Angina ant its pharmacotherapy

Pathophysiology of angina and its pharmacotherapy

1. RVS Chaitanya Koppala Angina

2. Definition Angina is the result of myocardial ischemia caused by an imbalance between myocardial blood supply and oxygen demand. It is a common presenting symptom (typically, chest pain) among patients with coronary artery disease. Type of chest pain: pressure or discomfort

3. ADAM.COM

4. Types of Angina Angina is classified broadly as stable or unstable , depending on its pattern of occurrence and severity. medmovie.com

5. Types of Angina (cont.) Stable angina occurs when increased physical activity (e.g., hurrying across a street or climbing a long stairs) which creates a greater demand for oxygen-rich blood to reach heart tissue. Unstable angina occurs with lesser degrees of exertion or while at rest. Unstable angina that occurs at rest is the most serious form. Formation of a blood clot at the site of a ruptured plaque in a coronary artery.

6. Pathophysiology Myocardial ischemia develops when coronary blood flow becomes inadequate to meet myocardial oxygen demand. This causes myocardial cells to switch from aerobic to anaerobic metabolism, with a progressive impairment of metabolic, mechanical, and electrical functions. Studies have shown that adenosine may be the main chemical mediator of anginal pain. During ischemia, ATP is degraded to adenosine, which, after diffusion to the extracellular space, causes arteriolar dilation and anginal pain.

7. Clinical Presentation Angina is a symptom of ischemic heart disease (IHD). Episodes of stable angina typically are brought on by exertion or emotion and are relieved with rest. An attack of stable angina lasts from 1 to 5 minutes and is described as - squeezing, - choking, - smothering, or - crushing pressure in the chest. Angina pain may radiate to the shoulders, arms, back, neck, or jaw. Patients with atherosclerosis also may experience sweating, shortness of breath (dyspnea).

8. Clinical Presentation (cont.)

9. Diagnosis A diagnosis of stable angina is based primarily on symptoms, such as chest pain. A diagnosis of unstable angina is made when there is - new onset angina that is severe and/or frequent; - chronic stable angina who develop more frequent, severe, prolonged, or more easily triggered episodes - angina at rest.

10. Diagnostic Tests and Procedures 1- ECG (Electrocardiogram) It detects and records the electrical activity of the heart. Certain electrical patterns that the ECG detects can suggest whether CAD is likely. However, some people with angina have a normal ECG. The ECG is usually normal between attacks. During an attack there may be a transient ST segment depression. If the angina is provoked by exertion, an exercise stress ECG should be performed.

11. Diagnostic Tests and Procedures Butterworth Publishers

12. Diagnostic Tests and Procedures 2- Stress ECG Testing Typically, this test involves taking an electrocardiogram (ECG) before, during, and after exercise on a treadmill or stationary bicycle. Patients who are at risk for a coronary event with exercise are, instead, given a drug to increase the heart rate.

13. Diagnostic Tests and Procedures 3- Coronary angiogram Is obtained by injecting contrast material into the bloodstream and taking x-rays of the coronary arteries. This enables the physician to see blockages, malformations, and stenosis in the vessels. 4- Blood Tests Blood tests check the levels of certain fats, cholesterol, sugar, and proteins in blood. Abnormal levels may indicate risk factors for CAD. Some studies suggest that high levels of CRP (C-reactive protein) in the blood may increase the risk for CAD and heart attack.

14. Goals of Treatment All treatments for people with coronary artery disease have the same goals: - to decrease the effects of the disease on the quality of life and alleviate symptoms. - to reduce mortality due to CAD progression.

15. Drug Therapy Currently, there are three main types of drugs used: 1) Nitrates 2) Beta blockers 3) Calcium channel blockers Nitrates or beta blockers are usually preferred for initial treatment of angina, and calcium channel blockers may be added if needed.

16. Drug Therapy (cont.) 1) Nitrates Nitrates improve blood flow by relaxing and dilating veins and arteries, including the coronary arteries. Examples: nitroglycerin and isosorbide dinitrate. Side effects:  The most common side effects of nitrates are headache, lightheadedness, flushing, and an increase in heart rate.

17. Drug Therapy (cont.) 2) Beta blockers Beta blockers reduce the heart rate, blood pressure, and the force of contractions, thereby decreasing the amount of oxygen the heart requires to pump blood. Examples: atenolol, metoprolol, nadolol and propranolol. Side effects: Cardiac effects -- worsen heart failure, bradycardia Noncardiac effects   -- constriction of airways, circulatory problems, Impotence, hallucinations, insomnia, and fatigue

18. Drug Therapy (cont.) 3) Calcium channel blockers Calcium channel blockers dilate arteries and lower blood pressure, which decreases the force of contractions. They also dilate veins, reducing the amount of blood returning to the heart, which reduces the workload of the heart. Examples: amlodipine, nifedipine, nicardipine, verapamil and diltiazem. Side effects: flushing, dizziness and lightheadedness, headache, peripheral edema and depression of cardiac function (with non-dihydropyridines) Patient information — Angina treatment , UpToDate.com (Patient Preview)

19. Other Measures in Managing CAD Anticoagulants Aspirin: (it helps to prevent blood clotting, keeping the narrowed arteries open and lowering the risk of a heart attack). Treat high blood pressure Treat high cholesterol Quit smoking Lose excess weight Reduce stress Exercise regularly

20. Other Treatment Options Percutaneous Coronary Intervention (previously called Angioplasty or Balloon Angioplasty) CABG (Coronary Artery Bypass Graft Surgery)

21. RVS Chaitanya Koppala Atherosclerosis

22. Introduction Atherosclerosis (also known as Arteriosclerotic Vascular Disease or ASVD) Artery wall thickens (build-up of fatty materials such as cholesterol) Affecting arterial blood vessels, a chronic inflammatory response in the walls of arteries Due to the accumulation of macrophage Promoted by Low-density lipoproteins Without adequate removal of fats and cholesterol from the macrophages

23. Hardening or furring of the arteries. Formation of multiple plaqueswithin the arteries. Restrict blood flow. These plaques can also burst, causing a blood clot. Often considered a heart problem Affect arteries anywhere in your body. Atherosclerosis is a preventable and treatable condition.

24. TERMS Arteriosclerosis is a general term describing any hardening (and loss of elasticity) of medium or large arteries Arteriolosclerosis is any hardening (and loss of elasticity) of arterioles (small arteries); Atherosclerosis is a hardening of an artery specifically due to an atheromatous plaque. Atherogenic is used for substances or processes that cause atherosclerosis. Atherogenesis is the developmental process of atheromatous plaques

25. Causes Atherosclerosis starts with damage or injury to the inner layer of an artery. The damage may be caused by: High blood pressure High cholesterol An irritant, such as nicotine Certain diseases, such as diabetes

26. Epidemiology Estimated 10-year risk of coronary artery disease according to various combinations of risk factor levels, expressed as the probability of an event in 10 years. According to United States data for the year 2004, for about 65% of men and 47% of women, the first symptom of atherosclerotic cardiovascular disease is heart attack or sudden cardiac death (death within one hour of onset of the symptom).

27. ATHEROSCLEROSIS is less prevalent in central and south America, Africa, and Asia. And more prevalent in united states and Japan. The mortality in U.S in 5 times higher than Japan Epidemiology

28. Pathophysiology Atherosclerosis develops as a chronic inflammatory response of the arterial wall to endothelial injury. Lesion progression occurs through interactions of modified lipoproteins, monocyte-derived macrophages, T-lymphocytes , and the normal cellular constituent of the arterial wall. The contemporary view of atherosclerosis is expressed by the response-to-injury hypothesis .

29. Response-to-injury hypothesis The following are the steps involved in the hypothesis: Chronic endothelial injury Accumulation of lipoproteins Monocyte adhesion to the endothelium SMC proliferations and ECM (extracellular matrix) production factor release platelet adhesion

30. Micrograph of an artery that supplies the heart With significant atherosclerosis and marked luminal narrowing

31. Symptoms Atherosclerosis develops gradually, typically begins in early adolescence, and is usually found in most major arteries. No atherosclerosis symptoms until an artery is so narrowed or clogged. Sometimes a blood clot completely obstructs blood flow, or even breaks apart and causes heart attack or stroke.

32. Atherosclerosis symptoms depend on which arteries are affected. For example: Atherosclerosis in heart arteries,  have symptoms similar to those of a heart attack, such as chest pain (angina). Atherosclerosis in the arteries leading to brain, have symptoms such as sudden numbness or weakness in your arms or legs, difficulty speaking or slurred speech, or drooping muscles in your face. Atherosclerosis in the arteries in arms and legs, produces decreased blood flow is called peripheral artery occlusive disease (PAOD).have symptoms such as leg pain when walking Sometimes atherosclerosis causes erectile dysfunction in men. Symptoms

33. Symptoms

34. Symptoms

35. Physiologic factors that increase risk Various anatomic, physiological & behavioral risk factors for atherosclerosis are known. These can be divided into various categories:, modifiable and non-modifiable. Modifiable Having diabetes or Impaired glucose tolerance (IGT) Dyslipoproteinemia (unhealthy patterns of serum proteins carrying fats & cholesterol): Tobacco smoking, increases risk by 200% after several pack years Having high blood pressure, on its own increasing risk by 60% Elevated serum C-reactive protein concentrations

36. 2. Non modifiable Advanced age Male sex Having close relatives who have had some complication of atherosclerosis (CVD/STROKE) Genetic abnormalities, e.g. familial hypercholesterolemia 3. Lesser or uncertain Being obese (in particular central obesity, A sedentary lifestyle Postmenopausal estrogen deficiency High carbohydrate intake Elevated serum levels of triglycerides Elevated serum lipoprotein concentrations Stress or symptoms of clinical depression Hyperthyroidism Elevated serum insulin levels Short sleep duration Physiologic factors that increase risk

37. Complications The complications of atherosclerosis depend on the location of the blocked arteries. For example: Coronary artery disease.   Carotid artery disease.   Peripheral artery disease (Arms and legs) Aneurysms (any where in body, formation of bulge in artery)

38. Tests and diagnosis Doctors may find signs of narrowed, enlarged or hardened arteries during a physical exam. These include: A weak or absent pulse below the narrowed area of the artery Decreased blood pressure in an affected limb Whooshing sounds (bruits) over the arteries, heard with a stethoscope Signs of a pulsating bulge (aneurysm) in the abdomen or behind knee Evidence of poor wound healing in the area where blood flow is restricted

39. Blood tests.  Lab tests can detect increased levels of cholesterol and blood sugar that may increase the risk of atherosclerosis. Doppler ultrasound.  Uses a special ultrasound device (Doppler ultrasound) to measure blood pressure at various points along arm or leg. These measurements can help doctor gauge the degree of any blockages, as well as the speed of blood flow in the arteries. Ankle-brachial index.  This test can tell if one have atherosclerosis in the arteries in your legs and feet. Doctor may compare the blood pressure in ankle with the blood pressure in the arm. This is known as the ankle-brachial index. An abnormal difference may indicate peripheral vascular disease, which is usually caused by atherosclerosis. Tests and diagnosis

40. Electrocardiogram (ECG).  An electrocardiogram records electrical signals as they travel through your heart. An ECG can often reveal evidence of a previous heart attack or one that's in progress. Angiogram.  To better view blood flow through heart, brain, arms or legs, doctor may inject a special dye into your arteries before an X-ray. This is known as an angiogram. The dye outlines narrow spots and blockages on the X-ray images. Other imaging tests.   doctor may use ultrasound, a computerized tomography (CT) scan or a magnetic resonance angiogram (MRA) to study the arteries. These tests can often show hardening and narrowing of large arteries, as well as aneurysms and calcium deposits in the artery walls. Tests and diagnosis

41. Lifestyle changes, such as eating a healthy diet and exercising, are often the first line of defense in treating atherosclerosis. But sometimes, medication or surgical procedures may be recommended as well. Various drugs can slow — or sometimes even reverse Cholesterol medications.  Aggressively lowering low-densitylipoprotein (LDL) cholesterol, the "bad" cholesterol, can slow, stop or even reverse the buildup of fatty deposits in arteries. Boosting your high-density lipoprotein (HDL) cholesterol, the "good" cholesterol, may help, too. cholesterol medications includes drugs known as statins and fibrates. Treatments and drugs

42. Anti-platelet medications.  Doctors may prescribe anti-platelet medications, such as aspirin, to reduce the likelihood that platelets will clump in narrowed arteries, form a blood clot and cause further blockage. Anticoagulants.  An anticoagulant, such as heparin or warfarin (Coumadin), can help thin blood to prevent clots from forming. Blood pressure medications.  Medications to control blood pressure — such as beta blockers, angiotensin-converting enzyme (ACE) inhibitors and calcium channel blockers — can help slow the progression of atherosclerosis Treatments and drugs

43. Other medications.   Such as diabetes. Leg pain during exercise, are prescribed. Symptoms or a blockage that threatens muscle or skin tissue survival, you may be a candidate for one of the following surgical procedures Treatments and drugs

44. Angioplasty.  In this procedure, your doctor inserts a long, thin tube (catheter) into the blocked or narrowed part of your artery. A mesh tube (stent) is usually left in the artery to help keep the artery open. Angioplasty may also be done with laser technology. Endarterectomy .  In some cases, fatty deposits must be surgically removed from the walls of a narrowed artery. When the procedure is done on arteries in the neck (the carotid arteries), it's known as carotid endarterectomy . Treatments and drugs

45. Thrombolytic therapy.  If you have an artery that's blocked by a blood clot, your doctor may insert a clot-dissolving drug into your artery at the point of the clot to break it up. Bypass surgery.  Your doctor may create a graft bypass using a vessel from another part of your body or a tube made of synthetic fabric. This allows blood to flow around the blocked or narrowed artery . Treatments and drugs

46. Lifestyle and home remedies Lifestyle changes can help prevent or slow the progression of atherosclerosis. Stop smoking.   Exercise most days of the week.   Eat healthy foods Manage stress Manage the condition of high cholesterol, high blood pressure, diabetes or other chronic disease

47. References: Harrison’s principle of internal medicine, 17 th edition. Robbins basic pathology, 8 th edition. www.wekiepedia.com/atherosclerosis www.mayoclinic.com/atherosclerois

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