Effect of diltiazem on exercise capacity after heart transplantation.

BACKGROUND: Sinus tachycardia (ST) is common after heart transplantation (HTx). The aim of the study was to evaluate the effect of diltiazem treatment during the first year after HTx on heart rate (HR), cardiac allograft function, and exercise capacity. METHODS: From the total cohort, 25 HTx recipients started diltiazem treatment 4±2 weeks after HTx and continued it for at least 1 year (diltiazem group). Each study case was matched to a control. All patients underwent hemodynamic assessment and cardiopulmonary exercise test (CPET) at 1 year after HTx. RESULTS: HR decreased in the diltiazem group from 99±11 bpm to 94±7 bpm (P=.03) and did not change in the controls (98±11 bpm vs 100±13 bpm, P=.14). The difference between the groups at 1 year after HTx was significant (P=.04). In the diltiazem group left ventricular (LV), stroke volume and ejection fraction increased (48±16 vs 55±17 mL, P=.02, and 60%±10% vs 62%±12% P=.03, respectively) but did not differ from controls. E/E' decreased (10.7±2.7 vs 7.3±1.9, P=.003) while cardiac index was higher (3.5±0.8 vs 3.1±0.5; P=.05) in the diltiazem group at 1-year follow-up. The absolute peak VO2 (21±4 vs 18±6 mL/kg/min; P=.05) and normalized peak VO2 (73%±17% vs 58%±14%; P=.004) were significantly higher in the diltiazem group. CONCLUSIONS: This study showed that diltiazem treatment reduces ST, may improve cardiac allograft function and exercise tolerance during the first year after HTx.

Hyponatremia after initiation and rechallenge with trimethoprim-sulfamethoxazole in an older adult.

PURPOSE: The purpose of this study is to describe a case report of a patient experiencing hyponatremia from trimethoprim-sulfamethoxazole (TMP-SMX) upon initial use and subsequent rechallenge. SUMMARY: An 82-year-old woman presented to the emergency department with altered mental status thought to be due to complicated cystitis and was treated with TMP-SMX 160 mg/800 mg orally twice daily for 7 days. Her basic metabolic panel prior to initiation of TMP-SMX was within normal limits, with the exception of her serum sodium of 132 mmol/L (range 133-145 mmol/L). The day after completing her 7-day course of TMP-SMX therapy the patient was evaluated by her primary care provider and another basic metabolic panel revealed a reduction in the serum sodium to 121 mmol/L. The patient's serum sodium concentrations increased to baseline 7 days after completion of the TMP-SMX therapy, and remained normal until she was treated in the emergency department several months later for another presumed urinary tract infection. She was again started on TMP-SMX therapy empirically, and within several days her serum sodium concentrations decreased from 138 mmol/L to a low of 129 mmol/L. The TMP-SMX therapy was discontinued upon negative urine culture results and her serum sodium increased to 134 mmol/L upon discharge. Based upon the Naranjo probability scale score of 9, TMP-SMX was the probable cause of the patient's hyponatremia. CONCLUSION: Our patient developed hyponatremia from TMP-SMX therapy upon initial use and rechallenge. Although hyponatremia appears to be rare with TMP-SMX therapy, providers should be aware of this potentially life-threatening adverse event.