BETA-BLOCKERS

This subject is divided into two parts as follows:

1. Selection of beta-blockers
2. Table for interchangeability of beta-blockers

For starters of the paragraph I have chosen a text from the Pharmaco-Therapeutic Guide (PTG) of 2016 PTG is a reference book composed of physicians under the direct and invariable participation and supervision of the pharmaceutical companies that produce all 5,000 medicinal preparation enrolled therein. The text of which I speak is the following, I quote: "All beta-blockers (except Nebivolol) after a prolonged use cause an increase in triglycerides and "bad" cholesterol (LDL) and decrease in "good" cholesterol (HDL) in plasma. Inhibit blood formation (hematopoiesis) performed by the bone marrow (leukocytes, platelets, red blood cells), kidney and liver function." If you wonder why your cholesterol is high, although the cardiologist has administered you the murderous for your health statins and despite that you have recently undergone a coronary artery bypass grafting operation your arteries are quickly filling again with cholesterol plaques, here's the answer.

1. Selection of beta-blockers

BETA-BLOCKERS

Fig.1. Selection of beta-blockers

In 1988 the Nobel Prize for medicine was given to James Black for the discovery of the first beta blocker (propranolol) and of the first H2 blocker (cimetidine). The beta-adrenergic antagonists (Beta-Blockers - BB) block the path of the stress from the brain to the body - we continue to be angry but that does not affect our body. Are the representatives of the beta-blockers all the same? Not at all! The term "beta-blocker" is a collective concept. Some features are common, others are completely different. Common is that they block the beta-adrenergic receptors but everything else is different. Some of them are non-selective, as they block both the beta1- and beta2-adrenoceptors (propranolol) while others have a much higher affinity to the beta-1 than to beta-2 receptors and therefore are determined as beta-1 selective (metoprolol, acebutolol, bisoprolol, nebivolol). However, selectivity is dependent on the dose as it diminishes or even disappears when using higher doses. Paradoxically, some BB can cause weak agonistic response (Intrinsic Sympathomimetic Activity - ISA) as they can both stimulate and block beta-adrenoreceptors. Some BB possess peripheral vasodilator activity, which is due to blockade of alpha-1 adrenoceptors (carvedilol) or mechanisms that are independent of this process (nebivolol). In addition, the BB can be lipophilic (fat-soluble), such as metoprolol, propranolol, timolol or hydrophilic (water-soluble), such as atenolol. This shows that even small chemical differences can lead to very different biological effects. Therefore BB are not interchangeable and each one should be used as intended.

Selection of beta-blocker in Ischemic Heart Disease (IHD)

After myocardial infarction some BB prolong life reducing the incidence of sudden cardiac death (used for secondary prevention). In the consensus for BB of the European Society of Cardiology on their use as secondary prevention after acute myocardial infarction, is written the following: "Positive results were obtained with propranolol, metoprolol, timolol, atsebutalol and carvedilol. On the contrary no benefit was registered in clinical trials with alprenolol, atenolol, oxprenolol or xamoterol." The beta-blockers which are useful for secondary prevention after myocardial infarction are fat-soluble - penetrating the blood-brain barrier and reaching the Central Nervous System (CNS). Those which have no effect are water-soluble and do not enter the CNS. Among those recommended in this consensus BB is not mentioned bisoprolol. It is fat-soluble, enters the CNS and is authorized for use in coronary artery disease but is less proven in this situation. That is why our usual choice after myocardial infarction is metoprolol or carvedilol. Nebivolol is not approved for use in Coronary Artery Disease (same as IHD).

Selection of a beta-blocker in Heart Failure (HF)

In HF are allowed four BB:
      - metoprolol succinate with extended release (metoprolol succinate CR/XL)
      - bisoprolol
      - carvedilol
      - nebivolol

Should be started with a low dose, slowly increased with time. If you start with a minimum dose and in two weeks it is increased slightly will be reached doses from which the patient's condition would deteriorate if the same are given to him suddenly. There are four permitted BB and one patient with HF. You are now allowed to administer these four doses rather only one of them. The principle is to give the BB which has been tested in people as the particular patient. Various BB were tested in various studies in different patient groups. If a person is suffering from HF due to myocardial infarction and has additionally residual angina the most proven drug in this situation is metoprolol. When the patient after myocardial infarction has developed heart failure and has severe arrhythmias, carvedilol prolongs his life. Carvedilol has been tested in patients with left ventricular ejection fraction less than only 15% (very severe condition). It has been proven it prolongs their lives.

Selection of beta-blocker in Arterial Hypertension (AH)

AH is a generalized spasm of the medium-sized arterial vessels (arterioles). It is therefore appropriate the use of vasodilator drugs for its treatment. Since stress expands vessels to the muscles then the BB that set it blocked acts vasoconstrictive. Only two BB (carvedilol and nebivolol) have properties that compensate for this disadvantage of the whole class. Carvedilol except that it is a beta-blocker is an alpha-blocker, and alpha-blockers are vasodilators. Nebivolol except being a beta-blocker stimulates the release of Nitric Oxide (NO) and it is the most potent natural vasodilator. Therefore these two vasodilator BB are preferred in the treatment of AH. If the hypertensive in question suffers also from Ischemic Heart Disease (IHD), the only choice remains the carvedilol as the nebivolol is not used to treat coronary artery disease.

Selection of beta-blocker in accompanying Diabetes Mellitus (DM)

The main consumers of blood glucose in the body is muscles and therefore BB by reducing blood flow to the muscles can lead to increased blood glucose. Only carvedilol and nebivolol, having vasodilatory properties do not significantly reduce blood flow to the muscles and therefore cause the least adverse changes in glucose homeostasis. If the diabetic patient in question suffers also from Ischemic Heart Disease (IHD), the only choice remains the carvedilol as the nebivolol is not used to treat coronary artery disease.

Selection of a beta-blocker with concomitant chronic arterial insufficiency of the limbs (CAIL).

Naturally, in CAIL can be used only the vasodilator BB such as carvedilol and nebivolol. Since patients with CAIL most commonly have also IHD as a choice remains only the carvedilol.

Selection of a beta-blocker with concomitant chronic obstructive pulmonary disease (COPD)

All BB can cause bronchospasm by blocking of the beta-2 receptors in the bronchi. The desired effect on the heart and kidneys is carried out by blocking the beta-1 receptors. That is why the more a BB selectively blocks the beta-1 receptors and weaker blocks beta-2 receptors, the less it will cause bronchospasm as a side effect. The most selective beta-blocker is nebivolol and the second in the ranking is bisoprolol. Therefore, in accompanying COPD are preferred these two drugs. If the patient has also coronary artery disease (IHD) remains in use only the bisoprolol.

Selection of a beta-blocker at a very high heart rate (HHR)

Of all the BB the highest anti-adrenergic activity has the bisoprolol. Through it the heart rate (HR) is slowed more than with the other BBs. On the contrary, the weakest anti-adrenergic activity has the nebivolol - it slows the heart rate less then the other BBs.

Selection of beta-blocker in ThyroToxicosis (TT)

Thyroid hormones enter cells and stimulate the synthesis of all types of adrenoceptors, which then appear on the membrane of the cells. That is why patients with hyperthyroidism have an accelerated heart rate and elevated blood pressure. Since at the cells’ surface in hyperthyroidism the concentration of all types of adrenoreceptors is increased must be used as much as possible non-selective beta-blocker such as propranolol, which will block most adrenoreceptors.

Selection of beta-blocker in the oesophageal varices (OV)

In varices of the esophagus is observed bleeding from the venous part of the abdominal blood vessels (portal hypertension). Blood in the veins comes from the arteries and most BB are vasoconstrictive and constrict arteries. It is therefore appropriate the use of any vasoconstrictive beta-blocker, as the most frequently applied again is propranolol.

Cases where stress is useful and we must not block it with BBs.

Patients who use beta blockers bear the heat more difficultly. Beta-blockers block the reflex tachycardia caused by hypovolemia and hamper perspiration, etc. Often the ambulances transport people taken from the street, requiring emergency surgery - for example due to perforated ulcer or bone fracture. If these patients have so far taken BB and are adapted thereof, these should not be stopped because of the operation. However, if the patient has not been administered BB it is desirable to not include such in case of upcoming risky surgical intervention. BBs block compensatory mechanisms necessary for our body for survival in trauma and blood loss. Figuratively speaking, regardless of the reason for this trauma and blood loss (surgical, traumatic, etc.), we all equally need the protective mechanism of stress to survive. It is not recommended preoperative inclusion of BB at high dose without titration.

2. Table for interchangeability of beta-blockers

At the first row of the table below are listed the beta-blockers which I included in the above table to the explanations for their choice of reception. I decided to publish this information because when a patient goes to an examination to another doctor he almost always rejects the prescribed medicine by the previous "specialist" and administers another beta-blocker. Is this always necessary? Not of course, especially if the replacement is a preparation which has the same generic (active) ingredient! In practice, this is the same drug but with a different name, only that it has another price, higher of course. In the vast majority of cases profiteering reasons prevail because the so-called "doctors" report their "activities" in front of the pharmaceutical companies to which they serve for various charity such as excursions (camouflaged as seminars, conferences and other events) and pathetic gifts in order to sell just their products rather than those of the competition, even if they are cheaper and better.

BETA-BLOCKERS

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