Pharmacology - Angina Treatment PDF
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Summary
This document provides an overview of pharmacological treatments for angina. It discusses the use of beta-blockers, calcium channel blockers, and newer options. The text covers mechanisms of action, combinations, and potential benefits/drawbacks of each.
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There is little evidence to suggest superiority of any particular β-blocker, but β- blockers with ISA should be avoided because the reduction in HR and O2 consumption would be minimal. They are contraindicated in Prinzmetal’s (variant) angina because...
There is little evidence to suggest superiority of any particular β-blocker, but β- blockers with ISA should be avoided because the reduction in HR and O2 consumption would be minimal. They are contraindicated in Prinzmetal’s (variant) angina because they block the β2-mediated coronary dilatation leaving the α1 receptors unopposed → ↑ coronary spasm. Mechanism of β-blockers in exertional angina They ↓ contractility, HR, and systolic BP → ↓ myocardial work and O2 demand. They ↑ diastolic (coronary) filling time. Cause redistribution of blood from normal to ischemic (subendocardial) regions Cytoprotective effect: they produce metabolic switch from myocardial fat utilization to carbohydrates utilization (i.e. improves myocardial metabolism). Combination of BBs and nitrates ↑ their efficiency & ↓ their side effects: β-blockers Nitrates Combination – HR ↓ ↑ (Reflex) ↓ or no effect – Contractility ↓ ↑ (Reflex) ↓ or no effect – Diastolic filling time ↑ ↓ ↑ or no effect – Blood pressure ↓ ↓ ↓↓ Calcium channel blockers (CCBs) They are considered first-line treatment for Prinzmetal’s (variant) angina. They are considered second-line alternative after beta-blockers in chronic stable angina in whom beta-blockers are contraindicated. Short acting dihydropyridines are associated with increased risk of ACS and should be avoided. Long acting dihydropyridines (e.g. amlodipine) and non- dihydropyridines (verapamil and diltiazem) are more preferred. Amlodipine is the CCB of best choice for symptomatic treatment of angina and/or hypertension in patients with chronic heart failure. █ Newer options for treatment of chronic angina pFOX inhibitors, potassium channel openers, and ranolazine are examples of new anti-anginal drugs. These drugs alter the balance between myocardial work and O2 supply by novel mechanism(s) of action. Their efficacy in treatment of angina is controversial; however they are approved for treatment of chronic stable angina in combination with β-blockers, CCBs, and nitrates. 170 pFOX inhibitors (metabolic mod ifiers): Trrimetazidin ne – Theey are teermed pFOX inhi bitors beccause they partially y inhibit fatty acidd oxidatioon in the myocardium m m. – Thiss “metabo olic switch h” from faats to carbbohydrate utilizationn requiress less O2 cconsumptiion. – By inhibition of fatty acid oxid ation, theyy ↓ intra acellular lactic aciidosis leadding to ↓ intracellular Ca2+ & Na+ acccumulation and ion disturbanc d ce, so they y prevent cell necro osis and preserve p conntractile fun nction. – It do oes not afffect HR, blood presssure or corronary bloo od flow. Potass sium cha annel ope eners: Nic corandil – Nico orandil is a new antia anginal dru ug with 2 proposed p mechanism m ms of actio on: It opens ATP-depen A ndent K+ c channels in the vasccular wall leading too VD of peripheral and coron nary arteriees. Nitrate-like e activity: it has a n nitrate com nd ↑ cGMP mponent an P like nitra ates but tolerance tot its effeccts is less m marked. – Likee nitrates, it should not n be used d with sild denafil. Ranola azine – It ↓ intracellular Ca2+ in g the late Na+ curreent that facilitates ndirectly byy reducing Ca22+ entry into myocard dial cells. T Na+ and Ca The reducttion in intrracellular N a2+ load reduces cardiiac contrac ctility and w work. – It do oes not afffect HR, blood presssure or corronary bloo od flow. Antiplatelets and a wering drrugs: see pharmaco cholesterol low ology of blo ood. Choice e of antian nginal drug gs in patie ents with another disease: Angina a with…. Most prreferred Least pre eferred Bronch hial asthma a Nitrates,, CCBs Beta-blocckers Heart fa ailure Amlodip pine Beta-blocckers, Vera apamil Hyperte ension Beta-blo ockers, CC CBs Nitrates Diabete es mellituss Nitrates,, Nifedipine e Beta-blocckers, Vera apamil 171 █ MAN NAGEMENT T OF ACUT TE MYOCAR RDIAL INFA ARCTION (AMI) ( Manife estations: persistentt central crushinng chest pain p + ST segment s elevatio on or depression + patholoogical Q wave + raised biochemical mark kers of my yocardial cell dea ath (tropon nin enzymee). All cases must beb hospita alized in a speciialized coronary care e unit. Non n-pharmacologic th herapy: Patientts presentiing within 12 hours of sympto om onset, the treatmment of ch hoice is percutaaneous co oronary in ntervention n (PCI, or coronarry angiopllasty). A balloon cathete er, guided by x-ray immaging, is introduced d into the occluded o aartery to open it. Pha armacolog gic therap py: Morphine sullfate (5 mg g i.v.): – T To producce analges sia and ↓ stress oof the patient p → ↓ sympa athetic ddischarge and heart work. – Morphine causes ve on → ↓ enodilatatio vvenous retturn and ca ardiac worrk. Oxyygen: receent evidenc ce suggessts that routtine O2 addministration has do oubtful sign nificance an nd did not reduce mo ortality. Nitrroglycerin ne and be ers: to eta-blocke limitt the infarc ct size. Antticoagulan nt drugs: heparin 1 10,000 IU ii.v. then 5000 5 IU/8h h s.c. esppecially whe en the patient is obe ese or if th here is histtory of prevvious MI. Thrrombolytic c (fibrino olytic) the erapy: stre eptokinase, urokinas se, or t-P PA as earlly as possiible (see blood). Sed datives: diazepam 5 mg i.v. Treatment off Complica ations: – C nic shock → dobutam Cardiogen mine i.v.i - Arrhythmia → lido ocaine i.v. 172