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12 Cards in this Set

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  • Back
Coronary artery disease
involves impairment of blood flow through the coronary arteries, most commonly by atheromas. Clinical presentations include silent ischemia, angina pectoris, acute coronary syndromes (unstable angina, MI), and sudden cardiac death. Diagnosis is by symptoms, ECG, stress testing, and sometimes coronary angiography. Prevention consists of modifying reversible risk factors (eg, hypercholesterolemia, physical inactivity, smoking). Treatment includes drugs and procedures to reduce ischemia and restore or improve coronary blood flow.
Acute Coronary Syndromes (ACS)
result from acute obstruction of a coronary artery. Consequences depend on degree of obstruction and range from unstable angina to non-ST-segment elevation MI (NSTEMI), ST-segment elevation MI (STEMI), and sudden cardiac death. Symptoms are similar in each of these syndromes (except sudden death) and include chest discomfort with or without dyspnea, nausea, and diaphoresis. Diagnosis is by ECG and the presence or absence of serologic markers. Treatment is antiplatelet drugs, anticoagulants, nitrates, β-blockers, and, for STEMI, emergency reperfusion via fibrinolytic drugs, percutaneous intervention, or, occasionally, coronary artery bypass graft surgery.
Angina Pectoris
is a clinical syndrome of precordial discomfort or pressure due to transient myocardial ischemia. It is typically precipitated by exertion and relieved by rest or sublingual nitroglycerin. Diagnosis is by symptoms, ECG, and myocardial imaging. Treatment may include nitrates, β-blockers, Ca channel blockers, and coronary angioplasty or coronary artery bypass graft surgery.
The aorta
originates at the left ventricle above the aortic valve (aortic root), travels upward (ascending thoracic aorta) to the 1st branch of the aorta (brachiocephalic or innominate artery), arches up and behind the heart (aortic arch), then turns downward distal to the left subclavian artery (descending aorta) through the thorax (thoracic aorta) and abdomen (abdominal aorta). The abdominal aorta ends by dividing into the 2 common iliac arteries.
Abdominal Aortic Branch Occlusion
Various branches of the aorta can be occluded by atherosclerosis, fibromuscular dysplasia, or other conditions, producing symptoms and signs of ischemia or infarction. Diagnosis is by imaging tests. Treatment is with embolectomy, angioplasty, or sometimes surgical bypass grafting.
are abnormal dilations of arteries caused by weakening of the arterial wall. Common causes include hypertension, atherosclerosis, infection, trauma, and hereditary or acquired connective tissue disorders. Aneurysms are usually asymptomatic but can cause pain and lead to ischemia, thromboembolism, spontaneous dissection, and rupture, which may be fatal. Diagnosis is by imaging tests (eg, ultrasonography, CT angiography, magnetic resonance angiography, aortography). Treatment of unruptured aneurysms is with risk factor modification (eg, strict BP control) plus surveillance imaging or with surgery, depending on size and location of the aneurysm and presence of symptoms. Treatment of ruptured aneurysms is immediate surgical repair and placement of a synthetic graft or endograft.
Abdominal Aortic Aneurysms (AAA)
account for 3⁄4 of aortic aneurysms and affect 0.5 to 3.2% of the population. Prevalence is 3 times greater in men. AAAs typically begin below the renal arteries but may include renal arterial ostia; about 50% involve the iliac arteries. Generally, aortic diameter ≥ 3 cm constitutes an AAA. Most AAAs are fusiform; some are saccular. Many are lined with laminated thrombi. AAAs involve all layers of the aorta and do not involve dissection; however, a thoracic aortic dissection may extend to the distal abdominal aorta.
etiology of AAA
The most common cause is weakening of the arterial wall, usually associated with atherosclerosis. Other causes include trauma, vasculitis, cystic medial necrosis, and postsurgical anastomotic disruption. Uncommonly, syphilis and localized bacterial or fungal infection, typically due to sepsis or infective endocarditis, weaken the arterial wall and cause infected (mycotic) aneurysms.

Smoking is the strongest risk factor. Other risk factors include hypertension, older age (peak incidence at age 70 to 80), family history (in 15 to 25%), Caucasian race, and male sex.
Thoracic aortic aneurysms (TAAs)
account for 1⁄4 of aortic aneurysms. Men and women are affected equally. About 40% of TAAs occur in the ascending thoracic aorta (between the aortic valve and brachiocephalic, or innominate, artery), 10% occur in the aortic arch (including the brachiocephalic, carotid, and subclavian arteries), 35% occur in the descending thoracic aorta (distal to the left subclavian artery), and 15% occur in the upper abdomen (as thoracoabdominal aneurysms).
Aortic Branch Aneurysms
may occur in any major aortic branch; such aneurysms are much less common than abdominal or thoracic aortic aneurysms. Risk factors include atherosclerosis, hypertension, cigarette smoking, and older age. Localized infection can cause mycotic aneurysms.

Subclavian artery aneurysms are sometimes associated with cervical ribs or thoracic outlet syndrome.

Splanchnic artery aneurysms are uncommon. About 60% occur in the splenic artery, 20% in the hepatic artery, and 5.5% in the superior mesenteric artery. Splenic artery aneurysms occur in more women than men (4:1). Causes include medial fibromuscular dysplasia, portal hypertension, multiple pregnancies, penetrating or blunt abdominal trauma, pancreatitis, and infection. Hepatic artery aneurysms occur in more men than women (2:1). They may result from previous abdominal trauma, illicit IV drug use, medial degeneration of the arterial wall, or periarterial inflammation. Renal artery aneurysms may dissect or rupture, causing acute occlusion
Aortic dissection
is the surging of blood through a tear in the aortic intima with separation of the intima and media and creation of a false lumen. The intimal tear may be a primary event or secondary to hemorrhage within the media. The dissection may occur anywhere along the aorta and extend proximally or distally into other arteries. Hypertension is an important contributor. Symptoms and signs include abrupt onset of tearing chest or back pain, and dissection may result in aortic regurgitation and compromised circulation in branch arteries. Diagnosis is by imaging tests (eg, transesophageal echocardiography, CT angiography, MRI, contrast aortography). Treatment always involves aggressive BP control and serial imaging to monitor progression of dissection; surgical repair of the aorta and placement of a synthetic graft is needed for ascending aortic dissection and for certain descending aortic dissections. One fifth of patients die before reaching the hospital, and up to 1⁄3 die of operative or perioperative complications.
is inflammation of the aorta, sometimes causing aneurysm or occlusion
is caused by several connective tissue disorders (eg, Takayasu's arteritis, temporal arteritis, ankylosing spondylitis, relapsing polychondritis) and infections (eg, bacterial endocarditis, syphilis, Rocky Mountain spotted fever, fungal infections). It is also a feature of Cogan's syndrome (inflammatory keratitis, vestibular and auditory dysfunction, and aortitis). Inflammation usually involves all layers of the aorta (intima, media, adventitia) and may lead to occlusion of the aorta or its branches or weakening of the arterial wall, resulting in aneurysms. Pathogenesis, symptoms and signs, diagnosis, and treatment differ by etiology.