Computed Tomography/Fluoroscopy Fusion and 3D Transesophageal Echocardiography-Guided Percutaneous Paravalvular Leak Closure.

Percutaneous paravalvular leak closure seems a safe alternative to surgery in frail patients. However, it is a challenging procedure that should be tailored to each patient with optimal imaging guidance. Transesophageal echocardiography during the procedure and computed tomography scan/fluoroscopy fusion provide guidance for critical steps, such as PVL localization and crossing. (Level of Difficulty: Advanced.).

Renin-angiotensin system blockade promotes a cardio-renal protection in albuminuric homozygous sickle cell patients.

The management of sickle cell nephropathy (SCN) at an early stage is an important issue to prevent renal and cardiovascular morbidity and mortality. This study aimed to evaluate in this population, whether angiotensin converting enzyme inhibitors (ACEIs) treatment could exert a cardio-renal protection in a SCN cohort. Forty-two SCN patients (urine albumin:creatinine ratio (ACR) > 10 mg/mmol) were treated with ACEIs for 6 months, then evaluated for ACR, measured glomerular filtration rate (mGFR) together with haematological and cardiovascular parameters. A 1-month washout was also performed in order to differentiate short- and long-term ACEIs effects. A decrease in ACR baseline value (>30%) was detected in 62% of cases (mean ACR: 46·4 ± 7·6 and 26·4 ± 3·9 mg/mmol at baseline and 6 months respectively; P = 0·002), whereas mGFR values were unchanged. ACR decrease was detected at 1 month following ACEI initiation (32·9 ± 6·9, P = 0·02) with a persistent trend after withdrawal (P = 0·08). ACEIs also decreased diastolic blood pressure (P = 0·007), pulse wave velocity (P = 0·01), tricuspid regurgitation velocity (TRV; P = 0·04), asymmetric dimethyl arginine (ADMA: P = 0·001) and haemoglobin (P = 0·01) while conventional haemolytic biomarkers were unchanged. Our data suggest that ACEIs are safe and effective at decreasing albuminuria in sickle cell patients with a beneficial effect on specific mortality risk factors, such as TRV and asymmetric dimethyl arginine.

Left atrial volume is not an index of left ventricular diastolic dysfunction in patients with sickle cell anaemia.

BACKGROUND: Left ventricular diastolic dysfunction (LVDD) is common in sickle cell anaemia (SCA). Left atrial (LA) size is widely used as an index of LVDD; however, LA enlargement in SCA might also be due to chronic volume overload. AIM: To investigate whether LA size can be used to diagnose LVDD in SCA. METHODS: One hundred and twenty-seven adults with stable SCA underwent echocardiographic assessment. LA volume was measured by the area-length method and indexed to body surface area (LAVi). Left ventricular (LV) filling pressures were assessed using the ratio of early peak diastolic velocities of mitral inflow and septal annular mitral plane (E/e'). Using mitral inflow profile and E/e', LV diastolic function was classified as normal or abnormal. LAVi>28mL/m(2) was used as the threshold to define LA enlargement. RESULTS: The mean age was 28.6±8.5years; there were 83 women. Mean LAVi was 48.3±11.1mL/m(2) and 124 (98%) patients had LA dilatation. In multivariable analysis, age, haemoglobin concentration and LV end-diastolic volume index were independent determinants of LAVi (R(2)=0.51; P<0.0001). E/e' was not linked to LAVi (P=0.43). Twenty patients had LVDD; when compared with patients without LVDD, they had a similar LAVi (52.2±14.7 and 47.5±10.2mL/m(2), respectively; P=0.29). Receiver operating characteristics curve analysis showed that LAVi could not be used to diagnose LVDD (area under curve=0.58; P=0.36). CONCLUSION: LA enlargement is common in SCA but appears not to be linked to LVDD. LAVi in this population is related to age, haemoglobin concentration and LV morphology.

Left atrial volume predicts abnormal exercise left ventricular filling pressure.

AIMS: Latent heart failure at rest can be observed in a number of patients upon exercise. Considering left atrial (LA) remodelling as the reflection of the cumulative effects of the LV filling pressure (FP) over time, our aim was to investigate whether the LA volume would predict abnormal exercise LVFP. METHODS AND RESULTS: Ninety patients (58.6 ± 10.8 years, 74 men) underwent exercise echocardiography. The LA maximal volume was measured by the Simpson method and indexed to body surface area. LVFP was assessed by the ratio between early peak diastolic velocities of mitral inflow and the septal annular mitral plane (E/e'). Exercise E/e' >13 was used as a threshold to define abnormal LVFP. Indexed LA volume was correlated with E/e' at rest (r = 0.37, P = 0.003), but the correlation was better with exercise E/e' (r = 0.54, P < 0.0001). In multivariate analysis, age, LV end-diastolic volume index, LVEF, and exercise E/e' were the independent determinants of LA volume index (R(2) = 0.47, P < 0.0001). Eleven patients had exercise E/e' >13; compared with the rest of the population, these patients were older and achieved a milder effort. LA volume index >33 mL/m(2) predicted an abnormal exercise LVFP with a 91% sensitivity and a 78% specificity. None of the patients with an LA volume index <26 mL/m(2) (n = 31, 34%) had an exercise E/e' >13. CONCLUSION: Exercise LVFP is a determinant of LA size. LA volume index seems to be helpful for predicting abnormal exercise LVFP. The potential use of LA remodelling to identify the patients benefitting most from exercise echocardiography should be investigated in larger studies.

Subclinical left ventricular systolic impairment in steady state young adult patients with sickle-cell anemia.

Chronic volume overload in sickle-cell anemia (SCA) is associated with left ventricular (LV) enlargement and hypertrophy. The effect of the disease on LV systolic function remains debated. The aim of our study was to investigate LV systolic function in SCA patients using 2D speckle-tracking imaging. We compared 30 steady state asymptomatic adult SCA patients (17 women, mean age 24.7 ± 5.1 years) with 30 age and sex-matched healthy subjects (17 women, mean age 25.0 ± 4.9 years). In addition to conventional echocardiographic parameters including LV ejection fraction (LVEF) and LV mass index (LVMi), global longitudinal strain (GLS) and strain rate (GLSR) were measured. GLS (-17.9 ± 2.0 vs. -19.7 ± 2.5 %, p = 0.004) and GLSR (-0.92 ± 0.09 vs. -1.07 ± 0.17 s(-1), p < 0.0001) values were lower in SCA patients while LVEF values (60.1 ± 3.8 vs. 61.7 ± 4.7 %, p = 0.30) were not different. LVMi was increased in SCA patients (100.7 ± 23.5 vs. 72.4 ± 15.2 g/m(2), p = 0.0001) and GLSR was significantly lower in the subgroup of patients with LV hypertrophy (-0.88 ± 0.09 vs. -0.96 ± 0.08 s(-1), p = 0.02). In SCA patients LVMi was correlated to GLS (r = 0.58, p = 0.001) and GLSR (r = 0.45, p = 0.015) pleading in favor of a pathological LV remodeling. Asymptomatic SCA patients exhibited a subclinical alteration of LV systolic function. Myocardial dysfunction appears to be linked to the degree of LV hypertrophy. 2D speckle-tracking imaging might be useful for long-term follow-up and to study the natural course of LV dysfunction in SCA patients.

[Chyluria presenting as milky urine and nephrotic-range proteinuria and milky urine: chyluria or glomerulopathy? Case report and literature review]. / Protéinurie de débit néphrotique et urines laiteuses: chylurie ou glomérulopathie? Cas clinique et analyse de la littérature.

A patient is admitted in hospital to explore a nephrotic proteinuria associated with milky urine. This is explained by a chyluria (presence of lymphatic fluid in the urines), which is due to a pyelolymphatic fistula probably linked to a lymphatic filariasis. Usually, the diagnosis of chyluria can be confirmed by the presence of urinary chylomicrons. The presence of an urinary-lymphatic fistula can be proved by different techniques (cystoscopy, retrograde pyelography, uroscanner, lymphoscintigraphy). The main cause of chyluria is parasitic infections (filarial infection, echinococcus, cysticercosis), but other causes can be found, such as granulomatosis, neoplasia, lymphatic malformations, or sequela of surgery or traumatism. Chyluria is one of the causes of post-nephronic nephrotic proteinuria. Depending on the impact of the chyluria for the patient, there will either be no treatment, or a treatment by sclerotherapy or surgery.