Bisoprolol is a cardioselective B1-blocker. It is used along with other B1-blockers to treat multiple heart diseases such as congestive heart failure, without having the unwanted effect of the B2 receptor blocking, which can affect multiple systems in the body.

Bisoprolol is considered to be one of the selective agents indicated in the treatment plan of compensated heart failure, along with carvedilol and metoprolol. Selective B- blockers are considered the first-line treatment for chronic stable angina. 

It is also FDA approved for the treatment of hypertension, post, or recent myocardial infarction (MI).

Other uses of bisoprolol that are not approved by the FDA include the treatment of migraine, tremor, arrhythmia, and use as an anxiolytic for some athletes and musicians.[1][2]

It correlates with decreased morbidity and mortality post-MI and reduces the risk of a stroke and coronary artery diseases in patients with heart diseases.

Selective B1 blocker drugs have a negative inotropic and chronotropic effect; they decrease the heart contractions and rate. As a net result, bisoprolol reduces the oxygen consumption of myocardial cells. B1 receptors are also present in the juxtaglomerular cells. By blocking these receptors, Bisoprolol leads to a decrease in the release of renin; as a result, it blocks the activation of the renin-angiotensin system. 

B1 adrenergic receptors are present in cardiac myocyte cells and juxtaglomerular cells. They couple with the G-stimulatory protein receptor (Gs receptor), and become stimulated by either norepinephrine or circulating catecholamine. Activation of B1 receptors in cardiac myocytes leads to positive chronotropic and inotropic effect, therefore, the net result will be increasing in heart rate contraction and the strength of myocyte contraction by the activation of Gs receptors, by the exchange of GTP to GDP, eventually it increases intracellular calcium concentration, and promote heart cell contraction.[3][4][5]

Activation of B1 receptors on juxtaglomerular cells leads to the activation of the renin-angiotensin system, and the release of Renin, therefore, increases the production of angiotensin I, which eventually converted by angiotensin-converting enzyme (ACE) to angiotensin II.

B2 receptors occur in multiple organs of the body and are activated by epinephrine, leading to different manifestations according to the location involved. In peripheral vessels, it causes vasodilation and decreases peripheral resistance, opposing the effect of alpha-1 receptors, which cause vasoconstriction on the peripheral vessels. On the bronchioles, it leads to extensive bronchodilation. B2 receptor activation in the liver and the muscles activate glycogenolysis and increasing the release of glucagon, therefore increase the sugar level in the blood.

Non-selective B blocker drugs block both the B1 receptor and B2 receptors, which lead to decrease cardiac output and decreases renin releasing from the kidney. And B2 receptor blockage leads to additional manifestations. Vasoconstriction of the peripheral vessels. In the lung, it causes contraction of the bronchial muscles, lead to bronchospasm in patients with COPD or Asthma. It is also lead to decrease glycogenolysis and glucagon release, which may lead to hypoglycemia.[2][6]

Cardioselective agents are either administered orally or intravenously. Bisoprolol is a low lipophilic agent, so it does not cross the blood-brain barrier with a high amount. And has long half-life extends from 9 to 12 hours. It is also having high bioavailability reaching 80 % compared to the majority of beta-blockers, which have lower bioavailability because the majority of beta-blockers have high first-pass metabolism in the liver.  

Bisoprolol administered orally as 5 or 10 mg tablet once per day. 

A common side effect of cardiovascular blockers is bradycardia, decreasing heart rate strength of contraction due to its negative chronotropic and inotropic effect.

It also decreases cardiac output; therefore, it decreases exercise capacity. Blocking beta receptors on the SA and AV node always carry a risk of heart block. It correlates less frequently with exacerbation of peripheral diseases such as the Raynaud phenomenon, bronchoconstriction, and hypoglycemia compared to non-selective beta-blockers.[7]

Other commonly encountered side effects include nausea, vomiting, and constipation.

Mask hypoglycemia is a dangerous side effect that happens in people with DM using beta-blockers. The drug blocks the normal signs of hypoglycemia such as tachycardia; therefore, it delays the normal response of the body to hypoglycemia, which may lead to fear complications.[8]

Cardioselective blockers are contraindicated in patients with complete heart block and should be monitored carefully in patients with second-degree heart block.

Patients with a history of recent fluid retention should not use beta-blockers without concomitant use of diuretics.

New studies suggest that cardioselective blockers are contraindicated in patients with severe asthma or COPD, while it is completely safe in patients with mild to moderate diseases.[9]

In patients with DM, it may lead to mask hypoglycemia, so careful monitoring is necessary.