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The process of atherosclerosis starts in early childhood. When the blockage of artery lumen is more than 70% than we call it to be critical stenosis.

factors for CAD


Major risk factors (Proven by Framingham study) :

  1. Smoking Q                                   
  2. Hypertension Q                                
  3. DM Q                   
  4. Hyperlipidemia Q (High LDL / HDL ratio is the best marker in hyperlipidemia) (AIIMS Nov 09) 

Minor risk factors include:

  1. Hyperinsulinemia Q   
  2. Increase homocysteine levelQ  (LQ 2012)     
  3. Cocaine use Q
  4. Increase fibrinogen
  5. Increase CRP                           
  6. Reduce HDL             
  7. Increase lipoprotein a.

Recent Advances: (Ref. Hari. 18th ed., pg - 1990) (LQ 2012)

  1. Plasma levels of CRP, as measured by a high-sensitivity assay (hsCRP), prospectively predict the risk of MI.
    CRP serves as a validated biomarker of risk but probably not as a direct contributor to pathogenesis.
  2. A high level of blood serum homocysteine ("homocystinemia") is a powerful risk factor for cardiovascular disease.
  3. Giving vitamins (folic acid, B6 (pyridoxine), and B12) to reduce homocysteine levels 

Precipitating factors.

  1. Fibrinogen Levels
    1. 'Fibrinogen levels correlate with coronary risk and provide information regarding coronary risk independent of lipoprotein profile.
    2. Elevated fibrinogen levels might promote a thrombotic diathesis '.
  2. Waist Hip Ratio:
    1. This refers to a characteristic 'male' distribution of adipose tissue i.e. excess of fat in the abdomen compared with that in hips.
    2. 'An elevated waist/hip ratio has been associated with symptomatic cardiovascular disease and cerebrovascular disease in both men and women.
  3. Hyper homocystinemia
    1. There is a strong positive correlation between atherosclerosis and circulating levels of Homocysteine'
    2. Major factor leading to hyperhomocysteinemia is folate deficiency
  4. Hyperlipidemia
    1. Primary Hyperlipidemia

Familial hyperlipidemia




Risk Of Coronary Artery Disease

Type I (Familial Hyper Chylomicronemia)

Not increased

Type II A (Familial Hyper Cholesterolemia)


Type II B (Familial Combined Hyperlipidemia)


Type III (Familial Dysbetalipoproteinemia


Type IV (Familial Hypertriglyceridemia)


Type V (Familial Mixed Hypertriglyceridemia)

Not increased

  1. Secondary hyperlipidemia

    1. Hypothyroid

    2. Nephrotic Syndrome

Hyperlipidemia in Nephrotic syndrome may accelerate atherosclerosis

  1. Hyperlipidemia in Nephrotic syndrome is a consequence of increased hepatic lipoprotein synthesis
  2. Low density lipoproteins and cholesterol are increased in majority of patients
  3. This Hyperlipidemia may accelerate atherosclerosis and progression of Renal disease  
Extra Edge:
  1. Hyperlipidemia in type V hyperlipoproteinemia is not associated with increased LDL.
  2. In type V hyper lipoproteinemia:
    1. VLDL and Chylomicrons are increased
    2. LDL is normal or decreased
  3. Predisposing factors for coronary artery disease include an increased lipoprotein ‘a’ (and not lipoprotein ‘b’).



(Ref. Hari. 18th ed.,  pg - 356)

  1. Xanthoma is a deposition of yellowish cholesterol-rich material in tendons or other body parts in various disease states.
  2. They are cutaneous manifestations of lipidosis in which there is an accumulation of lipids in large foam cells within the skin.
  3. Histology picture of xanthoma shows lipid laden foam cells with large areas of cholesterol clefts,
  4. They are associated with hyperlipidemias, both primary and secondary types.
  5. Tendon Xanthoma are associated with Type II hyperlipidaemia and chronic biliary obstruction.
  6. Palmar xanthomata and tuboeruptive xanthomata (over knees and elbows) occur in Type III hyperlipidaemia
  7. Eruptive with Type V hyperlipidemia


Abbreviations : ADH, autosomal dominant hypercholesterolemia; Apo, apolipoprotein; ARH, autosomal recessive hypercholesterolemia; FCHL, familial combined hyperlipidemia; FCS, familial chylomicronemia syndrome; FDB, familial defective ApoB; FDBL, familial dysbetalipoproteinemia; FH, familial hypercholesterolemia; FHTG, familial hypertriglyceridemia; LPL, lipoprotein lipase; LDLRAP, LDL receptor associated protein; GPIHBP1, glycosylphosphatidylinositol-anchoed high density lipoprotein binding protein 1; N, normal

Preventing Measures

  1. High fibre diet:
    1. Fibre supplements may reduce levels of total cholesterol and LDL Cholesterol, and may cause a reduction in coronary heart disease.
    2. However use of high fibre diet has not shown any benefit in overall mortality from CHD and has not yet been recommended for risk reduction in CHD by the American Heart Association (AHA)
  2. Sterol Esters:
    1. Sterol esters containing food have been documented to decrease Total Cholesterol levels and LDL cholesterol levels.
    2. They may be recommended in selected individual with hypercholesterolemia for lowering of total and LDL cholesterol levels and for secondary prevention after an atherosclerotic event.
    3. However the use of these agents require further monitoring as concerns have been raised regarding their tendency to decrease Beta carotene (vitamin A) and alpha tocopherol (vit-E) levels.
      A clear benefit in reduction of mortality has not been documented
  3. Omega 3 polyunsaturated fatty acids (ω3-PUFA) (AIIMS May 2011)
    1. Omega 3 PUFA have been documented to decrease total mortality and sudden death in patients with ischemic heart disease.
    2. Benefit are most prominently reported with Omega 3 PUF A's derived from marine sources namely Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)
    3. The supplemental use of Omega 3 Fatty acids (EPA plus DHA) has been recommended by the American Heart Association. 

Effect of omega 3 fatty acids on LDL levels

  1. In patients with high triglycerides omega 3 PUF A cause on increase in LDL cholesterol
  2. In patients with normal triglycerides omega 3 PUFA do not decrease LDL cholesterol
  3. When omega 3 PUF A are used in place of saturated fatty Acids LDL cholesterol levels decline (but this effect is same as that found with use of other types of PUFA). 
(Ref. Hari. 18th ed., pg - 3160)
  1. Omega-3 fatty acids lower plasma triglyceride levels, particularly in persons with hyper-triglyceridemia, by inhibiting the synthesis of very-low-density lipoprotein (VLDL) cholesterol and triglycerides in the liver.
  2. Four gm per day of omega-3 fatty acids reduced serum triglyceride concentrations by 25 to 30 percent, increased serum LDL cholesterol levels by 5 to 10 percent, and increased HDL cholesterol levels by 1 to 3 percent.
  3. Total cholesterol was not significantly affected.

Recent Advances:  (Ref. Hari. 18th ed., pg - 1998)


Chlamydia pneumoniae has been implicated in the pathogenesis of some cases of atherosclerosis.


Treatment of hyperlipidemia

  1. Triglycerides:
    1. A fibrate (gemfibrozil or fenofibrate) is the drug of choice to lower fasting triglycerides (Ref. Hari. 18th ed., Pg- 1996)
    2. Other drugs that lower triglycerides include statins, nicotinic acid, and high doses of omega-3 fatty acids. (Ref. Hari. 18th ed., Pg - 1997)
  2. LDL Cholesterol (Ref. Hari. 18th ed., Pg - 1996)
    1. Statins (HMG-CoA reductase inhibitors), which produce a 20–60% lowering of LDL cholesterol, are the first choice for medication.
    2. Side effects are rare and include an increase in hepatic transaminases and/or myopathy.
    3. Ezetimibe. The cholesterol absorption inhibitor ezetimibe should be the second choice. 
    4. Cholestyramine and Colestipol. The bile acid sequestrants cholestyramine and colestipol are more effective than ezetimibe but must be used with caution in patients with the metabolic syndrome because they can increase triglycerides. In general, bile sequestrants should not be administered when fasting triglycerides are >200 mg/dL.
    5. Nicotinic acid has modest LDL cholesterol–lowering capabilities (<20%).
    6. Fibrates are best employed to lower LDL cholesterol when both LDL cholesterol and triglycerides are elevated. Fenofibrate may be more effective than gemfibrozil in this group.
  3. HDL
    Nicotinic acid is the only currently available drug with predictable HDL cholesterol-raising properties. (Ref. Hari. 18th ed.Pg- 1997)
    Saroglitarzar = α and γ PPAR receptor agonist. It reduces blood sugar as well as lipids. It is a new drug, not given in Harrison 18th edition also. !!!

Recent Advances (Not given in Harrison 18th Edition): Icosapent Ethyl  has been approved for the treatment of hypertriglyceridemia. 

Abdominal aortic aneurysm (AAA)
(AIIMS May 2011)

  1. Abdomen (infrarenal) is the most common site of aortic aneurysm.
    1. Elastin, the principal load-bearing protein present in the wall of the aorta, is reduced in the abdominal aorta as compared to the thoracic aorta.
    2. The abdominal aorta does not possess vasa vasorum, hindering repair.
  2. Most are true aneurysms that involve all three layers (tunica intima, tunica media and tunica adventitia), and are generally asymptomatic before rupture.
  3. The prevalence of AAAs increases with age, with an average age of 65–70 at the time of diagnosis.
  4. AAAs have been attributed to atherosclerosis.
  5. There is a large risk of rupture once the size has reached 5 cm, though some AAAs may swell to over 15 cm in diameter before rupturing.
  6. Before rupture, an AAA may present as a large, pulsatile mass above the umbilicus. A bruit may be heard from the turbulent flow in a severe atherosclerotic aneurysm or if thrombosis occurs.
  7. Most of the time rupture is usually the first hint of AAA. Once an aneurysm has ruptured, it presents with a classic pain-hypotension-mass triad.
  8. The pain is classically in the abdomen, back or flank. It is usually acute, severe and constant, and may radiate through the abdomen to the back.
  9. The diagnosis of an abdominal aortic aneurysm by the use of ultrasound.
  10. Rupture could be indicated by the presence of free fluid in potential abdominal spaces, such as Morison's pouch, the splenorenal space, subdiaphragmatic spaces and peri-vesical spaces.
  11. A contrast-enhanced abdominal CT scan is needed for confirmation. 


  1. Medical treatment
    Strict blood pressure control.
  2. Surgical treatment
    The definitive treatment for an aortic aneurysm is surgical repair of the aorta.

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