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
05:39and ejection fractures lower than 45%.
05:45Most of this benefit
05:47came from reduced hospitalizations.
05:52Because of drugs such as Vericiguat,
05:56the prognosis of patients with heart failure
05:59with reduced ejection fraction
06:02has improved significantly
06:06in recent times.
06:09How much further doctors can take
06:12the treatment and well-being
06:14of patients with heart failure
06:15with reduced ejection fraction
06:18is anybody's guess at this time.
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06:31Until the next video,
06:33stay healthy and stay safe.
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