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Total Cholesterol (TC)
Triglycerides (TG)
HDL-cholesterol (HDL-C)
LDL-cholesterol (LDL-C)
VLDL-cholesterol (VLDL-C)
Non-HDL cholesterol = TC − HDL
Atherogenic Index = TG / HDL
LDL/HDL ratio
Total Cholesterol: < 200 mg/dL
Triglycerides: < 150 mg/dL
LDL: < 100 mg/dL (optimal)
HDL: > 40 mg/dL (men) ; > 50 mg/dL (women)
VLDL: ~ TG/5 (mg/dL)
Non-HDL cholesterol: < 130 mg/dL
Strongly associated with atherosclerosis
Major target of therapy (statins)
Seen in diabetes, metabolic syndrome, alcoholism, pancreatitis risk
Treated with fibrates, omega-3
Strong risk factor for coronary artery disease (CAD)
Best indicator in diabetics and metabolic syndrome
High TG
Low HDL
Small dense LDL
A chronic inflammatory disease of arteries characterized by formation of atheromatous plaques in the intima.
Endothelial injury
– Hypertension, smoking, diabetes, dyslipidemia
LDL infiltration into intima
– Oxidation of LDL by ROS
Macrophage uptake → foam cells
– Oxidized LDL taken up by scavenger receptors
Fatty streak formation
– Earliest visible lesion
Smooth muscle proliferation & collagen deposition
– Formation of fibrous cap
Plaque progression
– Narrowing of lumen
Plaque rupture → thrombosis
– Causes MI, stroke
Highly atherogenic
Attracts monocytes
Promotes inflammation
Leads to foam cell formation
Dyslipidemia (high LDL, low HDL)
Hypertension
Smoking
Diabetes mellitus
Obesity
Sedentary lifestyle
Diet high in saturated fats
Stress, alcohol
Age
Male sex
Family history
Genetic disorders (familial hypercholesterolemia)
High HDL
Exercise
Omega-3 fatty acids
Moderate alcohol
Antioxidants
Myocardial infarction
Stroke
Peripheral vascular disease
Aneurysm
Sudden cardiac death
Impairment of blood flow through the coronary arteries → myocardial ischemia.
Atherosclerosis (most common)
Vasospasm
Thrombosis
Embolism
Chest pain (angina pectoris)
Radiation to left arm, jaw
Dyspnea
Sweating, nausea
Silent ischemia (common in diabetics)
Predictable pain on exertion
Due to fixed atherosclerotic plaque
Pain at rest
Part of acute coronary syndrome
Plaque rupture + thrombosis (non-occlusive)
Due to coronary vasospasm
Episodes at rest
ST elevation during attack
Includes:
Unstable angina
NSTEMI
STEMI
All involve plaque rupture + thrombus.
Troponin I / T – most specific, rises early
CK-MB – useful for reinfarction
LDH-1 – late marker
Rupture of vulnerable plaque
Platelet activation + thrombus formation
Occlusion of coronary artery
Myocardial ischemia → necrosis
ST elevation
T-wave inversion
Q waves (late)
Same as atherosclerosis, plus:
Elevated lipoprotein(a)
High hs-CRP
Metabolic syndrome
LDL → atherogenic
HDL → protective
Lp(a) → strong genetic risk factor
LDL ("bad cholesterol") is the strongest lipid predictor of MI.
LDL enters the arterial wall → becomes oxidized LDL → triggers inflammation.
Oxidized LDL is taken up by macrophages → foam cells → fatty streak → atherosclerotic plaque.
Higher LDL = Faster plaque formation.
These particles penetrate arterial wall more easily.
Seen in:
Diabetes
Metabolic syndrome
Obesity
Strong association with early CAD and MI.
HDL removes cholesterol from plaques (reverse cholesterol transport).
Anti-inflammatory and antioxidant.
Low HDL → high risk of MI even if LDL is normal.
High TG → ↑ VLDL → formation of small dense LDL.
Increases risk of pancreatitis and contributes to CAD.
Very common in diabetes.
Lp(a) is similar to LDL but more thrombogenic.
Promotes:
Plaque growth
Thrombosis
Early MI (especially in young individuals)
A strong predictor of MI.
Ratio > 4 significantly increases risk.
Best used in population screenings.
Non-HDL = Total Cholesterol − HDL
Includes all atherogenic particles:
LDL
VLDL
IDL
Lp(a)
Best predictor of MI in diabetics and metabolic syndrome.
LDL enters intima
Oxidation → macrophage uptake
Foam cell formation → fatty streak
Smooth muscle proliferation → fibrous cap
Plaque grows → lumen narrows
Plaque rupture
Thrombus forms → occlusion → MI
Reduce LDL by upregulating LDL receptors
Stabilize plaques
Reduce inflammation
Proven to lower mortality after MI
Atherosclerosis has modifiable, non-modifiable, and emerging risk factors.
These cannot be changed.
Risk increases with age (men >45, women >55).
Males have higher risk
Women lose protection after menopause
Early CAD in first-degree relatives increases risk
Familial hypercholesterolemia
Familial combined hyperlipidemia
Lp(a) excess
These are responsible for majority of cases.
High LDL → strongest modifiable factor
Low HDL → increases risk
Damages endothelium
Accelerates plaque formation
Free radicals → endothelial injury
Increases platelet adhesion
Lowers HDL
Very strong risk factor
Glycation of LDL makes it more atherogenic
Endothelial dysfunction
Produces small dense LDL
Induces insulin resistance
Raises TG
Lowers HDL
Strong link with metabolic syndrome
Reduces HDL
Increases TG and LDL
Raises LDL sharply
Promotes plaque formation
Increasingly recognized in modern cardiology.
hs-CRP
IL-6
TNF-α
Strong genetic risk factor
Increases thrombosis tendency
Causes endothelial injury
Vitamin B6/B12/folate deficiency
Increases oxidation of LDL
Rheumatoid arthritis
Psoriasis
SLE
High HDL
Regular exercise
Omega-3 fatty acids
Antioxidant-rich diet
Mediterranean diet
Moderate alcohol intake (not for everyone)
High LDL = strongest modifiable risk factor for MI.
Low HDL increases CAD risk even if LDL is normal.
Lp(a) is a major genetic predictor of early MI.
Smoking + diabetes + high LDL → explosive risk combination.
Diabetics have small dense LDL, the most atherogenic form.
Atherosclerosis begins with endothelial injury.
Fatty streak is the earliest lesion of atherosclerosis.
Atherosclerosis prevention = reduce risk factors + stabilize plaques + improve vascular function.
Reduce saturated fats and trans-fats
Increase omega-3 fatty acids
Increase soluble fiber (oats, legumes)
Increase fruits & vegetables
Use unsaturated fats (olive, mustard oil)
Reduce red meat, processed foods, high-sugar meals
Target BMI < 25
Reduce central obesity (waist circumference: men < 90 cm, women < 80 cm)
150 min/week moderate aerobic exercise
Increases HDL
Reduces TG and BP
Eliminates a major inflammatory trigger
Improves HDL
Reduces MI risk dramatically
Small amounts may increase HDL
Avoid binge drinking
Maintain HbA1c < 7%
Prevents small dense LDL formation
BP target <130/80
ACE inhibitors / ARBs beneficial
Aim LDL < 100 mg/dL
In diabetics or CAD: LDL < 70 mg/dL
Vitamin B6, B12, folate
Lower LDL
Stabilize plaques
Anti-inflammatory
Lower triglycerides
Increase HDL
Lowers Lp(a)
Increases HDL
Used in secondary prevention
Prevents thrombosis on ruptured plaques
Lipid profile every 5 years
More frequent in diabetics, obese individuals, smokers
hs-CRP may help in borderline cases
These are rare genetic disorders resulting in abnormally low lipoprotein levels.
Absence of Apo B containing lipoproteins (chylomicrons, VLDL, LDL)
Fat malabsorption
Steatorrhea
Failure to thrive
Acanthocytosis
Peripheral neuropathy
Retinitis pigmentosa
Very low cholesterol
Almost no LDL/HDL/VLDL
Tangier disease
Apo A-I mutations
LCAT deficiency
Secondary (diabetes, smoking, obesity)
Very low HDL
Cholesterol deposits in tonsils (Tangier)
Low HDL
Corneal clouding
Hemolysis
Proteinuria / CKD
This classification is extremely high-yield.
Lipoprotein lipase (LPL) deficiency
OR
Apo C-II deficiency
Chylomicrons
Pancreatitis
Eruptive xanthomas
Lipemia retinalis
No ↑ risk of atherosclerosis
LDL receptor defect
OR
Apo B-100 defect
LDL
Tendon xanthomas
Premature CAD (young MI)
Very high LDL
Overproduction of VLDL + LDL
VLDL + LDL
Very common
High CAD risk
Seen in metabolic syndrome
Apo E2/E2 homozygosity (Apo E defect)
IDL + remnants
Palmar xanthomas (orange creases)
Tuberoeruptive xanthomas
High risk of atherosclerosis
Overproduction of VLDL
VLDL
High triglycerides
Pancreatitis risk
Common in diabetes
Increased VLDL + decreased LPL activity
VLDL + Chylomicrons
Pancreatitis
Eruptive xanthomas
Lipemia
Alcohol worsens it
| Type | Elevated Lipoprotein | Main Defect | Key Feature |
|---|---|---|---|
| I | Chylomicrons | LPL / Apo C-II | Pancreatitis |
| IIa | LDL | LDL receptor | Tendon xanthomas |
| IIb | LDL + VLDL | Overproduction | Common CAD |
| III | IDL / remnants | Apo E defect | Palmar xanthomas |
| IV | VLDL | Overproduction | High TG |
| V | VLDL + Chylomicrons | LPL impaired |
Pancreatitis |
LDL is the most atherogenic lipoprotein and the primary target for therapy.
HDL is protective because it performs reverse cholesterol transport.
Triglycerides correlate with pancreatitis risk, not directly with MI risk.
Non-HDL cholesterol (TC – HDL) is the best measure in diabetics and metabolic syndrome.
Small dense LDL particles (seen in diabetes) are the most dangerous for plaque formation.
Lipoprotein(a) is a strong genetic risk factor for premature MI.
Endothelial injury is the initiating event (smoking, hypertension, diabetes).
Oxidized LDL is central to plaque development → taken up by macrophages → foam cells.
Fatty streak is the earliest visible lesion of atherosclerosis.
Plaque rupture, not gradual narrowing, is the most common cause of MI.
Atherosclerosis is an inflammatory disease, not just lipid accumulation.
Diabetes produces small dense LDL, greatly accelerating atherosclerosis.
MI occurs due to rupture of a vulnerable plaque, not necessarily the largest plaque.
Troponins are the most sensitive and specific biomarkers for MI.
CK-MB helps detect reinfarction.
Stable angina occurs with exertion; unstable angina occurs even at rest.
Prinzmetal angina is due to coronary vasospasm (transient ST elevation).
Silent ischemia is common in long-standing diabetics.
High LDL = strong predictor of MI.
High HDL = protective (removes cholesterol from plaques).
Cholesterol-rich diets increase LDL and accelerate plaque growth.
Total cholesterol/HDL ratio > 4 increases MI risk sharply.
Lp(a) promotes thrombosis and early MI (familial risk).
Statins reduce MI risk, stabilize plaques, and lower inflammation.
Smoking cessation dramatically reduces risk within 2–3 years.
Exercise raises HDL, lowers TG, improves endothelial function.
Mediterranean diet lowers cardiovascular risk.
Hypertension, diabetes, and dyslipidemia must be tightly controlled.
(One-line memory)
Type I → Chylomicrons ↑ → pancreatitis, no atherosclerosis
Type IIa → LDL ↑ → tendon xanthomas, early MI
Type IIb → LDL + VLDL ↑ → common, high CAD risk
Type III → IDL ↑ → palmar xanthomas
Type IV → VLDL ↑ → hypertriglyceridemia
Type V → VLDL + chylomicrons ↑ → pancreatitis
Abetalipoproteinemia → no Apo B → absent chylomicrons/VLDL/LDL → fat malabsorption, acanthocytosis.
Tangier disease → HDL extremely low → orange tonsils.
LCAT deficiency → low HDL → corneal clouding and proteinuria.
High LDL
Low HDL
Hypertension
Smoking
Diabetes
Obesity (especially central)
High saturated fat intake
Sedentary lifestyle
Stress, alcohol excess
Age
Male sex
Family history
Genetic disorders
Elevated hs-CRP
High Lp(a)
Homocysteinemia
Chronic inflammatory diseases
LDL lowering (statins) reduces MI risk more than any other drug class.
HDL < 40 mg/dL is a strong, independent predictor of CAD.
Diabetes = atherosclerosis equivalent; treat LDL aggressively.
Small dense LDL = most atherogenic particle.
Type IIa hyperlipoproteinemia → very high LDL → premature MI.
Type I hyperlipoproteinemia → pancreatitis but no risk of atherosclerosis.
Palmar xanthomas = Type III dysbetalipoproteinemia.
A. HDL
B. Chylomicron
C. LDL
D. VLDL
Answer: C. LDL
A. LDL
B. VLDL
C. HDL
D. Lp(a)
Answer: C. HDL
A. High HDL, low LDL
B. Low HDL, high TG, small dense LDL
C. High HDL and high TG
D. High LDL only
Answer: B. Low HDL, high TG, small dense LDL
A. Fibrous cap
B. Fatty streak
C. Thrombus
D. Calcified plaque
Answer: B. Fatty streak
A. Large buoyant LDL
B. Small dense LDL
C. LDL-2
D. LDL-4
Answer: B. Small dense LDL
A. Lipoprotein lipase
B. Lecithin cholesterol acyltransferase
C. Myeloperoxidase / free radicals
D. Apo C-II
Answer: C. Myeloperoxidase / free radicals
A. HDL
B. Lp(a)
C. IDL
D. Chylomicron remnants
Answer: B. Lp(a)
A. Smoking
B. Obesity
C. Aerobic exercise
D. High saturated fat intake
Answer: C. Aerobic exercise
A. Type IIa
B. Type III
C. Type IV
D. Type V
Answer: D. Type V
(chylomicrons + VLDL)
A. Type I
B. Type IIa
C. Type III
D. Type V
Answer: C. Type III (Dysbetalipoproteinemia)
A. Type IIa
B. Type I
C. Type IV
D. Type V
Answer: A. Type IIa (Familial Hypercholesterolemia)
A. High LDL
B. High HDL
C. Very high triglycerides
D. High Lp(a)
Answer: C. Very high triglycerides
A. HDL
B. LDL
C. VLDL
D. All Apo B–containing lipoproteins
Answer: D. All Apo B–containing lipoproteins
A. High HDL
B. Low HDL
C. High LDL
D. High triglycerides
Answer: B. Low HDL
A. LDL
B. Chylomicrons
C. HDL
D. IDL
Answer: C. HDL
A. Plaque rupture
B. LDL deposition
C. Endothelial injury
D. Thrombosis
Answer: C. Endothelial injury
A. Monounsaturated fats
B. Omega-3 fatty acids
C. Saturated fats
D. Polyunsaturated fats
Answer: C. Saturated fats
A. HDL
B. LDL
C. Triglycerides
D. VLDL
Answer: B. LDL
A. Smoking cessation
B. Weight control
C. Tight glycemic control
D. Long-term anticoagulation
Answer: D. Long-term anticoagulation
(Only for selected high-risk cases, not general prevention.)
A. Fibrates
B. Statins
C. Niacin
D. Bile acid resins
Answer: B. Statins
A. Statins
B. Fibrates
C. PCSK9 inhibitors
D. Ezetimibe
Answer: B. Fibrates
A. Chylomicron
B. HDL
C. LDL
D. VLDL
Answer: A. Chylomicron
A. HDL
B. Oxidized LDL
C. VLDL
D. Apo E
Answer: B. Oxidized LDL
A. Hypothyroidism
B. Low HDL
C. High homocysteine
D. High bilirubin
Answer: D. High bilirubin (actually protective)
A. Hypoglycemia
B. Diabetes mellitus
C. Hypotension
D. Low protein diet
Answer: B. Diabetes mellitus
A 28-year-old man with no hypertension or diabetes presents with sudden chest pain. ECG shows anterior MI.
Lipid profile:
LDL = 240 mg/dL
HDL = 32 mg/dL
Triglycerides = 120 mg/dL
His father had MI at age 42.
Diagnosis:
➡️ Familial Hypercholesterolemia (Type IIa)
Reason: Very high LDL + early MI + family history.
A 56-year-old man experiences chest tightness while climbing stairs. Pain settles with rest.
Lipid profile:
LDL: 180 mg/dL
HDL: 38 mg/dL
Diagnosis:
➡️ Stable Angina (due to fixed atherosclerotic plaque)
A 68-year-old woman develops chest pain at rest. ECG shows ST depression.
Troponins are negative. LDL is 170 mg/dL.
Diagnosis:
➡️ Unstable Angina (ACS without enzyme rise)
A 60-year-old diabetic man presents with severe crushing chest pain at rest.
ECG: ST elevation in inferior leads.
Troponin-I positive.
Diagnosis:
➡️ STEMI (plaque rupture + thrombosis)
A 54-year-old man with Type 2 DM has no chest pain but complains of fatigue and breathlessness. ECG shows ST depression.
Diagnosis:
➡️ Silent Myocardial Ischemia
Reason: Neuropathy blunts pain sensation.
A 48-year-old obese man:
TG = 280 mg/dL
HDL = 29 mg/dL
Fasting glucose = 120 mg/dL
Waist circumference: 102 cm
Diagnosis:
➡️ Atherogenic Dyslipidemia associated with Metabolic Syndrome
A 35-year-old alcoholic presents with acute epigastric pain.
TG = 950 mg/dL
Amylase high.
Diagnosis:
➡️ Hypertriglyceridemia-induced pancreatitis (Type IV or V)
A 22-year-old man has multiple yellow papules over back and arms.
TG = 1250 mg/dL
Chylomicrons present.
Diagnosis:
➡️ Type V Hyperlipoproteinemia
(VLDL + Chylomicrons)
A 50-year-old man with orange-colored creases on palm.
Lipid profile:
TC = 350 mg/dL
TG = 400 mg/dL
IDL elevated
Diagnosis:
➡️ Type III Hyperlipoproteinemia (Dysbetalipoproteinemia)
A 40-year-old patient shows nodular swellings over Achilles tendon.
LDL = 280 mg/dL.
Diagnosis:
➡️ Familial Hypercholesterolemia (Type IIa)
A 6-year-old boy has extremely low HDL (3 mg/dL) and enlarged yellowish/orange tonsils.
Diagnosis:
➡️ Tangier disease (Hypoalphalipoproteinemia)
A young child has fat malabsorption, failure to thrive, ataxia, and RBC acanthocytes.
Diagnosis:
➡️ Abetalipoproteinemia
(Apo B absent → no chylomicrons/VLDL/LDL)
A 56-year-old woman after menopause has increased LDL despite normal body weight and diet.
Reason:
➡️ Loss of estrogen → estrogen protects HDL and LDL metabolism.
A 52-year-old diabetic woman has normal LDL (110 mg/dL) but still develops CAD.
Reason:
➡️ Presence of small dense LDL (highly atherogenic) even when LDL seems normal.
A 45-year-old man:
LDL = 118 mg/dL
HDL = 38 mg/dL
hs-CRP = significantly high
Interpretation:
➡️ High inflammatory state → unstable plaques → high CAD risk even if LDL borderline.
A 40-year-old woman presents with severe chest pain at rest, early morning.
ECG: transient ST elevation during pain.
Diagnosis:
➡️ Prinzmetal Angina (coronary vasospasm)
A 62-year-old non-diabetic smoker collapses suddenly. Autopsy: ruptured plaque with thrombus in LAD.
Mechanism:
➡️ Plaque rupture is the most common cause of MI.
A 58-year-old man on statins develops muscle aches.
CK-MB normal, CK (creatine kinase) elevated.
Diagnosis:
➡️ Statin-induced myopathy
A 40-year-old woman with fatigue and weight gain has:
LDL = 210 mg/dL
TSH = high.
Reason:
➡️ Hypothyroidism decreases LDL receptor expression → ↑ LDL.
A 50-year-old man with CAD is prescribed low-dose aspirin.
Why?
➡️ Prevents thrombosis over ruptured atherosclerotic plaques (secondary prevention).
A man switches to high-carb, low-fat diet.
After 3 months:
TG ↑, HDL ↓.
Reason:
➡️ Excess carbs → ↑ VLDL → ↑ TG → ↓ HDL.
A 32-year-old non-smoker with no diabetes presents with MI.
Lipid profile near-normal except:
Lp(a) = very high.
Diagnosis:
➡️ Genetic predisposition to premature CAD due to high Lp(a).
A 40-year-old man with normal LDL still gets MI. His father and brother had MI in their 40s.
Explanation:
➡️ Genetic risk overrides lipid levels (Lp(a), inflammation, endothelial function).
A 55-year-old man with CAD has homocysteine level elevated.
Mechanism:
➡️ Homocysteine damages endothelium → accelerates atherosclerosis.
(Linked with low B6/B12/folate)
A 42-year-old woman with rheumatoid arthritis develops CAD early.
Reason:
➡️ Chronic inflammation accelerates endothelial injury.
LDL.
HDL.
All atherogenic particles (LDL + VLDL + IDL + Lp(a)).
LDL = TC – HDL – (TG/5).
(Not valid if TG > 400 mg/dL.)
Exercise, estrogen, moderate alcohol.
Smoking, obesity, poorly controlled diabetes.
Total cholesterol / HDL ratio.
Low HDL + high TG + small dense LDL (common in Type 2 DM).
Endothelial injury.
Fatty streak.
Macrophages ingesting oxidized LDL.
Weak fibrous cap + inflammation.
Small dense LDL + endothelial dysfunction + chronic inflammation.
Highly atherogenic; promotes foam cell formation.
Coronary → carotid → femoral.
Inflamed, lipid-rich plaque with thin fibrous cap (“vulnerable plaque”).
Myocardial ischemia due to reduced coronary blood flow.
Predictable chest pain on exertion; relieved by rest.
Chest pain at rest; part of ACS; plaque rupture without biomarkers.
Coronary vasospasm causing transient ST elevation.
Plaque rupture with thrombosis.
Troponin I or T.
CK-MB.
Ischemia without pain (common in diabetics due to neuropathy).
High LDL.
Lipoprotein(a).
Reverse cholesterol transport + anti-inflammatory effect.
Highly atherogenic LDL seen in diabetes and metabolic syndrome.
Raises VLDL → increases small dense LDL.
Statins.
Aerobic exercise.
Mediterranean diet.
↓ HDL, ↑ oxidation of LDL.
Causes endothelial injury and plaque formation.
Vitamin B6, B12, folate deficiency.
Absence of Apo B lipoproteins (chylomicrons, VLDL, LDL).
Extremely low HDL + orange tonsils.
Low HDL + corneal clouding + renal disease.
(One-liners)
↑ Chylomicrons → pancreatitis (no CAD).
Very high LDL → tendon xanthomas + early CAD.
LDL + VLDL.
Palmar xanthomas (Apo E defect).
↑ VLDL + high triglycerides.
Chylomicrons + VLDL → pancreatitis.
Very high triglycerides (usually > 1000 mg/dL).
Chylomicrons.
Takes it back to liver (reverse transport).
Genetic factors — not diet.
Niacin.
Statins.
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