Heart failure-vericiguat explained—clearly and calmly. This video demystifies how vericiguat fits into modern treatment for heart failure with reduced ejection fraction (HFrEF). In plain language, we cover what the medicine does, who it’s for, and how it complements today’s “foundational four” therapies. What you’ll learn • What HFrEF means and why symptoms like breathlessness and swelling occur • How vericiguat—an sGC stimulator—supports the body’s NO-cGMP pathway to relax blood vessels and counter harmful heart remodeling • Which patients may benefit most (e.g., recently worsened heart failure despite standard therapy) • How vericiguat is used as an add-on, not a replacement, to guideline-directed therapy • What outcomes to expect (chiefly fewer hospitalizations) and common safety considerations discussed with your clinician Why this matters For many people, the right combination of medicines reduces symptoms, hospital visits, and risk. Understanding heart failure-vericiguat can help you ask sharper questions at your next appointment and partner more confidently in your care. Important notes This video is informational and not medical advice. Talk with your healthcare professional about whether vericiguat is appropriate for you, especially if you are pregnant, have low blood pressure or anemia, or take medications such as PDE-5 inhibitors. If you find this helpful, please like, share, and subscribe for more clear, evidence-based explanations on heart health.
00:00The treatment of heart failure with reduced ejection fraction has evolved in leaps and bounds over the past decade.
00:10In the past, doctors relied on drugs that aimed to improve the contractility of the heart muscle, such as digoxin.
00:20They then later improved the outcomes of patients with heart failure by introducing drugs that decrease the resistance in the arteries and the distal extremities.
00:40These drugs included drugs such as ACE inhibitors, an isosol by dinitrate combined with hydrolazine.
00:49Today, doctors target neurohormonal systems that are activated as compensatory mechanisms in heart failure.
00:59These include the RAAS, or renin-angiotensin-aldosterone system, and more recently, the nitric oxide CGMP-PKG system.
01:12As a result, the standard treatment of heart failure today includes the use of the foundational quadruple therapy of ARNIs, ACE inhibitors,
01:27and ARBs that work on the RAAS system, beta blockers that block the sympathetic nervous system,
01:37drugs that block the aldosterone in the body called mineralocorticoid receptor antagonists,
01:46and SGLT2 inhibitors that help the kidney to excrete salt.
01:51Heart failure with reduced ejection fraction occurs when the heart is unable to supply enough oxygenated blood to the tissues
02:02due to an inability to pump blood into the circulation.
02:09As a result, the body reacts by holding on to more fluid to help increase the amount of blood in the body
02:18to improve delivery.
02:22This, however, eventually fails as fluid leaks into the lung tissue and collects in the legs and in the abdomen.
02:33At the same time, our bodies increase the contractility of the heart muscle
02:40and the rate at which the heart pumps.
02:46Eventually, this also fails, leading to stretching of the heart muscle
02:53and remodeling and replacement of the heart muscle
03:00by fibrous tissue in a process called fibrosis.
03:06As this process progresses, the sympathetic nervous system is activated,
03:16causing the vessels in the extremities to narrow or to constrict.
03:24This, in turn, increases the work the heart has to do to supply the tissues with blood.
03:31Enter a new class of drug called a soluble guanulate cyclase stimulator.
03:41Soluble guanulate cyclase is an enzyme that works to convert guanazine triphosphate
03:49to cyclic guanazine monophosphate,
03:53which promotes blood vessels' relaxation
03:57and counters harmful remodeling and fibrosis of the heart muscle.
04:06CGMP, or cyclic guanazine monophosphate,
04:09acts on the enzyme called PKG, or protein kinase G,
04:15to reduce calcium signaling in the smooth muscle cells
04:19lining of blood vessels and in the heart.
04:23Reduced calcium signaling in the blood vessels and in the heart muscle
04:29causes them to relax.
04:32As a result, the heart faces less resistance,
04:37fills with blood more easily,
04:39and can pump blood easier to the tissues.
04:43Vericiguac is a drug that stimulates the system.
04:52It stimulates SGC, or soluble guanulate cyclase,
04:58to produce more CGMP,
05:01and this drives the reaction forward.
05:05It is considered an add-on drug
05:08to the four foundational drugs mentioned above
05:11for patients with recently worsening heart failure,
05:16such as those requiring hospitalizations or IV diuretics.
05:23In fact, the drug Vericiguat
05:27reduced the combined risk of cardiovascular debt
05:32or heart failure hospitalizations
05:35in people with symptomatic chronic heart failure
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