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Understanding the pathophysiology, diagnosis, and management of renovascular hypertension (RVH) is of paramount importance due to the severity of hypertension (HT) and renal insufficiency (RI). Moreover, adequate treatment by surgery and/or endovascular intervention can improve HT and revert RI. The comprehension of the pathophysiology of RVH had its origin on the experiments of Goldblatt which led to the recognition of the renin dependent, volume dependent, and mixed types. A continuum seems to exist, from an acute phase, supported by the endocrine renin angiotensin aldosterone system, evolving towards a chronic phase sustained by the local renin angiotensin system. The involved vasoconstrictor and mitogenic mechanisms may contribute to the arterial remodeling. The most common forms of pathology, i.e. atherosclerosis, fibromuscular dysplasia (FD), and Takayasu's arteritis, and their natural history, are described. The prevalence of RVH, ranging from 0.2% to more than 25%, depending on the clinical situation, is evidenced. Clinical symptoms and signs and the most important diagnostic tests are pointed out: functional tests (captopril test, postcaptopril renography, scintigraphy, and renin determinations) and anatomical tests (intravenous digital angiography and intrarterial angiography). New imaging techniques are also referred. A diagnostic work-up based on the index of clinical suspicion is described. The therapeutic goal is the resolution of the two main problems of RVH: hypertension and ischemic nephropathy. Revascularization is becoming mandatory either by percutaneous transluminal angioplasty mostly for FD and atheromatous non-ostial stenoses, or by surgery, which is preferred for patients with ostial or peripheral stenoses, aneuryms, occlusions and concomitant aortic disease. A better knowledge of RVH allows, not only diagnosis and treatment of one of the most frequent types of secondary hypertension, but also the control of the resulting ischemic nephropathy.
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PMID:[Renovascular arterial hypertension. From physiopathology to therapy]. 870 4

Clinical and angiographic characteristics of renovascular hypertension were studied in 95 patients. The patients were divided into 3 groups: 55 cases with aortic arteritis (group AA), 27 with fibromuscular dysplasia (group FMD) and 9 with atherosclerosis (group AS). The patients in group AS were significantly older in age and had longer history of hypertension. Abdominal bruit was heard significantly more often in group AA and serum potassium was significantly lower in group FMD. Angiographic data showed that in group AA lesions in thoracic aorta and abdominal aorta was found in 81.4% and those involving both renal arteries in 52.5%. In group FMD, 82.5% of patients had lesion in renal artery on one side and none had lesion in thoracic and abdominal aorta. In group AS, lesions were found mainly in thoracic and abdominal aorta, accounting for 77.7% and lesions in renal arteries were mainly unilateral. In group AA, lesions were found in 90 renal arteries altogether. Among them, 58.9% was in the proximal part of the renal artery; the lesion was either localized stenosis (67.8%) or obstruction (17.7%). In group FMD, lesions were found in 33 renal arteries altogether. Among them, 48.5% was in the middle or distal part of the renal artery and 27.3% resembled string of beads. In group AS, a total of 10 renal arteries were involved with 4 (40%) of ostial stenosis and 4 (40%) total obstruction.
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PMID:[Clinical and angiographic characteristics of renovascular hypertension]. 873 48

Renal artery stenosis may be caused by either atherosclerosis or fibromuscular dysplasia, and is responsible for hypertension or renal failure. Universal screening of all hypertensive patients is not recommended because of the relatively low prevalence of the disease. A selective approach is needed. The detection of renal artery stenosis requires noninvasive tests with a high predictive value (Doppler ultrasonography, intravenous angiography, spiral CT angiography, captopril renography) in patients in whom hypertension is severe, refractory to therapy, or associated with progressive renal insufficiency. Yet, after such screening, arteriography remains the gold standard of detecting and quantifying renal artery stenosis.
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PMID:[Screening of renal artery stenosis: which patients, by what methods?]. 876 15

The term "idiopathic" ventricular fibrillation is used to describe those episodes of unexpected sudden arrhythmic death due to ventricular fibrillation in patients with no demonstrable structural heart disease. Idiopathic ventricular fibrillation has been reported to account for 5-100% of all sudden arrhythmic deaths. Post mortem analysis have shown that about 80% of patients might have some kind of structural anomalies, mainly atherosclerosis, myocarditis, or right ventricular dysplasia. Follow-up of patients with idiopathic ventricular fibrillation has shown a high incidence of recurrent episodes of malignant ventricular arrhythmias. The absence of structural heart disease generally implies an excellent long-term prognosis if ventricular fibrillation can be avoided. Patients with an implantable defibrillator should have a mortality rate similar to the general population. New subsets of patients are being recognized as belonging with those previously classified as idiopathic ventricular fibrillation. More than 60 patients have been identified in different centers around the world with the so-called "right bundle branch block, ST segment elevation, and sudden death syndrome." Recurrence rate of malignant ventricular arrhythmias is very high in these patients, despite antiarrhythmic therapy. An implantable cardioverter-defibrillator seems the treatment of choice. Asymptomatic forms of the syndrome have been described. Follow-up in these asymptomatic patients has shown that some of them might become symptomatic during follow-up. Also, intermittent forms of the syndrome have been described, with transient normalization of the electrocardiogram. Administration of class I drugs in these patients unmasks the typical electrocardiographic pattern. In some of the patients previously classified as having idiopathic ventricular fibrillation, ajmaline or procainamide administration unmasks the electrocardiographic pattern of the syndrome, suggesting that its incidence may be higher than previously suspected.
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PMID:What to do in patients with no structural heart disease and sudden arrhythmic death? 882 Aug 39

Long-term outcome was studied in 233 patients who had undergone renal artery revascularization (51 with balloon angioplasty, 182 with surgery) between 1976 and 1992. Patients (excluding renal transplants) were treated for renal vascular hypertension without or with renal insufficiency (serum creatinine > 1.6 mg/dl. All patients still alive (n = 188) were contacted to determine current blood pressure, medications, serum creatinine, and subsequent significant medical events. In patients who had died the cause of death was determined and renal function status at the time of death noted from medical records. Some follow-up information was obtained on all 233 patients; follow-up serum creatinine data were obtained in 193 (82.8%) patients. Some 24 patients (10.3%) became dialysis-dependent. Using a multiple logistic regression analysis only, preoperative creatinine maintained significance (P < 0.001) for increased dialysis risk. There was no statistically significant association of dialysis for type of revascularization (percutaneous transluminal angioplasty, autogenous artery, saphenous vein, endarterectomy or synthetic material), simultaneous or previous aortic or other vascular surgery (carotid endarterectomy, femoropopliteal bypass, etc.), pathology (atherosclerosis or fibromuscular dysplasia), number of renal arteries stenosed or treated, length of follow-up, age, coronary artery disease, congestive heart failure, stroke, chronic lung disease or type II diabetes. It is concluded that, in patients with renal artery stenosis, the timing of renal artery revascularization relative to the level of renal function is the most important determinant for long-term renal salvage.
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PMID:Late renal function in patients undergoing renal revascularization for control of hypertension and/or renal preservation. 890 17

Most patients with hypertension in the United States have essential (primary) hypertension (95%), the cause of which is unknown. The remaining 5% of adults with hypertension have the secondary form of hypertension, the cause and pathophysiologic process of which are known. Internists and other primary care physicians refer to this as treatable or curable hypertension, because the hypertension can be managed or even controlled with medications. Similarly, the condition is called surgical hypertension by surgeons in the belief that once the cause is determined and identified, surgical intervention will result in cure of hypertension. Secondary causes of hypertension include renal parenchymal disease, renovascular diseases, coarctation of the aorta, Cushing's syndrome, primary hyperaldosteronism, pheochromocytoma, hyperthyroidism, and hyperparathyroidism. Occasionally included in this category are alcohol- and oral contraceptive-induced hypertension and hypothyroidism, but these conditions are not discussed herein. The evaluation of secondary hypertension is of interest and can bring together different facets of anatomy, physiology, pharmacology, and radiology in the medical and surgical treatment of these disorders. Despite enthusiasm that can be generated in the evaluation of these conditions, evaluation can be expensive and should not be conducted for all patients with hypertension. Features that aid in the diagnosis of secondary hypertension include the following: 1. Onset of hypertension before the age of 20 or after the age of 50 years. The presence of hypertension at a young age may suggest coarctation of the aorta, fibromuscular dysplasia, or an endocrine disorder. Hypertension found for the first time after the age of 50 years may suggest the presence of renovascular hypertension caused by atherosclerosis. 2. Markedly elevated blood pressure or hypertension with severe end-organ damage, as in grade III or IV retinopathy. These findings suggest the presence of renovascular hypertension or pheochromocytoma. 3. Specific body habitus and ancillary physical findings. For example, truncal obesity and purple striae occur with hypercortisolism, and exophthalmos is associated with hyperthyroidism. 4. Resistant or refractory hypertension (poor response to medical therapy usually necessitating use of more than three antihypertensive medications from three different classes). 5. Specific biochemical test that suggest the existence of certain disorders, such as hypercalcemia in hyperparathyroidism, hyperglycemia in Cushing's syndrome and pheochromocytoma, and unprovoked hypokalemia with renin-producing tumors, primary hyperaldosteronism, or renin-mediated renovascular hypertension. 6. Other characteristics that may suggest secondary hypertension such as abdominal diastolic bruits (renovascular hypertension), decreased femoral pulses (coarctation of the aorta), or bitemporal hemianopias (Cushing's disease). A combination of a good history and physical examination, astute observation, and accurate interpretation of available data usually are helpful in the diagnosis of a specific causation.
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PMID:Secondary hypertension: evaluation and treatment. 894 19

The authors describe the material and the use method of intravenous digital subtraction angiography (IVDSA) before presenting the obtained results. The morphologic abnormalities of the renal arteries evidenced in 105 patients, are distributed by different pathologies such as: atherosclerosis 48 patients; fibromuscular dysplasia 27 patients; Takayasu's aortoarteritis 8 patients (7.6%); renal artery aneurysms 5 patients (4.8%); renal arterial emboli 1 patient (0.9%); iatrogenic 6 patients (5.7%); small kidney/hypoplastic renal artery 10 patients (9.5%). The authors draw also attention to an anatomic variant-the early bifurcation of the renal artery that should be evaluated under the pathophysiologic point of view. From this experience some conclusions emerge. The IVDSA permits the ambulatory screening of the renal arteries abnormalities with additive value in the cost/benefit ratio, that is translated in the increasing number of hypertensive patients who are identified as having renal artery abnormalities. The pathologies more frequently identified are the atherosclerotic in the old male and the fibromuscular dysplasia in the young female. The pathophysiologic significance of the early bifurcation of the renal artery needs further elucidation. According to the authors experience, the IVDSA has a paramount position and can even be the first test to be performed in the workup diagnostic approach to the hypertensive patient with moderate and strong suspection of RVH.
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PMID:[Renovascular arterial hypertension. Importance of subtraction digital angiography in its diagnosis]. 899 93

Evaluation of percutaneous transluminal renal angioplasty (PTRA) is today based primarily on clinical criteria rather than direct investigation of luminal width. In this study, we examined renal blood flow by color-coded duplex sonography (CCD) in order to correlate blood pressure as well as renal function with the true renovascular patency. Fifty consecutive patients suspected of suffering from renovascular disease and treated by PTRA were included for a prospective sonographic study. In all PTRA was performed on 63 renal arteries. Thirty-seven patients were diagnosed to have atherosclerosis and 13 patients to have fibromuscular dysplasia (FMD). Examinations were performed using CCD before PTRA, and one day, three months, six months and 12 months after PTRA. If CCD showed a restenosis > or = 60%, CCD was non-conclusive or hypertension deteriorated, angiography and, if necessary, catheter re-intervention were performed. The primary patency rate after 12 months was 73%, and could be improved to 94% overall when treated restenosis (N = 22) were included. Restenosis was more frequent in patients with mild residual stenosis identified by CCD one day after PTRA (P = 0.002). There was neither a significant difference in the restenosis rate in patients with atherosclerosis versus FMD, nor in patients with ostial versus non-ostial lesions. Hypertension was improved or cured in 70% of patients with atherosclerosis, and in 85% of those with FMD. Nevertheless, hypertension deteriorated in 12% of the patients without restenosis, and no deterioration was present in 14% of the patients with restenosis. A decrease in serum creatinine levels by more than 15% was observed in 12 of 22 patients with impaired renal function and patent renal artery during follow-up. These results suggest that optimal therapeutic efficiency can be obtained using PTRA followed by systematic CCD.
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PMID:Patency of percutaneous transluminal renal angioplasty: a prospective sonographic study. 906 13

Visceral artery aneurysms are uncommon lesions that are rarely identified in the absence of symptoms. Between February 1972 and April 1992, nine patients (5 men and 4 women) with rupture of visceral artery aneurysms were treated. The average age was 62 years old (range 39 to 86 years old). The arteries involved were the splenic (4), the common hepatic (2), the left hepatic (1), the celiac (1), and the superior mesenteric (SMA) (1). No ruptured renal artery aneurysm was identified. Six patients presented with abdominal distension, pain, and hemodynamic instability. Three patients had recurrent gastrointestinal bleeding with erosion into the duodenum, the common bile duct or the pancreatic duct. All three had unnecessary gastrointestinal operations despite preoperative (2 patients) or intraoperative (1 patient) identification of a visceral artery aneurysm. One patient with an SMA aneurysm had ligation and bypass. Three patients with splenic artery aneurysms had splenectomy. The remaining five patients had either ligation or resection without arterial reconstruction. No end-organ dysfunction was identified. There was one death (11%) due to the SMA aneurysm. Pathological findings in four patients were cystic medial necrosis, diffuse deficiency of the internal elastic lamina, fibromuscular dysplasia, and atherosclerosis, respectively. The remainder were thought to be due to atherosclerosis on gross examination. Rupture of visceral artery aneurysms occurs infrequently and can be treated by simple ligation in most cases. Recognition that rupture of splanchnic arterial aneurysms into adjacent viscera can cause recurrent gastrointestinal bleeding may prevent both substantial delays in diagnosis and inappropriate therapy.
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PMID:Ruptured visceral artery aneurysms. 923 88

Arterial dissection is usually associated with pathological states such as malignant hypertension, severe atherosclerosis, severe trauma, Marfan syndrome, or Ehlers-Danlos syndrome. However, we report three cases in which renal artery dissection occurred in otherwise healthy, normotensive men. In two cases, the onset of symptoms of renal artery dissection was coincident with an unusual degree of physical activity. In the third case, the symptoms occurred while the patient was sitting but during a stressful business meeting. In each case, the patient experienced severe unilateral flank pain. Urolithiasis was suspected, but intravenous pyelography showed only ipsilateral impaired renal cortical perfusion, and the urinalyses showed no hematuria. The diagnosis of renal artery dissection was established by arteriography in two cases and by nephrectomy in one case. The latter case showed fibromuscular dysplasia by arteriography performed after the nephrectomy. The other two cases showed no evidence of fibromuscular dysplasia. We conclude that spontaneous renal artery dissection can occur in otherwise healthy individuals. Our experience and the reports of others indicate that this condition occurs mainly in men, conservative (nonsurgical) management is generally indicated, and the long-term prognosis is generally excellent. In some patients, an unusual degree of physical exertion might be the cause of renal artery dissection.
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PMID:Renal artery dissection causing renal infarction in otherwise healthy men. 939 33


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