Coronary Heart Disease

M Chadi Alraies M.D.

M Chadi Alraies

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The main reason to invest in prevention is to promote health and extend life, improve functioning and prevent suffering. 

"The Role of Prevention in Health Reform", Russell, Louise B., Ph.D., The New England Journal of Medicine, July 29, 1993;329 (5):352-354. (5):352-

M Chadi Alraies

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General considerations   

number one killer in the United States and worldwide. Every minute, an American dies of coronary heart disease. Coronary heart disease afflicts over 13 million Americans.
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dollars. M Chadi Alraies 4 . The estimated cost for cardiovascular disease in 1994 by the American Heart Association is 128 billion dollars.

M Chadi Alraies 5 . Her echocardiogram from 2 years ago showed moderate calcific aortic stenosis.6 m/s (normal. with an LDL cholesterol of 110 mg/dL (2.43 mmol/L). and there is 1+ peripheral edema. a regular pulse of 80/min.84 mmol/L). mean gradient of 44 mm Hg. and her 1exercise tolerance has not changed during the past year.2 cm2 (normal. and a respiratory rate of 16/min.5 m/s) a mean gradient of 30 mm Hg (normal. She denies all cardiac symptoms. She 82-yearhas hypertension and is on chronic -blocker therapy. Physical examination shows a blood pressure of 138/86 mm Hg. Abdominal examination is benign. her carotid upstrokes are normal. <5 mm Hg) and a valve area of 1. a single S2. and a valve area of 1. Her jugular venous pressure is 10 cm H2O. Laboratory data are remarkable for a total cholesterol of 210 mg/dL (5. Cardiac examination reveals a normal S1.0 cm2. >2 cm2) with normal left ventricular systolic function.2 m/s. <1.   An 82-year-old woman presents for her annual examination. She takes a daily 1-mile walk. and her lungs are clear. Echocardiography now shows a maximum aortic jet velocity of 4. with a maximum aortic velocity of 3. and a grade 3/6 early systolic murmur at the upper left sternal border that radiates to her carotids.

 Which is the most appropriate next step? A Reassurance  B Begin a cardiac rehabilitation program  C Begin hydrochlorothiazide  D Start statin therapy  E Refer for aortic valve replacement  M Chadi Alraies 6 .

Risk factors Abnormal lipids Smoking Hypertension Diabetes mellitus Abdominal obesity Psychosocial factors Consumption of too few fruits and vegetables. M Chadi Alraies 7 . Too much alcohol Lack of regular physical activity.

What is the number one preventable cause of cardiovascular disease worldwide? SMOKING! M Chadi Alraies 8 .

the risk of coronary heart disease decreases by 50% 50% M Chadi Alraies 9 .1 year after quitting.

Framingham score M Chadi Alraies 10 .

M Chadi Alraies 11 .

Women Men M Chadi Alraies 12 .

Define the metabolic syndrome? M Chadi Alraies 13 .

The metabolic syndrome  Three or more of the following: Abdominal obesity  Triglycerides 150 mg/dL  HDL cholesterol < 40 mg/dL for men and < 50 mg/dL for women  Fasting glucose 110 mg/dL  Hypertension.  M Chadi Alraies 14 .

Obesity    BMI = or > 30 kg/m2 kg/m2 33% of the adult population in the 2003²2004 33% 2003² survey. LowLow-fat diets appear to be at least as effective as other diets for weight loss M Chadi Alraies 15 .

hyperlipidemia. Physical examination reveals a blood pressure of 128/70 mm 128/ Hg. There is a grade 2/6 midsystolic murmur S2 that does not radiate and is best heard at the 2nd right intercostal space. dyspnea. Which of the following diagnostic tests is most appropriate at this time?      A No further testing at this time B Transthoracic echocardiography C Electron-beam CT ElectronD Treadmill stress echocardiogram E 24-hour ambulatory electrocardiographic monitoring 24M Chadi Alraies 16 . and edema. There is a normal S1 and a S1 physiologically split S2. Past medical history includes only hypertension. fatigue.   A 72-year-old woman is seen for a routine office evaluation to 72-yearestablish care. and a familial history of coronary artery disease. The rest of the physical examination is unrevealing. She does not smoke. There are no carotid bruits. She is active and walks daily and denies angina.

Pathophysiology M Chadi Alraies 17 .

Lipid metabolism in relation to formation of atherosclerotic lesions M Chadi Alraies 18 .

Formation of a fatty streak in an artery M Chadi Alraies 19 .

Formation of atheroma M Chadi Alraies 20 .

often related to the inflammatory process.Plaque rupture    Many atherosclerotic plaques remain stable or progress only gradually. The rupture causes« Turbulent flow  Extrusion of lipids and fatty gruel  Exposure of tissue factor  M Chadi Alraies 21 . Rupture.

M Chadi Alraies 22 . predispose to clinical events and portend a worse prognosis. Partial vessel occlusion (causing the symptoms of unstable angina or myocardial infarction) Restabilization often with more severe stenosis. which may result in elevation in serum troponin.  Transient occlusion and/or embolization of platelet and thrombin debris.Plaque rupture   All result in a cascade of events culminating in intravascular thrombosis. The outcome of these events is«    Complete vessel occlusion.

Plaque rupture

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Screening and Diagnosis

ElectroElectrocardiogram

Stress Test

Coronary Angiography

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A 22-year-old women who is 16 weeks pregnant is evaluated for 22-yeara 2-hour history of severe anterior chest pain radiating to her mid back. She is a tall, thin woman with a pectus abnormality of her chest and long, thin fingers. Her blood pressure is 140/80 140/ mm Hg, her pulse is 94/min and regular, and her respiratory rate 94/min is 24/min. Her chest wall is diffusely mildly tender to palpation. 24/min. Her lungs are clear to auscultation. Cardiac auscultation shows a normal S1, a physiologically split S2, and a grade 2/6 diastolic S1 S2 decrescendo murmur at the left sternal border. There is no peripheral edema. Her electrocardiogram shows only nonspecific STST-T changes. Oxygen saturation by pulse oximetry on room air is 99%. Her D-dimer level is mildly elevated. 99%. DWhich is the most likely cause of her chest pain? 
   

A Pulmonary embolus B Acute myocardial infarction C Aortic dissection D Costochondritis E Pericarditis
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Primary & Secondary Prevention of Coronary Heart Disease M Chadi Alraies 26 .

AHA/ACC Secondary Prevention for Patients With Coronary and Other Vascular Disease 2006 Update M Chadi Alraies 27 .

M Chadi Alraies 28 .

 M Chadi Alraies 29 . and  Carotid artery disease. Atherosclerotic vascular disease: Peripheral arterial disease.  Atherosclerotic aortic disease.Coronary and Other Vascular Disease   Established coronary disease.

Advise every tobacco user to quit.SMOKING        Goal: Complete cessation. M Chadi Alraies 30 . Arrange follow-up. referral to special programs. Urge avoidance of exposure to environmental tobacco smoke at work and home. No exposure to environmental tobacco smoke. Ask about tobacco use status at every visit. Assess the tobacco user·s willingness to quit. or followpharmacotherapy (including nicotine replacement and bupropion). Assist by counseling and developing a plan for quitting.

wheezing. and malaise of 3 days' duration. He has not had fever. scant clear-to-yellow 55-yearclear-tosputum.0 °F). On physical examination. and 37. pulse rate. temperature is 37.2 °C (99. The cardiopulmonary examination is normal. He has a 40-pack-year smoking history 40-packand has had similar symptoms three times in the past 6 months. feeling well in the intervals between episodes. chills. (99. including clear lungs on auscultation with no signs of consolidation. or recent contact with anyone who has been ill.   A 55-year-old man is evaluated for cough. or pleuritic chest pain. personalized message to the patient C Refer the patient to a behavioral-modification program behavioralD Prescribe bupropion M Chadi Alraies 31 . and blood pressure are normal. Which of the following is the most appropriate initial smokingsmokingcessation management step during this visit?     A Recommend nicotine gum B Provide a clear. respiration rate.

alcohol moderation.BLOOD PRESSURE CONTROL   Goal: For patients with blood pressure 140/ 140/90 mm Hg (or 130/80 mm Hg for 130/ individuals with chronic kidney disease or diabetes. increased physical activity. sodium reduction. and emphasis on increased consumption of fresh fruits. and low-fat dairy products. lowM Chadi Alraies 32 . vegetables. Initiate or maintain lifestyle modification³ modification³ weight control.

BLOOD PRESSURE CONTROL     Add blood pressure medication. Use JNC 7 M Chadi Alraies 33 . Treating initially with ß-blockers and/or ACE ßinhibitors. Addition of other drugs such as thiazides as needed to achieve goal blood pressure. pressure.

is normal. LDL cholesterol of 131 mg/dL (3. and HDL cholesterol of 35 mg/dL (0. He has no other medical conditions and takes only an 81-mg aspirin daily and 81occasional chondroitin sulfate for joint aches. Physical examination. The discomfort occurs with exercise.15 mmol/L).39 mmol/L). Electrocardiogram shows normal sinus rhythm with normal waveforms.   A 55-year-old man is evaluated for epigastric discomfort that has 55-yearbeen increasing in frequency despite the use of antacids. What is the most appropriate next step in the evaluation of this patient?      A Measurement of C-reactive protein CB Measurement of coronary calcium by electron-beam CT electronC Measurement of serum homocysteine D Exercise electrocardiographic stress test E Exercise echocardiogram M Chadi Alraies 34 . but at times he is able to exercise without provocation of his symptoms.91 mmol/L). including vital signs and cardiac examination. Lipid tests show total cholesterol of 199 mg/dL (5.

LIPID MANAGEMENT M Chadi Alraies 35 .

LDL ´The lower the betterµ M Chadi Alraies 36 .

HDL ´The higher the betterµ M Chadi Alraies 37 .

7. M Chadi Alraies 38 . 6. 5.<100 LDL-C <100 mg/dL non-HDLnon-HDL-C should be <130 mg/dL <130 Adding plant stanol/sterols (2 g/d) and viscous fiber (2 (>10 g/d) will further lower LDL-C. 3. Cholesterol (to <200 mg/d). Start dietary therapy. <200 LDL. 2.LIPID MANAGEMENT 1. (>10 LDLEncourage increased consumption of omega-3 fatty omegaacids in the form of fish or in capsule form (1 g/d) (1 for risk reduction. Reduce intake of saturated fats (to <7% of total <7 calories). 4.

LIPID MANAGEMENT  Assess fasting lipid profile in all patients. event. and within 24 hours of hospitalization for those with an acute cardiovascular or coronary event. M Chadi Alraies 39 .

LIPID MANAGEMENT  For hospitalized patients. LDLIf baseline LDL-C is 70 to 100 mg/dL. non-HDL<100 M Chadi Alraies 40 . intensify LDL-lowering drug onLDLLDLtherapy (may require LDL-lowering drug combination. initiate LDL-lowering drug therapy. If triglycerides are 200 to 499 mg/dL. LDL<70 If baseline LDL-C is 100 mg/dL. it is reasonable to treat to LDL-C LDLLDL<70 mg/dL. And« Further reduction of non-HDL-C to <100 mg/dL is reasonable. non-HDL-C should be <130 non-HDL<130 mg/dL. LDLLDLIf on-treatment LDL-C is 100 mg/dL. initiate lipid-lowering medication as lipidrecommended below before discharge according to the following schedule:        LDLLDL-C should be <100 mg/dL and« <100 Further reduction of LDL-C to <70 mg/dL is reasonable.

therapeutic options to prevent pancreatitis are fibrate or niacin before LDL-lowering therapy.LIPID MANAGEMENT  Therapeutic options to reduce non-HDL: nonMore intense LDL-C²lowering therapy LDL Niacin or  Fibrate therapy   If triglycerides are 500 mg/dL. LDL- M Chadi Alraies 41 .

simvastatin 40 mg a day reduces vascular events by more than 20%.  The PROVE-IT trial showed that vascular events PROVEwere reduced with more aggressive lipid lowering (atorvastatin 80 mg/d compared to pravastatin 40 mg/d following an acute coronary syndrome). providing more evidence of "lower is better"  The TNT (Treating to New Targets)  M Chadi Alraies 42 .(HMG(HMG-CoA) reductase inhibitors (statins)  Aggressive LDL lowering is associated with greater benefits. 20%. The Heart Protection Study (HPS).

(HMG(HMG-CoA) reductase inhibitors (statins)  Although true regression of plaque is uncommon even with intensive lipid therapy (as in the REVERSAL and ASTEROID trials). M Chadi Alraies 43 . progression can be prevented at least in the short run in many patients.

 M Chadi Alraies 44 . after adjustment to control for HDL. and in retrospective analyses of intervention trials such as the Coronary Primary Prevention Trial and the Multiple Risk Factor Intervention Trial 5-7 The data were consistent with a 2% to 3% decrease in CHD risk for each 1 mg/dL increase in HDL.HDL  Has been shown to be Cardioprotective in the Framingham Heart Study. other risk factors.

Treatment of low HDL   Niacin in high dosages (2²3 g/d or more) (2 Gemfibrozil (600 mg twice daily) (600 M Chadi Alraies 45 .

Examination of the abdomen and extremities is normal. Therapy with heparin. a subsequent 1STelectrocardiogram is normal. metoprolol. The lungs are clear and cardiac examination reveals a normal S1 and S2 and a faint mid-systolic click but no midmurmur. She has had similar pain previously. She has no family history of coronary artery disease.5 times the upper limit of normal. Her blood pressure is 128/70 mm Hg and pulse rate is 72/min. The patient is prescribed a daily aspirin and encouraged to stop using cocaine. She almost lost consciousness at work during the most recent episode. There is no neck vein distention or carotid bruits. She is otherwise healthy and takes no medications. Serum troponin concentration is 1. coronary angiography shows normal angiographic appearance of the arteries and normal left ventricular wall motion. The pain usually subsides spontaneously and occasionally is associated with diaphoresis but rarely dyspnea. and nitroglycerin is begun. aspirin. primarily in the morning and rarely with exertion.  A 32-year-old woman is brought to the hospital with chest pain at rest after a 32-yearparty. What additional medical therapy should be prescribed at discharge?      A Angiotensin-converting enzyme inhibitor AngiotensinB -blocker C Calcium-channel blocker CalciumD Clopidogrel M Chadi Alraies 46 . The next morning. Electrocardiogram shows a 1-mV inferior ST-segment elevation. She smokes a half pack of cigarettes a week and has occasionally inhaled cocaine.

walking breaks at work. Encourage resistance training 2 days per week.ACTIVITY    Encourage 30 to 60 minutes of moderatemoderateintensity aerobic activity. such as brisk walking all days of the week (5 days is acceptable). household work). M Chadi Alraies 47 . gardening. (5 Supplemented by an increase in daily lifestyle activities (eg.

M Chadi Alraies 48 . Encourage weight maintenance/reduction through an appropriate balance of physical activity. caloric intake.WEIGHT MANAGEMENT   Assess body mass index and/or waist circumference on each visit and consistently.

9) (18. M Chadi Alraies 49 .  Waist circumference: men <40 inches. With success.WEIGHT MANAGEMENT  Maintain/achieve« A BMI (18. women <35 <40 <35 inches.24.   The initial goal of weight loss therapy should be to reduce body weight by approximately 10% 10% from baseline. 24. further weight loss can be attempted if indicated through further assessment.5 .

DIABETES MANAGEMENT  Goal: HbA1c <7% HbA1 <7 M Chadi Alraies 50 .

ANTIPLATELET AGENTS/ ANTICOAGULANTS    Start aspirin 75 to 162 mg/d unless contraindicated. Doses higher than 162 mg/d can be continued for up to 1 year. aspirin should be started within 48 hours after surgery. For patients undergoing CABG. M Chadi Alraies 51 .

M Chadi Alraies 52 .ANTIPLATELET AGENTS/ ANTICOAGULANTS  Start and continue clopidogrel 75 mg/d in combination with aspirin for up to 12 months in patients after:  ACS. PCI with stent placement  Patients who have undergone percutaneous coronary intervention with stent placement should initially receive higher-dose aspirin at 325 highermg/d for 1 month for bare metal.

0 to 3.0 for paroxysmal or chronic atrial fibrillation or flutter Use of warfarin in conjunction with aspirin and/or clopidogrel is associated with increased risk of bleeding and should be monitored closely.ANTIPLATELET AGENTS/ ANTICOAGULANTS   Manage warfarin to international normalized ratio=2 ratio=2. M Chadi Alraies 53 .

hyperlipidemia. and daily aspirin. serum electrolyte levels. and renal function. On cardiopulmonary examination. The electrocardiogram is unchanged. Which of the following is the most appropriate next step in the preoperative evaluation of this patient?      A Plasma B-type natriuretic peptide measurement BB Echocardiography C Exercise stress testing D Nuclear imaging for LVEF E No further evaluation M Chadi Alraies 54 . walks 2 miles three to four times weekly. the pulse rate is 64/min. carvedilol. and 35%. There is no peripheral edema. His medical history includes inoperable coronary artery disease. and carries groceries up a flight of stairs to his apartment. Angina is stable. On physical examination. Jugular venous pressure is 6 cm.   A 68-year-old man recently diagnosed with adenocarcinoma of the cecum 68-yearundergoes preoperative evaluation before surgical resection. simvastatin. furosemide. heart failure with a left ventricular ejection fraction (LVEF) of 35%. Medications include lisinopril. using a cart. and the heart is regular without an S3. with a normal sinus rhythm and evidence of an old inferior infarction. 120/ 120/64 mm Hg. Laboratory studies. and he has no orthopnea or paroxysmal nocturnal dyspnea. the lungs are clear to auscultation. are normal. occurring approximately monthly. and blood pressure is 64/min. hypertension. He plays golf weekly. including S3 complete blood count.

RENIN-ANGIOTENSINRENIN-ANGIOTENSINALDOSTERONE SYSTEM BLOCKERS M Chadi Alraies 55 .

 HTN.  M Chadi Alraies 56 .ACE inhibitors  Start and continue indefinitely in all patients with« LV EF 40%. 40%.  DM  Chronic kidney disease.

Consider use in combination with ACE inhibitors in systolic-dysfunction heart failure. systolic- M Chadi Alraies 57 . 40%.Angiotensin receptor blockers     Intolerance of ACE inhibitors Heart failure Myocardial infarction with left ventricular ejection fraction 40%.

Jugular venous pressure is normal and the chest is clear. 2.7 mmol/L). 5. with normal S1 and S2 S1 S2 and no murmurs or extra heart sounds. 4. and LDL cholesterol 65 mg/dL (1. On 40%. and atorvastatin. A 55-year-old man with coronary artery disease is evaluated 2 55-yearweeks after having had a myocardial infarction. (1 mmol/L). On discharge.68 (88. sustained-release metoprolol.  1. sustainedisosorbide mononitrate.7 meq/L (5. Lisinopril therapy is stopped. Cardiac rhythm is regular.42 mol/L). examination. lisinopril. his heart rate is 60/min and his blood pressure is 60/min 130/ 130/70 mm Hg. 3. creatinine 1. his medications included aspirin.0 (5 mg/dL (88. Wich of the following medications should be started in this patient? Valsartan Spironolactone Amlodipine Eplerenone Hydralazine M Chadi Alraies 58 . Laboratory results from yesterday are potassium 5. Echocardiogram at that time showed inferior and posterior wall akinesis and a left ventricular ejection fraction of 40%.

 Left ventricular ejection fraction 40% 40%  Diabetes or heart failure.Aldosterone blockade  Use in post²myocardial infarction patients. post² without« Significant renal dysfunction or  Hyperkalemia  Already receiving therapeutic doses of an ACEI and BB.  M Chadi Alraies 59 .

Acute coronary syndrome. LV dysfunction Vascular disease Diabetes M Chadi Alraies 60 .ß-BLOCKERS      Myocardial infarction.

M Chadi Alraies 61 .INFLUENZA VACCINATION  Patients with cardiovascular disease should have an influenza vaccination.

M Chadi Alraies 62 .Antioxidant  (HOPE) trial found that vitamin E may even be harmful by increasing the likelihood of heart failure and other trials have suggested that vitamin E may hinder the effectiveness of statin therapy.

M Chadi Alraies 63 . Reduced with dietary supplements of folic acid (1 mg/d) in combination with vitamin B6 and B6 vitamin B12. RCT showed they are of little or no value in preventing vascular events.Elevated plasma homocysteine levels    Associated with an increased risk of vascular events. B12.

neither combined estrogen² estrogen² progesterone nor estrogen alone therapy is protective (in fact both cause harm). M Chadi Alraies 64 .Hormone replacement therapy HRT  In HERS trial.

may help omegaacids.Fish oil  Fish. and it is recommended that it be eaten three times a week by patients at risk. M Chadi Alraies 65 . protect against vascular disease. rich in omega-3 fatty acids.

7 mmol/L]). Blood pressure is 142/88 mm Hg. and low-density lipoprotein level is 158 mg/dL (4.36 (6 mmol/L). BMI is 35. Which of the following recommendations is most appropriate for this patient?      A Electron-beam CT ElectronB Exercise treadmill test C Hydrochlorothiazide D Intensive lifestyle modification E Intake of red wine M Chadi Alraies 66 . On examination.8 high(0 mmol/L). Laboratory studies indicate borderline hyperglycemia (fasting plasma glucose. 121 mg/dL [6.05 low(4 mmol/L).2. and waist circumference is 114 cm 35. The remainder of the 142/ physical examination is normal. Serum total cholesterol level is 246 mg/dL (6.   A 35-year-old man is evaluated during a routine examination. He 35-yeardoes not smoke and has no family history of early coronary artery disease. (45 in). high-density lipoprotein level is 31 mg/dL (0.

M Chadi Alraies 67 . cold weather. Precipitants include exercise. eating.Pathophysiology of Chronic Ischemia & Acute Coronary Syndromes   Chronic ischemia. including stable angina. is classically caused by supply and demand mismatch. and emotional stress.

  These episodes occur in the early morning or shortly after arising. M Chadi Alraies 68 .Pathophysiology of Chronic Ischemia & Acute Coronary Syndromes  ACS of unstable angina and MI caused by: caused Plaque disruption  Platelet and thrombin-mediated coronary thrombinthrombosis  Coronary spasm  Microvascular dysfunction.

M Chadi Alraies 69 .Pathophysiology of Chronic Ischemia & Acute Coronary Syndromes  Antithrombotic therapy is directed toward inhibition of platelet activity (aspirin. and fibrinolysis for STST-segment elevation myocardial infarction. inhibition of coagulation (unfractionated or lowlowmolecularmolecular-weight heparin). clopidogrel. IIb/IIIa receptor antagonists).

In patients with diagnosed CAD silent ischemic episodes have the same prognostic import as symptomatic ones.Types & Pathophysiology of myocardial ischemia presentation    Symptomatic. M Chadi Alraies 70 . causing angina pectoris. Completely silent.

Inotropic stimulation with dobutamine. May lead to LV failure.Myocardial Hibernation & Stunning       Areas of myocardium that are persistently underperfused. MRI. M Chadi Alraies 71 . Still viable May develop sustained contractile dysfunction. Identified by   Radionuclide testing. (PET). Reversible following coronary revascularization.

" is the occurrence of persistent contractile dysfunction following prolonged or repetitive episodes of myocardial ischemia.Myocardial Hibernation & Stunning  A related phenomenon. M Chadi Alraies 72 . termed "myocardial stunning.

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