Denotes abnormally  LEVELS of any or all LIPIDS &/or LIPOPROTEINS [LP] in blood Is the most common form of dyslipidemia Hypertriglyceridemia Hyper-cholesterolemia Mixed Hyperlipoprotienemia * Denotes usually  LDL * Unless specified in the familial types TGs & C CM, VLDL, IDL, LDL, HDL LProteinemia  LP  LipidsRisk Type I CMTGs- Type IIa LDLC  Type IIb VLDL & LDLTG & C  Type III IDLTGs & C  Type IV VLDLTGs  Type V VLDL & CMTGs & C_ TGs < 220 mg/dl C < 200 mg/dl LDL < 130 mg/dl HDL > 50 mg/dl

Very low Density lipoprotein [VLDL] Low Density lipoprotein [LDL] Chylomicrons [CM] High Density lipoproteins [HDL] % Lipid Composition ProteinCholesterolTriglyceridesPhospholipids OUTER CoatINNER Core Phospholipids Cholesterol Triglycerides Cholesterol esters Hydrophilic Gps. Lipophylic Gps. APOPROTEINS C TGs

Very low Density lipoprotein [VLDL] Low Density lipoprotein [LDL] Chylomicrons [CM] High Density lipoproteins [HDL] DENSITY [IDL] TYPE of Apoprotein B 48B100AI&II Beta LPAlpha LP Non-HDL CholesterolHDL Cholesterol ATHEROGENICATHEROPROTECTIVE

Begins as INFLAMMATORY REACTION triggered by; Endothelial dysfunction + Dyslipidemia MC Dysfunction Rolling Scrolling Diapedesis Expression LDL leak Trapping SR-A Engulf Ox -LDL No efflux

Progress as FIBRO- PROLIFERATIVE DISORDER Lumen Lipid Core Fibrous cap Shoulder Intima Media Elastic laminæ Internal External Rapidity of lipid accumulation & apoptosis Proliferative (fibrous) vs Inflammatory (proteolysis) Atheromatus Plaque Divide into > Lipid core < fibrous cap (thin) > Inflammatory cells

Switch into ATHER-THROMBOTIC INSULT at any stage of progression = ACSs, Stroke, …etc.

DYSLIPEDEMIA ENDOTHELIAL DYSFUNCTION MORBIDITY & MORTALITY OUTCOMES PREVENTED or DECREASED By CONTROLLING DYSLIPIDYMIA

Coronary  SUPPLY Pumping  Cardiac Work  DEMAND (O 2 ) IMPAIRED SUPPLY INCREASED DEMAND

Coronary  SUPPLY Pumping  Cardiac Work  DEMAND (O 2 ) Coronary Filling (in diastole)  by  diastolic time  diastolic pressure …etc Coronary Narrowing  by Spasm Atherosclerosis lesion IMPAIRED Cardiac Work  Heart Rate  Load; i.e  BP…etc.  Force; Hypertrophy INCREASED CORONARY HEART DISEASES [CHD]

FUNCTIONALSTRUCTURAL SPASM ATHEROSCLEROTIC PLAQUE + THROMBOSIS Vulnerable Stabilized CORONARY HEART DISEASES [CHD] Fissure at Classifications

FUNCTIONALSTRUCTURAL SPASM ATHEROSCLEROTIC PLAQUE + THROMBOSIS Vulnerable Stabilized CORONARY HEART DISEASES [CHD] SPASTIC ANGINA Prinzmetal’s Angina STABLE ANGINA UNSTABLE ANGINA MYOCARDIAL INFARCTION [AMI] Acute ~Subtotal / Total OCCLUSION ANGINA ACUTE CORONARY SYNDROME [ACS] Sustained Spasm

ANGINA Pectoris Chest pain (varying in severity) due to ischemia of heart muscle caused by obstruction or spasm of coronary arteries Constricting & tight, oppressive, crushing Starts in the centre behind the sternum or on left side of the front of chest & spread out to shoulder arm….. Weak relationship between severity of pain & degree of O 2 deprivation in the heart muscle (i.e., severe pain can occur with little or no risk of a heart attack, and a heart attack can occur without pain). Stable Angina Pain is due to (accumulation of metabolites K +, PGs, Kinins, Adenosine….) 2 ndry to the ischemia EFFORT ANGINA Prinzmetal’s Angina VARIANT ANGINA Occurs at rest Cyclic (vasospasm) due to contraction of VSMC >in younger women Develops by exertion Resolves at rest Lasts ~5 min Insidious onset Unstable Angina CRESCENDO ANGINA Occurs at rest / minimal exertion Severe / Lasting >10 min; Either of; * New onset (nothing for last 4–6 w) * Crescendo pattern; getting > severe / prolonged / frequent than previous By a Spasm or Stabilized Plaque Vulnerable Plaque

 ATP, Ion Pumps  Ca  Proteolysis, Membrane damage…. Necrosis ~~Action Potention, elect. Activities & functions Acute ~Subtotal / Total OCCLUSION Inflam. Mediators, ROS TNF , NF  B, …. Apoptosis ACUTE CORONARY SYNDROMES [ACS] ECG CHANGES AMI Cardiac Enzymes (Markers) +ve AMI -ve STEMINSTEMI Unstable Angina Umbrella term that covers a spectrum of acute clinical conditions ranging from Unstable angina (38%) NSTEMI (25%) STEMI (30%)