The persistence of a left-sided superior vena cava is the most common variant of systemic venous drainage. Increased utility of cardiac imaging, in particular cross-sectional techniques such as computed tomography and magnetic resonance (MR), will result in increased detection of the anomaly and its variants. Whilst in the typical form it is often haemodynamically insignificant, its discovery may have clinical significance nonetheless, and its mimics require exclusion. During cardiac development the anomaly results from a failure of the left anterior cardinal vein to obliterate. Recognized anatomical variants include the absence of the right superior vena cava and of an innominate bridging vein. Typical drainage is to the coronary sinus, dilatation of which may be the first hint to the anomaly. Clinical implications with respect to vascular access and arrhythmia are well described. A significant minority drain into the left atrium, potentially creating a haemodynamically significant lesion. Additionally, differentiation from anomalous left upper pulmonary venous drainage via a vertical vein is mandatory. A newly discovered variant runs an intra-atrial course with subsequent typical drainage, and if not recognized as such, may be confused with a left atrial mass. The use of 3D contrast-enhanced MR venography has proven extremely helpful in characterizing anomalous vasculature, and we demonstrate how such techniques can help delineate the anomaly and differentiate from its mimics.

IEFs are common, requiring further investigation in a substantial minority. The incidence of highly significant findings in this study was low (∼1%), and similar to the reported incidence in the computed tomography literature. No significant difference was found between the reporting rates of IEFs between different specialties.

Right-sided cardiac valvular disease has traditionally been considered less clinically important than mitral or aortic valve pathology. However, detectable tricuspid regurgitation (TR) is common and recent data suggest that significant TR can lead to functional impairment and reduced survival, particularly in patients with concomitant left-sided valvular disease. The tricuspid valve is a complex anatomical structure and advances in three dimensional echocardiography and cardiac MRI have contributed to a greater understanding of tricuspid valve pathology. These imaging techniques are invaluable in determining the aetiology and severity of TR, and provide an assessment of right ventricular function and pulmonary artery pressure. TR is more prevalent in women and those with a history of myocardial infarction and heart failure. It also occurs in about 10% of patients with rheumatic heart disease. Chronic severe TR may have a prolonged clinical course culminating in the development of fatigue and poor exercise tolerance due to a reduced cardiac output. Approximately 90% of cases of TR are secondary to either pulmonary hypertension or intrinsic right ventricular pathology and about 10% are due to primary tricuspid valve disease. Primary causes such as Ebstein's anomaly, rheumatic disease, myxomatous changes, carcinoid syndrome, endomyocardial fibrosis, and degenerative disease have characteristic morphological features readily identifiable by echocardiography. Ascertaining an accurate right ventricular systolic pressure is important in separating primary from secondary causes as significant TR with a pressure <40 mm Hg implies intrinsic valve disease. Cardiac MRI may be indicated in those with inadequate echocardiographic images and is also the gold standard for the evaluation of right ventricular function and morphology. The assessment of leaflet morphology, annular dimensions, and pulmonary artery pressure are particularly important for determining subsequent management. Along with appropriate treatment of the underlying cause of TR and pulmonary hypertension, management guidelines indicate a move towards more aggressive treatment of TR. In those undergoing left-sided valve surgery, tricuspid valve repair is universally recommended in the presence of severe coexistent TR; in those with isolated severe TR, surgery is recommended in the presence of symptoms or progressive right ventricular dilatation or dysfunction.

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We present a case of aortic and tricuspid native valve endocarditis in which Cardiobacterium valvarum was isolated from the blood culture of a 65-year-old man. Cardiobacterium valvarum is a fastidious, Gram-negative bacillus. The genus Cardiobacterium encompasses two speciesCardiobacterium valvarum and Cardiobacterium hominis. Although both species rarely feature as the aetiological agent of endocarditis, Cardiobacterium hominis has a higher incidence than Cardiobacterium valvarum. For this causative organism, we believe this is the first report of fatality prior to surgical intervention and the first clinical course to be complicated by cerebral vasculitis. Native valve endocarditis caused by Gram-negative bacilli is extremely rare and identification of isolates may require the use of reference laboratories with molecular identification techniques. Case reportA previously fit and well 65-year-old male was admitted with an 8 month history of intermittent back pain, worsening abdominal distension and non-specific symptoms of malaise, fatigue, slowed mobility and weight loss. He had not visited his general practitioner for over 30 years and had no known past medical or drug history. The patient was an occasional drinker and ex-smoker, having stopped 25 years previously. He had no history of recreational drug use. His dentition was extremely poor with widespread caries and gingivitis. He did not report any recent dental manipulation.At initial presentation, the patient had a temperature of 37.2 u C and a thin habitus and was pale. Blood pressure was 130/80 mmHg and his pulse was regular at 80 beats min 21 . On examination, a grade 4 harsh ejection systolic murmur and petechial rash over plantar areas of both feet were noted. During abdominal examination he was thought to have an expansile abdominal mass.Initial tests revealed a normal electrocardiogram and chest and abdominal radiographs. Laboratory results revealed a normocytic, normochromic anaemia [haemoglobin 10.9 g dl 21 (normal 13-18 g dl 21 ), mean corpuscular volume 92 fl (normal 76-96 fl)], total white blood cells 6.5610 9 l 21 (normal 4-11610 9 l 21 ) and normal clotting. C-reactive protein was raised at 34 mg l 21 (normal ,5) and showed an increasing trend throughout admission, peaking at 60 mg l 21 on day 13 of admission. He had renal failure with an elevated urea of 30.5 mmol l 21 (normal 2.5-6.7 mmol l 21 ), creatinine 278 mmol l 21 (normal 70-150 mmol l 21 ) and potassium 5.4 mmol l 21 (normal 3.5-5 mmol l 21 ). Sodium was 133 mmol l 21 (normal 135-145 mmol l 21 ).Urine and blood cultures were taken in the emergency department (bioMérieux BactT/Alert; aerobic and anaerobic bottles; one set of cultures). An urgent computerized tomography (CT) scan of the aorta was performed to investigate the expansile mass and lower back pain. This showed no abdominal aortic aneurysm. Incidentally, the CT scan revealed a massively dilated bladder with bilateral hydronephrosis, splenomegaly, renal cysts and pulmonary nodules with an appearance suggestive of an inflamm...