Drugs used in cardiovascular diseases
MOA
Example & MOA cellular Therapeutic
Drug Group Physiologica
kinetics Biochemical
l
Beta Blocker propranolol Blocks the effect of NA
Short half life, and Adr on beta - and
Non-Selective beta-2 receptors, pure
needs to be taken
3-4 times a day antagonist, in heart,
lungs, blood vessels
and liver, JG cells. Also
blocks beta cells in
brain
Beta Blocker atenolol Blocks the effect of NA
bisoprolol and Adr on beta-1
Cardioselective
Long half life, able to receptors, pure
be taken 1-2 a day antagonist. Also blocks
beta cells in brain and
release of renin from
JG cells
1
Adverse
uses effects & CI
Blocks conduction SNS and somatic Diabetes, heart
through AV node anxiety tachycardia block, heart failure,
Blocks conduction in primarily on HR and COPD, asthma, PVD
SA node SV) Angina pectoris
Decreases (decreases O2
contractility consumption)
Decrease O2 Supraventricular
demand by heart arrhythmia (block NA
and slow AV
conduction)
Blocks conduction Hypertension Type I diabetes,
through AV node (primarily on HR and heart block, COPD,
Blocks conduction in SV, renin) asthma, PVD, even
SA node Angina pectoris though theoretically
Decreases (decreases O2 safe
contractility consumption)
Decrease O2 Supraventricular
demand by heart. arrhythmia (block NA
Looses beta 1 and slow AV
selectivity at higher conduction). Bisoprolol
does and so start has good outcomes in
blocking beta 2 reducing mortality in
receptors heart failure patients
 MOA
Example & MOA cellular Therapeutic Adverse
Drug Group Physiologica
kinetics Biochemical uses effects & CI
l
Calcium verapamil Blocks the entry of Blocks conduction Hypertension SA or AV nodal
calcium into the through AV node (primarily on vascular problems
Channel diltiazem
vascular smooth Blocks conduction in resistance) Headache, ankle
short acting but
Blockers - used as a slow muscle cells arterioles SA node Angina pectoris oedema (not true
Cardiac And release formulation, and the myocardium. Decreases (decreases O2 oedema,
Vascular liver metabolism contractility consumption) vasodilatation)
Decrease O2 Supraventricular
demand by heart arrhythmia (block NA
Decreases TPR and slow AV
conduction)

Calcium nifedipine (short Blocks the entry of Potent peripheral Hypertension Headache, ankle
Channel acting used only as calcium into the vasodilator (primarily on vascular oedema (not true
a slow release vascular smooth Can cause an resistance) oedema,
Blockers- formulation) muscle cells and increase heart rate Angina pectoris vasodilatation,
Vascular Selective amlodipine (long decreases TPR. Causes (decreases O2 cannot be
Dihydropyridines VSM relaxation. consumption) by mobilised). Slight
acting only needs to
decreasing afterload tachycardia
be used once daily)

Organic Nitrates glyceryl trinitrate Increases cGMP levels Decreases in wall Angina pectoris Headache, tolerance
short acting by nitric oxide effect. stress decrease O2 (decreases O2 to effect
Short Acting Mainly acts to demand and angina consumption) by Hypotension,
Cannot be taken
orally, bioavailability increases venous is relieved. Also decreasing preload and tachycardia
< 5%. Taken SL. capacitance. More shunts blood to after load (less effect Do not use with
High first pass, not blood is stored, less ischaemic areas of Used to abort exercise sildenafil!!
given orally blood returns to heart, heart. Causes induced angina
EDP drops, wall stress vasodilatation, Drop
decreases in TPR, increases HR

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 MOA
Example & MOA cellular Therapeutic Adverse
Drug Group Physiologica
kinetics Biochemical uses effects & CI
l
Organic Nitrates Isosorbide Nitric oxide donor Decreases in wall Angina pectoris Headache, tolerance
long- increases cGMP stress decrease O2 (decreases O2 to effect
(Long Acting) mononitrate
through guanylate demand and angina consumption) by Hypotension,
acting taken orally,
bioavailability = cyclase. Mainly acts to is relieved. Also decreasing preload and tachycardia
100%. No first pass increases venous shunts blood to after load (less effect). Do not use with
capacitance. More ischaemic areas of Used as long term sildenafil!!
blood is stored, less heart. Causes prophylactic
blood returns to heart, vasodilatation, Drop Used with hydralazine
EDP drops, wall stress in TPR, increases HR in heart failure in
decreases patients with CI to
ACE/ARB

ACE Inhibitors captopril Blocks the conversion Decreases total Hypertension Dry cough
Short half life, of AI to active AII. AII peripheral (primarily on TPR (bradykinin)
needs to be taken normally is a resistance and Heart failure by Angioedema, rash.
2-3 times a day vasoconstrictor and reduce the amount decreasing after load CI in severe renal
release aldosterone of Na and water and pre load failure and
lisinopril /
reabsorbed in the Heart failure as above, pregnancy
ramipril (long kidney. Increases improves survival and hyperkalaemia
acting only needs to bradykinin, which is QoL. Ramipril in high especially with K
be used once daily vasodilator and risk patients sparing diuretics
irritant

Angiotensin valsartan Blocks the binding of Decreases total Hypertension Rash. CI in severe
AII to its AT1 receptor, peripheral (primarily on TPR renal failure and
Receptor losartan
competitive resistance and Heart failure by pregnancy. Side
long acting only
Blockers (ARB) needs to be used antagonist / AII reduces the amount decreasing after load effect similar
once daily normally is a of Na and water and pre load placebo. ACE without
vasoconstrictor and reabsorbed in the Heart failure as above, the cough
releases aldosterone kidney. Does not improves survival and Hyperkalaemia with
produce bradykinin QoL K sparing diuretics

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 MOA
Example & MOA cellular Therapeutic
Drug Group Physiologica
kinetics Biochemical
l
Beta Blocker carvedilol Blocks conduction
through AV node
Non Selective and needs to be built up
slowly to prevent Blocks conduction in
Alpha Blocker SA node
heart failure
Decreases contractility
Decrease O2 demand
by heart. Block action
of NA on VSM
Alpha-1 doxazosin Blocks the binding of
only needs to be noradrenaline to the
Receptor arteriolar VSM alpha 1
used once daily
Blockers adrenergic receptor,
competitive antagonist.
Blocks the increase in
intracellular IP3 and Ca
Alpha-2 alpha methyldopa An alpha 2 presynaptic Decreases total
Needs to be taken agonist, Blocks the
Receptor release of
twice daily. Liver
Agonist metabolism noradrenaline in the
vasomotor centre, SNS
activity falls.
Decreases release of
noradrenaline in the
vasomotor centre, SNS
activity decreases
4
Adverse
uses effects & CI
Blocks the effect of Hypertension but Diabetes, heart
NA and Adr on mainly in heart failure, block, heart failure,
beta1 and beta 2 stops catecholamine COPD, asthma, PVD
and alpha 1 SNS induced
receptors, pure remodelling
antagonist, in heart, Lowers heart rate,
lungs, blood vessels decreases diastolic
and liver, JG cells. filling time, allows
more coronary blood
flow, anti ischaemic
Decreases total Hypertension Depression.
peripheral (primarily on TPR Tiredness (blockade
resistance, but also Only as third line drug. of alpha 1 receptors
causes first dose Also useful in patients in brain). Orthostatic
hypotension and with benign prostatic hypotension
orthostatic hypertrophy (BPH)
hypotension (blocks
reflex increase SNS
after postural
changes)
Hypertension Depression.
peripheral (primarily on TPR via Tiredness (reduction
resistance, but also reduction of central of noradrenaline in
causes first dose SNS. Used for brain). Orthostatic
hypotension and hypertension hypotension
orthostatic associated with
hypotension (blocks pregnancy
reflex increase SNS
after postural
changes)
 MOA
Example & MOA cellular Therapeutic
Drug Group Physiologica
kinetics Biochemical
l
Cardiac digoxin Increases the entry of
taken once daily, calcium into the
Glycosides myocardium by
excreted in the
kidney and inhibiting the
metabolised in liver membrane Na/K
ATPase pump. The
increase in intracellular
Na less Ca being
expelled from the cell.
Increases activity of
vagal nerve to SA/AV
node and increases
sensitivity of SA and
AV node to
acetylcholine
Loop Diuretics furosemide Blocks the Na/K/Cl co
transporter in the
ascending limb of loop
of Henle. Also causes
calcium loss and
magnesium excretion
Thiazide hydro- Blocks the Na/Cl
reabsorption in the
Diuretics chlorothiazide
distal convoluted
indapamide tubule. Also reabsorbs
calcium and increases
potassium excretion.
Increases serum uric
acid by competing with
uric acid for secretion
in proximal convoluted
tubule
5
Adverse
uses effects & CI
Blocks conduction Heart failure (primarily SA or AV nodal
through AV node with atrial fibrillation) problems
and decreases SA Supraventricular Headache,
node firing, heart arrhythmia, slow AV confusion, visual
rate decreases. conduction. Used with disturbances. Narrow
Contractility and SV verapamil or diltiazem therapeutic index
increase marginally. Caution in
O2 demand by heart hypokalaemia, effects
Increases potentiated
Is a high ceiling Used in heart failure to Hypokalaemia,
diuretic with a large mobilise oedema, hyperuricaemia
dose response. prevent pulmonary Volume depletion
Given IV or oral congestion. Also used hyponatraemia
for hypercalcaemia
Is a low ceiling Used in mild heart Hypokalaemia,
diuretic with a low failure to mobilise hyperuricaemia.
dose response. In oedema, prevent Decrease release of
hypertension causes congestion. Also used insulin and increases
a drop in TPR after for diabetes insipidus. blood glucose.
2-3 weeks. Often Main use is for Sulphur drug
added to ACE and hypertension, Used
Bblockers to with loop diuretics in
augment heart failure
antihypertensive
effect
 MOA
Example & MOA cellular Therapeutic Adverse
Drug Group Physiologica
kinetics Biochemical uses effects & CI
l
Aldosterone spirinolactone Structurally similar to Is a very low ceiling Used with HCTZ in Hyperkalaemia,
aldosterone. Blocks diuretic. Is seldom hypertension. Also gynaecomastia,
Antagonists the aldosterone used as a diuretic used in heart failure inhibits testosterone
induces Na/ K alone but not in with ACE inhibitors to synthesise
exchange in the hypertension prevent aldosterone
collecting duct. Also escape. Major impact
causes loss of H ions on mortality in heart
failure

Potassium amiloride Blocks the Na/ K Is a very low ceiling Used with HCTZ in Hyperkalaemia, not
exchange in the diuretic and is hypertension. to be given with ACE
Sparing triamterene
collecting duct. Also seldom used as a inhibitors
Diuretics causes loss of H ions diuretic alone. Only Alkalosis
used in combination
with HCTZ to
prevent K loss in
hypertension

Fibrates bezafibrate Reduces the synthesis
gemfibrozil of VLDL and increases
synthesis of HDL. Also
stimulates the activity
of lipoprotein lipase
which increases
adipose tissue
deposition of FFA and
lipids, thus serum trigs
drop.
Primarily reduces Only used as add or if Well tolerated,
triglycerides but there is very high trigs mylagia can occur,
also reduced LDL. or/and very low HDL, and life-threatening
HDL increases by rhabdomyolysis can
10-15%. More cause renal failure
effective than stains and death if
in increasing HDL. combined with
Little effect on LDL statin. Also
sometimes cause
increase in liver
enzymes

6
 MOA
Example & MOA cellular Therapeutic Adverse
Drug Group Physiologica
kinetics Biochemical uses effects & CI
l
HMG Co A simvastatin Inhibits HMG Co A Primarily lowers The most effective Well tolerated,
reductase in the liver, total cholesterol and drugs in lowering LDL. mylagia can occur,
Reductase atorvastatin
the rate-limiting LDL. Triglycerides The percentage and life-threatening
Inhibitors rosuvastatin
enzyme for production also reduced but not decrease in LDL is rhabdomyolysis can
of cholesterol. The as much as LDL. roughly associated cause renal failure
reduction in cholesterol HDL remains with a similar drop in and death (rare).
induces an increase in unchanged CVD events (stroke, Also sometimes
synthesis of liver LDL CAD, MI and mortality) cause transient
receptors and Atorvastatin 10 = increase in liver
cholesterol levels drop simvastatin 20 = 31% enzymes
drop in LDL

GIT Cholesterol ezetemibe absorbed, blocks
cholesterol in the gut
Inhibitors (high proportion of
cholesterol) The
reduction in liver
cholesterol induces an
increase in synthesis of
liver LDL receptors and
LDL cholesterol levels
drop
Primarily lowers Only used as add on to well tolerated,
total cholesterol and reduce LDL in familial
LDL. Triglycerides hyper-
reduced but not as cholesterolaemia.
much as LDL. HDL Percentage decrease in
remains unchanged. LDL is about 20%

GP IIb/IIIa eptifibatide Blocks the binding of Used only as Injectable Bleeding, restenosis
fibrin to GP IIb/IIIa. drugs for the ACS,
inhibitors tirofiban
Inhibits the activation prior to stenting and
of platelets CABG

7
 MOA
Example & MOA cellular Therapeutic
Drug Group Physiologica
kinetics Biochemical
l
COX I aspirin Blocks the activity of
Used in low dose as cyclo-oxygenase in all
Platelet tissues, but because
a once daily dose
Inhibitors platelets only produce
TXA2, this effects most
platelets. Aspirin is the
only COX inhibitor to
irreversible bind to and
inhibit platelet cyclo-
oxygenase.
ADP Inhibitors prasugrel; Blocks the action of
clopidogrel ADP on ADP receptors
and therefore inhibits
Ticagrelor
platelets aggregation
Heparin enoxaparin Accelerates the action
heparin of antithrombin III by
a thousand fold. Blocks
the active factors IIa
(thrombin) that
converts soluble
fibrinogen to fibrin.
Also blocks the activity
of Xa. Also XII, XI, IX
8
Adverse
uses effects & CI
Because platelets Used to prevent GIT most common.
cannot regenerate platelet aggregation in Reflux, asthma,
new COX, the TIA, MI, stroke, PVD, renal, Perforation,
production of TXA2 colon cancer ulcers and bleeds
is inhibited at these rare but fatal
doses prostacyclin is
not affected
Used in addition to bleeding
aspirin to prevent
stroke. CVD and PVD
Difference between Used before the action Bleeding is the major
HMW and LMW are oral anticoagulants problem, can cause
that LMW less work osteoporosis
activity on Used for DVT,
thrombin, and more prophylaxis for hip
selective on Xa. surgery and in high
Immediate onset of risk patients
action. Antagonised
by protamine
 MOA
Example & MOA cellular Therapeutic Adverse
Drug Group Physiologica
kinetics Biochemical uses effects & CI
l
Oral warfarin Blocks the liver Onset of action Used for long term Strictly CI in
High protein metabolism of factor about three days. prophylaxis of DVT, pregnancy. High risk
Anticoagulant II, VII, IX, X. Inhibits Depends on serum atrial fibrillation, of foetal
binding,
metabolised in liver the activity of vitamin half life of clotting pulmonary embolism, abnormalities.
K epoxide reductase factors. Only liver prevents CAD long Bleeding is major
which converts vitamin production is term in conjunctions side effect, but
K to its active form. impacted by with aspirin?. Also in dermatitis can occur.
Also inhibits protein C warfarin. Many drug patients with history of
which increases risk of interaction liver DVT and traumatic
thrombosis early in metabolism and DVT, and
treatment high protein immobilization
binding. Monitor
prothrombin time.
Also INR increased
by double.

Oral dabigatran Direct factor IIa, Xa Not necessary to Used for long term Bleeding is major
inhibitor First oral monitor prophylaxis of side effect, Early
Anticoagulant rivaroxaban
anticoagulant prothrombin time or reducing clotting with outcome data
o INR atrial fibrillation, Still suggests caution in
being tested in prosthetic valves,
pulmonary embolism may increase risk
(PE) in patients with fatal bleeds
history of DVT

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 MOA
Example & MOA cellular Therapeutic Adverse
Drug Group Physiologica
kinetics Biochemical uses effects & CI
l
Fibrinolytics streptokinase Converts inactive Only attacks Used for the treatment Bleeding, especially
tissue plasminogen to established clots of pulmonary haemorrhagic
plasmin, which breaks and no effect on embolism and STEMI . stroke.
plasminogen
down fibrin to fibrin new clot formation. Streptokinase e can
activator (t-PA) degradation products. Injected. induce antibodies,
alteplase cause allergy and
inactivate after initial
use. Do not use in
unstable angina,
may convert non-
STEMI to full
infarction

Parasympatholy atropine Generally decrease Blocks post stop vagal induced Dry mouth,
salivation, mydriasis, ganglionic effects and decrease tachycardia,
tics hyoscine
decreases peristalsis, muscarinic salivation in surgery constipation, urine
prevent bladder receptors. hyoscine – irritable retention
voiding, increase heart decreases IP3 bowel syndrome Blurred vision,
rate, bronchodilation, mydriasis, glaucoma
decrease salivary gland
secretion, increase
bladder sphincter tone

Alpha 1 adrenaline Increase conduction Mimics the effect of increase CO and HR Tremor anxiety,
only used IV through AV node and NA and Adr on Both used in arrhythmia, heart
Beta 1/2 conduction in SA node beta-1 in heart and cardiogenic shock, failure
Agonists Increases contractility JG cells. anaphylaxis
Increase O2 demand
by heart.
direct alpha 1 effects
stimulate beta 2
receptors

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 MOA
Example & MOA cellular Therapeutic Adverse
Drug Group Physiologica
kinetics Biochemical uses effects & CI
l
Beta 2 Agonist salbutamol Stimulate beta 2 Mimics the effect of Increase airway Tremor anxiety,
receptors in the Adr on beta-2 in diameter, used in arrhythmia,
MDI, tabs,
bronchioles. Increases lungs and skeletal asthma and COPD. tachycardia, mainly
syrup cAMP muscle, and liver. Also prevents at high doses
IV Also inhibits uterine premature labour in through beta-1
contractions pre term women. cardiac effects

Beta 1 Agonists dopamine – Increase conduction Mimics the effect of –increase CO and HR Tremor anxiety,
only used IV through AV node and NA and Adr on Both used in arrhythmia, heart
conduction in SA node beta-1 in heart and cardiogenic shock failure
Increases contractility JG cells.
dopamine – beta 1
Increase O2 demand
agonist, increase CO
by heart.
and renal perfusion
(dopamine presynaptic
effect). Higher doses
causes
vasoconstriction
through direct alpha 1
effects

Anti-Arrhythmic lignocaine Amide local Blocks conduction Used in ventricular Causes CNS
anaesthetic in, ventricle tachycardia and problem, convulsion,
Amide Type intravenous
metabolised in liver. Generally does not fibrillation. Used CI in AV node and
Local only Blocks the entry of depress prophylactically may SA node
Class Ib sodium into myocardial myocardium, and no increase mortality in
cells does not lengthen effect on atrium MI patients
APD. Class In. Blocks
in the inactivated
state, therefore
purkinje and
ventricular

11
 MOA
Example & MOA cellular Therapeutic Adverse
Drug Group Physiologica
kinetics Biochemical uses effects & CI
l
Anti-Arrhythmic amiodarone Prolongs depolarisation Blocks conduction in Used in all Causes thyroid
(potassium into all parts of the Supraventricular problems (increase
taken once
myocardial cells, Class heart, including arrhythmia and to and decrease)
daily III). Also Ca blocker atrium, ventricle prevent ventricular Pulmonary fibrosis
extremely long and Na entry (Class I) Generally does not tachycardia and may be fatal
half life and beta-blocker. depress arrhythmia. Can cause Also causes torsades
Class III agent, action myocardium (3 AV, SA node block in des pointes, in LVH
and onset very slow. weeks) and peak some patients QT prolongation.
Increase AP duration. effect after 2-3 Maintain sinus rhythm Many drug
In addition, QT months after cardioversion in interactions with
prolongation. atrial fibrillation. warfarin and digoxin
Caution in
hypokalaemia

Anti-Arrhythmic sotalol Prolongs depolarisation Blocks conduction in Used in Non selective beta
(potassium into all parts of the Supraventricular blocker with all SE
taken 2-3
myocardial cells, Class heart, including arrhythmia and to and CI.
times daily III). Also Na entry atrium, ventricle prevent ventricular Also causes torsades
(Class I) but mainly Generally does not tachycardia des pointes, in LVH
beta-blocker. (Class II) depress QT prolongation.
Increase AP duration myocardium Which is more
and QT prolongation. prominent than
amiodarone

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