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DR. SUBASINI UTHIRAPATHY Angina Pectoris

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Dr. Subasini uthirapathy

Dr. Subasini uthirapathyAngina PectorisAngina PectorisSymptoms of patient with ischemic heart diseaseManifested by sudden, severe, pressing sub-sternal pain that often radiates to the left shoulder, along the flexor surface of the left arm.Usually precipitated by exercise, excitement or a heavy meal2symptoms - patient with anginaCentral chest tightness or heaviness, which may be brought on by exertion or relieved by rest. It may radiate to one or both arms, the neck, jaw or teeth. Other associated symptoms include: dyspnoea (shortness of breath), nausea, sweatiness and faintnessModifiable risk factors hyperlipidaemia smoking hypertension lack of exercise poor diet personality obesity heavy alcohol consumption contraceptive pill stress.Non-modifiable risk factors age gender positive family history diabetes mellitus ethnicity Age Indian origin Sedentary job/possible lack of exercise Smoking Gender men are at increased risk.Types of AnginaClassical Angina (Typical angina) or stable anginaPain is commonly induced by exercise, excitement or a heavy mealSecondary to advanced atherosclerosis of the coronary vessels.Associated with ST segment depression on ECGClassical angina (stable angina)Obstruction is stablePatients symptoms also stableAlways ppted exertional/emotional or walking or exerciseAngina pain starts, patients take rest, - demand will be able to meet oxygen supplySublingual nitrates within 2-3 mts angina will disappearVariant Angina(Prinzmetal angina)Pain is induced while at rest. Associated with ST-segment elevation on ECGSecondary to vasospasm of the coronary vessels.Not related with exertion or tachycardiaPatients taking rest it may produced (vasospasicity)Unstable AnginaMay involve coronary spasm and may also have the component of atherosclerosisThe duration of manifestation is longer than other first two and has the manifestation of MIUnstable anginaUnstable coronary plugAtheromatic plug surface may be platelet aggregation with irregular fibrin deposition or it rupture the outer surface or ulceration thrombus formationIt is produced severe ischemic, deeper sub endothelial myocardium vessel may undergo occlude completely.Lost more than 30 mts undergo MIEtiologyDecreased oxygen supplyIncreased oxygen demandDeterminant of Myocardial oxygen supplyDeterminant of oxygen demand wall stress - Intraventricular pressure - Ventricular volume - Wall thicknessHeart rateContractilityVascular toneTreatment PlanDecrease the risk factor like atherosclerosis, hypertension, smokingIncrease oxygen supplyDecrease oxygen demandAnti-Anginal drugsAgents which decrease o2 demand and increase o2 supplyNitrates GTN and Isosorbide dinitrateCalcium Channel BlockersVerapamil, diltiazem, nifedipine, amlodipine, niodipine etcAgents which decrease o2 demandBeta Blockers Propanolol, metoprolol,atenolol etc.

Nitrates and NitritesClassification Nitrates1. rapidly acting nitrates used to terminate acute attack of anginaEg. Nitroglycerine and Amyl nitrateRoute: sublingually (3-5 mts)2. Long acting Nitrateseg. Erythrytyl tetranitrate Isosorbide dinitrate Penta erythrytyl tetranitrateRoute: orally or topically

MOA (Nitrates)At therapeutic doses the main effect of nitrates is to act on vascular smooth muscle to dilate the veins, thus reducing central venous pressure (preload) and ventricular end-diastolic volume. The overall effect is to lower myocardial contraction, wall stress and oxygen demand, thereby relieving the angina. Nitrates also promote vasodilation of the coronary blood vessels.MOA (Nitrates)Coronary artery dilatation

Relieved coronary vasospasm

Increased coronary blood flow

Increased oxygen supply

MOA ( Nitrates)Reduction of Peripheral resistance

Decrease blood flow

Decrease after load

Decrease work load

Decrease oxygen consumptionMOA(molecular level)Organic nitrates

No

Guanalyl Cyclase

cGMP

cGMP dependent proteinkinase dephosphorylation of MLCK

Intracellular Ca++

Vascular SM relaxationRoute of administrationSublingual route: Rational and effective for the treatment of acute attack of anginaOral route: to provide convenient and prolonged prophylaxis against attack of anginaIV route: useful in the treatment of coronary vasospasm and Ischemic syndromeTopical route: used to provide gradual absorption of the drug for prolonged prophylactic purposeEg. Buccal mucosa 3-6 mts Transdermal 8-10 hrs.

Adverse effectsThrobbing headacheFlushing of the faceDizziness especially at the beginning of treatment (palpitation weakness, fainting)Postural hypotension (due to pooling of blood below portion of the body)Less commonly nausea, vomiting, heartburn, flushing.Methmoglobinemia`Reflex Tachycardia

Clinical IndicationsStable anginaCoronary vasospasmLVF accompanying MIHypertension during cardiac surgery

0.5 mg SL0.4 -0.8 mg SL sprayIV begin with 5mcg/ mintsContraindicationsRenal ischemiaAcute Myocardial infarctionPatients receiving other antihypertensive agentBeta BlockersHemodynamic effects1. decrease Heart rate2. decrease pressure and cardiac contractility3. decrease cardiac outputBeta Blockers (BB)Atenolol (Tenormin)Metoprolol (Lopressor)Propranolol (Inderal)Nadolol (corgard)MOA (Beta blockers)Decrease heart rate & Contractility

Duration of diastole decrease workload coronary blood flow oxygen supply o2 supplyContraindicationsCongestive heart failureAsthma (COPD)Complete heart blockDiabetic mellitusDepressionSide effects1. CVS: bradycardia, hypotension 2 or 3 degree heart block heart failure2. Metabolic: Altered glucose and lipid metabolic3. CNS: dizziness, fatigue, mental depression, lethargy, drowsiness4. Others: Impotence, wheezing, dysponeaReflex Tachycardia- nitrates+BetaB

Calcium Channel BlockersThree types Ca+ channels in smooth muscles Voltage sensitive, receptor operated and leak channelVoltage sensitive are again 3 types L-Type, T-Type and N-TypeNormally, L-Type of channels admit Ca+ and causes depolarization excitation-contraction coupling through phosphorylation of myosin light chain contraction of vascular smooth muscle elevation of BPCCBs block L-Type channel:Smooth Muscle relaxationNegative chronotropic, ionotropic and dromotropic effects in heartDHPs have highest smooth muscle relaxation and vasodilator action followed by verapamil and diltiazemOther actions: DHPs have diuretic action

Classification

Ca++ Channel BlockersCoronary artery dilatationReduction of peripheral resistance ( decrease after load)Commonly used CCBNifedipineVerapamilDiltiazamNicardifineFelodipine

Calcium Channel Blockers (CCB):

Calcium Channel Blockers (CCB):Verapamil, diltiazem, nifedipine, felodipine, amlodipine, nimodipine etc.

MOA: Blocks influx of Ca++ in smooth muscle cells relaxation of SMCs decrease BPUnwanted effectNausea, vomitingDizzynessFlushing of the faceTachycardia due to hypotensionContraindicationsCardiogenic shockRecent MIHeart failureAtrio ventricular blockCombination TherapyNitrates and BB = EDVCCA and BB = BPCCA and Nitrates = preload & afterload afterload Triple drugs therapyNitrates + CCB + BBNitrates - preloadNifedipine afterloadBB - Heart rate & contraictility

Newer group of drugsTrimetazidine (modify myocardial metabolism)RanolazineClinically reduces the frequency of angina attacks in persons with stable angina.Both drugs reduces ischemic symptoms in angina pts by preventing myocardial sodium and calcium overload. The End -Thank you