (OSA) patients. In total, nine OSA patients, mean+/-sd age 49+/-9 yrs, apnoea/hypopnoea index 52+/-32 events.h(-1), were studied on 2 nights, one with trazodone at 100 mg and one with a placebo, in a double blind randomised fashion. While receiving continuous positive airway pressure (CPAP), repeated arousals were induced: 1) by increasing inspired CO(2) and 2) by stepwise decreases in CPAP level. Respiratory effort was measured with an oesophageal balloon. End-tidal CO(2 )tension (P(ET,CO(2))) was monitored with a nasal catheter. During trazodone nights, compared with placebo nights, the arousals occurred at a higher P(ET,CO(2)) level (mean+/-sd 7.30+/-0.57 versus 6.62+/-0.64 kPa (54.9+/-4.3 versus 49.8+/-4.8 mmHg), respectively). When arousals were triggered by increasing inspired CO(2) level, the maximal oesophageal pressure swing was greater (19.4+/-4.0 versus 13.1+/-4.9 cm H(2)O) and the oesophageal pressure nadir before the arousals was lower (-5.1+/-4.7 versus -0.38+/-4.2 cm H(2)O) with trazodone. When arousals were induced by stepwise CPAP drops, the maximal oesophageal pressure swings before the arousals did not differ. Trazodone at 100 mg increased the effort-related arousal threshold in response to hypercapnia in obstructive sleep apnoea patients and allowed them to tolerate higher CO(2) levels.