MECH: COX inhibitor. Inhibits TXA2 synth. which reduces platelet aggregation.

USE: Stable angina (33% red. risk of MI). Unstable or acute MI, reduces vascular mortality (23%), nonfatal reinfarction (49%), nonfatal stroke (46%). Primary prevention (44% red. risk of first MI).

MECH: Inhibits platelet aggregation by ADP. Liquifies blood by decr. plasma firinogen and incr. RBC deformability.

Adverse Effects: Neutropenia. TTP (rarely).

MECH: Selective, irreversable inhibitor of ADP binding to platelet receptors blocking ADP activation of glycoprotein IIb/IIIa complex (which binds to fibrinogen).

USE: Super Aspirin--almost too good of an anticoag. Used in stent patients.

MECH: Irreversable binding to P2Y12 receptor (G coupled receptor for ADP).

USE: Approved in 2009 for ACS patients who have been stented--only for patients <75 y.o., >60kg and no Hx of stroke or TIA. (Fatal bleeding is a big problem--mitigates the positive effects of drug.)

MECH: Incr. platelet cAMP. Inh. uptake of adenosine by RBCs and vasc. endothelium, inh. phosphodiesterase. Incr. coronary artery vasodilation! (vasodilation of coronary arteries can enhance excercise-induced ischemia bc. damaged endothelium will not vasodilate so undamaged endothelial segments will dialate and "steal" blood from damaged.

USE: Used in stress testing.

GENERAL: First ACE-I, 3x day dosage.

MECH: Decr. Angiotensin II effects including, Vasoconstriction, aldosterone induction, vasopressin and sympathetic effects. Incr. Bradykinin by inhibition of Kininase II (Angiotensin II), this promotes vasodilation, tPA and prostoglandin secretion [However Renin blockers also cause increase in Bradykinin so this mechanism is disputed].

AE: Dry cough, hypotension, hyperkalemia (decr. aldo), angioedema--swelling of skin aroung mouth, mucosa of mouth, throat and tongue.

MECH: Decr. Angiotensin II effects including, Vasoconstriction, aldosterone induction, vasopressin and sympathetic effects. Incr. Bradykinin by inhibition of Kininase II (Angiotensin II), this promotes vasodilation, tPA and prostoglandin secretion [However Renin blockers also cause increase in Bradykinin so this mechanism is disputed].

AE: Dry cough, hypotension, hyperkalemia (decr. aldo), angioedema--swelling of skin aroung mouth, mucosa of mouth, throat and tongue.

MECH: Decr. Angiotensin II effects including, Vasoconstriction, aldosterone induction, vasopressin and sympathetic effects. Incr. Bradykinin by inhibition of Kininase II (Angiotensin II), this promotes vasodilation, tPA and prostoglandin secretion [However Renin blockers also cause increase in Bradykinin so this mechanism is disputed].

AE: Dry cough, hypotension, hyperkalemia (decr. aldo), angioedema--swelling of skin aroung mouth, mucosa of mouth, throat and tongue.

MECH: Decr. Angiotensin II effects including, Vasoconstriction, aldosterone induction, vasopressin and sympathetic effects. Incr. Bradykinin by inhibition of Kininase II (Angiotensin II), this promotes vasodilation, tPA and prostoglandin secretion [However Renin blockers also cause increase in Bradykinin so this mechanism is disputed].

AE: Dry cough, hypotension, hyperkalemia (decr. aldo), angioedema--swelling of skin aroung mouth, mucosa of mouth, throat and tongue.

MECH: Decr. Angiotensin II effects including, Vasoconstriction, aldosterone induction, vasopressin and sympathetic effects. Incr. Bradykinin by inhibition of Kininase II (Angiotensin II), this promotes vasodilation, tPA and prostoglandin secretion [However Renin blockers also cause increase in Bradykinin so this mechanism is disputed].

AE: Dry cough, hypotension, hyperkalemia (decr. aldo), angioedema--swelling of skin aroung mouth, mucosa of mouth, throat and tongue.

MECH: Decr. Angiotensin II effects including, Vasoconstriction, aldosterone induction, vasopressin and sympathetic effects. Incr. Bradykinin by inhibition of Kininase II (Angiotensin II), this promotes vasodilation, tPA and prostoglandin secretion [However Renin blockers also cause increase in Bradykinin so this mechanism is disputed].

AE: Dry cough, hypotension, hyperkalemia (decr. aldo), angioedema--swelling of skin aroung mouth, mucosa of mouth, throat and tongue.

MECH: Beta blockade (Beta-1 selective) decr. heart rate and contractility reducing myocardial oxygen demand. Small degree of periph. vasoconstriction due to beta 2 blockade, but not significant. Class II antiarrythmic due to inh. of sympathetic influence on cardiac electrical activity. Also increase action potential duration and effective refractory period.

USE: Prevent MI, angina, ischemia. Increase survival post MI (due to anti-ischemic and anti-arrythmic effects).

CONTRA: Severe bradyc, AV block, sick sinus syndrome (episodes of brady with tachy), unstable LV failure (chronic LV fail is indication). Asthma and bronchospastic disease, severe depression, periph. vasc. dis.

AE: Fatigue, decr. exercise tol., insomnia, worse claudication, impotence.

MECH: Beta blockade (Beta-1 selective) decr. heart rate and contractility reducing myocardial oxygen demand. Small degree of periph. vasoconstriction due to beta 2 blockade, but not significant. Class II antiarrythmic due to inh. of sympathetic influence on cardiac electrical activity. Also increase action potential duration and effective refractory period.

USE: Prevent MI, angina, ischemia. Increase survival post MI (due to anti-ischemic and anti-arrythmic effects).

CONTRA: Severe bradyc, AV block, sick sinus syndrome (episodes of brady with tachy), unstable LV failure (chronic LV fail is indication). Asthma and bronchospastic disease, severe depression, periph. vasc. dis.

AE: Fatigue, decr. exercise tol., insomnia, worse claudication, impotence.

MECH: Beta blockade (Beta-1 selective) decr. heart rate and contractility reducing myocardial oxygen demand. Small degree of periph. vasoconstriction due to beta 2 blockade, but not significant. Class II antiarrythmic due to inh. of sympathetic influence on cardiac electrical activity. Also increase action potential duration and effective refractory period.

USE: Prevent MI, angina, ischemia. Increase survival post MI (due to anti-ischemic and anti-arrythmic effects).

CONTRA: Severe bradyc, AV block, sick sinus syndrome (episodes of brady with tachy), unstable LV failure (chronic LV fail is indication). Asthma and bronchospastic disease, severe depression, periph. vasc. dis.

AE: Fatigue, decr. exercise tol., insomnia, worse claudication, impotence.

MECH: Beta blockade decr. heart rate and contractility reducing myocardial oxygen demand. Small degree of periph. vasoconstriction due to beta 2 blockade, but not significant. Class II antiarrythmic due to inh. of sympathetic influence on cardiac electrical activity. Also increase action potential duration and effective refractory period.

USE: Prevent MI, angina, ischemia. Increase survival post MI (due to anti-ischemic and anti-arrythmic effects).

CONTRA: Severe bradyc, AV block, sick sinus syndrome (episodes of brady with tachy), unstable LV failure (chronic LV fail is indication). Asthma and bronchospastic disease, severe depression, periph. vasc. dis.

AE: Fatigue, decr. exercise tol., insomnia, worse claudication, impotence.

MECH: Beta blockade decr. heart rate and contractility reducing myocardial oxygen demand. Small degree of periph. vasoconstriction due to beta 2 blockade, but not significant. Class II antiarrythmic due to inh. of sympathetic influence on cardiac electrical activity. Also increase action potential duration and effective refractory period.

USE: Prevent MI, angina, ischemia. Increase survival post MI (due to anti-ischemic and anti-arrythmic effects).

CONTRA: Severe bradyc, AV block, sick sinus syndrome (episodes of brady with tachy), unstable LV failure (chronic LV fail is indication). Asthma and bronchospastic disease, severe depression, periph. vasc. dis.

AE: Fatigue, decr. exercise tol., insomnia, worse claudication, impotence.

MECH: Interaction with enzymes and intracellular sulfhydryl groups that reduce nitrate groups to NO. NO activates smooth musc. guanylyl cyclase, incr. cGMP. cGMP inh. Ca entry resulting in sm. muscle relaxation.

DO NOT require healthy endothelium. Incr. O2 to myocardium. Incr. use of collaterals. Incr. venous vasodilation in periphery (reducing preload, work). ALSO, inhibits platelet aggregation, inhibits leukocyte-endothelial interactions (anti-infl.).

USE: As needed due to tolerance.

CONTRA: Conditions that depend on preload: Hypertrophic cardiomyopathy, aortic stenosis, hypotension, USE OF PHOSPHODIESTERASE INHIBITORS (VIAGRA) WHICH INCR. cGMP EVEN MORE!

AE: Headache, hypotension, Bezold-Jarisch reflex causing brady (hypotension in extremities causes baroreceptor symp. increase in HR and Contr., but ventricular stretch receptors counteract due to decr. volume causing acute hypotension.

MECH: (Dihydropyridine) Vasoselective reduction of transmembrane influx of Ca via L-type voltage-gated calcium channels in coronary arteries thus reducing tension in sm. muscle. Also Nifedipine has some neg. inotrope action.

USE: HTN.

CONTRA: Decompensated HF.

AE: Hypotension, worsening heart failure, peripheral edema, constipation, headache, flushing, AV block.

MECH: (Dihydropyridine-2ng gen.) Vasoselective reduction of transmembrane influx of Ca via L-type voltage-gated calcium channels in coronary arteries thus reducing tension in sm. muscle.

USE: HTN.

CONTRA: Decompensated HF.

AE: Hypotension, worsening heart failure, peripheral edema, constipation, headache, flushing, AV block.

MECH: (Dihydropyridine-2ng gen.) Vasoselective reduction of transmembrane influx of Ca via L-type voltage-gated calcium channels in coronary arteries thus reducing tension in sm. muscle.

USE: HTN.

CONTRA: Decompensated HF.

AE: Hypotension, worsening heart failure, peripheral edema, constipation, headache, flushing, AV block.

MECH: (Dihydropyridine-2ng gen.) Vasoselective reduction of transmembrane influx of Ca via L-type voltage-gated calcium channels in coronary arteries thus reducing tension in sm. muscle.

USE: HTN.

CONTRA: Decompensated HF.

AE: Hypotension, worsening heart failure, peripheral edema, constipation, headache, flushing, AV block.

MECH: (Non-dihydropyridine) Vasoselective reduction of transmembrane influx of Ca via L-type voltage-gated calcium channels in coronary arteries thus reducing tension in sm. muscle. ALSO, negative inotropes and chronotropes--slow sinus rate and AV node conduction.

USE: HTN.

CONTRA: Decompensated HF, bradycardia, sinus node dysfunction, AV block.

AE: Hypotension, worsening heart failure, peripheral edema, constipation, headache, flushing, AV block.

MECH: (Non-dihydropyridine) Vasoselective reduction of transmembrane influx of Ca via L-type voltage-gated calcium channels in coronary arteries thus reducing tension in sm. muscle. ALSO, negative inotropes and chronotropes--slow sinus rate and AV node conduction.

USE: HTN.

CONTRA: Decompensated HF, bradycardia, sinus node dysfunction, AV block.

AE: Hypotension, worsening heart failure, peripheral edema, constipation, headache, flushing, AV block.

MECH: Decr. perfusion causes incr. extracellular [K]. Less negative depolarization, shorter action potential duration. More negative in phase 2 and 3. Sets up gradient betw. ischemic and normal cells. Systolic current of injury from normal to ischemic cells, AKA positive current in systole flows from normal cells to ischemic cells. On a curved surface, transmural ischemia will sum in a positive vector directed outward from endo to epicardium toward electrode lead and positive ST segment deflection.

THERAPY: Primary goal: open artery as quickly as possible--catheterization within 90 mins. (Fibrinolytics considered when angioplasty not available.) 1) Give oxygen. 2) Nitrates (except in pts. with sub 90 BP). 3) Analgesia (morphine) reduces catecholamine surge. 4) Aspirin--antithrombotic effect, 162 mg RRR of 23% in one month. 5) Beta blockers--decr. myocardial O2 demand, decr. size of infarct, decr. rate of reinfarction, decr. ventricular arrythmias (CONTRA: cocaine associated MI; bradycardia, <100 BP; LV dysfunction, AV block, active asthma). 6) Thrombolytics: Who gets?: Pts. with STEMI with <12hr. symptoms, ST elev. of >0.1mV in 2 contiguous leads or two adjacent limb leads OR new LBBB. Myriad contraindications mostly associated with bleeding risk. 7) ACE-I--within 24hrs, ant. wall MI, pulm. congestion or LVEF <40%. 8) Heparin--Adjunct of thrombolytics (SE: Bleeding, HIT). Requires frequent monitoring, many interactions. (DABIGATRAN is non-inferior, direct thrombin inhibitor).

MECH: Direct thrombin inhibitor. Not influenced by diet. Non-inferior to Warfarin. Fewer drug interactions. Does not require constant monitoring.

AE: Dyspepsia.