For many of our patients with moderate or severe asthma, we continue to prescribe the long-acting beta agonists. In many instances they provide dramatic, sometimes life-altering benefit. But we also take seriously the new warnings about the risks associated with their use. When we recommend their use, we do so as part of a comprehensive program of asthma management. This program includes avoiding as much as possible the triggers that cause your asthma and allergies to flare; periodic review of your medications to ensure the optimal treatment regimen; monitoring for deteriorations in your asthma; and developing a plan to deal with flare-ups before they become dangerously severe (your “asthma action plan”). You can help by taking your medications as prescribed, being alert to signs that your asthma is worsening, communicating with your asthma providers when you are not doing well, and keeping your regular follow-up medical appointments. We share with you the same goal: an active and safe life unrestricted by asthma or its treatments. Together we can achieve this goal, using the best available treatment program.
Ivabradine blocks the hyperpolarization-activated cyclic nucleotide-gated (HCN) channel responsible for the cardiac pacemaker I(f) ‘funny' current, which regulates heart rate without any effect on ventricular repolarization or myocardial contractility. It is indicated to reduce the risk of hospitalization for worsening heart failure in patients with stable, symptomatic chronic heart failure with LVEF ≤35%, who are in sinus rhythm with resting heart rate ≥70 bpm and either are on maximally tolerated doses of beta-blockers or have a contraindication to beta-blocker use.
These receptors, like those in the heart, are coupled to a Gs-protein , which stimulates the formation of cAMP . Although increased cAMP enhances cardiac myocyte contraction (see above), in vascular smooth muscle an increase in cAMP leads to smooth muscle relaxation. The reason for this is that cAMP inhibits myosin light chain kinase that is responsible for phosphorylating smooth muscle myosin. Therefore, increases in intracellular cAMP caused by β 2 -agonists inhibits myosin light chain kinase thereby producing less contractile force (., promoting relaxation).