Antianginal

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An antianginal is a drug used in the treatment of angina pectoris , a symptom of ischaemic heart disease.

Contents

Myocardial ischemia arises from the dysfunction of coronary macrovascular or microvascular components, leading to a compromised supply of oxygen and nutrients to the myocardium. The underlying pathophysiological mechanisms encompass a range of factors, including atherosclerosis in epicardial coronary arteries, vasospasm in large or small vessels, and microvascular dysfunction—whose clinical significance is increasingly acknowledged. The diverse clinical presentations of myocardial ischemia collectively fall under the term chronic coronary syndromes.

Addressing these conditions involves a multifaceted approach, where the most common antianginal medications alleviate symptoms by inducing coronary vasodilation and modifying the determinants of myocardial oxygen consumption, such as heart rate, myocardial wall stress, and ventricular contractility. Additionally, these medications can alter cardiac substrate metabolism to alleviate ischemia by enhancing the efficiency of myocardial oxygen utilization. While there is consensus on the prognostic importance of lifestyle interventions and preventive measures like aspirin and statin therapy, determining the optimal antianginal treatment for chronic coronary syndrome patients remains less defined.

The majority of individuals experiencing stable angina can effectively address their condition through lifestyle modifications, particularly by embracing smoking cessation and incorporating regular exercise into their routine. Alongside these lifestyle changes, the use of antianginal drugs is a common approach. However, findings from randomized controlled trials reveal that the efficacy of various antianginal drugs is comparable, with none demonstrating a significant reduction in mortality or the risk of myocardial infarction (MI). Despite this, prevailing guidelines lean towards recommending beta-blockers and calcium channel blockers as the preferred first-line treatment.

The European Society of Cardiology (ESC) guidelines for managing stable coronary artery disease provide well-defined classes of recommendation with corresponding levels of evidence. In a parallel vein, the National Institute for Health and Care Excellence (NICE) guidelines for stable angina management consider cost-effectiveness in their recommendations, designating terms such as first-line and second-line therapy. Notably, both sets of guidelines advocate for the use of low-dose aspirin and statins as disease-modifying agents.

This article aims to critically examine and evaluate the pharmacological recommendations outlined in these guidelines for the management of patients with stable angina. By delving into the nuances of these recommendations, we seek to provide a comprehensive understanding of the rationale behind the suggested pharmacological interventions for stable angina, shedding light on their respective strengths and considerations in clinical practice. [1]

Political Considerations

The 2019 guidelines from the European Society of Cardiology (ESC) advocate for a personalized approach in which antianginal medications are tailored to an individual patient's comorbidities and hemodynamic profile. It's noteworthy that, although antianginal medications do not improve survival, their effectiveness in symptom reduction significantly depends on the underlying mechanism of angina.

Key considerations in antianginal therapies involve enhancing coronary vascular oxygen supply to the ischemic myocardium, reducing heart rate, myocardial work, and oxygen consumption, as well as optimizing the energetic efficiency of cardiomyocytes. Despite current guidelines recommending β-blockers and calcium-channel blockers as first-line therapy, there is a lack of evidence demonstrating their superiority over second-line therapies.

In this comprehensive review, it is crucial to emphasize that, thus far, neither drugs nor interventions that reduce ischemia have been shown to prolong survival in patients with chronic coronary syndromes.

Examples

Drugs used are nitrates, beta blockers, or calcium channel blockers.

Nitrates

Nitrates cause vasodilation [2] of the venous capacitance vessels by stimulating the endothelium-derived relaxing factor (EDRF). Used to relieve both exertional and vasospastic angina by allowing venous pooling, reducing the pressure in the ventricles and so reducing wall tension and oxygen requirements in, the heart. Short-acting nitrates are used to abort angina attacks that have occurred, while longer-acting nitrates are used in the prophylactic management of the condition.

Agents include glyceryl trinitrate (GTN), pentaerythritol tetranitrate, isosorbide dinitrate and isosorbide mononitrate.

Beta blockers

Beta blockers are used in the prophylaxis [3] of exertional angina by reducing the myocardial oxygen demand below the level that would provoke an angina attack.

They are contraindicated in variant angina and can precipitate heart failure. They are also contraindicated in severe asthmatics due to bronchoconstriction, and should be used cautiously in diabetics as they can mask symptoms of hypoglycemia.

Agents include either cardioselectives such as acebutolol or metoprolol, or non-cardioselectives such as oxprenolol or sotalol.

Calcium channel blockers

Calcium ion (Ca++) antagonists (Calcium channel blockers) are used in the treatment of chronic stable angina, and most effectively in the treatment of variant angina (directly preventing coronary artery vasospasm). They are not used in the treatment of unstable angina .

In vitro, they dilate the coronary and peripheral arteries and have negative inotropic and chronotropic effects - decreasing afterload, improving myocardial efficiency, reducing heart rate and improving coronary blood flow. In vivo, the vasodilation and hypotension trigger the baroreceptor reflex. Therefore, the net effect is the interplay of direct and reflex actions.

Examples include Class I agents (e.g., verapamil), Class II agents (e.g., amlodipine, [4] nifedipine), or the Class III agent diltiazem.

Nifedipine is more a potent vasodilator and more effective in angina. It is in the class of dihydropyridines and does not affect refractory period on SA node conduction.

Related Research Articles

<span class="mw-page-title-main">Coronary artery disease</span> Reduction of blood flow to the heart

Coronary artery disease (CAD), also called coronary heart disease (CHD), ischemic heart disease (IHD), myocardial ischemia, or simply heart disease, involves the reduction of blood flow to the heart muscle due to build-up of atherosclerotic plaque in the arteries of the heart. It is the most common of the cardiovascular diseases. Types include stable angina, unstable angina, and myocardial infarction.

<span class="mw-page-title-main">Angina</span> Chest discomfort due to not enough blood flow to heart muscle

Angina, also known as angina pectoris, is chest pain or pressure, usually caused by insufficient blood flow to the heart muscle (myocardium). It is most commonly a symptom of coronary artery disease.

An antiplatelet drug (antiaggregant), also known as a platelet agglutination inhibitor or platelet aggregation inhibitor, is a member of a class of pharmaceuticals that decrease platelet aggregation and inhibit thrombus formation. They are effective in the arterial circulation where classical Vitamin K antagonist anticoagulants have minimal effect.

Calcium channel blockers (CCB), calcium channel antagonists or calcium antagonists are a group of medications that disrupt the movement of calcium through calcium channels. Calcium channel blockers are used as antihypertensive drugs, i.e., as medications to decrease blood pressure in patients with hypertension. CCBs are particularly effective against large vessel stiffness, one of the common causes of elevated systolic blood pressure in elderly patients. Calcium channel blockers are also frequently used to alter heart rate, to prevent peripheral and cerebral vasospasm, and to reduce chest pain caused by angina pectoris.

<span class="mw-page-title-main">Ischemia</span> Restriction in blood supply to tissues

Ischemia or ischaemia is a restriction in blood supply to any tissue, muscle group, or organ of the body, causing a shortage of oxygen that is needed for cellular metabolism. Ischemia is generally caused by problems with blood vessels, with resultant damage to or dysfunction of tissue i.e. hypoxia and microvascular dysfunction. It also implies local hypoxia in a part of a body resulting from constriction.

<span class="mw-page-title-main">Amlodipine</span> Medication against high blood pressure

Amlodipine, sold under the brand name Norvasc among others, is a calcium channel blocker medication used to treat high blood pressure, coronary artery disease (CAD) and variant angina. It is taken orally.

Microvascular angina, previously known as cardiac syndrome X, is angina with signs associated with decreased blood flow to heart tissue but with normal coronary arteries.

<span class="mw-page-title-main">Diltiazem</span> Calcium channel blocker medication

Diltiazem, sold under the brand name Cardizem among others, is a nondihydropyridine calcium channel blocker medication used to treat high blood pressure, angina, and certain heart arrhythmias. It may also be used in hyperthyroidism if beta blockers cannot be used. It is taken by mouth or injection into a vein. When given by injection, effects typically begin within a few minutes and last a few hours.

Vasospasm refers to a condition in which an arterial spasm leads to vasoconstriction. This can lead to tissue ischemia and tissue death (necrosis). Cerebral vasospasm may arise in the context of subarachnoid hemorrhage. Symptomatic vasospasm or delayed cerebral ischemia is a major contributor to post-operative stroke and death especially after aneurysmal subarachnoid hemorrhage. Vasospasm typically appears 4 to 10 days after subarachnoid hemorrhage.

<span class="mw-page-title-main">Acute coronary syndrome</span> Medical condition

Acute coronary syndrome (ACS) is a syndrome due to decreased blood flow in the coronary arteries such that part of the heart muscle is unable to function properly or dies. The most common symptom is centrally located pressure-like chest pain, often radiating to the left shoulder or angle of the jaw, and associated with nausea and sweating. Many people with acute coronary syndromes present with symptoms other than chest pain, particularly women, older people, and people with diabetes mellitus.

<span class="mw-page-title-main">Variant angina</span> Medical condition

Variant angina, also known as Prinzmetal angina,vasospastic angina, angina inversa, coronary vessel spasm, or coronary artery vasospasm, is a syndrome typically consisting of angina. Variant angina differs from stable angina in that it commonly occurs in individuals who are at rest or even asleep, whereas stable angina is generally triggered by exertion or intense exercise. Variant angina is caused by vasospasm, a narrowing of the coronary arteries due to contraction of the heart's smooth muscle tissue in the vessel walls. In comparison, stable angina is caused by the permanent occlusion of these vessels by atherosclerosis, which is the buildup of fatty plaque and hardening of the arteries.

<span class="mw-page-title-main">Unstable angina</span> Medical condition

Unstable angina is a type of angina pectoris that is irregular or more easily provoked. It is classified as a type of acute coronary syndrome.

<span class="mw-page-title-main">Ivabradine</span> Heart medication

Ivabradine, sold under the brand name Procoralan among others, is a medication, which is a pacemaker current (If) inhibitor, used for the symptomatic management of heart-related chest pain and heart failure. Patients who qualify for use of Ivabradine for coronary heart failure are patients who have symptomatic heart failure, with reduced ejection volume, and heart rate at least 70 bpm, and the condition not able to be fully managed by beta blockers.

Coronary vasospasm refers to when a coronary artery suddenly undergoes either complete or sub-total temporary occlusion.

Myocardial stunning or transient post-ischemic myocardial dysfunction is a state of mechanical cardiac dysfunction that can occur in a portion of myocardium without necrosis after a brief interruption in perfusion, despite the timely restoration of normal coronary blood flow. In this situation, even after ischemia has been relieved and myocardial blood flow (MBF) returns to normal, myocardial function is still depressed for a variable period of time, usually days to weeks. This reversible reduction of function of heart contraction after reperfusion is not accounted for by tissue damage or reduced blood flow, but rather, its thought to represent a perfusion-contraction "mismatch". Myocardial stunning was first described in laboratory canine experiments in the 1970s where LV wall abnormalities were observed following coronary artery occlusion and subsequent reperfusion.

<span class="mw-page-title-main">Nitrovasodilator</span> Drug that causes vasodilation by releasing nitric oxide

A nitrovasodilator is a pharmaceutical agent that causes vasodilation by donation of nitric oxide (NO), and is mostly used for the treatment and prevention of angina pectoris.

<span class="mw-page-title-main">Coronary ischemia</span> Medical condition

Coronary ischemia, myocardial ischemia, or cardiac ischemia, is a medical term for a reduced blood flow in the coronary circulation through the coronary arteries. Coronary ischemia is linked to heart disease, and heart attacks. Coronary arteries deliver oxygen-rich blood to the heart muscle. Reduced blood flow to the heart associated with coronary ischemia can result in inadequate oxygen supply to the heart muscle. When oxygen supply to the heart is unable to keep up with oxygen demand from the muscle, the result is the characteristic symptoms of coronary ischemia, the most common of which is chest pain. Chest pain due to coronary ischemia commonly radiates to the arm or neck. Certain individuals such as women, diabetics, and the elderly may present with more varied symptoms. If blood flow through the coronary arteries is stopped completely, cardiac muscle cells may die, known as a myocardial infarction, or heart attack.

<span class="mw-page-title-main">Acute decompensated heart failure</span> Medical condition

Acute decompensated heart failure (ADHF) is a sudden worsening of the signs and symptoms of heart failure, which typically includes difficulty breathing (dyspnea), leg or feet swelling, and fatigue. ADHF is a common and potentially serious cause of acute respiratory distress. The condition is caused by severe congestion of multiple organs by fluid that is inadequately circulated by the failing heart. An attack of decompensation can be caused by underlying medical illness, such as myocardial infarction, an abnormal heart rhythm, infection, or thyroid disease.

<span class="mw-page-title-main">Management of acute coronary syndrome</span>

Management of acute coronary syndrome is targeted against the effects of reduced blood flow to the affected area of the heart muscle, usually because of a blood clot in one of the coronary arteries, the vessels that supply oxygenated blood to the myocardium. This is achieved with urgent hospitalization and medical therapy, including drugs that relieve chest pain and reduce the size of the infarct, and drugs that inhibit clot formation; for a subset of patients invasive measures are also employed. Basic principles of management are the same for all types of acute coronary syndrome. However, some important aspects of treatment depend on the presence or absence of elevation of the ST segment on the electrocardiogram, which classifies cases upon presentation to either ST segment elevation myocardial infarction (STEMI) or non-ST elevation acute coronary syndrome (NST-ACS); the latter includes unstable angina and non-ST elevation myocardial infarction (NSTEMI). Treatment is generally more aggressive for STEMI patients, and reperfusion therapy is more often reserved for them. Long-term therapy is necessary for prevention of recurrent events and complications.

The Canadian Cardiovascular Societygrading of angina pectoris is a classification system used to grade the severity of exertional angina.

References

  1. ↑ Rousan, Talla A; Thadani, Udho (April 2019). "Stable Angina Medial Therapy Management". Eur Cardiol. 14 (1): 18–22. doi:10.15420/ecr.2018.26.1. PMC   6523058 . PMID   31131033.
  2. ↑ Pfister M, Seiler C, Fleisch M, Göbel H, Lüscher T, Meier B (October 1998). "Nitrate induced coronary vasodilatation: differential effects of sublingual application by capsule or spray". Heart. 80 (4): 365–9. doi:10.1136/hrt.80.4.365. PMC   1728824 . PMID   9875113.
  3. ↑ O'Rourke ST (October 2007). "Antianginal actions of beta-adrenoceptor antagonists". Am J Pharm Educ. 71 (5): 95. doi:10.5688/aj710595. PMC   2064893 . PMID   17998992.
  4. ↑ "NORVASC- amlodipine besylate tablet". DailyMed. 14 March 2019. Retrieved 19 December 2019. Exertional Angina: In patients with exertional angina, NORVASC reduces the total peripheral resistance (afterload) against which the heart works and reduces the rate pressure product, and thus myocardial oxygen demand, at any given level of exercise.
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