Heart failure is an abnormal change in the structure or function of the heart caused by a variety of causes, which eventually leads to dysfunction of ventricular contraction or diastolic function, resulting in a complex set of clinical syndromes.
The main manifestations are dyspnea, fatigue, and fluid retention, such as lung congestion, systemic congestion, and peripheral edema. In recent years, the drugs that have sprung up in the field of heart failure, such as candesartan and sakuba valsartan, have played an increasingly important role.
Candesartan
Candesartan, a novel angiotensin II receptor antagonist, selectively acts on the type 1 receptor of angiotensin II., antagonizes the vasoconstriction of angiotensin II receptors, and the reabsorption of sodium salts by renal tubules.
It has outstanding advantages such as fast oral absorption, high bioavailability, long duration of action, and few adverse reactions, and has played a very important role in the treatment of essential hypertension. In addition, candesartan can delay, or even reverse, carotid intimal thickening and resistance to heart failure in patients with essential hypertension.
In heart failure, the adrenaline system, the renin-angiotensin-aldosterone system, and cytokines are all activated, and the continuous activation of these vasoactive factors is an important cause of heart failure.
Candesartan can directly act on the heart, kidneys, and angiotensin II receptors on the blood vessel wall, block the angiotensin II to constrict blood vessels, stimulate the adrenal cortex to secrete aldosterone, reduce water and sodium retention, thereby reducing preload; reduce norepinephrine release, reduce sympathetic activity, increase the sensitivity of arterial pressure reflexes, reduce excessive sympathetic tension, and reduce heart rate.
Anti-cardiac and vascular remodeling, delay or reverse myocardial hypertrophy, reduce left ventricular mass index, improve cardiac function, improve hemodynamic abnormalities, alleviate clinical symptoms, reduce myocardial stiffness and improve ventricular diastolic compliance by inhibiting the accumulation of collagen synthesis and collagen crosslinking, rather than antihypertensive effect; can effectively reduce the incidence of cardiovascular events and the mortality rate of patients with heart failure.
Clinical studies have shown that after 8 weeks of oral candesartan in patients with heart failure, not only the clinical symptoms and cardiac function indicators are significantly improved, but also the heart is reduced and the ventricular remodeling is reduced. It is explained that the addition of candesartan on the basis of cardiac diuresis is conducive to better improving the symptoms of patients with heart failure, as well as the classification of hemodynamic status and cardiac function, improving the quality of life, and reducing the cardiovascular mortality rate. Especially in patients with hypertensive heart disease complicated by heart failure, it can also effectively reduce blood pressure.
Shakuba Tri valsartan
Sacuba tri valsartan, belonging to the angiotensin receptor - cerebral lining peptidase inhibitor, is mainly composed of sakubatro and valsartan in a 1:1 ratio of compound. Sakubatrex can increase the level of natriuretic peptides by inhibiting cerebral lininge, which plays a role in sodium excretion, diuresis, and vasodilation.
Valsartan can inhibit the renin-angiotensin-aldosterone system, exerting the effects of sodium excretion, diuresis, and reducing aldosterone release. Through synergistic action, the two improve heart failure (grade 2-4 cardiac function, ejection fraction
In addition, it also has a good effect on acute myocardial infarction, inhibiting myocardial remodeling by reducing myocardial fibrosis and hypertrophy after myocardial infarction, compared with conventional acute myocardial infarction treatment, sakuba tridriad valsartan reduces the incidence of cardiovascular death, heart failure, and re-hospitalization rate due to heart failure in patients after acute myocardial infarction.
Reducing the risk after acute myocardial infarction may be achieved through hemodynamic mechanisms, such as reducing left ventricular wall tension. Other studies have shown that the combination of the two drugs of sacobatripto and valsartan may also have a favorable effect on coronary artery circulation by inhibiting the decomposition of C-type natriuretic peptides and inhibiting the effect of adenylates, thereby increasing intracellular guanylate concentration. C-type natriuretic peptides are important substrates of cerebral liningase and play an important role in the regulation of coronary artery tone and blood flow.
In addition, the results of application in > 55-year-old patients with simple systolic hypertension show that in the course of treatment of 4 to 12 weeks, sakuba trisacsartan has a more significant advantage in reducing systolic blood pressure, diastolic blood pressure, dynamic systolic blood pressure and dynamic diastolic blood pressure in the course of treatment of 4 to 12 weeks.
In addition, the effect of lowering systolic blood pressure in the sakuba triac saltan group can even last up to 52 weeks, and the study showed that sakuba valsartan can be used as an optional drug in patients with hypertension over 55 years of age. At present, the treatment of high blood pressure by sakubatri valsartan has been written into the guidelines.
In short, candesartan and sakuba tridansartan play an important role in improving heart failure and protecting cardiovascular disease through a variety of mechanisms of action. It not only effectively improves the clinical symptoms of patients with heart failure, but also reduces the rate of re-hospitalization and case fatality rate of heart failure, which is worth further practice in the clinic.