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(Circulation. 2006;114:1793.)
© 2006 American Heart Association, Inc.

Issue Highlights

An extract of the first 250 words of the full text is provided, because this article has no abstract.

	PHOSPHODIESTERASE-5 INHIBITOR IN EISENMENGER SYNDROME: A PRELIMINARY OBSERVATIONAL STUDY, by Mukhopadhyay et al.

 
The hemodynamic effects of phosphodiesterase-5 (PDE-5) inhibitors in patients with Eisenmenger syndrome are unknown. Mukhopadhyay and colleagues present a preliminary observational study on the effects of tadalafil, a PDE-5 inhibitor with a half-life of approximately 18 hours, on acute hemodynamics, tolerability, and efficacy over a 12-week period in patients with Eisenmenger syndrome. Pulmonary vascular resistance (PVR) fell immediately in 13 of 16 subjects; all those who responded in the short term had a further decline in PVR over the 12-week study period, with less right-to-left shunting and improvement in the systemic arterial oxygen saturation. No patients had adverse events. This preliminary investigation, the first to assess the hemodynamic effects of PDE-5 inhibitors in Eisenmenger syndrome, suggests that a daily single dose of tadalafil may be effective in decreasing PVR in selected patients with Eisenmenger syndrome. See p 1807.

	TRANSCRIPTIONAL PROFILING IN CORONARY ARTERY DISEASE: INDICATIONS FOR NOVEL MARKERS OF CORONARY COLLATERALIZATION, by Chittenden et al.

 
Coronary collaterals have been shown to reduce ischemic damage; many patients, however, do not develop sufficient collaterals. The factors responsible for the presence or absence of collaterals are poorly understood. Recent studies have suggested that circulating monocytes may be important. In the study by Chittenden et al in this issue of Circulation, a comprehensive characterization of monocyte transcriptome in patients with and without collaterals was performed using high-throughput expression profiling and redundancy-based data mining techniques. From this analysis, molecular markers were identified. Correlative serum markers were also determined to validate the gene expression studies. These findings support the contention that genetic factors heavily influence coronary collateral vessel growth in humans. . . . [Full Text of this Article]

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