2. ANGINA PECTORIS A Chronic disease of CVS Occurs with Interminent chest pain spread along the Chest, Shoulders and Arms.
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4. Angina pectoris, or angina, as it is commonly referred to, and coronary artery disease or arteriosclerosis are closely related.
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6. Various Chemical Factors released from Ischeamic Muscle like K+ H+ Adenosine are responsible to stimulate the Nociceptorsi.e Chest Pain when the muscles contract with interrupted supply of blood. Also the same mediators that cause Coronary Vasodilation are responsible for this Pain.
7. Also may occur due to accumulation of the waste products in the heart muscle and stimulate local nerve endings. The usual discomfort is regarded as a pressure, heaviness, tightness, squeezing, burning or choking sensation. The angina – coronary occlusion occurs which leads to the Anginal attack over a period of time.
9. CORONARY CIRCULATION Most tissues can increase O2 extraction with demand. Heart extracts near maximal amount of O2 at rest. Therefore can increase O2 demand by increasing the Coronary Blood Flow. Various Coronary Arteries of Heart
10. Types Of Angina Pectoris Stable Angina Unstable Angina Variant Angina (Prinzmetal’s Angina) Anginal Equivalent Syndrome Syndrome- X Silent Ischemia
11. STABLE ANGINA Predictable Occurs on exercise, emotion or eating. Caused by increase demand of the heart and by a fixed narrowing of coronary vessels, almost always by atheroma. Coronary obstruction is ‘fixed’ Blood flow fails to increase during increased demand despite the local factors mediated ‘vasodilation’ and so ischeamic pain is felt.
12. So, the diastolic pressure increases and this causes a endocrinal ‘crunch’ and thus causing Ischeamatic pain in this region. Thus, a form of acutely developing and rapidly reversible left ventricular failure results which is relieved by taking rest and reducing the myocardial workload.
13. UNSTABLE ANGINA This is characterized by Pain that occurs with less excertion , cumulating pain at rest. The pathology is similar to that involved in Myocardial Infraction, namely platelet-fibrin thrombus associated with a ruptured atheromatous plaque, but without complete occulation of the vessels. The risk of infraction is subtanial, and the main aim of therapy is to reduce this.
14. VARIANT ANGINA (PRINZMETAL’S ANGINA) Uncommon Occurs at rest generally during sleep Caused by Large Coronary Artery Spasm Usually associated with atheromatous disease Abnormally reactive and hypertrophied segments in the Coronary Artery Drugs aimed at preventing & relieving Coronary Spasm.
15. ANGINAL EQUIVALENT SYNDROME Patient’s with exertionaldyspnea rather than exertional chest pain Caused by exercise induced left ventricular dysfunction
16. ANGINA: SYNDROME X Typical , exertional angina with positive exercise stress test Anatomically normal coronary arteries Reduced capacity of vasodilation in microvasculature Calcium channel blockers and Beta blockers are effective.
17. ANGINA: SILENT ISCHEMIA Very Common More episodes of Silent than Painful angina in the same patient. Difficult to diagnose Gnerally Exercise testing.
18. DIAGNOSIS STRESS (EXERCISE) TEST. ECG (ELECTROCARDIOGRAPHY) CHEST X-RAY CARDIAC ANGIOGRAPHY/ CARDIAC CATHETERIZATION ERGONOVINE TEST BLOOD TEST (BIO-MARKERS)
19. 1. EXERCISE TEST/STRESS TEST Used to measure heart’s response to exercise Patient asked to walk on a treadmill while the physician takes the ECG So any changes in heart function can be determined Alternatively the patient recieves an injection of a radioisotope (generally Thallium) which makes the heart visible to a special-linked camera 90% accurate But doesn’t identify the exactly where and how the coronary arteries are blocked.
20. 2. ELECTROCARDIOGRAM (ECG) Measures electrical activity of the heart Provides info about the changes or damages to the heart muscle Doesn’t detect the narrowing of the coronary arteries During an Anginal attack the ECG may show S-T phase depression. T- phase inversion and/or Ventricular arrythmia ECG- more abnormal with Unstable Angina where the elevation in S-T segment is found.
22. 3. CHEST X-RAY Performed to rule out any lung disease or heart damage that may be causing the pain. Also may reveal enlargement of heart
23. 4. CARDIAC ANGIOGRAPHY/ CARDIAC CATHETERIZATION Shows the precise size and location of blockages within the Coronary arteries A cathereter is inserted through the blood vessels from the forearm or groin It is snaked through arteries till it reaches the heart A fluid is pumped So the arteries and the heart are clearly visible
24. 5. ERGONOVINE TEST Generally done if the person is assumed to suffer from Coronary Spasm Done along with angiography The artery-narrowing drug—Ergonovine or Ach is given to cause Coronary Spasm The persons response to ergonovanine is measured
25. 6. BLOOD TEST/BIOMARKERS Blood test for amount of Lipids within the blood Because lipids major cause of anginal attack Lipid profile for :- 1. HDL 2. LDL 3. TRIGLYCERIDES Recently the newer biomarkers like the C-reactive proteinandB-type natriuretic protein have been found out and the tests for each of them is done These tests are predictive of the moratality of heart disease
26. TREATMENT 3 Classes of drugs used according their mode of action NITRATES - ADRENOCEPTOR ANTAGONISTS CALCIUM CHANNEL ANTAGONISTS ANTIPLATELET DRUGS
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28. Improving Oxygen Demand:Supply Ratio a. Relaxation of resistance vessels (small arteries and arterioles) ↓TPR -> ↓BP -> ↓Afterload (Nitrates, calcium channel blockers and beta-blockers) b. Relaxation of capacitance vessels (veins and venules) ↓Venous return, ↓heart size, ↓Preload (Nitrates and calcium channel blockers) c. Blockade or attenuation of sympathetic influence on the heart ↓Contactility, ↓HR, ↓O2 demand (Beta-blockers) d. Coronary Dilation, Important mechanism for relieving vasospastic angina, ↑O2 supply (Nitrates)
29. NITRATES Prodrugs Sources of Nitric Oxide Eg:- Nitroglycerin, IsosorbideDinitrate Isosorbide-5-Mononitrate Mechanism Of Action
31. Nitrates mainly give Vasoldilation effect The specificity of their action is in dilating the collaterals Unlike other vasodilators (dipyridamole) which dilate only the arteries but not the collaterals
39. -ADRENOCEPTOR ANTAGONOSTS Important in prophylaxis of angina and treating unstable angina Decrease O2 consumption by the heart Effects on coronary vessels-not important Avoided in variant angina As they increase the chances of spasm Eg:- Atenolol Propranolol
43. ANTICOAGULANTS Anticoagulants are often called "blood thinners," although they don't really thin blood. They decrease the blood's ability to clot. Eg Heparin, Dalteparin, Enoxaparin, Warfarin, Aspirin
45. COMBINATION THERAPY Nitrates + -blockers :- in stable angina Ca++ channel blockers + -blockers :-in stable angina when the treatment with nitrates and -blockers has failed. Ca++ channel blockers + Nitrates :- in unstable angina All 3 together:- when the combinations of 2 drugs has failed, where:- Nitrates:- decrease Preload Ca++ channel Blockers:- decrease Afterload -blockers:- decrease heart rate and myocardial contractions
49. NEWER DRUGS RANOLAZINE (Ranexa™; CV Therapeutics, Inc.), a drug that has been in development for 20 years. It is a Sodium Channel Blocker. NICORANDIL, a potassium channel activator, and also has a Nitrogen Donating Moeity. IVABRADINE, inhibits the If channel in the sinus node and thereby causes bradycardia without any negative inotropic effects.
