Thiamine deficiency in patients with congestive heart failure receiving long-term furosemide therapy: a pilot study.

PURPOSE: To test the hypothesis that long-term furosemide therapy in patients with congestive heart failure (CHF) is associated with clinically significant thiamine deficiency via urinary loss. DESIGN: (1) Biochemical evaluation of thiamine status in hospitalized patients with CHF treated with long-term furosemide and in age-matched control patients. (2) Uncontrolled trial of the effect of intravenous thiamine on cardiac performance in a subset of six patients with CHF. SETTING: General medical ward of a teaching community hospital. PATIENTS: Twenty-three patients with chronic CHF receiving furosemide, and 16 age-matched control patients without heart failure and not taking diuretics. Daily furosemide doses were 80 to 240 mg, and duration of furosemide therapy was 3 to 14 months. Patients with identifiable causes of inadequate thiamine intake, absorption, or utilization or increased metabolic requirements were excluded. INTERVENTION: A 7-day course of intravenous thiamine, 100 mg twice daily, in six consenting patients with CHF. RESULTS: A high thiamine pyrophosphate effect (TPPE), indicating thiamine deficiency, was found in 21 of 23 furosemide-treated patients and in two of 16 controls (p less than 0.001). The mean (+/- SE) TPPE (normal: 0% to 15%) in furosemide-treated and control patients was 27.7 +/- 2.5% and 7.1 +/- 1.6%, respectively (p less than 0.001). Despite the high TPPE, the mean (+/- SE) urinary thiamine excretion in the furosemide-treated patients (n = 18) was inappropriately high (defined as greater than 130 micrograms/g creatinine), 410 +/- 95 micrograms/g creatinine, even in comparison with that in the controls (n = 14): 236 +/- 69 micrograms/g creatinine. In six patients treated with intravenous thiamine, the elevated TPPE decreased to normal, from a mean (+/- SE) of 27.0 +/- 3.8% to 4.5 +/- 1.3% (p less than 0.001), indicating normal thiamine utilization capacity. Left ventricular ejection fraction increased in four of five of these patients studied by echocardiography. CONCLUSIONS: These preliminary findings suggest that long-term furosemide therapy may be associated with clinically significant thiamine deficiency due to urinary loss and contribute to impaired cardiac performance in patients with CHF. This deficit may be prevented or corrected by appropriate thiamine supplements.

Dilated cardiomyopathy associated with Chlamydia trachomatis infection.

A 26-year-old man was admitted to hospital with acute myocarditis complicated by congestive heart failure, and atrial and ventricular arrhythmias. Detailed investigations to determine the aetiological factors involved yielded negative results, except for serological evidence of infection with Chlamydia trachomatis. During the follow-up period, dilated cardiomyopathy developed. To the best of our knowledge a similar case has not been reported previously.

Hypertrophic apical cardiomyopathy: a subtype of hypertrophic cardiomyopathy.

This is the first report of hypertrophic apical cardiomyopathy outside of Japan. Electrocardiographic, vectorcardiographic, echocardiographic, hemodynamic and angiographic investigations support the view that this entity is a subset of hypertrophic cardiomyopathy that differs from hypertrophic obstructive cardiomyopathy and left-ventricular cavity obliteration. The ECG recorded giant negative T waves associated with prominent R waves in the precordial leads and septal Q waves were absent, with a normal mean QRS axis in the frontal plane. The vectorcardiogram showed a QRS loop oriented to the left anteriorly and inferiorly, while the T loop was characteristically discordant, elongated and situated in the right posterior quadrant. An M-mode ECG scan along the left-ventricular long axis revealed a marked increase in both septal and posterior wall thickness and excursions toward the apex. A characteristic spadelike configuration was observed in the left ventriculogram at end-diastole. Pressure studies at rest and after ventricular ectopic beats and isoproterenol provocation revealed no significant peak systolic pressure gradient within the left ventricle. This may have certain therapeutic implications.