Transcript Coronary Artery Disease and Acute Coronary Syndrome Myocardial Infarction
Coronary Artery Disease and Acute Coronary Syndrome Myocardial Infarction
(relates to Chapter 33, “Nursing Management: Coronary Artery Disease and Acute Coronary Syndrome,” in the textbook)
Description
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Cardiovascular diseases are the major cause of death in Canada Heart attacks are still the leading cause of all cardiovascular disease deaths and deaths in general
Etiology and Pathophysiology Developmental Stages
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Complicated lesion
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Final stage in development
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The most dangerous
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Plaque consists of a core of lipid materials within an area of dead tissue
Etiology and Pathophysiology Developmental Stages
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Complicated lesion
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With the incorporation of lipids, thrombi, damaged tissue, and accumulation of calcium, the growing lesion becomes complex
Etiology and Pathophysiology Collateral Circulation
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Normally some arterial branching, termed collateral circulation, exists within the coronary circulation
Etiology and Pathophysiology Collateral Circulation
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Growth of collateral circulation is attributed to two factors:
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The inherited predisposition to develop new vessels
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The presence of chronic ischemia
Etiology and Pathophysiology Collateral Circulation
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When occlusion of the coronary arteries occurs slowly over a long period, there is a greater chance of adequate collateral circulation developing
Collateral Circulation Fig. 33-5
Clinical Manifestations of CAD
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Angina Pectoris Acute Coronary Syndrome Sudden Cardiac Death
Clinical Manifestations
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Stable Angina
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Results when the lack of oxygen supply is temporary and reversible
Clinical Manifestations
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Acute Coronary Syndrome (ACS)
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Develops when the oxygen supply is prolonged and not immediately reversible
Clinical Manifestations
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ACS encompasses:
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Unstable angina
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Non-ST-segment-elevation myocardial infarction (NSTEMI)
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ST-segment-elevation (STEMI)
Relationships Among CAD, Stable Angina, and MI Fig. 33-8
Etiology and Pathophysiology
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Myocardial ischemia:
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O 2 demand > O 2 supply
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Primary reason for insufficient blood flow is narrowing of coronary arteries by atherosclerosis
Etiology and Pathophysiology
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In CAD the coronary arteries are unable to dilate to meet increased metabolic needs because they are already chronically dilated beyond the obstructed area
Etiology and Pathophysiology
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For ischemia to occur, the artery is usually 75% or more stenosed In addition, the diseased heart has difficulty increasing the rate of blood flow
Etiology and Pathophysiology
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Coronary spasm
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The constriction is transient and reversible
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Causes either subtotal or total narrowing
Etiology and Pathophysiology
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Myocardial cyanosis occurs within the 1 st 10 seconds of coronary occlusion ECG changes Total occlusion
anaerobic metabolism and lactic acid accumulation
Etiology and Pathophysiology
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Myocardial Infarction
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Occurs as a result of sustained ischemia, causing irreversible cellular death
Etiology and Pathophysiology
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Myocardial Infarction
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The degree of altered function depends on the area of the heart involved and the size of the infarct
Etiology and Pathophysiology
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Myocardial Infarction
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Contractile function of the heart stops in the areas of myocardial necrosis
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Most involve the left ventricle (LV)
Etiology and Pathophysiology
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Myocardial Infarction
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Transmural MI
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Involves the entire thickness of the myocardium
Transmural MI Fig. 33-11
Etiology and Pathophysiology
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Myocardial Infarction
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Subendocardial MI
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The damage has not penetrated through the entire thickness
Etiology and Pathophysiology
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Myocardial Infarction
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Infarctions are described by the area of occurrence
Etiology and Pathophysiology Healing Process
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Within 24 hours, leukocytes infiltrate the area of cell death
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Enzymes are released from the dead cardiac cells (important indicators of MI)
Etiology and Pathophysiology Healing Process
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Proteolytic enzymes of neutrophils and macrophages remove all necrotic tissue by 2 nd or 3 rd day
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Development of collateral circulation improves areas of poor perfusion
Etiology and Pathophysiology Healing Process
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Necrotic zone identifiable by ECG changes and nuclear scanning
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10 to 14 days after MI, scar tissue is still weak
Etiology and Pathophysiology Healing Process
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By 6 weeks after MI, scar tissue has replaced necrotic tissue
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Area is said to be healed
Etiology and Pathophysiology Healing Process
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Ventricular remodeling
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In an attempt to compensate for the infarcted muscle, the normal myocardium will hypertrophy and dilate
Types of Angina Silent Ischemia
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Up to 80% of patients with myocardial ischemia are asymptomatic
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Associated with diabetes mellitus and hypertension
Types of Angina Prinzmetal’s Angina
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When spasm occurs:
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Pain
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Marked, transient ST segment elevation with angina (unlike with AMI; ↑ST = MI)
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May occur during REM sleep
Clinical Manifestations Myocardial Infarction
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Pain
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Severe, immobilizing chest pain not relieved by rest, position change, or nitrate administration
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The hallmark of an MI
Location of Chest Pain Fig. 33-12
Clinical Manifestations Myocardial Infarction
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Nausea and vomiting
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Can result from reflex stimulation of the vomiting center by the severe pain
Clinical Manifestations Myocardial Infarction
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Sympathetic nervous system stimulation
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catecholamines released during initial phases of MI
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Results in diaphoresis and vasoconstriction
Clinical Manifestations Myocardial Infarction
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Fever
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May
within 1 st 24 hours up to 100.4
°
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May last as long as 1 week
Clinical Manifestations Myocardial Infarction
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Fever
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Systemic manifestation of the inflammatory process caused by cell death
Clinical Manifestations Myocardial Infarction
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Cardiovascular manifestations
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BP and heart rate initially
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Later the BP may drop from
CO
Clinical Manifestations Myocardial Infarction
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Cardiovascular manifestations
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urine output
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Crackles
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Hepatic engorgement
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Peripheral edema
Complications of Myocardial Infarction
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Arrhythmias
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Most common complication
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Present in 80% of MI patients
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Most common cause of death in the prehospital period
Complications of Myocardial Infarction
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Congestive heart failure
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A complication that occurs when the pumping power of the heart has diminished
Complications of Myocardial Infarction
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Cardiogenic shock
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Occurs when inadequate oxygen and nutrients are supplied to the tissues because of severe LV failure
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Requires aggressive management
Complications of Myocardial Infarction
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Papillary muscle dysfunction
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Causes mitral valve regurgitation
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Condition aggravates an already compromised LV
Complications of Myocardial Infarction
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Ventricular aneurysm
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Results when the infarcted myocardial wall becomes thinned and bulges out during contraction
Complications of Myocardial Infarction
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Pericarditis
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An inflammation of the visceral and/or parietal pericardium
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May result in cardiac compression,
LV filling and emptying, and cardiac failure
Complications of Myocardial Infarction
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Dressler syndrome
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Characterized by pericarditis with effusion and fever that develops 1 to 4 weeks after MI
Complications of Myocardial Infarction
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Pulmonary embolism
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Source of the thrombus may be the roughened endocardium or leg veins
Diagnostic Studies Myocardial Infarction
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History of pain Risk factors Health history ECG: ST elevation, greater than 1 mm above PR Interval; T Wave inversion (flipped T Waves); Pathological Q-wave (Q wave greater than ¼ size of R wave) Serum cardiac markers: CK-MB: indicates muscle damage (rises 3-12 hours post AMI – returns to normal 2-3 days) Triponen: is a myocardial muscle protein (rises as quickly as CK; remains elevated for 2 weeks) Myoglobin: rises 3 hours after AMI; lacks cardiac specificity
Collaborative Care Angina
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Percutaneous coronary intervention
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Surgical intervention alternative
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Performed with local anesthesia
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Ambulatory 24 hours after the procedure
Collaborative Care Angina
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Stent placement
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Used to treat abrupt or threatened abrupt closure and restenosis following PCI
Collaborative Care Angina
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Atherectomy
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The plaque is shaved off using a type of rotational blade
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Decreases the incidence of abrupt closure as compared with PCI
Collaborative Care Angina
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Laser angioplasty
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Performed with a catheter containing fibers that carry laser energy
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Used to precisely dissolve the blockage
Collaborative Care Angina
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Myocardial revascularization (CABG)
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Primary surgical treatment for CAD
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Patient with CAD who has failed medical management or has advanced disease is considered a candidate
Collaborative Care Angina
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MIDCABG procedure
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Minimally invasive direct coronary artery bypass grafting (MIDCABG)
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Alternative to traditional CABG
Collaborative Care Myocardial Infarction
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Fibrinolytic therapy Cardiac catheterization Percutaneous coronary intervention
Collaborative Care Myocardial Infarction
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Drug Therapy
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IV nitroglycerin
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Antiarrhythmic drugs
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Morphine
Collaborative Care Myocardial Infarction
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Drug Therapy
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-Adrenergic blockers
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Angiotensin-converting enzyme inhibitors
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Stool softeners
Collaborative Care Myocardial Infarction
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Nutritional Therapy
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Diet restricted in saturated fats and cholesterol
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Low sodium
Nursing Management Angina and Myocardial Infarction Nursing Implementation: MI
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Acute Intervention
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Morphine
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Continuous ECG
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Frequent vital signs
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Rest and comfort
Nursing Management Angina and Myocardial Infarction Nursing Implementation: MI
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Acute Intervention
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Anxiety
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Emotional and behavioral reactions
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Communicate with family
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Provide support
Nursing Management Angina and Myocardial Infarction Nursing Implementation: MI
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Ambulatory and Home Care
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Rehabilitation
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Cardiac rehabilitation
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Physical exercise
Nursing Management Angina and Myocardial Infarction Nursing Implementation: MI
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Ambulatory and Home Care
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Resumption of sexual activity
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Emotional readiness
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Physical training
Nursing Management Angina and Myocardial Infarction Evaluation
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Pain level Cardiac pump effectiveness Anxiety control Energy conservation Health orientation
Women and Coronary Artery Disease
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About 500,000 deaths occur in women per year
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Kills almost 10 times more women than breast cancer
Women and Coronary Artery Disease
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Manifest CAD 10 years later in life than men
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Most have symptoms of angina rather than MI
Women and Coronary Artery Disease
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Diabetes mellitus found to be the single most powerful predictor of CAD in women