Tetsuro Shirai

Adrenal insufficiency causes life‑threatening arrhythmia with prolongation of QT interval

A 63-year-old woman who had hypopituitarism was re-admitted to our hospital because of fever, diarrhea and disturbance of consciousness with life-threatening arrhythmia due to prolongation of the QT interval. She has been treated with hydrocortisone consequently, and has shown few ventricular arrhythmias with normalization of the QT interval. There have been several reports showing the case of prolonged QT interval with adrenal insufficiency, but there are few reports of isolated adrenocorticotropic hormone deficiency without any electrolytes imbalance that showed polymorphic ventricular tachycardia associated with QT prolongation. We discuss some possible mechanisms of how adrenal insufficiency causes life-threatening arrhythmia. Since lack of glucocorticoid hormone might induce prolongation of the QT interval, patients with adrenal insufficiency should be paid attention as candidates of lethal arrhythmias particularly when exposed to excessive stresses.

Resetting of tachycardia cycle by single and double ventricular extrastimuli in recurrent sustained ventricular tachycardia.

In two cases with recurrent sustained ventricular tachycardia (VT) due to re‐entry, the response pattern to extrastimuli during the tachycardia was studied. In each case, right ventricular extrastimuli with longer coupling intervals during VT were followed by fully compensatory pauses and with shorter coupling intervals reset the tachycardia cycle. In one case, a plateau was produced by a single extrostimulus, resembling that seen in the response curve of sinus node automaticity as well as ectopic atrial tachycardia. Two successive stimuli produced three definite zones, i.e., fully compensatory, reset producing a plateau, and progressive prolongation zones with shortening of the coupling intervals between the two stimuli, and terminated the tachycardia with further shortening of the coupling intervals. In conclusion, resetting phenomenon was confirmed on two cases with re‐entrant VT. This phenomenon cannot be used as a criterion to determine the mechanism responsible for VT.

Impact of Oral Treatment on Physical Function in Older Patients Hospitalized for Heart Failure: A Randomized Clinical Trial.

Background Frailty is a characteristic of older patients with heart failure, who undergo functional decline during hospitalization. At present, continuous intravenous infusion of diuretics is widely used for the treatment of hospitalized patients with heart failure. In this prospective, randomized, open-label controlled trial, we tested whether an early switch from continuous intravenous infusion therapy to oral treatment with diuretics prevents functional decline in patients hospitalized for heart failure. Methods A total of 59 patients hospitalized for heart failure were randomized to either continuous intravenous infusion (n = 30) or oral medication (n = 29) within 48 h of admission. The primary outcome was the Barthel index, a universally utilized scale to assess the functional status of patients in their activities of daily living, assessed at 10 days. Secondary outcomes included the number of daily steps counted using pedometers and average hospital costs. Results Barthel index scores were significantly higher in the oral medication group than in the intravenous group (78.1 ± 20.8 vs. 59.6 ± 34.2, P = 0.029). The number of daily steps was significantly higher in the oral treatment group relative to the intravenous group (P < 0.001), and the average hospital costs were similar between the randomized groups. Multivariate analysis revealed that oral medication was a significant independent predictor of Barthel index score at day 10, and the number of daily steps was significantly associated with the patient’s functional outcome. Conclusions This trial showed that, in patients hospitalized for heart failure, oral medication increased functional independence during hospitalization compared with sustained continuous intravenous infusion, most likely because the release from the infusion line enabled the patients to be more mobile. Notably, these beneficial effects were achieved without increasing hospital costs.

Measurement of adenylate cyclase activity in the right ventricular endomyocardial biopsy samples from patients with chronic congestive heart failure.

A highly sensitive fluorometric assay technique was adopted in order to examine the adenylate cyclase activity in the minute right ventricular endomyocardial biopsy samples from patients with chronic congestive heart failure (n = 10). Norepinephrine (10–4 M) and adenosine (10–3 M) were incubated for 30 min with 10 μl of membrane preparation (1–2 mg protein/mg) to analyze the extent of the receptor‐coupled adenylate cyclase activity. Forskolin (10–4 M) stimulation was used to estimate the maximum adenylate cyclase activity (pmol/mg protein/min, mean ± SE). The new microanalytical cyclic AMP assay involves four steps: enzymatic destruction of noncyclic adenine nucleotides and phosphorylated metabolites, conversion of cyclic AMP to ATP, amplification of ATP by enzymatic cycling, and fluorometric measurement of NADPH, which is generated in proportion to initial cyclic AMP levels. Basal and forskolin‐stimulated maximum adenylate cyclase activities were 75 ± 8 and 123 ± 15, respectively. Norepinephrine increased the adenylate cyclase activity to 107 ± 14, while adenosine tended to decrease it to 65 ± 7. In addition, elimination of adenosine by adenosine deaminase (10 U/ml) slightly increased the adenylate cyclase activity to 82 ± 9. These results indicate that the adenylate cyclase activity can be measured in minute endomyocardial biopsy samples. Use of this new approach shows promise of becoming a new and potentially important way to predict the efficacy of pharmacological treatment. J. Clin. Lab. Anal. 14:48–52, 2000.