However, longer follow up analysis (10–15 years) could possibly demonstrate a significant decrease in the death rates in the intervention group. In addition, there were too few events for further sub-group analysis according to age or risk factors. Future larger studies should focus on recognising those who would benefit the most from price TBC-11251 this proactive screening strategy. Finally, the cost-effectiveness analysis of this strategy has not yet been reported. A critical question that needs to be answered before adopting a similar screening program on a wider scale is how much this strategy cost? Hopefully, with even more specific target
population and widely available screening tools, this strategy may further reduce its cost and optimize its efficacy. What have we learnt? STOP-HF provides an excellent model to the global community on how to integrate primary care simple screening
with secondary and tertiary level targeted diagnostic and therapeutic system. This integration includes screening of high-risk groups, use of a sensitive screening tool, early diagnostic modalities, early therapeutic interventions, and proper assessment of the hard clinical outcomes. However, to reach for the Holy Grail of reducing the global HF burden, more studies are needed across multiple sites around the world with different levels of health care services. More specific, higher-risk groups may show more benefit from this approach with a lesser cost to the public health systems.
Stimulators of soluble guanylate cyclase (sCG) are novel pharmacological agents that directly stimulate sGC. Ongoing research on sGC stimulators led to the development of the more
potent and more specific sGC stimulator, riociguat. Recently, the US Food and Drug Administration has approved riociguat to treat pulmonary arterial hypertension in adults. Support for the approval of riociguat comes from the recently published PATENT-1 (Pulmonary Arterial Hypertension Soluble Guanylate Cyclase–Stimulator Trial 1) study. Background Pulmonary arterial hypertension (PAH) is associated with the impairment of the nitric oxide (NO)-soluble guanylate cyclase (sGC)-cyclic guanosine monophosphate Drug_discovery (cGMP) pathway, supporting a role for therapeutic interventions which target this pathway. 1–2 Until recently, the only practical therapeutic strategy to enhance the NO–sGC–cGMP pathway was the use of phosphodiesterase-5 (PDE-5) inhibitors, such as sildenafil, tadalafil, and vardenafil to slow cGMP degradation. The clinical benefits associated with the PDE-5 inhibitor have led to interest in testing whether other agents that modulate NO signaling might be similarly beneficial in PAH. This is important considering the finding that up to 60% of patients with PAH do not respond to therapy with the PDE-5 inhibitor sildenafil, with some indication that pulmonary cGMP production is markedly impaired.