cardiac medication Flashcards
Dyslipidemia screening
Men and women ≥ 40 yrs. of age (or post menopausal women)
Ethnicity: South Asian and First Nations people are at increased risk (consider earlier screening)
Patients with the following conditions (regardless of age):
DM
Obesity (BMI ≧ 30)
Chronic kidney disease (eGFR ≦ 60 mL/min)
FHx of premature CAD (Men < 55 yrs., Women < 65 yrs. in a 1st degree relative) & those that have a family hx. of dyslipidemia
Known atherosclerosis: CAD, MI, PCI/CABG, PVD, CVA/TIA, carotid arterial disease, AAA
Stigmata of dyslipidemia (arcus cornea, xanthelasma)
Inflammatory disease (RA, SLE, IBD)
HIV (Rx: HARRT)
Current tobacco use
HTN (includes hypertensive diseases in pregnancy i.e. preeclampsia)
Erectile dysfunction, COPD
screening of dyslipidemia
Lipid profile (non-fasting state)
TC (total cholesterol)
LDL-C (low density lipoprotein)
HDL-C (high density lipoprotein)
non-HDL-C (non-HDL-cholesterol)
TG
FBG, HbA1C level
Electrolytes (eGFR)
Lipoprotein (a) – once in a person’s lifetime at initial screening
non-HDL-C =
TC minus HDL-C
Apolipoprotein B (ApoB)
main component of LDL and VLDL (very low density lipoprotein)
Framingham Risk Score
High Risk: FRS of ≥ 20%
Intermediate Risk: 10%-19.9%
Low Risk: < 10%
Statin Indications
Atherosclerotic Cardiovascular Disease (ASCVD)
Most people with DM
- Age ≥ 40 yr.; Age ≥ 30 yr. + DM x 15 yrs.
- Microvascular disease
CKD: Age ≥ 50 yr. and eGFR < 60 mL/min
LDL ≥ 5.0 mmol/L
MOA of statin
Competitively block HMG-CoA reductase, a key rate limiting enzyme in cholesterol synthesis
Block the conversion of HMG-CoA to mevalonic acid
Reduce hepatic cholesterol synthesis
Upregulation of LDL receptors, increases hepatic uptake of LDL-C from circulation
Pleiotropic effects of statins
Improve endothelial function
Increase NO bioavailability
Inhibit inflammatory response
Stabilize atherosclerotic plaques
Contraindications to Prescribing Statins
Active or Chronic Liver Disease
Pregnancy and during breastfeeding
side effects of statins
Myalgia
Myositis (inflammation of skeletal muscles)
Rhabdomyolysis
Baseline Testing before initiating statins
TSH (hypothyroidism is a risk factor for statin intolerance)
Liver function
Renal function/creatinine: (CKD are at higher risk of statin)
Monitor labs at minimum every 6 months, with any changes in therapy, or if suspected adverse effects
Repeat a lipid profile in 4-6 weeks to reassess if at target
Primary prevention treatment threshold
IF non-HDL-C > 2.6 mmol/L or LDL-C ≥ 2.0 mmol/L or ApoB ≥ 0.8 g/L and on maximally tolerated statin dose, the next step is to discuss add-on therapy
First line add on therapy in primary prevention is Ezetimibe
Note that PCSK9 inhibitors are not recommended in primary prevention
Secondary prevention treatment threshold
IF the non-HDL-C ≥ 2.4 mmol/L or LDL-C ≥ 1.8 mmol/L or ApoB ≥ 0.7g/L, the next step is to intensity therapy with addition of ezetimibe and/or PCSK9 inhibitor
Ezetimibe
Inhibits absorption of dietary cholesterol in the small intestine
Metabolized in both the small intestine and liver but not by CYP450 enzyme system
PCSK9 Inhibitors
Monoclonal antibody that inhibits PCSK9, a protein that targets LDL receptors, and clears LDL from the blood
PCSK9 Inhibitors side effects
urticaria, rash, angioedema
Hypertriglyceridemia medication
Fibric Acids (fenofibrate)
contraindication: Severe Renal or Hepatic Disease
*Can increase serum Cr
ASA MOA
COX inhibitor - Irreversibly inhibits platelet aggregation
ASA side effects
GI bleeding, dyspepsia, thrombocytopenia, allergic RXN (aspirin induced asthma)
ASA is indicated for
ASA is indicated for the secondary prevention of CV disease
Antiplatelet Therapy (APT)
Selectively inhibit ADP (adenosine diphosphate) induced platelet aggregation
Platelet P2Y12 receptor antagonists: Clopidogrel, Ticagrelor, Prasugrel
ACE Inhibitors MOA
Prevent the conversion of angiotensin I to II; Angiotensin II is a potent vasoconstrictor
ACEi cause arterial and venous vasodilation
Block the breakdown of bradykinin
e.g. ramipril, perindopril
Adverse effects of ACEi
Angioedema (life threatening)
ACE induced cough (ARBs can be used in patients with ACE induced cough)
Renal dysfunction, hyperkalemia
Hypotension
Cautious use in patients with RAS, single kidney, CKD (contraindicated in bilateral RAS)
Contraindicated in pregnancy (fetal malformations/death)
Beta-Blockers MOA
↓myocardial oxygen demand, ↓ HR, ↓contractility
adverse effects of beta-blockers
Bradycardia (contraindicated in heart 2nd/3rd degree heart block)
Hypotension
Fatigue, Sleep disturbance, Nausea
Sexual dysfunction
Bronchospasm
Worsen claudication symptoms
nitrates MOA
↑ myocardial oxygen via vasodilation of coronary arteries (release of NO)
MOA of calcium channel blockers
CCBs ↑ myocardial oxygen by vasodilation of coronary arteries
Amlodipine is used to treat
angina & HTN (no arrhythmic action)
side effects of amlodipine
HA, ↓BP, peripheral edema
Non-dihydropyridines: Diltiazem, Verapamil
control HR by prolonging the refractory period of AV node; Arrhythmic use – i.e. managing SVT/tachyarrhythmia’s
side effects of Non-dihydropyridines (Diltiazem, Verapamil)
↓ HR, ↓ BP, AV block
↓ HR and contractility - worsen HF