Artery/arterial stenosis

Remonda L, Held O, Schroth G. Carotid artery stenosis, occlusion, and pseudoocclusion first-pass, gadolinium-enhanced, three-dimensional MR angiography— preliminary study. Radiology 1998 209 95-102 [see comment]. 

FIGURE 4.5 A 72-year-old man with medical history remarkable for hypertension and dyslipidemia presented with posterior circulation infarct (a). CTA and posterior circulation angiography (left vertebral artery injection) performed demonstrated severe mid-basilar artery stenosis (b and c). Left vertebral artery injection demonstrated near-complete reversal of the stenosis after a drug-eluting balloon expandable stent (Cypher, Cordis Johnson Johnson) was deployed (d). 

Aleksic M, Rueger MA, Lehnhardt EG, Sobesky J, Matoussevitch V, Neveling M, Heiss WD, Bmnkwall J, Jacobs AH. Primary stroke unit treatment followed by very early carotid endarterectomy for carotid artery stenosis after acute stroke. Cerebrovasc Dis 2006 22 276-281. 

McPherson CM, Woo D, Cohen PL, Panciob AM, Kissela BM, CarrozzeUa JA, Tomsick TA, ZuccareUo M. Early carotid endarterectomy for critical carotid artery stenosis after thrombolysis therapy in acute ischemic stroke in the middle cerebral artery. Stroke 2001 32 2075-2080. 

Gasecki AP, Eerguson GG, EUasziw M, Clagett GP, Pox AJ, Hachinski V, Barnett HJ. Early endarterectomy for severe carotid artery stenosis after a nondisabling stroke Results from the North American symptomatic carotid endarterectomy trial. J Vase Surg 1994 20 288-295. 

Full-dose heparin may be used when there are selected indications, such as cardiac sources with a high risk of recurrent embohsm, arterial dissection, or high-grade arterial stenosis prior to surgery (Level of Evidence IV). 

Markus H, Mac Kinnon A. Asymptomatic embolization detected by Doppler ultrasound predicts stroke risk in symptomatic carotid artery stenosis. Stroke 2005 36 971-975. 

Suwanwela N, Can U, Furie KL, Southern JF, Macdonald NR, Ogilvy CS, Hansen CJ, Buonanno FS, Abbott WM, Koroshetz WJ, Kistler JR Carotid Doppler ultrasound criteria for internal carotid artery stenosis based on residual lumen diameter calculated from en bloc carotid endarterectomy specimens. Stroke 1996 27(11) 1965-1969. 

Pan XM, Saloner D, Reilly LM, Bowersox JC, Murray SP, Anderson CM, Gooding GA, Rapp JH. Assessment of carotid artery stenosis by ultrasonography, conventional angiography, and magnetic resonance angiography correlation with ex vivo measurement of plaque stenosis. J Vase Surg 1995 21(l) 82-88 [discussion 88-89]. 

Henderson RD, Steinman DA, Ehasziw M, Barnett HJ. Effect of contralateral carotid artery stenosis on carotid ultrasound velocity measurements. Stroke 2000 31(ll) 2636-2640. 

Polak IF, Dobkin GR, O Leary DH, Wang AM, Cutler SS. Internal carotid artery stenosis accuracy and reproducibility of color-Doppler-assisted duplex imaging. Radiology 1989 173(3) 793-798. 

Despite their clear benefits, ACE inhibitors are still underutilized in HF. One reason is undue concern or confusion regarding absolute versus relative contraindications for their use. Absolute contraindications include a history of angioedema, bilateral renal artery stenosis, and pregnancy. Relative contraindications include unilateral renal artery stenosis, renal insufficiency, hypotension, hyperkalemia, and cough. Relative contraindications provide a warning that close monitoring is required, but they do not necessarily preclude their use. 

The benefit of carotid endarterectomy for prevention of recurrent stroke has been studied previously in major trials.25,26 A recent meta-analysis has been completed that has combined these clinical trials to evaluate 6,092 patients.27 Carotid endarterectomy has been shown to be beneficial for preventing ipsilateral stroke in patients with symptomatic carotid artery stenosis of 70% or greater and is recommended in these patients. In patients with symptomatic stenosis of 50% to 69%, a moderate reduction in risk is seen in clinical trials. In all patients with stenosis of 50% to 69% and a recent stroke, carotid endarterectomy is appropriate. In other patients, surgical risk factors and surgeon skill should be considered prior to surgery. The patient should have, at a minimum, a life expectancy of 5 years, and the surgical risk of stroke and/or death should be less than 6%. Carotid endarterectomy is not beneficial for symptomatic carotid stenosis less than 50% and should not be considered in these patients. 

There are data to suggest that patients with asymptomatic carotid artery stenosis of 60% or more benefit from carotid endarterectomy if it is performed by a qualified surgeon with low complication rates (less than 3%). At this time, there is considerable controversy over how this information can be applied to clinical practice. A current review recommends considering carotid endarterectomy in patients with carotid artery stenosis... 

Coronary artery bypass graft surgery Thoracic surgery whereby parts of a saphenous vein from a leg or internal mammary artery from the arm are placed as conduits to restore blood flow between the aorta and one or more coronary arteries to bypass the coronary artery stenosis (occlusion). 

Percutaneous coronary intervention A minimally invasive procedure whereby access to the coronary arteries is obtained through the femoral artery up the aorta to the coronary os. Contrast media is used to visualize the coronary artery stenosis using a coronary angiogram. A guidewire is used to cross the stenosis and a small balloon is inflated and/or stent is deployed to break up atherosclerotic plaque and restore coronary artery blood flow. The stent is left in place to prevent acute closure and restenosis of the coronary artery. Newer stents are coated with antiproliferative drugs, such as paclitaxel and sirolimus, which further reduce the risk of restenosis of the coronary artery. 

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. 

High-risk NSTE ACS patients should undergo early coronary angiography (within 24 to 48 hours) and revascularization if a significant coronary artery stenosis is found. Moderate-risk patients with positive biochemical... 

Patients with renal artery stenosis may have an abdominal systolic-diastolic bruit. 

Acute renal failure is a rare but serious side effect of ACE inhibitors preexisting kidney disease increases the risk. Bilateral renal artery stenosis or unilateral stenosis of a solitary functioning kidney renders patients dependent on the vasoconstrictive effect of angiotensin II on efferent arterioles, making these patients particularly susceptible to acute renal failure. 

ACE inhibitors, ARBs, and direct renin inhibitors are contraindicated in sexually active girls because of potential teratogenic effect and in those who might have bilateral renal artery stenosis or unilateral stenosis in a solitary kidney. 

The action of nitrates appears to be mediated indirectly through reduction of MVo2 secondary to venodilation and arterial-arteriolar dilation, leading to a reduction in wall stress from reduced ventricular volume and pressure. Direct actions on the coronary circulation include dilation of large and small intramural coronary arteries, collateral dilation, coronary artery stenosis dilation, abolition of normal tone in narrowed vessels, and relief of spasm. 

Transcranial Doppler can determine the presence of intracranial sclerosis (e.g., middle cerebral artery stenosis). 

Isolated renal hypoperfusion Bilateral renal artery stenosis (unilateral renal artery stenosis in solitary kidney) Emboli Cholesterol Thrombotic Medications Cyclosporine Angiotensin-converting enzyme inhibitors Nonsteroidal antiinflammatory drugs Radiocontrast media... 

Undesired effects. The magnitude of the antihypertensive effect of ACE inhibitors depends on the functional state of the RAA system. When the latter has been activated by loss of electrolytes and water (resulting from treatment with diuretic drugs), cardiac failure, or renal arterial stenosis, administration of ACE inhibitors may initially cause an excessive fall in blood pressure. In renal arterial stenosis, the RAA system may be needed for maintaining renal function and ACE inhibitors may precipitate renal failure. Dry cough is a fairly frequent side effect, possibly caused by reduced inactivation of kinins in the bronchial mucosa. Rarely, disturbances of taste sensation, exanthema, neutropenia, proteinuria, and angioneurotic edema may occur. In most cases, ACE inhibitors are well tolerated and effective. Newer analogues include lisinopril, perindo-pril, ramipril, quinapril, fosinopril, benazepril, cilazapril, and trandolapril. 

Renal function impairment Some hypertensive patients with renal disease, particularly those with severe renal artery stenosis, have developed increases in BUN and serum creatinine after reduction of BP. 

Flow through moderately severe coronary artery stenosis is commonly normal at rest but becomes inadequate for the increased metabolic requirements and blood flow during stress. Coronary blood flow normally increases to four times resting baseline flow rates after coronary artery vasodilators such as dipyridamole and adenosine. A stenosis restricts maximal blood flow capacity compared to normal coronary arteries, thereby causing a disparity in regional perfusion of areas supplied by a stenotic artery compared to normal coronary arteries. This disparity manifests as a relative perfusion defect during stress, corresponding to the ischemic myocardial territory supplied by a stenotic artery. Furthermore, the quantitative severity of the relative perfusion defect is proportional to the severity of the stenosis under conditions of maximal coronary flow after dipyridamole or adenosine stress [24]. 

---