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Seyed Mohammad HashemiProfessor of Cardiology
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A careful historyhistory and physical examination is critical to accurately establish the diagnosisdiagnosis of angina pectoris and to exclude other causes of chest pain.
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Angina is caused by myocardial ischemia which occurs whenever myocardial oxygen demand exceeds oxygen supply
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Angina is often elicited by activities and situations which increase increase myocardial oxygen demandmyocardial oxygen demand, including physical activity, cold, emotional stress, sexual intercourse, meals, or lying down .
It has been strongly recommended that patients also be questioned about cocaine use .
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Angina is often characterized more as a discomfortdiscomfort than pain, and may be difficult to describe
squeezing, tightness, pressure, constriction, strangling, burning, heart burn, fullness in the chest,, lump in throat, ache, heavy weight on chest (elephant sitting on chest)
Levine sign
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Angina often radiates to other parts of the body including the upper abdomen (epigastric), shoulders, arms (upper and forearm), wrist, fingers, neck and throat, lower jaw and teeth (but not upper jaw), and rarely to the back (specifically the interscapular region).
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Visceral Pain Visceral fibers enter the spinal cord at
several levels leading to poorly localized, poorly characterized pain. (discomfort, heaviness, dull, aching)
Heart, blood vessels, esophagus and visceral pleura are innervated by visceral fibers
Because of dorsal fibers can overlap three levels above or below, disease of thoracic origin can produce pain anywhere from the jaw to the epigastrum
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Parietal Pain Parietal painParietal pain, in contrast to visceral
pain, is described as sharpsharp and can be localizedlocalized to the dermatome superficial to the site of the painful stimulus.
The dermis and parietal pleura are innervated by parietal fibers.
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Angina occurs more commonly in the morningmorning due to a morning diurnal increase in sympathetic tone. Enhanced sympathetic activity raises heart rate, blood pressure, vessel tone and resistance (resulting in a reduced vessel diameter which causes any fixed lesion to be more occlusive), and platelet aggregability.
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More than 5 min and less than 20 min.
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The most common : shortness of shortness of breathbreath, may reflect mild pulmonary congestion resulting from ischemia-mediated diastolic dysfunction.
Other symptoms may include belching, nausea, indigestion, diaphoresis, dizziness, lightheadedness, clamminess, and fatigue.
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04/21/23
16
Relief of symptoms (To improve quality of life)
Prevention or slowing of disease progression
Prevention of future cardiac events, such as MI, unstable angina, or the need for revascularization
Improvement in survival
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Nonpharmacologic and lifestyle measures
Medical therapy, Percutaneous coronary
intervention (PCI), surgical revascularization
(CABG).
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1. Treatment of hypertension according to Joint National Conference VI guidelines Blood pressure <140/90 or 130/85
mm Hg if heart failure or renal insufficiency; <130/85 mm Hg if diabetes
2. Smoking cessation therapy Smoking Complete cessation
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3. Management of diabetes Diabetes management HbA1c <7%
4. Comprehensive cardiac rehabilitation program (including exercise) Physical activity Minimum goal: 30 min 3 or 4 d/w Optimal goal: daily
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5. LDL-lowering therapy in patients with documented or suspected CAD and LDL cholesterol ≥130 mg/dl, with a target LDL of <100 mg/dl Lipid management Primary goal: LDL <100
mg/dl Secondary goal: If triglycerides ≥200 mg/dl, then non-HDL should be <130 mg/dl
Therapy to lower non-HDL cholesterol in patients with documented or suspected CAD and triglycerides >200 mg/dl, with a target non-HDL cholesterol <130 mg/dl
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6. Weight reduction in obese patients in the presence of hypertension, hyperlipidemia, or diabetes mellitus Weight management BMI 18.5–24.9
kg/m2
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1. Folate therapy in patients with elevated homocysteine levels
2. Identification and appropriate treatment of clinical depression to improve CAD outcomes
3. Intervention directed at psychosocial stress reduction
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1. Initiation of hormone replacement therapy in postmenopausal women for the purpose of reducing cardiovascular risk A
2. Vitamins C and E supplementation A 3. Chelation therapy C 4. Garlic C 5. Acupuncture C 6. Coenzyme Q C
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occurrence of mild angina during the first stages of exercise with disappearance of chest pain at higher workloads despite a greater exercise.
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Exercise Training Enhanced external
counterpulsation (EECP) Endothelial function Promotes coronary collateral
formation Peripheral vascular
resistance Ventricular function Placebo effect
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Transmyocardial revascularization (TMR) Sympathetic denervation Angiogenesis
Spinal cord stimulation (SCS) Neurotransmission
of painful stimuli Release of
endogenous opiates Redistributes myocardial
blood flow to ischemic areas
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Surgical surgeons use the laser to make
between 20 and 40 tiny (one-millimeter-wide)
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improved perfusion by stimulation of angiogenesis
potential placebo effect anesthetic effect mediated by the
destruction of sympathetic nerves carrying pain-sensitive afferent fibers
Peri-procedural infarction.
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Percutaneous
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EECPEECP
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Increases arterial blood pressure and retrograde aortic blood flow during diastole (diastolic augmentation).
Cuffs are wrapped around the patients legs and sequential pressure (300mmHg) is applied in early diastole.
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Angina class III/IV Refractory to medical therapy Reversible ischemia of the free wall not amenable for revascularization
Excluded if LVEF<20% or had current major illness