Drug Therapy Of Ischemic Heart Disease Flashcards
Compare ECG of classic & priznmetal anginal
C, ST depression
P, ST elevation with oaradixical T wave normalization
What is the direct cause of anginal pain?
By accumulation of metabolites in cardiac muscle
The distinguishing feature of unstable angina from MI is
No in serum markers in angina
Describe mechanism of action of nitrates
Nitrates bind to certain receptors on vessel wall, they release nitric oxide which bind with -SH group forming S-nitrosothiol that activates guanyl cyclase inc cGMP, dec IC Ca++, resulting SM relaxation.
Describe pharmacological actions of nitrates
- Relaxation of vascular SM, venodilators (dec preload) & arteriodilators (dec afterload)
- Brief relaxation of other smooth musces (GIT: Sphincter of Oddi & cardiac opening of oesophagus)
Describe mechanism of antianginal effect of nitrates
Dec O2 demand: venodilators & arteriodilators (in high doses) causing dec preload & afterload
Inc O2 supply: VD of large epicardial vessels & collateral & redistribution of blood to ischemic areas by dec VR, dec ventricular filling & dec coronary art compression in subendocardium (by pooling of blood in splanchnic area & extermities
Antiplatelet effect
Mention indications of nitrates
All types of angina
Congestive HF & acute pulmonary edema
Hypertensive emergencies
Acute MI (dec size)
Mention adverse effects of nitrates
- Throbbing headache+ flushing
- Withdrawal angina
- Postural hypotension
- Reflex tachycardia in high dose
- Methemoglobenemia
- Rapid tolerance
GR: Occurrence if throbbing headache with nitrates &ttt
Due to VD of meningeal arteries ttt aspirin
GR: Occurrence if reflex tachycardia with nitrates &ttt
Due to dec BP leads to worse angina ttt BB
GR: Occurrence if rapid tolerance with nitrates &ttt
Due to -SH group depletion & VC caused by activation of adrenegic system by RAAS
Nitrate free interval 8hrs/d
GR: Occurrence if Methemogobinemia with nitrates &ttt
More with nitrites due to oxidation
Methylene blue
Mention contraindications of nitrates
- With sildenafil
- HOCM
- RT vent innfarction
- In volume depletion & severe aortic stenosis (cautiously)
With nitrates a maximum of …. Is taken within …., if no effect ….
3 tablets
15 min
Refer ti hospital
GR: NG & ISDN are not given oral
Extensive 1st pass metabolism
Mention preparations of NG & ISDN & their indications
- Subligual/spray: 1st choice in acute attack & immediate prphylaxis
- Transdermal patch/oral slow release: for CHF & long term prophyalxis
- IV: AHF or unstable angina
What is the difference between ISDN & ISMN
With ISMN
No 2st pass metabolism, high bioavailability, delayed onset & longer action.
Mechanism of antianginal effect of BB
Dec O2 demand: ded HR, BP, lipolysis & fat utilization
Inc O2 supply by inc coronary filling in diatole (by dec HR), Redistribution of coronary blood flow to subendocardial ischemic areas
Antiplatelet activity
All BB are effective except ….
BB with ISA may inc HR
Role of BB in Long term prophylaxis of IHD
Dec frequency & severity of attacks
Control HR at rest
Blunt inc HR & BP during exercise
Describe mechanism of action of CCBs
They act on alpha1 subunit of L-type Ca channel in conductive tissue, cardiac myocytes & vascular SM including coronaries.
Mention a short & a long-acting DHP CCB
S, nifedipine
L, amlodipine
Describe selectivity of DHPs & nonDHPs
DHP, Vessels>myocardium>SAN&AVN
NonDHP, SAN&AVN>myocardium=vessels
Mention vascukar effects of CCBs
Peripheral arteriolar VD, dec PR & ABP
Mora with DHP
Compare cardiac effects of DHP & non DHP
DHP, No effects on nodes, reflex tachycardia (more with short-acting) & mild inhibition of contractility.
Non-DHP, dec SAN & AVN conduction, bradycardia & suppress contractility
Verapamil is more ….. than diltiazem
Cardio-depressant
Mention other actions of CCBs
Relaxation of Git, bronchial, urinary, uterine SM
Inhibit platelet aggregation
Compare adverse effects of DHP & nonDHP
DHP, Reflex tachycardia…worsen angina Hypotenion….flushing & headache Ankle edema,dizziness & tinnitus Non-DHP, Bradycardia & heart block Hypotension, heart failure Constipation (verapamil)
Mention therapeutic uses of CCBs
Angina (of choice in vasospastic) diltiazem & long acting DHP
Hypertension
Supraventricular arrhythmia (verapamil): PSVT & AF & Af
HOCM (Verapamil)
Describe antianginal effect of CCBs
Dec O2 demand by ive ino & chronotropic effect (more with verapamil), dec peripheral resistance (more with DHP)
Inc coronary blood flow due to diltation of epicardial coronary vessels
Mention other uses of CCBs
Peripheral vascular disaese, prevention of premature labour, migraine prophylaxis
Describe mechansim & precautions of trimetazidine
It switches myocardial metabolism from fatty acid oxidation (more O2 demand to glucose oxidation, so dec demand. Given in combination with other antianginal drugs.
Reduce dose by 50% in renal impairment
CI parkiaonism
Describe mechanism, indications & precautions of ivaradine
Selectively inhibits pacemaker I-funny current leading to dec cardiac pacemaker activity & dec HR
Indicated, systolic HF & IHD
CI with CCBs (inhibit their metabolism) used cautiously with BB
Drugs dec atheroscelerosis & MI risk
Antiplatelet
Hypolipedmic agents
Anticoagulants
Management of ACS
Antiplatlet Anticoagulant ACEI Antianginal Statins Fibrinolytics (within 6 hr)
Revascularization and angioplasty may be needed EXCEPT in
Vasospastic angina
Describe mechanism, indications & side effects of ranolazine
Inhibits late phase of Na current, dec Na & Ca overload, improve diasoltic function & improve O2 supply & demand balance
Used in chronic angina
Side effect, prolong QT interval, drug interactions (extensively metabolised by CYP3A4)
