Alkylation of the alpha-carbanion of (R)-(-)-tert-butyl methyl sulfoxide (4) with n-propyl bromide afforded (+)-n-butyl tert-butyl sulfoxide (1) to which the absolute configuration (R) was ascribed. This assignment was confirmed by X-ray analysis of the complex 6 obtained from the enantiomerically pure sulfoxide (-)-1 and mercury chloride. Vibrational absorption and circular dichroism spectra of (+)-1 were measured in CDCl3 solution in the 2000-900 cm(-1) region and compared with the ab initio predictions of absorption and VCD spectra obtained with density functional theory using the B3LYP/6-31G basis set for different conformers of (R)-1. This comparison indicated also that (+)-1 is of the (R)-configuration.

Therapeutic target with β blockers in heart failure, i.e., target heart rate reduction or β‐blocker dose, is controversial. To resolve this controversy, the authors studied 152 heart failure patients on β blockers who were divided into four groups based on median peak exercise heart rate reduction as compared with predicted and prescription of at least 50% recommended β‐blocker dose. Event‐free survival (vs. death or assist device placement or urgent transplantation) was compared. Baseline and peak exercise heart rates were 74±14 and 116±21 bpm, respectively. Median heart rate reduction at peak exercise was 35%. When median or higher peak heart rate reduction was achieved, there were no significant survival differences noted between patients on different β‐blocker doses. With below‐median peak heart rate reduction, there was a strong trend toward better event‐free survival with higher β‐blocker doses. In conclusion, the results suggest that higher heart rate reduction is associated with better outcomes for heart failure patients overall and, for patients with persistently elevated heart rates, higher β‐blocker doses provided additional benefit.

Anemic heart failure patients with systolic dysfunction are known to have reduced exercise capacity. Whether this is related to poor hemodynamic adaptation to anemia is not known. Peak exercise oxygen consumption (VO2) and hemodynamics at rest and peak exercise were assessed among 209 patients and compared among those who were (n=90) and were not (n=119) anemic. Peak VO2 was significantly lower among anemic patients (11.7±3.3 mL/min/kg vs 13.4±3.1 mL/min/kg; P=.01). At rest, right atrial pressure was higher (10±5 mm Hg vs 8±4 mm Hg; P=.02) and venous oxygen saturation lower (62%±8% vs 58%±10%; P<.01) among anemic patients. At peak exercise, anemic patients had a higher wedge pressure (27±9 mm Hg vs 24±10 mm Hg; P=.04). No significant differences in stroke volume, cardiac index, systemic vascular resistance, or oxygen saturation were noted between the 2 groups. In conclusion, the relative hemodynamic response to exercise among anemic heart failure patients appears blunted and may contribute to worse exercise tolerance.

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