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ANGINA PECTORIS
By:- PARTH SHAH M.Pharm(Pharmacology)
ANGINA PECTORISA Chronic disease of CVS
Occurs with Interminent chest pain spread along the Chest, Shoulders and Arms.
•Angina pectoris, or angina, as it is commonly referred to, and coronary artery disease or arteriosclerosis are closely related.
•Angina occurs in people who have some form of blockage in the coronary arteries. In other words, it occurs in people with coronary heart disease.
•Angina pectoris: a heart condition marked by paroxysms of chest pain due to reduced oxygen to the heart
• It occurs when the Oxygen Supply to the Myocardium is insufficient for its needs.
Factors affecting Oxygen Demand Supply Ratio
Various Chemical Factors released from Ischeamic Muscle like
1. K+2. H+3. Adenosine are responsible to stimulate the
Nociceptors i.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.
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.
ANGINA-CORONARY OCCLUSION
CORONARY OCCLUSION
CORONARY CIRCULATIONMost 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
Types Of Angina Pectoris1. Stable Angina
2. Unstable Angina
3. Variant Angina (Prinzmetal’s
Angina)
4. Anginal Equivalent Syndrome
5. Syndrome- X
6. Silent Ischemia
STABLE ANGINAPredictableOccurs 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.
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.
UNSTABLE ANGINAThis 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.
VARIANT ANGINA (PRINZMETAL’S ANGINA)UncommonOccurs at rest generally during sleepCaused by Large Coronary Artery SpasmUsually associated with atheromatous
diseaseAbnormally reactive and
hypertrophied segments in the Coronary Artery
Drugs aimed at preventing & relieving Coronary Spasm.
ANGINAL EQUIVALENT SYNDROMEPatient’s with exertional dyspnea rather
than exertional chest pain
Caused by exercise induced left ventricular dysfunction
ANGINA: SYNDROME XTypical , exertional angina with positive
exercise stress testAnatomically normal coronary arteriesReduced capacity of vasodilation in
microvasculatureCalcium channel blockers and Beta blockers
are effective.
ANGINA: SILENT ISCHEMIAVery Common
More episodes of Silent than Painful angina
in the same patient.
Difficult to diagnose
Gnerally Exercise testing.
DIAGNOSIS1. STRESS (EXERCISE) TEST.2. ECG (ELECTROCARDIOGRAPHY)3. CHEST X-RAY4. CARDIAC ANGIOGRAPHY/ CARDIAC
CATHETERIZATION5. ERGONOVINE TEST6. BLOOD TEST (BIO-MARKERS)
1. EXERCISE TEST/STRESS TESTUsed to measure heart’s response to exercisePatient asked to walk on a treadmill while the
physician takes the ECG So any changes in heart function can be
determinedAlternatively the patient recieves an injection
of a radioisotope (generally Thallium) which makes the heart visible to a special-linked camera
90% accurateBut doesn’t identify the exactly where and
how the coronary arteries are blocked.
2. ELECTROCARDIOGRAM (ECG)Measures electrical activity of the heartProvides info about the changes or damages
to the heart muscleDoesn’t detect the narrowing of the coronary
arteriesDuring an Anginal attack the ECG may show 1. S-T phase depression.2. T- phase inversion and/or3. Ventricular arrythmia ECG- more abnormal with Unstable Angina
where the elevation in S-T segment is found.
STABLE ANGINA
At Rest
After Excercise
3. CHEST X-RAYPerformed to rule out any lung disease or
heart damage that may be causing the pain.Also may reveal enlargement of heart
4. CARDIAC ANGIOGRAPHY/ CARDIAC CATHETERIZATIONShows the precise size and location of
blockages within the Coronary arteriesA cathereter is inserted through the blood
vessels from the forearm or groinIt is snaked through arteries till it reaches
the heartA fluid is pumpedSo the arteries and the heart are clearly
visible
5. ERGONOVINE TESTGenerally done if the person is assumed to
suffer from Coronary SpasmDone along with angiographyThe artery-narrowing drug—Ergonovine or
Ach is given to cause Coronary SpasmThe persons response to ergonovanine is
measured
6. BLOOD TEST/BIOMARKERSBlood test for amount of Lipids within the
bloodBecause lipids major cause of anginal attackLipid profile for :- 1. HDL 2. LDL 3.
TRIGLYCERIDES Recently the newer biomarkers like the C-
reactive protein and B-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
TREATMENT3 Classes of drugs used according their mode
of action
1. NITRATES2. - ADRENOCEPTOR ANTAGONISTS3. CALCIUM CHANNEL ANTAGONISTS4. ANTIPLATELET DRUGS
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)
NITRATESProdrugsSources of Nitric OxideEg:- Nitroglycerin, Isosorbide Dinitrate Isosorbide-5-Mononitrate
Mechanism Of Action
PHARMACO-LOGICAL ACTIONS OF NITRATES
Nitrates mainly give Vasoldilation effectThe specificity of their action is in dilating the
collateralsUnlike other vasodilators (dipyridamole) which
dilate only the arteries but not the collaterals
TOXICITY OF NITRATESHeadacheIncreased mortalityRecurrence of Myocardial InfractionDizzinessFlushingRapid heart beatRestlessnessDry mouthSkin rashNausea
MARKETED FORMULATIONSGTN Sorbitrate (PIRAMAL)Vasovin (TORRENT)
ISMO retard (PIRAMAL)Angicor (NOVARTIS)
Nitroglyceride
Isosorbide-5-monophosphate
CALCIUM CHANNEL ANTAGONISTSDisrupt Ca++ through Ca++ channels-ve ionotrpic effect2 types:-1. Dihydropyridine (amlodipine, nifedipine,
nicardipine)2. Non-Dihydropyridine
1. Phenylalkylamine (verapamil, gallopamil)2. Benzodiazapenes (diltiazem)3. Non-selective (bepridil, mibefradil)
MECHANISM OF ACTION
Pharmacological Actions
TOXIC EFFECTS
MARKETED PREPARATIONSCalaptin (PIRAMAL)Vasopten (TORRENT)Coriem XL (RANBAXY)Dicard (INTAS)Amtas (INTAS)Cadeut (PFIZER)
Verapamil
Diltiazem
Amplodipine
-ADRENOCEPTOR ANTAGONOSTSImportant in prophylaxis of angina and
treating unstable anginaDecrease O2 consumption by the heartEffects on coronary vessels-not importantAvoided in variant anginaAs they increase the chances of spasmEg:-
Atenolol Propranolol
PHARMACOLOGICAL ACTIONS
MECHANISM OF ACTION
MARKETED PREPARATIONSBetacard ( TORRENT)
Aten (ZYDUS CADILA)
Betacap (SUN PHARMA)
Cardilax (INTAS)
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
COMPARITIVE TOXIC EFFECTS
COMBINATION THERAPY1. Nitrates + -blockers :- in stable angina2. Ca++ channel blockers + -blockers :-in
stable angina when the treatment with nitrates and -blockers has failed.
3. Ca++ channel blockers + Nitrates :- in unstable angina
4. All 3 together:- when the combinations of 2 drugs has failed, where:-
1. Nitrates:- decrease Preload2. Ca++ channel Blockers:- decrease Afterload3. -blockers:- decrease heart rate and
myocardial contractions
Recommended Drug therapy for Angina with other medications
NEWER DRUGSRANOLAZINE (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.
THANK YOU!!!!