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C oronary Artery Disease

C oronary Artery Disease. Punit Goel, MD Asst Professor in Cardiology, University of Missouri Hospital & Clinics Staff Cardiologist, Harry Truman VA Hospital. Epidemiology Risk factors Pathogenesis Spectrum Prevention. Atherosclerosis is the leading cause of death and disability

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C oronary Artery Disease

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  1. Coronary Artery Disease Punit Goel, MD Asst Professor in Cardiology, University of Missouri Hospital & Clinics Staff Cardiologist, Harry Truman VA Hospital

  2. Epidemiology Risk factors Pathogenesis Spectrum Prevention

  3. Atherosclerosis is the leading cause of death and disability in the developed and developing world Clinical manifestations depend on the particular vascular bed affected Coronary vasculature angina, MI, sudden death Cerebral TIA, stroke Peripheral claudication, gangrene Renal hypertension

  4. Atherothrombotic disease is often a diffuse condition involving • multiple vascular beds • Multi-territory atherothrombosis • 3-8% have symptomatic atherosclerosis in all • three territories • 23-32% have involvement in two territories

  5. Epidemiology Risk factors Pathogenesis Spectrum Prevention

  6. Epidemiology The three major clinical manifestations of atherosclerotic CVD are: CHD CVA PVD

  7. Disease impact: In 1997, more than 5mn Americans had CVD Currently one in five American has some form of CVD Each year 1mn deaths are due to CVD (42% of all deaths!) One-sixth of CVD deaths are in persons <65 yrs of age Annually 1.5mn Americans have MI 0.5mn die from CHD 0.5mn have stroke 0.15mn die from stroke

  8. Death rates from CHD has decreased by 40% since 1968 CVD still remains the leading cause of death in developed nations CHD & stroke are the 2nd and 3rd leading causes of mortality even in the developing regions

  9. Economic impact: Despite age adjusted decline in CVD mortality, there is paradoxic increase in economic burden due to: 1) aging population causing actual number of CVD cases to remain stable 2) technologic advances causing more aggressive and extensive treatment

  10. Epidemiology Risk factors Pathogenesis Spectrum Prevention

  11. Concept of “risk factors” for CAD evolved from prospective epidemiological studies in US and Europe which demonstrated consistent association among characteristics observed at one point of time in apparently healthy individuals and subsequent incidence of CAD in these patients. But, presence of a risk factor does not necessarily imply a direct causal relationship.

  12. ATP III classifies Risk factors for CVD into three categories: -Underlying -Major (traditional) -Emerging

  13. Underlying risk factors include: Obesity Disinclination to exercise Atherogenic diet

  14. Major (traditional risk factors): -Age -Male gender -Dyslipidemia High LDL cholesterol Low HDL cholesterol -DM -HTN -Smoking -Family history of premature CAD in first degree relative

  15. Emerging risk factors: -Metabolic syndrome -Triglyceride -Lp(a) -Lp-PLA2 -Fibrinogen -Homocysteine -Urine microalbuminuria/creatinine ratio -Hs CRP -Impaired fasting glucose (100-125 mg/dl per ADA) -Markers of subclinical ASCVD ABI Exercise testing EBCT/MRI Carotid IMT

  16. Dyslipidemia Better term than hyperlipidemia as it includes the risk of having low HDL Serum total cholesterol (TC) is a composite of: LDL cholesterol- directly related to CVD HDL cholesterol- inversely related to CVD VLDL cholesterol- related to CVD in patients with DM and low HDL Best single predictor for CVD risk is TC/HDL ratio. Ideal ratio is <3, intermediate 3-5, high risk >5 This ratio is also the best predictor of treatment benefits

  17. Hypertension Potent risk factor for all CVD and dominant risk factor for stroke. Graded relationship between level of BP and outcomes. SBP rises with age, whereas DBP plateaus in the late middle life and decreases somewhat then. Trials for isolated systolic hypertension have shown benefits for both stroke and CHD

  18. Systolic and diastolic hypertension increase the RR for CVD by 1.6 times For combined Systolic and diastolic HTN the RR is 2.0 The risk for CVD is increased even in individuals with “high normal BP” (130-39/85-89 mm Hg)

  19. Smoking This habit increases the risk of vascular outcomes by 2 fold. Both, regular and filter cigarettes have same adverse effects. Low tar/low nicotine products have not been shown to reduce the risk Unlike other modifiable risk factors, cigarette smoking can be eliminated entirely Benefits of quitting smoking are dramatic. Risk in ex-smokers falls to near non-smoking levels in 2 yrs.

  20. Obesity It contributes independently to CVD risk and also aggravates known CVD risk factors. Measures of obesity include: BMI Waist: hip ratio.

  21. Synergy of risk factors: The CHD death risk in men who smoke, have DBP>90 mm Hg, TC>250 mg/dl, the actual risk is 82/1000 v/s 43/1000 if all the three risk factors are added Thus there is multiplicative effect of multiple risk factors acting in concert. Also control of one risk factor provides substantial benefit in persons with multiple risk factors

  22. Diabetes Mellitus Patients with either type I or type II diabetes have increased risk for CVD Risk of CHD is increased 2-fold in young men and 3-fold in young women with type 2 diabetes Type II diabetics have one or more metabolic abnormalities (hypertriglyceridemia, low HDL, hypertension) They may also have normal LDL levels but LDL particles are dense and small thus being more atherogenic

  23. (Circulation 1998;97:1837)

  24. Metabolic syndrome: -Abdominal obesity: waist circumference Men >40 inches Women >35 inches -Triglycerides >150 mg/dl -HDL Men <40 mg/dl Women <50 mg/dl -BP >130/85 mm Hg -Fasting glucose >100 mg/dl (presence of 3 or more criteria constitutes metabolic syndrome)

  25. Epidemiology Risk factors Pathogenesis Spectrum Prevention

  26. Pathogenesis Atherosclerosis is a progressive disease The term was first proposed by pathologist Felix Marchand in 1904 Athero= gruel/porridge, sclerosis=hardening The process begins in childhood and has clinical manifestations in late adulthood Advanced lesions are a result of three processes: 1. Lipid accumulation 2. Accumulation of intimal SMC, macrophages, T-lymphocytes 3. Formation of connective tissue matrix by proliferated SMC

  27. Atherosclerotic disease can lead to stenosis and occlusion as in most muscular arteries or cause ectasia or aneurysm formation as in elastic vessels (aorta) Even in a given arterial bed it tends to involve certain predisposed areas- proximal LAD, proximal renal arteries, carotid bifurcation The process develops over years to decades and progression is not linear and smooth but discontinuous with periods of quiescence and rapid evolution. Manifestations may be varied from asymptomatic to chronic stable angina/claudication to dramatic acute MI/ stroke/sudden death.

  28. Normal arterial wall has three layers: intima- limited by internal elastic lamina media- between internal and external elastic lamina adventitia Intima is the site at which the atherosclerotic lesions form Lesions can form in one of the two ways: Positive remodelling- intimal thickening associated with dilatation of the artery, so the lumen remains large Negative remodeling- asymmetrical intimal thickening with lumen encroachment

  29. Endothelium: Largest and the most extensive tissue in the body which performs several functions. -“Barrier” between blood and arterial wall -non-thrombogenic surface by secreting PGI2 -highly active metabolic tissue capable of forming several vasoactive substances and connective tissue macromolecules Endothelial cells have receptor for several molecules: LDL Growth factors Pharmacological agents

  30. Initiation of atherosclerosis Lipoprotien accumulation and modification fatty streak formation lipid oxidation nonenzymatic glycation Leukocyte recruitment (T lymphocytes, macro) foam cell formation Evolution and complications SMC involvement

  31. LDL Binds to receptor on endothelial cell surface Internalized Oxidized to oxidized-LDL Ingested by Increased adherence Macrophages and migration of T-cells, monocytes from the lumen into the wall Foam Cell

  32. Smooth muscle cell Accumulation of SMC in the intima is the sine qua non for atherosclerosis. It proliferates in the intima to form intermediate and advanced lesions of atherosclerosis Smooth muscle cell can exist as contractile phenotype or synthetic phenotype. It is the principal contributor to the reparative and fibroproliferative process in the development of atherosclerosis For the lesions to form, the SMC migrates from the media to intima

  33. Vulnerable plaques Thin fibrous cap Large lipid core High macrophage content Stable plaques Thick cap Dense extracellular matrix Less lipid rich core

  34. Epidemiology Risk factors Pathogenesis Spectrum Prevention

  35. Spectrum of coronary artery disease Silent ischemia Chronic stable angina Acute coronary syndromes Unstable angina NSTEMI STEMI

  36. Clinical presentation of CHD depends on age and gender Women: Angina is most common first CHD event followed by MI Men: MI is the most common first event followed by angina. Sudden cardiac death is not uncommon

  37. Acute myocardial infarction (AMI) One of the most common diagnosis in hospitalized patients in industrialized nations Mortality of acute MI is 30% and one-half of these deaths occur before hospitalization Mortality after admission has decreased by 30% in last 2 decades 1 in 25 pts (4%) who survive till hospital discharge die within one year

  38. Pathophysiology AMI results when thrombus (occlusive/nonocclusive) develops at the site of ruptured plaque Vulnerable plaque Rupture Coagulation cascade platelet adhesion, activation activation,aggregation Fibrin and platelet clot Coronary occlusion MI

  39. Amount of myocardial damage depends upon: -territory supplied by the occluded vessel -collateral circulation -duration of occlusion -partial/total occlusion -oxygen demand of jeopardized myocardium

  40. Presentation: Chest pain- most common, similar to anginal pain but more severe and prolonged described as severe, crushing/squeezing/pressure ‘worst pain’ ever Chest pain may be absent in pts with DM or in elderly Atypical presentations: confusion, syncope, profound wkness, arrhythmia

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