1/43. Penetrating atherosclerotic ulcer at the proximal aorta complicated with cardiac tamponade and aortic valve regurgitation.A 56-year-old man had a penetrating atherosclerotic ulcer originating in the proximal ascending aorta, which is an unusual case of penetrating aortic ulcer complicated with the aortic valve regurgitation and cardiac tamponade. This hemodynamically unstable patient was successfully treated by conservative management to control his blood pressure and was also monitored closely with follow-up imaging studies.- - - - - - - - - - ranking = 1keywords = pressure (Clic here for more details about this article) |
2/43. Successful Wallstent implantation for extensive iatrogenic renal artery dissection in a patient with fibromuscular dysplasia.PURPOSE: To describe a case of renal artery stenosis with fibromuscular dysplasia (FMD) and extensive iatrogenic dissection treated with Wallstent implantation. methods AND RESULTS: An 83-year-old woman with a history of coronary artery disease and hypertension presented at another facility with exertional angina and poorly controlled hypertension. Renal arteriography uncovered a critical right renal artery stenosis with severe FMD. However, angioplasty resulted in extensive dissection of the renal artery, for which the patient was referred to our institution. The renal artery was recanalized via the left brachial approach with restoration of flow using a Wallstent and a Palmaz stent. The patient's blood pressure was controllable after this procedure, and follow-up duplex imaging with flow velocities at 6 months showed patent right renal artery stents. CONCLUSIONS: Owing to its length and flexibility, the Wallstent endoprosthesis was a useful treatment modality in this case of extensive renal artery dissection.- - - - - - - - - - ranking = 1keywords = pressure (Clic here for more details about this article) |
3/43. cholesterol embolism in a patient with inflammatory abdominal aortic aneurysm.A 66-year-old man whose renal function had progressively deteriorated had an elevated blood pressure and also was found to have an inflammatory abdominal aortic aneurysm (AAA). Blood examination revealed that he had eosinophilia. livedo reticularis of the toes developed, and a skin biopsy specimen showed embolization of atheromatous plaques in the arterioles of the subcutaneous tissue. Progressive enlargement of inflammatory AAA may have dislodged the atheromatous plaques, resulting in cholesterol embolism.- - - - - - - - - - ranking = 1keywords = pressure (Clic here for more details about this article) |
4/43. Coexistence of atherosclerotic renal artery stenosis with primary hyperaldosteronism.The discovery of two forms of secondary hypertension in the same patient is unusual and suggests similar pathophysiological mechanisms, a predisposition to one type in the presence of the other or a chance occurrence. We describe two patients with renal artery stenosis who after successful correction of the stenotic lesions were discovered to have primary hyperaldosteronism associated with bilateral adrenal hyperplasia. Initially prior to revascularisation of the renal artery stenosis, the diagnosis of primary hyperaldosteronism was not evident. Both patients were subjected to further diagnostic evaluation after the appearance of hypokalaemia in one patient and continued resistant hypertension in both patients. The addition of spironolactone therapy reduced blood pressure impressively in both patients. Clinicians should be aware of the possibility that these two forms of secondary hypertension may be present in the same patient and that optimal blood pressure control requires diagnostic assessment and intervention for both disorders.- - - - - - - - - - ranking = 2keywords = pressure (Clic here for more details about this article) |
5/43. Primary hyperaldosteronism without suppressed renin due to secondary hypertensive kidney damage.Primary hyperaldosteronism is characterized by high plasma and urinary aldosterone and suppressed PRA. renin suppression is due to aldosterone-dependent sodium retention and mild extracellular volume expansion. We observed three patients with primary hyperaldosteronism, severe refractory hypertension, and normal to high normal PRA levels whose aldosterone/renin ratios were still elevated because of disproportionately high aldosterone levels. All available medical data on the patients as well as publications on the aldosterone/renin relationship in primary hyperaldosteronism were reviewed to explain the unusual findings. In one patient, histologically proven renal arteriolosclerosis was the probable cause of the escape of PRA from suppression by an aldosterone-producing adenoma. In the other two patients, hypertensive kidney damage due to primary hyperaldosteronism was the most likely explanation for the inappropriately high PRA, as in patient 1. All patients had high normal or slightly elevated serum creatinine levels and responded to 200 mg spironolactone/day with increased serum creatinine and hyperkalemia. hyperkalemia was probably due to a decreased filtered load of sodium and a spironolactone-induced decrease in mineralocorticoid function. Two patients were cured of hyperaldosteronism by unilateral adrenalectomy but still need some antihypertensive therapy, whereas one patient has probable bilateral adrenal disease, with normal blood pressure on a low dose of spironolactone. In patients with severe hypertension due to primary hyperaldosteronism, PRA can escape suppression if hypertensive kidney damage supervenes. An increased aldosterone/PRA ratio is still useful in screening for primary hyperaldosteronism. These patients may respond to spironolactone therapy with a strong increase in serum creatinine and potassium. Early specific treatment of primary hyperaldosteronism is therefore indicated, and even a patient with advanced hypertension will profit from adrenalectomy or cautious spironolactone treatment.- - - - - - - - - - ranking = 1keywords = pressure (Clic here for more details about this article) |
6/43. Fatal lipid embolism following intraarterial angiography at an early stage of arteriosclerosis.Intraarterial angiography was performed on a patient with peripheral arterial occlusive disease (Fontaine IIb). No relevant risk factors were known, and a previous angiography had been undertaken without incident. After administration of contrast medium, the patient complained of acute pain in the lower abdomen and both legs, and a sudden rise in blood pressure was observed. The patient subsequently lost consciousness and died within 1.5 h. Postmortem examination showed that death was due to peripheral atheromatous microembolism of lipids, and not cholesterol as is usual in these cases. The differential diagnosis is discussed and a review of the literature is presented.- - - - - - - - - - ranking = 1keywords = pressure (Clic here for more details about this article) |
7/43. renal artery stenosis: a complication of needle puncture for manometry. Case of subintimal dissection with spontaneous resolution.After aortorenal bypass for renovascular hypertension secondary to atherosclerosis of the renal artery of a solitary left kidney a high-grade stenosing lesion developed distal to the site of insertion of a Dacron graft. In the immediate postoperative period the blood pressure was restored to normal, but one week later hypertension recurred. An arteriogram disclosed an area of stenosis 1 cm distal to the site of insertion of the graft in the renal artery. During the next year, serial arteriograms were made, renal function remained normal, and hypertension gradually abated. One year after the discovery of the postbypass stenosis, an arteriogram showed disappearance of the constricting lesion. The postoperative stenosis was, in all probability, caused by subintimal dissection secondary to needle puncture for strain gauge manometry.- - - - - - - - - - ranking = 1keywords = pressure (Clic here for more details about this article) |
8/43. Spontaneous expulsive suprachoroidal hemorrhage.PURPOSE: To present a 90-year-old patient with spontaneous expulsive suprachoroidal hemorrhage (SESCH). This unique case suggests a mechanism of SESCH, which is still under debate. methods: The patient, who had corneal inflammatory disease and diabetes mellitus, atherosclerosis, and glaucoma, presented with active ocular bleeding and expulsion of intraocular tissues. Almost the entire cornea was absent, except for several small and irregular areas in its periphery. Histopathologic evaluation of the eviscerated contents was performed. RESULTS: Clinicopathologic evaluation revealed acute inflammation of the corneal remains as well as intraocular inflammation. Inflammatory necrosis of choroidal vessels was evident. CONCLUSION: The findings point to the assumption that choroidal bleeding, secondary to vascular inflammatory necrosis, was the initial event in this case of spontaneous expulsive suprachoroidal hemorrhage. Presumedly, the intraocular pressure level was very high owing to continuous bleeding, which could result in a very large, rather than localized, tearing of the peripherally inflamed cornea.- - - - - - - - - - ranking = 1keywords = pressure (Clic here for more details about this article) |
9/43. A technique to access severely diseased arteries.cardiac catheterization performed in patients with severe peripheral vascular disease may represent a difficult technical challenge and is associated with a higher incidence of vascular complications. We describe a technique that uses angioplasty equipment to access severely diseased arteries. This technique allows a percutaneous transluminal coronary angioplasty (PTCA) guide wire to be steered across vascular lesions under direct visualization of the lumen and continuous pressure monitoring, potentially reducing the risk of vascular complications.- - - - - - - - - - ranking = 1keywords = pressure (Clic here for more details about this article) |
10/43. Post-reperfusion rapidly progressive glomerulonephritis in post-transplant IgA nephropathy.Rapidly progressive glomerulonephritis (RPGN) is a rare occurrence in IgA nephropathy (IgAN) in renal transplant patients on immunosuppressive therapy. RPGN post ischemia-reperfusion has not been previously reported. We report a 62 year old male patient on azathioprine therapy, 9 years after left cadaveric renal transplantation due to end stage renal disease of unknown etiology, who presented with progressive deterioration in renal function and hematuria. Renal biopsy was consistent with IgAN. Duplex and CT scan demonstrated a decreased renal graft perfusion, due to severe atherosclerosis and stenosis of iliac arteries. The patient underwent left axilo-femoral bypass graft surgery with improvement in kidney graft perfusion and function. However, few weeks later, patient presented with pulmonary edema and advanced renal failure and he was initiated on hemodialysis. Repeated renal biopsy demonstrated crescentic GN. To the best of our knowledge, this is the first report of RPGN following reversal of ischemia and reperfusion. There was no evidence for atherembolic disease which is not uncommon after vascular surgery and it has been reported to be rarely associated to crescentic GN. Theoretical explanations for exacerbation of IgAN to crescentic GN, following successful reperfusion, could be enhancement of capillary damage, inflammation and oxidative stress. Putative mechanisms for these phenomena may be interaction of reperfusion-induced hyperfiltration, high intraglomerular capillary pressure, oxidative stress, increased polymorphonucler cells infiltration and inflammation; the presence of IgA immune deposits and azathioprine metabolites, both can also be associated to enhancement of oxidative stress.- - - - - - - - - - ranking = 1keywords = pressure (Clic here for more details about this article) |
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