Angina pectoris

DEFINITION,ETIOLOGY, EPEDIMIOLOGY,RISK FACTORS,PATHOGENESIS, PHARMACOLOGICAL & NON-PHARMACOLOGICAL TREATMENT.

1. ANGINA PECTORIS BY HEENA PARVEEN

2. ANGINA PECTORIS ANGINA—Classical symptom of MI. It refers to severe pain in the chest esp. during exercise/effort due to MI. The pain may radiate to the neck, left arm, Back throat, Jaw . Angina Pectoris  was first brought to the notice of the medical profession by William Heberden in 1772.

3. ETIOLOGY Coronary artery spasm Atherosclerosis Cocaine use Blockage of Coronary artery by blood clot/ Compression Inflammation /Infection of coronary artery Poor functioning of tiny blood vessels.

4. RISK FACTORS

5. SIGNS & SYMPTOMS

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7. INVESTIGATIONS CHEST X-RAY. COMPLETE BLOOD COUNT. SERUM CHOLESTEROL & LIPID PROFILE. STABLE ANGINA: Rest & E xcercise ecg . Myocardial perfusion scanning. Stress echocardiography. Coronary arteriography . Angiography ---Reveals which coronary artery is affected.

8. Types of Angina Pectoris Type Definition Pattern EKG Causes Stable/Classical Angina/ Exertional Angina/Angina of Effort Occurs as a result of Increased myocardial oxygen demand in atherosclerotic narrowing of coronary arteries. Excessive stress, Emotion, Excessive physical exertion. Depressed ST-segment during attack. Predictable. >70% lumen narrowing by uncomplicated as Plaque . Unstable Angina /Uncommon/ Atypical/Crescendo/Pre-infarction Angina. It is type wherein recurrent attacks occurs even when the person is at rest. Progressive atherosclerotic narrowing of arteries. Transient ST-elevation during Angina. -ST depression T-wave changes Uncomplicated As a plaque is with a Coronary spasm. Variant Angina/ Prinzmetal’s Angina/ Vasospastic Angina,. More common in Women. Vasospasm of coronary arteries which occurs due to release of humoral vasoconstrictory agents by mast cells in coronary adventitia. Charactersied by pain at rest & has no relationship with Physical activity. May lead to death due to severe MI/Acute arrhthmias . Elevated ST-segment during attack. As plaque destabilisation : Rupture, Haemorrhage , Thrombosis.

9. ECG CANGES IN ANGINA PECTORIS

10. PATHOPHYSIOLOGY

11. NON-PHARMACOLOGICAL TREATMENT   TENS (Trans- cutaeneous electrical nerve stimulation) S pinal cord stimulation, M usic   therapy , R elaxation

12. PHARMACOLOGICAL TREATMENT 1)Nitrate compounds : Short acting-- Trinitoglycerine , Amylnitrate Long acting— Isosorbide mononitrate , Isosorbide dinitrate , Pentaerythritol tetranitrate . 2)Beta-blockers : Propanolol , Atenolol , Nodolol,Bisoprolol . 3)Ca+2 channel blockers : Verapamil,Diltiazem,Nifedipine . 4)K+ channel activators : Nicorandil 5)Anti-platelets : Aspirin, Dypiridamole . 6) Cytoprotectives : Ranolazine , Oxyphedrine , Trimetazidine .

13. K + channel activators : Nicorandil These drugs cause the opening of the K+ channels resulting in rapid outflow of K+ ions --- Hyperpolarisation & increasing the negativity in the cell -----Smooth muscle relaxation. K+channels are of –Voltage sensitive K+ channels. ATP sensitive K+ channels.( Nicorandil ) Ca+2 Activated K + channels. Na+2 Activated K+ channels . Nicorandil activates Guanylyl cyclase to enhance the production of cGMP in epcardial coronary arteries— Vasodilation leading to improved coronary blood flow , without causing significant effect on cardiac contractility, Conduction , Heart rate , Blood flow, BP .

14. P/K Adverse effects Contraindicated Uses ORAL Bioavailability—75-80%. 25% Plasma protein bound. Raoid first pass metabolism. Elimination half life—1 hr. Facial flushing, Palpitations, Headache, Diarrhoea , Weakness, N&V, Mouth ulcers. Cardiogenic shock, Low BP, Hypovolemia Angina, Hypertension, Alopecia, Bronchia Asthma, Premature labour , CHF, MI.

15. TH9 Q