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Coronary Heart Disease

M Chadi Alraies M.D.

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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.
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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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The estimated cost for cardiovascular disease in 1994 by the American Heart Association is 128 billion dollars.

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An 82-year-old woman presents for her annual examination. She has hypertension and is on chronic β-blocker therapy. She denies all cardiac symptoms. She takes a daily 1-mile walk, and her exercise tolerance has not changed during the past year. Physical examination shows a blood pressure of 138/86 mm Hg, a regular pulse of 80/min, and a respiratory rate of 16/min. Her jugular venous pressure is 10 cm H2O, her carotid upstrokes are normal, and her lungs are clear. Cardiac examination reveals a normal S1, a single S2, and a grade 3/6 early systolic murmur at the upper left sternal border that radiates to her carotids. Abdominal examination is benign, and there is 1+ peripheral edema. Laboratory data are remarkable for a total cholesterol of 210 mg/dL (5.43 mmol/L), with an LDL cholesterol of 110 mg/dL (2.84 mmol/L). Her echocardiogram from 2 years ago showed M Chadi Alraies 5 moderate calcific aortic stenosis, with a

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

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Risk factors
Abnormal lipids Smoking Hypertension Diabetes mellitus Abdominal obesity Psychosocial factors Consumption of too few fruits and vegetables. Too much alcohol Lack of regular physical activity.
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What is the number one preventable cause of cardiovascular disease worldwide?

SMOKING!
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1 year after quitting, the risk of coronary heart disease decreases by 50%
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Framingham score

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Women

Men

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Define the metabolic syndrome?

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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.

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Obesity
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BMI = or > 30 kg/m2 33% of the adult population in the 2003–2004 survey. Low-fat diets appear to be at least as effective as other diets for weight loss

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

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Pathophysiology
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Lipid metabolism in relation to formation of atherosclerotic lesions

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Formation of a fatty streak in an artery

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Formation of atheroma

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Plaque rupture

Many atherosclerotic plaques remain stable or progress only gradually. Rupture, often related to the inflammatory process. The rupture causes…
Turbulent flow  Extrusion of lipids and fatty gruel  Exposure of tissue factor

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Plaque rupture
 

All result in a cascade of events culminating in intravascular thrombosis. The outcome of these events is…
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Complete vessel occlusion. Partial vessel occlusion (causing the symptoms of unstable angina or myocardial infarction) Restabilization often with more severe stenosis.

Transient occlusion and/or embolization of platelet and thrombin debris, which may result in elevation in serum troponin, predispose to clinical events and portend a 22 worse prognosis. M Chadi Alraies

Plaque rupture

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Screening and Diagnosis
me as ur es
me asu res
blo od

show s
sp ec ifi c
coronaries
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ele ctrical

to he ar t

Electrocardiogram
s lse pu im

Stress Test
su pp ly

Coronary Angiography
ng in Narrow i

of of es es St Siit

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A 22-year-old women who is 16 weeks pregnant is evaluated for a 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 mm Hg, her pulse is 94/min and regular, and her respiratory rate is 24/min. Her chest wall is diffusely mildly tender to palpation. Her lungs are clear to auscultation. Cardiac auscultation shows a normal S1, a physiologically split S2, and a grade 2/6 diastolic decrescendo murmur at the left sternal border. There is no peripheral edema. Her electrocardiogram shows only nonspecific ST-T changes. Oxygen saturation by pulse oximetry on room air is 99%. Her D-dimer level is mildly elevated. Which is the most likely cause of her chest pain?

A Pulmonary embolusM Chadi Alraies

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Primary & Secondary Prevention of Coronary Heart Disease
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AHA/ACC Secondary Prevention for Patients With Coronary and Other Vascular Disease 2006 Update
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Coronary and Other Vascular Disease
 

Established coronary disease. Atherosclerotic vascular disease:
Peripheral arterial disease,  Atherosclerotic aortic disease, and  Carotid artery disease.

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SMOKING
     

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

A 55-year-old man is evaluated for cough, scant clear-to-yellow sputum, and malaise of 3 days' duration. He has not had fever, chills, wheezing, or pleuritic chest pain, or recent contact with anyone who has been ill. He has a 40-pack-year smoking history and has had similar symptoms three times in the past 6 months, feeling well in the intervals between episodes. On physical examination, temperature is 37.2 °C (99.0 °F), and pulse rate, respiration rate, and blood pressure are normal. The cardiopulmonary examination is normal, including clear lungs on auscultation with no signs of consolidation. Which of the following is the most appropriate initial smoking-cessation management step during this visit?
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A Recommend nicotine gum B Provide a clear, personalized message to the patient M Chadi Alraies

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BLOOD PRESSURE CONTROL

Goal: For patients with blood pressure 140/90 mm Hg (or 130/80 mm Hg for individuals with chronic kidney disease or diabetes. Initiate or maintain lifestyle modification—weight control; increased physical activity; alcohol moderation; sodium reduction; and emphasis on increased consumption of fresh fruits, vegetables, and lowM Chadi Alraies

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

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A 55-year-old man is evaluated for epigastric discomfort that has been increasing in frequency despite the use of antacids. The discomfort occurs with exercise, but at times he is able to exercise without provocation of his symptoms. He has no other medical conditions and takes only an 81-mg aspirin daily and occasional chondroitin sulfate for joint aches. Physical examination, including vital signs and cardiac examination, is normal. Electrocardiogram shows normal sinus rhythm with normal waveforms. Lipid tests show total cholesterol of 199 mg/dL (5.15 mmol/L), LDL cholesterol of 131 mg/dL (3.39 mmol/L), and HDL cholesterol of 35 mg/dL (0.91 mmol/L). What is the most appropriate next step in the evaluation of this patient?
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A Measurement of C-reactive protein B Measurement of coronary calcium by electron-beam M Chadi Alraies CT

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LIPID MANAGEMENT

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LDL
“The lower the better”

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HDL
“The higher the better”

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LIPID MANAGEMENT
1. 2. 3. 4. 5. 6.

7.

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

Assess fasting lipid profile in all patients, and within 24 hours of hospitalization for those with an acute cardiovascular or coronary event.

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LIPID MANAGEMENT

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

LIPID MANAGEMENT

Therapeutic options to reduce nonHDL:
More intense LDL-C–lowering therapy  Niacin or     Fibrate therapy

If triglycerides are 500 mg/dL, therapeutic options to prevent pancreatitis are fibrate or niacin before LDL-lowering therapy.
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(HMG-CoA) reductase inhibitors (statins)

Aggressive LDL lowering is associated with greater benefits.
The Heart Protection Study (HPS), simvastatin 40 mg a day reduces vascular events by more than 20%.  The PROVE-IT trial showed that vascular events were 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" M Chadi Alraies 42

(HMG-CoA) reductase inhibitors (statins)

Although true regression of plaque is uncommon even with intensive lipid therapy (as in the REVERSAL and ASTEROID trials), progression can be prevented at least in the short run in many patients.

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HDL

Has been shown to be Cardioprotective in the Framingham Heart Study, 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, after adjustment to control for other risk factors.
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Treatment of low HDL

Niacin in high dosages (2–3 g/d or more) Gemfibrozil (600 mg twice daily)

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A 32-year-old woman is brought to the hospital with chest pain at rest after a party. She has had similar pain previously, primarily in the morning and rarely with exertion. The pain usually subsides spontaneously and occasionally is associated with diaphoresis but rarely dyspnea. She almost lost consciousness at work during the most recent episode. She smokes a half pack of cigarettes a week and has occasionally inhaled cocaine. She is otherwise healthy and takes no medications. She has no family history of coronary artery disease. Her blood pressure is 128/70 mm Hg and pulse rate is 72/min. There is no neck vein distention or carotid bruits. The lungs are clear and cardiac examination reveals a normal S1 and S2 and a faint mid-systolic click but no murmur. Examination of the abdomen and extremities is normal. Electrocardiogram shows a 1-mV inferior STsegment elevation; a subsequent electrocardiogram is normal. Serum troponin concentration is 1.5 times the upper limit of normal. Therapy with heparin, aspirin, metoprolol, and nitroglycerin is begun. The next morning, coronary angiography shows normal angiographic appearance of the arteries and normal left ventricular wall motion. The patient is prescribed a daily aspirin and encouraged to stop using cocaine. What additional medical M Chadi Alraies should be prescribed at therapy discharge?
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ACTIVITY

Encourage 30 to 60 minutes of moderate-intensity aerobic activity, such as brisk walking all days of the week (5 days is acceptable). Supplemented by an increase in daily lifestyle activities (eg, walking breaks at work, gardening, household work). Encourage resistance training 2 days per week.
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WEIGHT MANAGEMENT

Assess body mass index and/or waist circumference on each visit and consistently. Encourage weight maintenance/reduction through an appropriate balance of physical activity, caloric intake.

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WEIGHT MANAGEMENT

Maintain/achieve…
A BMI (18.5 - 24.9)  Waist circumference: men <40 inches, women <35 inches.

The initial goal of weight loss therapy should be to reduce body weight by approximately 10% from baseline. With success, further weight loss can be attempted if indicated through further assessment.
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DIABETES MANAGEMENT

Goal: HbA1c <7%

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ANTIPLATELET AGENTS/ ANTICOAGULANTS

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

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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 mg/d for 1 month for bare metal.
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ANTIPLATELET AGENTS/ ANTICOAGULANTS

Manage warfarin to international normalized ratio=2.0 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.
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A 68-year-old man recently diagnosed with adenocarcinoma of the cecum undergoes preoperative evaluation before surgical resection. His medical history includes inoperable coronary artery disease, heart failure with a left ventricular ejection fraction (LVEF) of 35%, hypertension, and hyperlipidemia. Angina is stable, occurring approximately monthly, and he has no orthopnea or paroxysmal nocturnal dyspnea. Medications include lisinopril, carvedilol, furosemide, simvastatin, and daily aspirin. He plays golf weekly, using a cart, walks 2 miles three to four times weekly, and carries groceries up a flight of stairs to his apartment. On physical examination, the pulse rate is 64/min, and blood pressure is 120/64 mm Hg. Jugular venous pressure is 6 cm. On cardiopulmonary examination, the lungs are clear to auscultation, and the heart is regular without an S3. There is no peripheral edema. Laboratory studies, including complete blood count, serum electrolyte levels, and renal function, are normal. The electrocardiogram is unchanged, with a normal sinus rhythm and evidence of an old inferior infarction. Which of the following is the most appropriate next step in the preoperative evaluation of this patient?
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A Plasma B-type natriuretic peptide measurement B Echocardiography M C Exercise stress testing Chadi Alraies

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RENIN-ANGIOTENSINALDOSTERONE SYSTEM BLOCKERS

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ACE inhibitors

Start and continue indefinitely in all patients with…
LV EF 40%.  HTN,  DM  Chronic kidney disease.

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

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 3. 4.

A 55-year-old man with coronary artery disease is evaluated 2 weeks after having had a myocardial infarction. On discharge, his medications included aspirin, sustained-release metoprolol, isosorbide mononitrate, lisinopril, and atorvastatin. Echocardiogram at that time showed inferior and posterior wall akinesis and a left ventricular ejection fraction of 40%. On examination, his heart rate is 60/min and his blood pressure is 130/70 mm Hg. Jugular venous pressure is normal and the chest is clear. Cardiac rhythm is regular, with normal S1 and S2 and no murmurs or extra heart sounds. Laboratory results from yesterday are potassium 5.7 meq/L (5.7 mmol/L), creatinine 1.0 mg/dL (88.42 µmol/L), and LDL cholesterol 65 mg/dL (1.68 mmol/L). Lisinopril therapy is stopped. Wich of the following medications should be started in this patient? Valsartan M Chadi Alraies 58 Spironolactone

Aldosterone blockade

Use in post–myocardial infarction patients, without…
Significant renal dysfunction or  Hyperkalemia  Already receiving therapeutic doses of an ACEI and BB.  Left ventricular ejection fraction 40%  Diabetes or heart failure.

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ß-BLOCKERS
    

Myocardial infarction, Acute coronary syndrome, LV dysfunction Vascular disease Diabetes

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INFLUENZA VACCINATION

Patients with cardiovascular disease should have an influenza vaccination.

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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.

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Elevated plasma homocysteine levels

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

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Hormone replacement therapy HRT

In HERS trial, neither combined estrogen–progesterone nor estrogen alone therapy is protective (in fact both cause harm).

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Fish oil

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

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A 35-year-old man is evaluated during a routine examination. He does not smoke and has no family history of early coronary artery disease. On examination, BMI is 35.2, and waist circumference is 114 cm (45 in). Blood pressure is 142/88 mm Hg. The remainder of the physical examination is normal. Laboratory studies indicate borderline hyperglycemia (fasting plasma glucose, 121 mg/dL [6.7 mmol/L]). Serum total cholesterol level is 246 mg/dL (6.36 mmol/L), high-density lipoprotein level is 31 mg/dL (0.8 mmol/L), and low-density lipoprotein level is 158 mg/dL (4.05 mmol/L). Which of the following recommendations is most appropriate for this patient?
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A Electron-beam CT B Exercise treadmill test C Hydrochlorothiazide M Chadi Alraies D Intensive lifestyle modification

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Pathophysiology of Chronic Ischemia & Acute Coronary Syndromes

Chronic ischemia, including stable angina, is classically caused by supply and demand mismatch. Precipitants include exercise, eating, cold weather, and emotional stress.

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ACS of unstable angina and MI caused by:
Plaque disruption  Platelet and thrombin-mediated coronary thrombosis  Coronary spasm  Microvascular dysfunction.

Pathophysiology of Chronic Ischemia & Acute Coronary Syndromes

These episodes occur in the early morning or shortly after arising.
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Pathophysiology of Chronic Ischemia & Acute Coronary Syndromes

Antithrombotic therapy is directed toward inhibition of platelet activity (aspirin, clopidogrel, IIb/IIIa receptor antagonists), inhibition of coagulation (unfractionated or lowmolecular-weight heparin), and fibrinolysis for ST-segment elevation myocardial infarction.
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Types & Pathophysiology of myocardial ischemia presentation

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Symptomatic, causing angina pectoris. Completely silent. In patients with diagnosed CAD silent ischemic episodes have the same prognostic import as symptomatic ones.
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Myocardial Hibernation & Stunning
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Areas of myocardium that are persistently underperfused. Still viable May develop sustained contractile dysfunction. May lead to LV failure. Reversible following coronary revascularization. Identified by
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Radionuclide testing, (PET), MRI, M Chadi Alraies Inotropic stimulation with dobutamine.

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Myocardial Hibernation & Stunning

A related phenomenon, termed "myocardial stunning," is the occurrence of persistent contractile dysfunction following prolonged or repetitive episodes of myocardial ischemia.

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