Summary
Cardiovascular drugs- ALL summary
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This is a document of all classes of Cardiovascular drugs with their MOA, Side effects, Contraindications and Uses.
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DRUG FOR DYSLIPIDAEMIASDrug Class Drug Name MOA Pharmacological Effects Therapeutic Uses Adverse Effects
HMG CoA Statin - Competitively inhibit HMG-CoA - Lower blood cholesterol levels by Hypercholesterolaemia - Elevation of liver aminotransferase
win
Reductase reductase enzyme (an early & rate Reducing instrinsic cholesterol synthesis - Reduce LDL cholesterol enzyme, therefore the enzyme levels
Inhibitor limiting step in intrinsic cholesterol - Useful alone, or with should be monitored
synthesis) the blood (which reduces LDL levels) resins, niacin or Caution for patients who have
- Reduce the conversion of HMG-CoA to Modest decrease in plasma triglycerides ezetimibe underlying hepatic diseases or are
mevalonate which causes the Small increase in HDL alcoholics
me
reduction in intrinsic cholesterol Additional actions:
synthesis - Decrease in oxidative - Myopathy/rhendomyolysis/increased
- Increase the expression of LDL
& stress & improvement in CK Enzyme
receptors, which increases the uptake endothelial function Especially in those with heavy
of cholesterol from systemic - Modulation of physical activity
circulation & inflammatory response Can have generalized discomfort
and vascular or weakness in skeletal muscles
inflammation Can proceed to myoglobinuria &
- Maintenance of plaque renal injury if not discountinued
& stability Higher chance of myopathy if use
together with other drugs (e.g.
Standard practice of initiating fibrates)
myopathy if (
reducatse inhibitor therapy
immediately after acute statins + fibrates
coronary syndrome regardless
of lipid levels
Fibrates Clofibrates Act as ligands for the nuclear transcription receptor PPAR- - Reduction in VLDL Hypertriglyceridemias - Myositis, myopathy, or
-
- Moderate increase in HDL - Predominantly VLDL rhabdomyositis
Upregulate transcription of LPL enzyme (which converts VLDL > LDL) - Moderate decrease in LDL / increase in LDL Dysbetalipoproteinemia & - Cholelithiasis (gallstones);
cholesterol gallstones, reflecting an
Enhanced VLDL catabolism ( VLDL) increase in the cholesterol content of
bile
- Hepatitis
Increased apo A1 & A2 (moderate HDL)
- Rash
Modest reduction of LDL in most patients, Increase in LDL in others (especially combined
hyperlipidemia) as triglycerides are reduced
Bile Acid Chloestyramine Inhibit bile acid reabsorption at terminal ileum - Useful only for isolated increase in LDL Primary Hypercholesterolemia - GI
um
Sequestrants are normally efficiently reabsorbed in the jejunum and - Resins are also used in Constipation and Bloating
(Bile acid- ileum combination with other (COMMON),
binding drugs to achieve further Heartburn and diarrhea &
resins) hypocholesterolemic steatorrhea (OCCASIONALLY)
itself is not absorbed effect Malabsorption of vitamin K (fat-
soluble vitamin) (RARE), leading to
& Relief of pruritus in patients hypoprothrombinemia.
Enhanced conversion of cholesterol > bile acids who have cholestasis and bile (Prothrombin time should be
salt accumulation measured frequently in patients
liver, which is normally controlled by negative feedback by bile acids who are taking resins and
anticoagulants)
Upregulation of LDL receptors
creased uptake of LDL and IDL from plasma results from upregulation of LDL receptors, - Impairment of absorption of other
particularly in liver. drugs
-
(e.g. digitalis glycosides, thiazides,
of
Decreased cholesterol in circulation warfarin, tetracycline)
In general, additional medication
should be given 1 hour before or
at least 2 hours after the resin to
ensure adequate absorption.
Intestinal Ezetimibe - Selectively inhibits intestinal absorption of cholesterol and phytosterols - Reduction in LDL cholesterol Primary Hypercholesterolemia Not Stated
sterol ~ - Targets transport protein NPC1L1 - synergistic with
absorption reductase inhibitors,
inhibitor producing decrements
in cholesterol beyond
that achieved with the
reductase inhibitor
, inotropic (increases contractility), chronotropic (increases heart rate), dromotropic (increases rate of conduction t
DRUGS FOR ISCHEMIC HEART DISEASE
Drug Class Drug Name MOA Pharmacological Effects Therapeutic Uses Adverse Effects
Nitrate Nitroglycerin - Systemic Circulation: - Acute relief of angina - Tolerance
(Vasodilator) / Glyceryl - Orally for maintenance - Vasodilating effects:
Trinitrate de to slow onset and long Throbbing headache (dilated
(GTN) duration of action cerebral vessels)
Flushing (dilated peripheral
vessels)
Reflex Tachycardia (indirect
action)
Orthostatic/Postural
Hypotension (No arterial
tone due arterial vasodilation
> reduced CO > lower
Isosorbide - Coronary Circulation: blood flow to brain >
Dinirate results in blackout)
Coronary vasodilation > Increased myocardial O2 supply Coronary steal syndrome
(Vasodilation of systemic and
Preload is the initial stretching of the
cardiac myocytes (muscle cells) prior to
* *tf unobstructed coronary
arteries, causing
obstructed/atherosclerotic
contraction. It is related to ventricular arteries to cannot further
filling. Afterload is the force or load against vasodilate, thus blood
which the heart has to contract to eject supplying the ischemic zones
Calcium Verapamil - Inhibit calcium entry through calcium channels present on cell membranes -
the blood
Systemic Circulation - Acute relief of angina -
¥ are shunted away, further
worsening the ischemia)
Heart
Channel (L-type CCB) Decreased contractility and
Blockers Cardiac tissue (cardiac myocytes, conducting tissues SA & AV Nodal tissue) heart failure
Vascular tissue (arteriole smooth muscles) [no effect on veins] Bradycardia and AV block
- Vessels
Vasodilation causing
hypotension, dizziness,
edema, flushing.
- Heart
Diltiazem
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