Tilt test results in young and elderly patients with syncope of unknown origin.

The effects of aging on the results of prolonged drug-free tilt testing were studied in 175 consecutive patients with unexplained syncope divided into 3 groups: 59 patients < 40 years old; 57 patients between 40 and 60 years; and 59 patients > 60 years old. Tilt-induced vaso-vagal syncope occurred respectively in 17 (29%), 20 (35%), and 18 patients (31%) in the 3 age groups. Vasodepressor, mixed, and cardioinhibitory vaso-vagal syncope occurred similarly in the 3 groups; organic heart disease and systemic hypertension were more frequent in elderly patients without affecting the incidence of tilt-induced syncope. Blood pressure and heart rate variations during syncope were similar in the 3 age groups; in the first 20 minutes of tilt testing, before the appearance of the vaso-vagal reflex, elderly patients showed greater reduction in blood pressure and smaller increase in heart rate than younger patients. Our data indicate that increasing age determines a different blood pressure and heart rate behavior during tilt testing, but apparently does not influence the incidence of vaso-vagal syncope in patients with syncope of undetermined etiology. As the proportion of patients with a positive isoproterenol tilt test was reported to decline with age, our results suggest that the reduced incidence of syncope during isoproterenol tilt testing could be the expression of impaired autonomic response among elderly syncope patients.

Effect of high-dose furosemide in refractory congestive heart failure.

High-dose firosemide is considered effective in primary renal sodium retention but is not generally recommended in congestive heart failure. In order to evaluate efficacy and safety of high-dose furosemide (greater than 500 mg/day), the authors studied 20 patients (pts) resistant to therapy (including furosemide less than 500 mg/day) selected from 161 pts admitted for chronic heart failure. All refractory pts (15 men and 5 women, mean age sixty +/- 12 years) were in NYHA class IV and showed hyponatremia (130 +/- 5 mEq/L) and impaired renal function (BUN 31 +/- 14 mg/dL, serum creatinine 1.3 +/- 0.3 mg/dL and BUN/creatinine ratio 23 +/- 7). In addition to digitalis, dopamine, angiotensin-converting enzyme inhibitors, or vasodilators, IV high-dose furosemide (775 +/- 419 mg/day, 500-2000) was given for ten +/- five days under daily clinical and laboratory monitoring. Three pts died of low-output syndrome while 16 pts were upgraded to NYHA class III and 1 pt to class II; a mean weight reduction of 7.3 +/- 2.9 kg in ten + five days (0.80 +/- 0.4 kg/day) and a mean diuresis increase of 88 +/- 57% occurred. The maximal dose of furosemide did not correlate with serum creatinine but did correlate with BUN/creatinine ratio (r = 0.78, p less than .001). Pts were discharged on with chronic heart failure, and 43% in the subgroup in NYHA class IV with hyponatremia. High dose furosemide was effective for rapid removal of excess water and salt in "furosemide-resistant" congestive heart failure. The relationship between renal impairment and maximal furosemide doses seems to confirm the role of renal pharmacokinetics in the appearance of furosemide resistance.

Prognostic value of hyponatremia in patients with severe chronic heart failure.

In order to evaluate the incidence and the prognostic value of hyponatremia (hypoNa) in patients (pts) with severe chronic heart failure (SCHF), the authors studied 161 consecutive pts (113M, 48F ages sixty-seven +/- ten) with SCHF in NYHA class III-IV. The cause of SCHF was ischemic in 64 pts, hypertensive in 39, valvular in 14, alcohol-related in 3, and idiopathic in 41. Pretreatment hypoNa (less than 135 mmol/L) was found in 64/161 pts (40%) (Group I); Na+ was less than 125 in 10 pts, 125-130 in 19, and 131-135 mmol/L in 35; 42/64 pts (66%) of Group I were in NYHA class IV at admission. In the pts with pretreatment Na+ less than 125 mmol/L, hypoNa was persistent and refractory to high-dose furosemide (less than 500 mg/day) and water restriction. Cardiovascular mortality of Group I pts was 69% within twenty-four months (34 pts died of low-output syndrom and 10 suddenly). All pts with Na+ less than 130 mmol/L died within six months. The 20 pts who normalized Na+ are alive, and in NYHA class II-III (follow-up: twenty-six +/- fifteen, six to sixty months). Pts without hypoNa were 97/161 (Group II), and 58/97 (60%) are alive (follow-up: thirty +/- eighteen, five to fifty-eight months), whereas 39 pts died (27 suddenly, 9 of low-output syndrome, and 3 of extracardiac disease) within twenty-four months. The mortality rate of Group II was significantly lower (40% vs 69%, p less than 0.001) compared with Group I. The two groups were similar for age, sex, and cause and duration of SCHF.(ABSTRACT TRUNCATED AT 250 WORDS)