Download Free Medical Antianginal Drugs PowerPoint Presentation

Antianginal Drugs PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : Check out this medical presentation on Angina, which is titled "Antianginal Drugs", to know about the drugs for atherosclerotic disease, also known as coronary artery disease (CAD) or ischemic heart disease (IHD), is the most common cause of mortality worldwide.

Tags : Angina, Antianginal Drugs, atherosclerotic disease, coronary artery disease, CAD, ischemic heart disease, IHD

Published on : May 25, 2021 | Views : 3491 | Downloads : 5

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

Antianginal drugs By: Dr Meherunisa Associate professor CIMS
Slide 2-

23-May-16 Angina Atherosclerotic disease, also known as coronary artery disease (CAD) or ischemic heart disease (IHD), is the most common cause of mortality worldwide. Atherosclerotic lesions in coronary arteries can obstruct blood flow, leading to an imbalance in myocardial oxygen supply and demand that presents as stable angina (ischaemic chest pain) an acute coronary syndrome
Slide 3-

23-May-16 Angina unstable angina. myocardial infarction (MI) (heart attack): caused by the complete occlusion of the coronary artery and associated death of tissue Spasms of vascular smooth muscle may also impede cardiac blood flow, reducing perfusion and causing ischemia and anginal pain.
Slide 4-

23-May-16 Angina Is a characteristic sudden, severe, pressing-like substernal chest pain radiating to the neck, jaw, back, and arms. Patients may also present with dyspnea or atypical symptoms such as indigestion, nausea, vomiting, or diaphoresis. is caused by inadequate blood flow through the coronary blood vessels, is a consequence of myocardial O2 demand exceeding supply.
Slide 5-

23-May-16 Angina Transient, self-limited episodes (15 seconds to 15 minutes) of myocardial ischemia (stable angina) do not result in cellular death; such as occurs in myocardial infarction (MI). however, acute coronary syndromes and chronic ischemia can lead to deterioration of cardiac function, heart failure, arrhythmias, and sudden death.
Slide 6-

Types of Angina Angina pectoris has three patterns: Stable, effort-induced, classic, or typical angina. Unstable angina, preinfarction or crescendo angina. Prinzmetal, variant, vasospastic, or rest angina. They are caused by varying combinations of increased myocardial demand and decreased myocardial perfusion. 23-May-16
Slide 7-

Stable angina: the most common (90%) is chest pain caused by a temporary inadequacy of blood flow to the myocardium, The underlying cause is usually occlusion of the coronary arteries by atherosclerosis Usually lasts 1-15 minutes, and is provoked by exercise, stress, extreme cold or heat, heavy meals, alcohol, or smoking. Rx: is promptly relieved by rest or nitroglycerin (a vasodilator). Stable Angina
Slide 8-

Unstable angina (Acute coronary syndrome) lies between stable angina and MI. The pathology is similar to that involved in MI: a platelet-fibrin thrombus associated with a raptured atherosclerotic plaque, but without complete occlusion of the blood vessel. chest pains occur with increased frequency, duration, and intensity. precipitated by progressively less effort. 23-May-16
Slide 9-

Unstable angina (Acute coronary syndrome) Any episode of rest angina longer than 20 minutes, any new-onset angina, any increasing (crescendo) angina, or even sudden development of shortness of breath is suggestive of unstable angina. The symptoms are NOT relieved by rest or nitroglycerin. requires hospital admission and more aggressive therapy to prevent death and progression to MI. 23-May-16
Slide 10-

23-May-16 Prinzmetal's or variant or vasospastic angina is an uncommon pattern of episodic angina that occurs at rest and is due to coronary artery spasm. Symptoms are caused by decreased blood flow to the heart muscle from the spasm of the coronary artery. Although individuals with this form of angina may have significant coronary atherosclerosis, the angina attacks are unrelated to physical activity, heart rate, or blood pressure.
Slide 11-

23-May-16 Prinzmetal's or variant or vasospastic angina generally responds promptly to coronary vasodilators, such as nitroglycerin and calcium-channel blockers. but β-blockers are contraindicated???
Slide 12-

Determinants of the volume of oxygen required by the heart. Determinant of myocardial O2 demand Preload- diastolic filling pressure (blood volume and venous tone) Afterload-peripheral vascular resistance Heart rate Wall tension Ejection time 23-May-16
Slide 13-

Angina-precipitating factors: exercise, emotional stress, sex ↑HR, Contraction ↑ work of the ↑sympathetic activity force, wall tension, TPR heart ↑ myocardial O2 demand ≠ myocardial O2 supply Ischemia 23-May-16
Slide 14-

Increase blood flow to ischemic heart muscle and/or Decrease myocardial oxygen demand Four types of drugs, used either alone or in combination, are commonly used to manage patients with stable angina: β-blockers, CCBs, organic nitrates, and the sodium channel blocking drug, ranolazine. These agents help to balance the cardiac oxygen supply and demand equation by affecting blood pressure, venous return, heart rate, and contractility. Therapeutic strategies
Slide 15-

Lipid lowering drugs, particularly statins, can be given if elevated plasma cholesterol levels are detected Antiplatelet drugs, especially low-dose (75mg) aspirin to reduce the possibility of thrombosis. Fibrinolytic drugs (e.g. heparin) are used in unstable angina Therapeutic strategies
Slide 16-

23-May-16 Newer Therapeutic strategies Trimetazidine: Partial fatty acid oxidation inhibitors (pFOX inhibitors). A newer strategy attempts to increase the efficiency of oxygen utilization by shifting the energy substrate preference of the heart from fatty acids to glucose. Ranolazine: inhibition of late sodium current. Ivabradine: selectively reduces heart rate with no other detectable hemodynamic effects, act by inhibition of the SA pacemaker current, If. Nicorandil, Potassium channel activators,
Slide 17-

Treatment algorithm for improving symptoms in patients with stable angina. 23-May-16
Slide 18-

23-May-16 Organic nitrates Nitroglyserine, Isosorbid dinitrate, Isosorbid mononitrate They are effective in all types of angina pectoris. at therapeutic doses :has 2 major effects Dilation of the large veins resulting in pooling of blood in the veins which diminish the preload and reduces the work of the heart Dilates the coronary vasculature providing increased blood supply to the heart muscle ↓ Preload ↓ Afterload Relieving vasospasm Redistribution blood flow The total effect is a decrease in myocardial oxygen consumption because of decreased cardiac work
Slide 19-

A. Mechanism of action relax vascular smooth muscle by their intracellular conversion to nitrite ions, to nitric oxide, activates guanylate cyclase (GC) and increases the cGMP. dephosphorylation of the myosin light chain, vascular smooth muscle relaxation. 23-May-16
Slide 20-

23-May-16 Pharmacokinetics of Nitroglycerine Prototype: nitrate significant first-pass effect metabolism of nitroglycerin occurs in the liver with PO forms Therefore, it is common to take the drug either sublingually or via a transdermal patch, The time to onset of action varies from 1 minute for nitroglycerin to more than 1 hour for isosorbide mononitrate. Isosorbide mononitrate owes its improved bioavailability and long duration of action to its stability against hepatic breakdown. Oral isosorbide dinitrate undergoes denitration to two mononitrates, both of which possess antianginal activity.
Slide 21-

Time to peak effect and duration of action 23-May-16
Slide 22-

Common nitrate preparations Glyceryl trinitrate can be taken by sublingual tablet or spray The effects start within minutes and last ~30 min Transdermal patches and I.V preparations are also available Isosorbide mononitrate is a longer acting preparation which is given orally (half-life 4hrs), and slow release preparations are available. Side effects: nitrates can cause Headache in about 30% - 60% of patients because of the pronounced vasodilation. High doses can cause postural hypotension, flushing & tachycardia
Slide 23-

23-May-16 Nitrate Tolerance Tolerance develops rapidly. The blood vessels become desensitized to vasodilation. providing a daily “nitrate-free interval” to restore sensitivity to the drug. This interval is typically 10 to 12 hours, usually at night, because demand on the heart is decreased at that time. Nitroglycerin patches are worn for 12 hours then removed for 12 hours. However, variant angina worsens early in the morning, perhaps due to circadian catecholamine surges. Therefore, the nitrate-free interval in these patients should occur in the late afternoon.
Slide 24-

23-May-16 Beta Blockers Atenolol, metoprolol, propranolol, bisoprolol Are used only for prophylactic therapy of angina; they are of no value in an acute attack. Effective in preventing exercise-induced angina. But are ineffective against the vasospastic form Cardioselective β-blockers, such as metoprolol or atenolol, are preferred. Thus, Propranolol is not preferred
Slide 25-

23-May-16 Beta Blockers Agents with intrinsic sympathomimetic activity (for example, pindolol) are less effective and should be avoided in angina. The dose should be gradually tapered off over 5 to 10 days to avoid rebound angina or hypertension.
Slide 26-

23-May-16 Mechanism of Action Suppress the activation of the heart by blocking B1 receptors I. Decrease the HR, resulting in: decreased myocardial oxygen demand. increased oxygen delivery to the heart. Decrease myocardial contractility, helping to conserve energy or decrease demand Reduce the work of the heart by decreasing COP and causing a slight decrease in BP ↓ HR, ↓contractility, ↓systolic wall tension, ↑perfusion time
Slide 27-

23-May-16 Reasons for Using Nitrates and β-Blockers in Combination in Angina β-Blockers prevent reflex tachycardia and contractility produced by nitrate-induced hypotension. Nitrates prevent any coronary vasospasm produced by β- Blockers. Nitrates prevent increases in left ventricular filling pressure or preload resulting from the negative inotropic effects produced by β-Blockers .
Slide 28-

23-May-16 Calcium Channel Blockers (CCBs) ex : amlodipine, diltiazem, felodipine, nicardipine, nifedipine, verapamil Mechanism of Action Calcium is essential for muscular contraction. The CCBs protect the tissue by inhibiting the entrance of Ca+2 into cardiac and smooth muscle cells of the coronary and systemic arterial beds. All CCBs are therefore arteriodilators that cause a decrease in vascular resistance. Cause peripheral arterial vasodilation Reduce myocardial contractility (-ve inotropic action) Result: decreased myocardial oxygen demand
Slide 29-

Mechanism of Action 23-May-16
Slide 30-

23-May-16 Calcium-channel blockers Verapamil mainly affects the myocardium, whereas nifedipine exerts a greater effect on smooth muscle in the peripheral vasculature. Diltiazem is intermediate in its actions. They lower blood pressure may worsen heart failure due to their - ve inotropic effect. All ↓ afterload, coronary vasodilation Verapamil & deltiazem: ↓HR, ↓contractility→↓O2 demand
Slide 31-

23-May-16 Calcium Channel Blockers a dihydropyridine derivative A- Nifedipine a dihydropyridine derivative. functions mainly as an arteriolar vasodilator. This drug has minimal effect on cardiac conduction or heart rate. Used in variant angina caused by spontaneous coronary spasm Other members of this class, amlodipine, nicardipine, and felodipine, have similar cardiovascular characteristics except for amlodipine, which does not affect heart rate or cardiac output.
Slide 32-

23-May-16 Calcium Channel Blockers B- nondihydropyridine derivative/ Verpamil The diphenylalkylamine slows cardiac atrioventricular (AV) conduction directly, and decreases HR, contractility, BP, and oxygen demand. causes greater -ve inotropic effects than nifedipine, but it is a weaker vasodilator. is extensively metabolized by the liver. is contraindicated in patients with preexisting depressed cardiac function or AV conduction abnormalities. Drug Interaction: verapamil increases digoxin levels. It also causes constipation.
Slide 33-

23-May-16 Calcium Channel Blockers C- nondihydropyridine derivative/ Deltiazem Its cardiovascular effects similar to verpamil Reduce the HR but lesser than verpamil Reduce BP Relieve coronary artery spasm so used in variant angina Can be used in angina in patients with concomitant diseases I. First-line agents for treatment of: angina, hypertension, supraventricular tachycardia II. Short-term management of atrial fibrillation and flutter Very acceptable side effect and safety profile, May cause: hypotension, palpitations, tachycardia or bradycardia, constipation, nausea, dyspnea
Slide 34-

23-May-16 Newer Antianginal Drugs Sodium Channel Blocker, Ranolazine Ranolazine inhibits the late phase of the sodium current (late INa), improving the oxygen supply and demand equation. Inhibition of late INa reduces intracellular sodium and calcium overload, thereby improving diastolic function. It has antianginal as well as antiarrhythmic properties. Ranolazine is extensively metabolized, mainly by the CYP3A family and also by CYP2D6. It is also a substrate of P- glycoprotein. As such, ranolazine is subject to numerous drug interactions. ranolazine can prolong the QT interval.
Slide 35-

23-May-16
Slide 36-

Thank you 23-May-16