Aortic aneurysms

Acute myocardial infarction Angiopathy Aortic aneurysm Aortic balloon assist devices Giant hemangiomas Peripheral vascular disease Postcardiac arrest Prosthetic devices Raynaud s syndrome Infectious Arbovirus Aspergillus Candida albicans Cytomegalovirus Ebola virus... 

Suggested Alternatives for Differential Diagnosis Abdominal aneurysm, aortic dissection, pleural effusion, subarachnoid hemorrhage, superior vena cava syndrome, hantavirus pulmonary syndrome, mediastinitis, fulminate mediastinal tumors pneumonia, gastroenteritis, meningitis, ecthyma, rat bite fever, spider bite, leprosy, plague, tularemia, coccidioidomycosis, diphtheria, glanders, histoplasmosis, psittacosis, typhoid fever, and rickettsial pox. 

Parodi, RE. et al.. Oral administration of diferuloylmethane (curcumin) suppresses proinflammatory cytokines and destructive connective tissue remodeling in experimental abdominal aortic aneurysms, Ann. Vase. Surg., 20, 360, 2006. 

CV RRR, normal S1r S2 no murmurs, rubs, or gallops Abd Soft, non-tender, non-distended positive for bowel sounds, no hepatosplenomegaly or abdominal aortic aneurysm... 

Aortic aneurysm, prosthetic heart valve, vascular or orthopedic prosthesis... 

Growing clinical data also points to the importance of IL-8 in atherogenesis. IL-8 has been found in atheromatous lesions from patients with atherosclerotic disease including carotid artery stenosis (103), CAD (118), abdominal aortic aneurysms (AAA) (103,104,114), and peripheral vascular disease (PVD) (104). Furthermore, studies using plaque explant samples have yielded more direct evidence for IL-8 involvement. Media from cultured AAA tissue induced IL-8-dependent human aortic endothelial cell (HAEC) chemotaxis (122). Homocysteine, implicated as a possible biomarker for CAD, is also capable of inducing IL-8 (123-125) by direct stimulation of endothelial cells (123,124) and monocytes (125). When patients with hyperhomocysteinemia were treated with low-dose folic acid, decreases in homocysteine levels correlated with decreases in IL-8 levels (126). Statins significantly decrease serum levels of IL-6, IL-8, and MCP-1, as well as expression of IL-6, IL-8, and MCP-1 mRNA by peripheral blood monocytes and HUVECs (127). Thus, IL-8 may be an underappreciated factor in the pathogenesis of atherosclerosis. 

Koch AE, Kunkel SL, Pearce WH, et al. Enhanced production of the chemotactic cytokines interleukin-8 and monocyte chemoattractant protein-1 in human abdominal aortic aneurysms. Am J Pathol 1993 142(5) 1423—1431. 

Szekanecz Z, Shah MR, Harlow LA, Pearce WH, Koch AE. Interleukin-8 and tumor necrosis factor-alpha are involved in human aortic endothelial cell migration. The possible role of these cytokines in human aortic aneurysmal blood vessel growth. Pathobiology 1994 62(3) 134-139. 

The response-to-injury hypothesis states that risk factors such as oxidized LDL, mechanical injury to the endothelium, excessive homocysteine, immunologic attack, or infection-induced changes in endothelial and intimal function lead to endothelial dysfunction and a series of cellular interactions that culminate in atherosclerosis. The eventual clinical outcomes may include angina, myocardial infarction, arrhythmias, stroke, peripheral arterial disease, abdominal aortic aneurysm, and sudden death. 

A complete history and physical examination should assess (1) presence or absence of cardiovascular risk factors or definite cardiovascular disease in the individual (2) family history of premature cardiovascular disease or lipid disorders (3) presence or absence of secondary causes of hyperlipidemia, including concurrent medications and (4) presence or absence of xanthomas, abdominal pain, or history of pancreatitis, renal or liver disease, peripheral vascular disease, abdominal aortic aneurysm, or cerebral vascular disease (carotid bruits, stroke, or transient ischemic attack). 

The goals of treatment are to lower total and LDL cholesterol in order to reduce the risk of first or recurrent events such as myocardial infarction, angina, heart failure, ischemic stroke, or other forms of peripheral arterial disease such as carotid stenosis or abdominal aortic aneurysm. 

Goal BP values are <140/90 for most patients, but <130/80 for patients with diabetes mellitus, significant chronic kidney disease, known coronary artery disease (myocardial infarction [MI], angina), noncoronary atherosclerotic vascular disease (ischemic stroke, transient ischemic attack, peripheral arterial disease [PAD], abdominal aortic aneurysm), or a 10% or greater Framingham 10-year risk of fatal coronary heart disease or nonfatal MI. Patients with LV dysfunction have a BP goal of <120/80 mm Hg. 

Because their actions are so broad, including blocking of sympathetic and parasympathetic systems, their therapeutic use has been largely supplanted by more specific drags. They may still be used in the control of blood pressure in patients with acute dissecting aortic aneurysm and for the induction of hypotension in surgery. 

Hypersensitivity to any component of the product pheochromocytoma (because the drug may stimulate secretion of catecholamines from the tumor through its antihypertensive action) acute Ml dissecting aortic aneurysm. 

Hydralazine (Apresoline/ Others) [Antihypertensive/ Vasodilator] Uses Mod-severe HTN CHF (w/ Isordil) Action Peripheral vasodilator Dose Adults. Initial 10 mg PO qid, T to 25 mg qid 300 mg/d max Peds. 0.75-3 mg/kg/24 h POq6—12h -i in renal impair V CBC ANA before Caution [C, +] -1- Hqjatic Fxn CAD T tox w/ MAOI, indomethacin, BBs Contra Dissecting aortic aneurysm, mitral valveAheumatic heart Dz Disp Tabs, inj SE SLE-like synd w/ chronic high doses SVT following IM route, p ipheral neuropathy Interactions T Effects W/ antih5 pertensives, diazoxide, diuretics, MAOIs, nitrates. 

The major cardiovascuiar manifestations are mitral valve prolapse and ioss of eiasticity of the aortic root, which mayiead to progressive aneurysm andpotentiaiiyfatai aortic dissection. 

Osteolathyrism is a disease characterized by lameness, skeletal deformities, aortic aneurysms, and slowing or cessation of body growth. Certain aminonitriles are known to cause osteolathyrism in several animal species aminoacetonitrile, 3-aminopropionitrile, and 3-amino-2-methylpropionitrile are potent inducers of this disease. It is believed that the basis of their ability to cause osteolathyrism is due to their ability to inhibit lysine oxidase, an enzyme important in cross-linking of collagen and formation of connective tissue. While no reports of these substances causing osteolathyrism in humans have appeared, it seems plausible that these substances could cause this disease in humans because they are known to cause it in a variety of experimental animals. 

Myocardial ischemia has been reportedly precipitated by intramuscular administration of betamethasone (SEDA-21, 413 23). It has been suggested that longterm glucocorticoid therapy accelerates atherosclerosis and the formation of aortic aneurysms, with a high risk of rupture (SEDA-20, 369 24). 

Sato O, Takagi A, Miyata T, Takayama Y. Aortic aneurysms in patients with autoimmune disorders treated with corticosteroids. Eur J Vase Endovasc Surg 1995 10(3) 366-9. 

S. E., Shete, S. S., and Milewicz, D. M. (2003). Mapping a locus for familial thoracic aortic aneurysms and dissections (TAAD2) to 3p24-25. Circulation 107, 3184-3190. 

CHD = myocardial infarction (Ml), significant myocardial ischemia (angina), history of coronary artery bypass graft (CABG), history of coronary angioplasty, angiographic evidence of lesions, carotid endarterectomy, abdominal aortic aneurysm, peripharal vascular disease (claudication), thrombotic/embolic stroke, transient ischemic attack (TIA)... 

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