Reversible Cortical Blindness as a Prominent Manifestation of Cerebral Embolism due to Infective Endocarditis

Introduction. Infective endocarditis in the left heart may be complicated by stroke, due to embolisation from infectious valvular vegetations. Infarction of both occipital lobes, which are supplied by the posterior cerebral arteries, is infrequent, and is the cause of cortical blindness from lesion of the visual cortex. Cortical blindness is characterized by intact pupillary reflexes, a normal fundoscopy, and, rarely, denial of visual loss. Case Presentation. We report the case of a 58-year-old woman, recipient of a mechanical aortic valve, who presented with fever, multiple organ dysfunction, and cortical blindness. Transesophageal echocardiography and blood cultures confirmed the diagnosis of infective endocarditis caused by methicillin-sensitive Staphylococcus aureus. Computed tomography of the brain without contrast revealed the presence of infarctions in both occipital lobes. It is noteworthy that the visual loss resolved after treatment of endocarditis. Conclusions. A stroke occurring in a patient presenting with fever and a history of valvular heart disease strongly suggests the presence of infective endocarditis. Bilateral thromboembolic infarcts of the occipital lobes cause cortical blindness, that can resolve after treatment of endocarditis

Recainam, A potent new antiarrhythmic agent: Effects on complex ventricular arrhythmias

The antiarrhythmic efficacy and safety of intravenous recainam, a newly synthesized compound displaying potent class I antiarrhythmic activity, were tested in 10 hospitalized patients with frequent (>30/h) complex ventricular ectopic beats. There were seven men and three women of average age 57 years (range 21 to 74); five had ischemic heart disease, three had cardiomyopathy and two had valvular heart disease. Recainam was given as a 3.0 mg/kg per 40 min loading infusion followed by a 0.9 mg/kg per h maintenance infusion over a 24 hour observation period. Arrhythmia response was assessed both in the short term (comparing 2 hours before and 1 hour after drug loading) and in the long term (comparing 48 hours before drug loading and 23 hours of maintenance infusion).The median frequency of total premature ventricular complexes decreased in the short term by 99.6% (from 392.5 to 1.5/h, p < 0.005) and in the long term by 99.7% (from 435 to 1.3/h, p < 0.01). Repetitive beats were suppressed by a median of 100% both in the short term (p < 0.006) and during 24 hour infusion (from 80.9 to 0/h, p < 0.003). More than 90% suppression of repetitive beats occurred in all 10 patients (100%) and more than 90% suppression of total arrhythmias occurred in 9 patients (90%) during the maintenance period. Electrocardiographic PR and QRS intervals increased by 19% (p < 0.001) and 24% (p < 0.003), respectively, during therapy, but the JTc interval decreased (p < 0.001). Plasma recainam concentrations averaged 5.2 ± 0.9 μg/ml after loading and 3.0 ± 0.5 μg/ml during maintenance therapy. No adverse symptoms occurred.In summary, recainam is a promising, highly efficacious and well tolerated agent when administered intravenously for short-term and maintenance suppression of complex ventricular arrhythmias. The efficacy of oral and intravenous recainam for arrhythmia management deserves further evaluation

Etiology of Anemia in Patients With Advanced Heart Failure

ObjectivesWe prospectively investigated the causes of anemia in patients with advanced congestive heart failure (CHF).BackgroundAnemia is common in patients with advanced CHF, and its etiology is generally considered to be multifactorial. However, despite its importance, precise information is lacking regarding the prevalence of putative etiologic factors.MethodsPatients who were hospitalized for decompensated advanced CHF and who were stabilized after their initial treatment underwent evaluation of “clinically significant” anemia, defined as a hemoglobin content <12 g/dl for men and <11.5 g/dl for women. Patients with a serum creatinine concentration >3 mg/dl or patients with concurrent diseases that are known to cause anemia were not included. The initial evaluation included measurements of vitamin B12, folic acid, thyroid-stimulating hormone, erythropoietin, lactate dehydrogenase, Coombs test, multiple fecal occult tests, and bone marrow aspiration. Patients without diagnosis by these methods underwent red cell mass measurement with 51Cr assay.ResultsThe mean age of the 37 patients was 57.9 ± 10.9 years and mean left ventricular ejection fraction 22.5 ± 5.9%. Iron deficiency anemia was confirmed by bone marrow aspiration in 27 patients (73%), 2 patients (5.4%) had dilutional anemia, and 1 patient (2.7%) had drug-induced anemia. No specific cause was identified in 7 patients (18.9%) who were considered to have “anemia of chronic disease.” Serum ferritin for the iron-deficient patients was not a reliable marker of iron deficiency in this population.ConclusionsIn this group of patients, iron deficiency was the most common cause of anemia. The iron status of patients with end-stage chronic CHF should be thoroughly evaluated and corrected before considering other therapeutic interventions

Occurrence of exercise-induced and spontaneous wide complex tachycardia during therapy with flecainide for complex ventricular arrhythmias: A probable proarrhythmic effect

Flecainide acetate, a new antiarrhythmic agent, possesses favorable pharmacokinetic and hemodynamic properties and demonstrates highly favorable antiarrhythmic activity in patients with ventricular arrhythmias. However, the proarrhythmic potential of flecainide deserves further evaluation. In 7 (13%) of 55 consecutive patients treated with oral flecainide, 200 to 600 mg/day, for complex ventricular arrhythmias (including sustained ventricular tachycardia in 14), we observed the appearance of new or more sustained exercise-induced (five patients) or spontaneous (two patients) wide complex tachycardia. The mechanism of wide complex tachycardia appeared to be ventricular tachycardia in all seven. In our series, episodes were self-remitting or successfully treated. In four patients, wide complex tachycardia did not recur during exercise testing during alternative antiarrhythmic therapy (three patients) or no antiarrhythmic therapy (one patient). These observations raise the possibility of flecainide-related proarrhythmia, manifested as an increased propensity to exercise (activity)-induced wide complex tachycardia, which was not reliably predicted by results of Holter recordings or programmed electrical stimulation. Patients with complex ventricular arrhythmias beginning long-term treatment with oral flecainide should be considered for treadmill exercise testing together with ambulatory monitoring as part of the initial assessment of drug efficacy.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/26728/1/0000278.pd

Wegener&apos;s granulomatosis presenting as a renal mass

Wegener’s granulomatosis is a systemic necrotizing vasculitis that usually involves the kidneys, typically causing segmental necrotizing glomerulonephritis. An association between Wegener’s granulomatosis and renal cell carcinoma was recently reported. We describe a case of Wegener’s granulomatosis presenting as a renal mass in a 72-year-old woman. Histologic examination of the mass revealed granulomatous inflammation, an extremely rare manifestation of this disease. We also review the incidence of renal mass in Wegener’s granulomatosis and highlight the importance of excluding the coexistence of renal cell carcinoma

Stauffer&apos;s syndrome as a prominent manifestation of renal cancer: a case report

Background: Renal cell carcinoma is associated with a wide spectrum of para-neoplastic syndromes, which may be precursors of primary or recurrent disease. Non-metastatic hepatic dysfunction in patients suffering from renal cell carcinoma is known as Stauffer&apos;s syndrome. It is associated with the production of cytokines by the tumour, and several biochemical abnormalities, including elevated serum alkaline phosphatase. Case presentation: We describe a 36-year-old woman presenting with various non-specific, systemic disease manifestations, and elevated liver enzymes due to cholestasis as the main laboratory abnormality. Imaging studies showed a solid mass in the left kidney, which, after surgical excision, was identified as renal cell carcinoma. No metastasis was found. Conclusion: Stauffer syndrome may precede other manifestations of renal cell carcinoma. In case of unexplained abnormal liver function, particularly in presence of systemic symptoms, underlying renal cell carcinoma should be excluded by focused investigations. © 2009 Kranidiotis et al; licensee BioMed Central Ltd