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Renal artery stenosis (RAS) is most commonly caused by atherosclerosis, which is also the most common cause of chronic heart failure (CHF). One-third of patients with CHF are reported to have significant renovascular disease. The presence of RAS confers a worse outcome in studies of hypertension and coronary disease, though data are lacking for patients with CHF. As the kidney is intricately involved in the fluid retention that occurs in CHF, an adverse effect of RAS on outcome would be expected. Presentations of RAS in CHF include flash pulmonary oedema, hypertension, worsening of CHF, and worsening renal function. RAS commonly progresses and may cause worsening of renal function in patients with CHF and previously stable renal function. A variety of investigations that can safely and accurately identify RAS in CHF are available, although none is recommended in current guidelines for the management of CHF. Treatment for RAS, whether for hypertension, for renal dysfunction, or for pulmonary oedema, is at the discretion of the physician due to the lack of adequate randomized controlled trials demonstrating the efficacy and safety of intervention. As it is not clear how RAS should be managed in CHF, screening cannot be advocated. Currently, a multicentre randomized outcome trial, which includes a cohort of patients with RAS and CHF, is in progress to provide answers in this area of uncertainty.
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PMID:Atherosclerotic renovascular disease in chronic heart failure: should we intervene? 1597 92

It is illusory to think that one year is long enough to establish all the truths that will guide our clinical practice in vascular medicine. On the contrary, one year was long enough to contradict what the preceding twelve months had set out to demonstrate. Consequently, promising trials in the treatment of abdominal aortic aneurysms by endoprostheses have been the object of contradictory debate with regards to the long-term benefits. In fundamental research, circulating progenitors of endothelial cells have been shown to be a marker of atherosclerosis, but is it a better marker than LDL-cholesterol values? The demonstration that these progenitors are of value in the treatment of essential ischaemia of the lower limbs is awaited. Finally, ximelagatran, a direct thrombin antagonist, seemed to have all the qualities of an ideal anticoagulant: easy to use, safe... until the report of raised hepatic enzymes, the clinical relevance of which remains to be determined. In the good news section: the Systolic Pressure Index, an unquestioned marker of arterial disease. Its reduction was known to be correlated with the prevalence of cardiovascular complications. However, it has now been shown that an increase in the index is also associated with cardiovascular complications, a real U-shaped curve. Renal arterial stenosis should be considered in patients with left ventricular failure presenting with flash pulmonary oedema. In the absence of cardiac pathology, BNP would seem to be a good biological marker of haemodynamically significant renal arterial stenosis. Finally, should superficial femoral artery stenosis be treated by an active stent. To date, there is no formal proof.
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PMID:[The best of vascular medicine in 2005]. 1647 63

Fibromuscular dysplasia (FMD) and aortoarteritis are the most frequent causes of secondary hypertension induced by renal artery stenosis (RAS). Revascularization of this disease entity usually cures arterial hypertension. Demographic evolution leads to an increasing incidence of atherosclerotic RAS, one of the major causes of end-stage renal failure. Furthermore, atherosclerotic RAS leads to deterioration of primary hypertension, progression of atherosclerosis manifestation such as occlusive and aneurysmatic peripheral artery disease, and chronic or acute organ damage such as left ventricular hypertrophy and recurrent flash pulmonary edema. Despite the lack of sufficiently powered randomized controlled trials, each hemodynamically relevant RAS (eg, > or = 70%) should be considered for stent angioplasty in patients without end-stage ischemic nephropathy or limited life expectancy due to concomitant disease (eg, cancer). Drug-eluting stents will probably reduce the overall low in-stent restenosis rate of 10% to 20%. Interventions in patients with dialysis-dependent end-stage nephropathy are left to appropriate clinical study protocols.
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PMID:Renal artery stenosis. 1748 11

The prevalence of atherosclerotic renal artery stenosis (RAS) is more common than was previously thought, particularly in patients with known coronary, cerebrovascular, or peripheral vascular atherosclerosis. Clinical subsets in which RAS is more common include patients with uncontrolled hypertension, renal insufficiency, and/or sudden onset ("flash") pulmonary edema. Renal artery atherosclerosis progresses over time and is associated with loss of renal function regardless of medical therapy. Patients with symptomatic (hypertension, renal insufficiency, or flash pulmonary edema) and hemodynamically significant RAS are potential candidates for revascularization. The current standard of care is stent placement for aorto-ostial atherosclerotic lesions. Procedure success rates are very high (> or =95%), with infrequent major complication rates. Five-year primary patency rates are 80% to 85%, and secondary patency rates exceed 90%. The key element in managing patients with RAS is selecting those most likely to benefit, that is, those with blood pressure control, preservation or improvement of renal function, and control of flash pulmonary edema from renal revascularization. This article will highlight the anatomical features, physiologic parameters, and biomarkers that may be helpful in optimally selecting patients for renal artery revascularization.
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PMID:Catheter-based therapy for atherosclerotic renal artery stenosis. 1776 75

The most common cause of obstructive renal artery disease is atherosclerosis, accounting for 90 % of cases of renal artery stenosis. Atherosclerotic renal artery stenosis can be associated with renovascular hypertension, ischemic nephropathy, or both or it may occur alone. The prevalence of atherosclerotic renal artery stenosis among hypertensive patients is estimated between 1 and 5 %, but the frequency rises among patients with refractory hypertension (20 %) coronary heart disease (15 to 20 %) or peripheral arterial disease (30 to 40 %). The gold standard for diagnosing renal artery disease is contrast renal arteriography. MR angiography, CT angiography and color duplex ultrasonography have the highest sensitivity and specifity among the non invasive screening methods. Therapy is based on consequent medical treatment of hypertension, antiplatelet therapy and modification of risk factors for atherosclerosis. Revascularisation is advised in patients with severe hypertension, in patients with pulmonary edema and cases of acute worsening of renal function. Percutaneous angioplasty with stent implantation is the method of choice for revascularisation. The prognosis of patients with atherosclerotic renal artery stenosis is determined by cardiovascular and renal complications.
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PMID:[Atherosclerotic renal artery stenosis]. 1798 55

Sleep plays a large role in patients with heart failure. In normal subjects, sleep is usually in a supine position with reduced sympathetic drive, elevated vagal tone and as such a relatively lower cardiac output and minute ventilation, allowing for recuperation. Patients with heart failure may not experience the same degree of autonomic activity change and the supine position may place a large strain on the pulmonary system. More than half of all heart failure patients have one of two types of sleep apnea: either obstructive or central sleep apnea. Some patients have both types. Obstructive sleep apnea is likely to be a cause of heart failure due to large negative intrathoracic pressures, apnea related hypoxemia and hypercapnia, terminated by an arousal and surge in systemic blood pressure associated with endothelial damage and resultant premature atherosclerosis. Reversal of obstructive sleep apnea improves blood pressure, systolic contraction and autonomic dysfunction however mortality studies are lacking. Central sleep apnea with Cheyne Stokes pattern of respiration (CSA-CSR) occurs as a result of increased central controller (brainstem driving ventilation) and plant (ventilation driving CO2) gain in the setting of a delayed feed back (i.e., low cardiac output). It is thought this type of apnea is a result of moderately to severely impaired cardiac function and is possibly indicative of high mortality. Treatment of CSA-CSR is best undertaken by treating the underlying cardiac condition which may include with medications, pacemakers, transplantation or continuous positive airway pressure (CPAP). In such patients CPAP exerts unique effects to assist cardiac function and reduce pulmonary edema. Whether CPAP improves survival in this heart failure population remains to be determined.
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PMID:Sleep in heart failure. 1911 Jan 35

A reduction in the diameter of the renal arteries can lead to hypertension, renal dysfunction and/or pulmonary edema. About 90% of patients with renal artery stenosis have atherosclerosis, and 10% have fibromuscular dysplasia. Atherosclerotic renal artery stenosis is a common condition that typically occurs in patients at high risk of cardiovascular disease with coexistent vascular disease at nonrenal sites. Patients who undergo revascularization to treat hypertension associated with atherosclerotic stenosis need to continue medication with statins, antiplatelet agents and renin-angiotensin antagonists after the procedure to prevent renal and cardiovascular events. Two recent trials compared renal outcomes in patients with atherosclerotic stenosis who were treated with antihypertensive medication plus stenting with those in patients who were treated with medication alone. Available results favor a conservative approach (medication only) for most patients with atherosclerotic renal artery stenosis. These results, however, concern patients with stable clinical conditions and, in many cases, only moderate renal artery lesions. Blood pressure outcome after angioplasty is more favorable in patients with fibromuscular renal artery disease, who usually do not have renal failure, than in those with atherosclerosis.
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PMID:Diagnosis and treatment of renal artery stenosis. 2010 Dec 56

A renal artery stenosis (RAS) is common among patients with atherosclerosis, up to a third of patients undergoing cardiac catheterization. Fibromuscular dysplasia is the next cause of RAS, commonly found in young women. Atherosclerosis RAS generally progresses overtime and is often associated with loss of renal mass and worsening renal function (RF). Percutaneous renal artery stent placement is the preferred method of revascularization for hemodynamically significant RAS according to ACC and AHA guidelines. Several randomized trials have shown the superiority of endovascular procedures to medical therapy alone. However, two studies ASTRAL and STAR studies were recently published and did not find any difference between renal stenting and medical therapy. But these studies have a lot of limitations and flaws as we will discuss (poor indications, poor results, numerous complications, failures, poor technique, inexperienced operators, ecc.). Despite these questionable studies, renal stenting keeps indications in patients with: uncontrolled hypertension; ischemic nephropathy; cardiac disturbance syndrome (e.g. "flash" pulmonary edema, uncontrolled heart failure or uncontrolled angina pectoris); solitary kidney. To improve the clinical response rates, a better selection of the patients and lesions is mandatory with: good non-invasive or invasive imaging; physiologic lesion assessment using transluminal pressure gradients; measurements of biomarkers (e.g., BNP); fractional flow reserve study. A problem remains after renal angioplasty stenting, the deterioration of the RF in 20-30% of the patients. Atheroembolism seems to play an important role and is probably the main cause of this R.F deterioration. The use of protection devices alone or in combination with IIb IIa inhibitors has been proposed and seems promising as shown in different recent reports. Renal angioplasty and stenting is still indicated but we need: a better patient and lesion selection; improvements in techniques and maybe the use of protection devices to reduce the risk of RF deterioration after renal stenting.
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PMID:Renal angioplasty and stenting: is it still indicated after ASTRAL and STAR studies? 2092 31

The predominant cause of renal artery stenosis (RAS) is atherosclerosis. Clinical manifestations of atherosclerotic RAS are both direct (hypertension and kidney dysfunction) and indirect (increased cardiovascular events and mortality). However, in many cases, atherosclerotic RAS seems to be an incidental finding with no discernable effects. Antihypertensive medications such as renin-angiotensin-aldosterone system inhibitors, along with statins and aspirin, have significantly improved the medical treatment of atherosclerotic RAS. However, revascularization is still advocated in a variety of clinical settings such as the preservation of renal function, recurrent episodes of "flash" pulmonary edema, and in patients with refractory hypertension. Current management guidelines indicate "resistant hypertension" as an indication for renal artery revascularization. A large number of observational studies support revascularization for both control of high blood pressure and/or preservation of renal function. Unfortunately, the favorable effects of revascularization on these end points seen in the observational studies were not reproduced in randomized controlled trials compared to medical therapy alone. The ability for revascularization to improve control of congestive heart failure or to prevent hard cardiovascular end points (eg, myocardial infarction or stroke) has not been tested in the randomized clinical trials published to date. Hence, the efficacy of intervention remains controversial, which poses a dilemma, especially given the large number of elderly patients with resistant systolic hypertension.
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PMID:Revascularization in renal artery stenosis. 2231 44

Renovascular hypertension (hypertension induced by renal artery stenosis) is a form of secondary hypertension caused by overactivation of the renin-angiotensin system by the ischemic kidney. Prevalence of renal artery stenosis (RAS) is estimated to be between 2% (unselected hypertensives) and 40% (older patients with other atherosclerotic comorbidities). Most cases of RAS are caused by atherosclerosis; other causes, including fibromuscular dysplasia, vasculitis, thromboembolism and aneurysms, are less frequent. The most frequent clinical presentation of RAS is hypertension. Acute kidney injury, rapid loss of kidney function and episodes of flash pulmonary edema are other symptoms of RAS, especially in bilateral disease. In current practice, RAS therapy includes antiplatelet (aspirin) and lipid-lowering (statin) therapy as well as angiotensin II receptor blockers or angiotensin-converting enzyme inhibitors as a first choice of antihypertensive agents. Angiotensin blockade, however, is contraindicated in bilateral RAS and in RAS of the solitary kidney. This review summarizes the current status and perspectives on the epidemiology and management of renovascular hypertension.
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PMID:Epidemiology and optimal management in patients with renal artery stenosis. 2302 22


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