Therapeutic Strategies for Angina Pectoris
This guide outlines the established therapeutic strategies for managing angina pectoris, a clinical syndrome characterized by chest discomfort caused by transient myocardial ischemia. Effective management aims to reduce the frequency and severity of anginal episodes, improve exercise tolerance, prevent myocardial infarction and death, and enhance the patient’s quality of life.
Angina pectoris typically occurs when the myocardial oxygen demand exceeds the oxygen supply. The primary cause is usually obstructive coronary artery disease (CAD). Therapeutic interventions are therefore directed at either reducing myocardial oxygen demand or increasing myocardial oxygen supply, or both.
Understanding the Goals of Angina Treatment
The treatment of angina pectorus has two main objectives:
- Symptom Relief: Alleviate acute anginal episodes and reduce their frequency and severity to improve the patient’s daily life and functional capacity.
- Prognostic Improvement: Prevent serious cardiovascular events such as myocardial infarction, stroke, and cardiovascular death, often by addressing the underlying atherosclerotic process and managing risk factors.
Achieving these goals typically involves a multi-faceted approach including lifestyle modifications, pharmacological therapy, and potentially revascularization procedures.
Overview of Therapeutic Strategies
Contemporary management of angina incorporates several key strategies:
- Lifestyle Modifications: Addressing modifiable risk factors for atherosclerosis is fundamental. This includes smoking cessation, dietary changes (lowering saturated fat, cholesterol, and sodium intake), regular physical activity (as tolerated), weight management, and stress reduction.
- Pharmacological Therapy: Medications are cornerstone for both symptom control and prognostic improvement. Drugs primarily work by altering the balance of myocardial oxygen supply and demand, preventing thrombosis, controlling blood pressure, and managing lipid levels.
- Revascularization Procedures: For patients with significant coronary artery stenosis that is not adequately controlled by medical therapy or who have high-risk anatomy, percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG) may be necessary to improve blood flow to the myocardium.
Major Groups of Drugs Used in Angina Treatment
Pharmacological therapy for angina pectoris relies on several key drug classes, often used in combination depending on the type of angina (stable, unstable, variant) and the patient’s comorbidities. The primary groups include:
- Nitrates: Potent vasodilators, primarily reducing preload and afterload, thereby decreasing myocardial oxygen demand. They also have effects on coronary arteries.
- Beta-Adrenergic Blockers (Beta-Blockers): Reduce heart rate, contractility, and blood pressure, significantly decreasing myocardial oxygen demand. They are cornerstones for stable angina prophylaxis.
- Calcium Channel Blockers (CCBs): Reduce contractility (non-dihydropyridines like verapamil, diltiazem) and cause vasodilation (dihydropyridines like amlodipine, nifedipine), decreasing oxygen demand and/or increasing oxygen supply (especially in variant angina).
- Antiplatelet Agents: Prevent platelet aggregation and reduce the risk of thrombotic events, crucial for preventing MI and improving prognosis in patients with CAD. Aspirin is standard therapy. P2Y12 inhibitors (e.g., clopidogrel, prasugrel, ticagrelor) are also used, particularly after PCI or in acute coronary syndromes.
- Lipid-Lowering Agents: Primarily statins, which slow the progression of atherosclerosis and reduce plaque instability, significantly improving prognosis.
- Renin-Angiotensin-Aldosterone System (RAAS) Inhibitors: ACE inhibitors or ARBs are often used, particularly in patients with hypertension, diabetes, left ventricular dysfunction, or chronic kidney disease, contributing to blood pressure control and cardiovascular risk reduction.
- Newer Anti-Anginal Agents: Drugs like Ranolazine act via different mechanisms to improve oxygen supply-demand balance without significantly affecting heart rate or blood pressure.
This guide will now focus specifically on the first group: Nitrates.
Pharmacokinetics of Nitrates
Nitrates used in angina therapy are organic nitrates that are converted within the body to nitric oxide (NO), a potent vasodilator. They are classified based on their duration of action and route of administration:
- Short-Acting Nitrates: Primarily used for acute angina relief and situational prophylaxis.
- Example: Nitroglycerin (Glyceryl Trinitrate)
- Routes: Sublingual tablets/spray, intravenous
- Long-Acting Nitrates: Used for chronic prophylaxis of angina.
- Examples: Isosorbide dinitrate, Isosorbide mononitrate, Nitroglycerin transdermal patches/ointments, Nitroglycerin extended-release oral capsules.
- Routes: Oral, sublingual (for isosorbide dinitrate), transdermal, buccal.
Pharmacokinetics:
- Absorption: Varies significantly by route.
- Sublingual/Buccal Nitroglycerin: Rapidly absorbed into the systemic circulation, bypassing the liver, leading to quick onset of action (1-3 minutes). High bioavailability.
- Oral Nitroglycerin: Undergoes extensive first-pass metabolism in the liver via nitrate reductase enzymes. Bioavailability is low and erratic, hence specific oral formulations (extended-release) or alternative routes are preferred for long-term therapy.
- Oral Isosorbide Dinitrate: Also undergoes significant first-pass metabolism to active metabolites, isosorbide-2-mononitrate and isosorbide-5-mononitrate. Bioavailability is about 25%.
- Oral Isosorbide Mononitrate: Does not undergo significant first-pass metabolism. Its bioavailability is nearly 100%, making it more predictable.
- Transdermal Nitroglycerin: Absorbed through the skin, providing sustained release for several hours.
- Intravenous Nitroglycerin: Directly enters systemic circulation, providing immediate and precisely titratable concentrations.
- Distribution: Distributed widely throughout the body. Volume of distribution varies by nitrate.
- Metabolism: Primarily hepatic, mediated by glutathione S-transferase and nitrate reductase enzymes. Organic nitrates are denitrated, yielding inorganic nitrite and eventually nitric oxide, but also inactive metabolites. The rate of metabolism is rapid for nitroglycerin (especially orally), less so for isosorbide dinitrate, and even slower for isosorbide mononitrate. Isosorbide dinitrate is metabolized to the active mononitrates (2- and 5-mononitrates), which have longer half-lives than the parent compound.
- Excretion: Metabolites are primarily excreted by the kidneys. Half-lives vary: Nitroglycerin has a very short half-life (1-4 minutes). Isosorbide dinitrate has a half-life of 1 hour, but its active metabolite, isosorbide-5-mononitrate, has a half-life of 4-6 hours. Isosorbide mononitrate has a half-life of 4-5 hours. The longer half-lives of the mononitrates make oral isosorbide mononitrate particularly suitable for sustained effects.
Mechanism of Action and Organ-System Effects of Nitrates
Mechanism of Action:
Nitrates are prodrugs. When administered, they are bioactivated within smooth muscle cells (and endothelium) to release or generate nitric oxide (NO). This process requires specific enzymes, notably aldehyde dehydrogenase-2 (ALDH-2), particularly for nitroglycerin.
Nitric Oxide (NO) is a potent vasodilator. It exerts its effects by:
- Activating guanylyl cyclase in smooth muscle cells.
- Increased activity of guanylyl cyclase leads to a rise in the intracellular concentration of cyclic guanosine monophosphate (cGMP).
- Increased cGMP activates protein kinase G (PKG).
- PKG phosphorylates various proteins involved in calcium homeostasis and smooth muscle contraction. This leads to a decrease in intracellular calcium concentration and desensitization of the contractile apparatus to calcium.
- The net result is relaxation of vascular smooth muscle.
Organ-System Effects:
The primary effects of nitrates are due to smooth muscle relaxation, particularly in the vascular system:
- Cardiovascular System:
- Venodilation: This is the most prominent effect at typical therapeutic doses. Relaxation of venous smooth muscle leads to pooling of blood in the peripheral veins (increased venous capacitance). This reduces the amount of blood returning to the heart (preload). A reduced preload decreases ventricular volume and wall tension, significantly lowering myocardial oxygen demand.
- Arterial Dilation: Nitrates also relax arterial smooth muscle, though this effect is usually less pronounced than venodilation at lower doses. Dilation of peripheral arterioles reduces resistance to left ventricular ejection (afterload). A reduced afterload also decreases myocardial oxygen demand and improves myocardial perfusion by reducing extravascular compression of coronary vessels during systole.
- Coronary Artery Effects: Nitrates can dilate epicardial coronary arteries, including collateral vessels, which can potentially increase blood flow to ischemic areas. This effect is particularly helpful in vasospastic (variant or Prinzmetal’s) angina. In stable angina with fixed atherosclerotic stenosis, the ability to increase flow through the stenotic segment is limited, but redistribution of flow towards ischemic areas can occur, and the primary benefit remains the reduction in oxygen demand.
- Effect on Heart Rate and Contractility: Primarily indirect effects. The reduction in blood pressure (due to venodilation and arterial dilation) can trigger a reflex sympathetic activation, potentially leading to a reflex tachycardia and increased contractility. This reflex can be counteracted by concomitant use of beta-blockers.
- Other Smooth Muscle: Nitrates can relax smooth muscle in other parts of the body, including:
- Bronchial smooth muscle (minor bronchodilation).
- Gastrointestinal smooth muscle (relieving spasm).
- Biliary tract smooth muscle.
- Ureteral smooth muscle.
Mechanism of action contributes to the development of nitrate tolerance with continuous exposure. The exact mechanisms are complex but may involve depletion of intracellular sulfhydryl groups necessary for NO generation (especially for nitroglycerin), desensitization of guanylyl cyclase, or activation of counter-regulatory mechanisms. Nitrate-free intervals are typically required for long-acting nitrates to restore sensitivity.
Clinical Uses and Method of Administration of Nitrates
Nitrates have several important clinical uses in cardiovascular medicine beyond angina, but their primary role remains in the management of myocardial ischemia.
Clinical Uses:
- Angina Pectoris:
- Acute Symptom Relief: Short-acting nitrates (especially sublingual nitroglycerin) are the cornerstone for rapidly alleviating an ongoing anginal attack.
- Prophylaxis of Effort Angina: Short-acting nitrates can be taken before engaging in activities known to precipitate angina (situational prophylaxis).
- Chronic Prophylaxis of Angina: Long-acting nitrates are used to reduce the frequency and severity of anginal episodes over time. They are often used in combination with beta-blockers or calcium channel blockers.
- Vasospastic (Prinzmetal’s) Angina: Nitrates are effective in preventing and treating episodes of coronary artery spasm.
- Acute Coronary Syndromes (ACS): Intravenous nitroglycerin is used in unstable angina and non-ST-elevation myocardial infarction (NSTEMI) to relieve ischemia and control blood pressure, and in STEMI as an adjunct therapy if hypertension or heart failure is present.
- Heart Failure: Nitrates, particularly in combination with hydralazine, can be used to reduce preload and improve symptoms in certain patients with heart failure.
- Hypertensive Emergencies: IV nitroglycerin is sometimes used when hypertension is complicated by myocardial ischemia or acute heart failure.
Method of Administration:
The route of administration is chosen based on the desired onset and duration of action:
- Sublingual (SL): Nitroglycerin tablets or spray are placed under the tongue. This is the preferred route for acute angina relief due to rapid absorption and onset (1-3 minutes). The dose can be repeated every 5 minutes, up to 3 doses. If pain persists after 3 doses, the patient should seek urgent medical attention (indicating potential ACS).
- Buccal: Nitroglycerin preparations placed between the cheek and gum allow for sustained absorption. Used for prophylaxis.
- Oral: Isosorbide dinitrate and isosorbide mononitrate are available in oral tablet or capsule forms for sustained prophylaxis. Due to first-pass metabolism, higher doses are needed compared to sublingual nitroglycerin. Extended-release oral nitroglycerin is also available. To prevent tolerance, oral nitrates (and transdermal) are typically administered with a daily “nitrate-free interval” (e.g., 8-14 hours, often overnight).
- Transdermal: Nitroglycerin patches or ointment applied to the skin provide a sustained release of the drug for prophylaxis. Patches should be removed for a nitrate-free interval daily.
- Intravenous (IV): Nitroglycerin is administered intravenously in hospitalized patients with persistent ischemia (e.g., unstable angina, NSTEMI, STEMI), refractory angina, or hypertensive emergencies. This allows for precise dose titration.
Major Toxic Effects of Nitrates and Nitrites
While generally well-tolerated, nitrates and nitrites can cause adverse effects, primarily related to their vasodilatory properties.
Common Adverse Effects:
- Headache: The most common side effect, often described as throbbing. It is due to vasodilation of cerebral arteries. This often diminishes with continued use but can be severe enough to limit use.
- Flushing: Reddening of the skin, especially of the face and neck, due to cutaneous vasodilation.
- Dizziness/Lightheadedness: Can occur due to orthostatic hypotension (a drop in blood pressure upon standing).
- Orthostatic Hypotension: Significant drop in blood pressure when moving from a lying or sitting position to standing, leading to dizziness or fainting.
- Reflex Tachycardia: The drop in blood pressure can trigger a reflex increase in heart rate as the body attempts to compensate. This can sometimes worsen angina by increasing oxygen demand.
Less Common or More Serious Effects:
- Syncope: Fainting due to severe hypotension.
- Palpitations: Awareness of heartbeats due to reflex tachycardia.
- Nausea and Vomiting: Can occur, particularly with higher doses.
Specific Toxic Effects / Overdose:
- Profound Hypotension and Shock: Excessive vasodilation can lead to severe, life-threatening hypotension, especially with overdose or in volume-depleted patients.
- Methaemoglobinaemia: This is a rare but serious complication, particularly with very high doses or with nitrites (less common with organic nitrates used therapeutically). Nitrites can oxidize the ferrous iron (Fe²⁺) in hemoglobin to ferric iron (Fe³⁺), forming methaemoglobin, which cannot bind oxygen. This results in functional anaemia and tissue hypoxia, even if arterial pO2 is normal. Symptoms include cyanosis, dyspnea, headache, confusion, and can be life-threatening. Methylene blue is the antidote.
- Increased Intracranial Pressure: Due to cerebral vasodilation, nitrates can increase intracranial pressure, potentially problematic in patients with pre-existing conditions affecting cerebral pressure.
- Nitrate Tolerance: As discussed, continuous exposure (without a nitrate-free interval) leads to a reduced effectiveness of the drug. This is a major limitation of long-acting nitrate therapy.
Drug Interactions:
- Absolute Contraindication: Nitrates are absolutely contraindicated with concurrent use of phosphodiesterase-5 (PDE5) inhibitors such as sildenafil, tadalafil, vardenafil, or avanafil (used for erectile dysfunction or pulmonary hypertension). PDE5 inhibitors block the degradation of cGMP. When combined with nitrates, which increase cGMP production, this leads to dangerously synergistic vasodilation, causing profound and potentially fatal hypotension and cardiovascular collapse. This interaction can occur up to 24 hours (for sildenafil/vardenafil) or even longer (48 hours for tadalafil) after PDE5 inhibitor use.
- Other Hypotensive Agents: Concurrent use with other drugs that lower blood pressure (e.g., beta-blockers, CCBs, antihypertensives, alcohol) can potentiate hypotension.
- Other Vasodilators: Additive hypotensive effects.
Conclusion
The management of angina pectoris is a critical aspect of caring for patients with coronary artery disease. Therapeutic strategies encompass lifestyle changes, revascularization when indicated, and importantly, pharmacological interventions. Nitrates remain a cornerstone of this pharmacological approach, highly effective for both the acute relief and chronic prevention of anginal symptoms by modulating the balance of myocardial oxygen supply and demand through their potent vasodilating actions. While generally safe and effective, understanding their pharmacokinetics, mechanism of action, proper administration techniques, and potential adverse effects, including the crucial interaction with PDE5 inhibitors and the issue of tolerance, is essential for their safe and optimal use in clinical practice. They are often used in combination with other drug classes as part of a comprehensive management plan tailored to the individual patient’s needs and underlying pathophysiology.
Calcium Channel Blockers (CCBs) in Angina Treatment
Calcium channel blockers are a class of drugs that block the influx of calcium ions into smooth muscle cells and cardiac myocytes. Calcium entry through L-type calcium channels plays a critical role in smooth muscle contraction (leading to vasoconstriction) and in cardiac electrical activity (particularly in the sinoatrial and atrioventricular nodes) and contractility. By blocking these channels, CCBs induce vasodilation and, for certain types, affect cardiac function.
Role of CCBs in Angina
CCBs primarily exert their antianginal effects through two main mechanisms:
- Vasodilation: By blocking calcium entry into vascular smooth muscle cells, CCBs cause relaxation and dilation of both systemic arteries (reducing afterload) and coronary arteries. Reducing afterload decreases the workload on the heart, lowering oxygen demand. Dilation of coronary arteries can improve blood flow, increasing oxygen supply, which is particularly beneficial in vasospastic angina (Prinzmetal’s angina), where coronary artery spasm is the primary cause of ischemia.
- Reduction in Myocardial Oxygen Demand (for Non-Dihydropyridine CCBs): Certain CCBs also block calcium channels in the heart itself. This leads to decreased heart rate and contractility, directly reducing myocardial oxygen demand.
CCBs are classified into two main types based on their predominant effects:
- Dihydropyridines (DHPs): Primarily act on vascular smooth muscle, causing potent vasodilation. Examples include Amlodipine, Nifedipine, Felodipine. They have minimal effect on cardiac conduction or heart rate at therapeutic doses.
- Non-Dihydropyridines (Non-DHPs): Act on both vascular smooth muscle and cardiac muscle. They cause vasodilation but also significantly decrease heart rate, slow AV nodal conduction, and reduce myocardial contractility. Examples include Verapamil and Diltiazem.
Given these mechanisms, CCBs are effective in treating angina pectoris, especially:
- In patients who cannot tolerate Beta-Blockers.
- When Beta-Blockers alone are not sufficient to control symptoms.
- In patients with vasospastic angina, where DHPs are particularly beneficial due to their potent vasodilatory effects on coronary arteries.
- Non-DHPs are useful when both reducing oxygen demand (via heart rate/contractility) and increasing supply (via vasodilation) are needed, but caution is required when combining with Beta-Blockers due to the risk of excessive bradycardia or heart block.
Commonly Used Calcium Channel Blockers for Angina
Here is a description of some commonly used CCBs in angina treatment, detailing their pharmacokinetics, indications, contraindications, and adverse effects.
1. Amlodipine
- Class: Dihydropyridine (DHP)
- Pharmacokinetics: Well absorbed orally; bioavailability is 64-90%. Highly protein bound (approx. 97.5%). Extensively metabolized in the liver to inactive metabolites. Excreted primarily in urine (approx. 60% as metabolites, 10% as unchanged drug). Long elimination half-life (30-50 hours), allowing for once-daily dosing.
- Indications: Stable angina, Vasospastic angina (Prinzmetal’s angina), Hypertension.
- Contraindications: Severe hypotension, Cardiogenic shock, Known hypersensitivity to dihydropyridines.
- Adverse Effects: Peripheral edema (most common, dose-dependent), Headache, Flushing, Dizziness, Palpitations (reflex tachycardia possible, though less common with Amlodipine due to its slow onset of action).
2. Nifedipine
- Class: Dihydropyridine (DHP)
- Pharmacokinetics: Rapidly and almost completely absorbed orally, but undergoes significant first-pass metabolism, resulting in bioavailability of 45-56%. Highly protein bound (approx. 92-98%). Extensively metabolized in the liver to inactive metabolites. Excreted primarily in urine (approx. 60-80% as metabolites) and feces. Elimination half-life of standard preparations is short (2-5 hours), requiring frequent dosing. Extended-release (ER) or sustained-release (SR) formulations have slower absorption and release, providing a longer duration of action suitable for angina and hypertension treatment and mitigating the risk of reflex tachycardia associated with rapid onset.
- Indications: Stable angina, Vasospastic angina (Prinzmetal’s angina), Hypertension (ER/SR formulations). Note: Short-acting nifedipine is generally not recommended for chronic angina management due to rapid onset causing potential reflex tachycardia and increased cardiac events in some studies; ER/SR formulations are preferred.
- Contraindications: Severe hypotension, Cardiogenic shock, Acute unstable angina or within a few weeks of myocardial infarction (for short-acting formulations), Known hypersensitivity to dihydropyridines.
- Adverse Effects: Peripheral edema, Headache, Flushing, Dizziness, Reflex tachycardia (especially with fast-acting formulations), Hypotension, Constipation (less common than with Verapamil).
3. Verapamil
- Class: Non-Dihydropyridine (Non-DHP)
- Pharmacokinetics: Well absorbed orally (90%), but undergoes extensive first-pass metabolism, resulting in bioavailability of 20-35%. Protein bound (approx. 90%). Extensively metabolized in the liver via CYP enzymes; forms active metabolites (e.g., norverapamil). Excreted primarily in urine (approx. 70% as metabolites). Elimination half-life varies with dose and duration of therapy (single dose: 2-8 hours; chronic dosing: 4.5-12 hours).
- Indications: Stable angina, Vasospastic angina, Supraventricular tachyarrhythmias (rate control), Hypertension.
- Contraindications: Severe left ventricular dysfunction, Hypotension, Cardiogenic shock, Sick sinus syndrome (unless a pacemaker is in place), Second- or third-degree AV block (unless a pacemaker is in place), Atrial flutter or fibrillation with an accessory bypass tract (e.g., Wolff-Parkinson-White syndrome).
- Adverse Effects: Constipation (very common), Bradycardia, Hypotension, Dizziness, Fatigue, AV block, Peripheral edema (less common than with DHPs). Caution needed when combining with Beta-Blockers or Digoxin due to additive effects on heart rate and AV conduction.
4. Diltiazem
- Class: Non-Dihydropyridine (Non-DHP)
- Pharmacokinetics: Well absorbed orally (80%), undergoes significant first-pass metabolism, resulting in bioavailability of 40-65%. Protein bound (approx. 70-80%). Metabolized in the liver via CYP enzymes; forms both active and inactive metabolites. Excreted primarily in urine (approx. 35% as metabolites) and feces (approx. 65% as metabolites). Elimination half-life varies with formulation (immediate-release: 3-4.5 hours; extended-release formulations have longer half-lives suitable for once or twice-daily dosing).
- Indications: Stable angina, Vasospastic angina, Supraventricular tachyarrhythmias (rate control), Hypertension.
- Contraindications: Severe left ventricular dysfunction, Hypotension, Cardiogenic shock, Sick sinus syndrome (unless a pacemaker is in place), Second- or third-degree AV block (unless a pacemaker is in place), Atrial flutter or fibrillation with an accessory bypass tract.
- Adverse Effects: Peripheral edema (more common than Verapamil, less common than DHPs), Bradycardia, Hypotension, Dizziness, Headache, AV block. Caution needed when combining with Beta-Blockers or Digoxin. Less constipating than Verapamil.
In summary, CCBs are valuable agents for angina treatment, particularly useful for vasospastic angina or when Beta-Blockers are contraindicated or insufficient. The choice between DHP and non-DHP CCBs depends on the patient’s specific clinical presentation, including heart rate, left ventricular function, and the presence of concomitant conditions like arrhythmias or hypertension.
Beta-Blockers (BBs) in Angina Treatment
Beta-adrenergic receptor blockers, or Beta-Blockers, reduce the effects of stress hormones like adrenaline (epinephrine) and noradrenaline (norepinephrine) on the heart and blood vessels by blocking beta-adrenergic receptors. In the heart, these receptors are primarily beta-1, while beta-2 receptors are predominantly found in bronchial smooth muscle and peripheral blood vessels.
Role of BBs in Angina
Beta-blockers are considered a cornerstone in the management of chronic stable angina, particularly for reducing the frequency of anginal episodes and improving exercise tolerance. Their primary antianginal effect is achieved by significantly reducing myocardial oxygen demand through several mechanisms:
- Decreased Heart Rate: By blocking beta-1 receptors in the SA node, BBs slow the heart rate, especially during exertion. A lower heart rate reduces oxygen consumption per minute.
- Decreased Myocardial Contractility: BBs reduce the force of contraction, further decreasing the work performed by the heart and thus lowering oxygen demand.
- Reduced Blood Pressure: By reducing heart rate, contractility, and renin release, BBs can lower blood pressure, which reduces afterload and subsequent wall tension, contributing to reduced oxygen demand.
- Prolonged Diastole: By slowing the heart rate, BBs increase the duration of diastole. This is crucial because the majority of coronary blood flow to the left ventricle occurs during diastole. A longer diastolic period allows for better perfusion of the myocardium, potentially increasing oxygen supply, especially in the subendocardium which is most vulnerable to ischemia.
Due to these effects, Beta-Blockers are highly effective in preventing exercise-induced angina. They are generally recommended as first-line therapy for most patients with chronic stable angina unless contraindicated. Certain Beta-Blockers (those with intrinsic sympathomimetic activity, ISA) are less commonly used for angina as they may not effectively reduce heart rate during exercise. Cardioselective Beta-1 blockers (like metoprolol and atenolol) are often preferred as they have less effect on bronchial muscle (beta-2 receptors), which is important for patients with concomitant respiratory conditions, although selectivity is lost at higher doses.
Conclusion
Calcium Channel Blockers and Beta-Blockers are essential pharmacological agents in the comprehensive management of angina pectoris. Beta-Blockers are typically the first-line choice for chronic stable angina due to their proven efficacy in reducing myocardial oxygen demand and improving prognosis in patients with underlying CAD. Calcium Channel Blockers offer complementary benefits through vasodilation and are particularly valuable for vasospastic angina, as an alternative or adjunct therapy for stable angina when Beta-Blockers are insufficient or contraindicated, or for managing concomitant hypertension or certain arrhythmias. The selection of the appropriate drug or combination of drugs depends on the specific type of angina, the patient’s comorbidities, tolerance, and potential drug interactions, requiring careful clinical assessment and individualized treatment planning by healthcare professionals.
