No abstract

AimsPatients with chronic heart failure are often characterized by impaired renal function, also referred to as cardiorenal syndrome (CRS). The aim of this study was to assess whether novel markers of kidney injury are elevated in chronic heart failure and CRS. Methods and resultsThe new renal biomarkers kidney injury molecule-1 (KIM-1), N-acetyl-ß-D-glucosaminidase (NAG) and neutrophil gelatinase-associated lipocalin (NGAL) were assessed from urine samples of 173 individuals. Patients with chronic heart failure (n ¼ 150) were characterized by decreased ejection fraction (32 + 9% vs. controls 62 + 4%, P , 0.001) and increased plasma N-terminal pro-brain natriuretic peptide (median 1460 pg/mL, interquartile range (IQR) 630 -3000 pg/mL vs. controls 56, IQR 25 -64l pg/mL, P , 0.001). Urinary analysis showed that KIM-1 was significantly elevated in heart failure patients compared with healthy controls (1100, IQR 620-1920 vs. 550, IQR 320 -740 ng/g urinary creatinine, P , 0.001). Further, KIM-1 increased significantly with decreasing left ventricular function (r ¼ 20.37, P , 0.001) and severity of New York Heart Association (NYHA)-class (r ¼ 0.5, P , 0.001). N-acetyl-ß-D-glucosaminidase showed a weaker response but correlated significantly with left ventricular dysfunction (r ¼ 20.18, P ¼ 0.015) and more severe clinical condition (r ¼ 0.22, P ¼ 0.04). In contrast, NGAL showed no significant correlation. Kidney injury molecule-1 and NAG were also predictors of all-cause mortality and the composite of all-cause mortality and rehospitalization for heart failure (all P , 0.05). ConclusionsKidney injury molecule-1 and NAG are elevated in symptomatic heart failure. This finding may be present in patients with apparently normal kidney function and indicates tubular injury in chronic heart failure. Kidney injury molecule-1 and NAG are potential markers of CRS with additional prognostic value.--

Sleep-disordered breathing was associated with less myocardial salvage and a smaller reduction in infarct size. These findings suggest a contribution of SDB to impaired healing of MI.

Objective: To compare the extent and distribution of focal fibrosis by gadolinium contrast-enhanced magnetic resonance imaging (MRI; delayed hyperenhancement) in severe left ventricular (LV) hypertrophy in patients with pressure overload caused by aortic stenosis (AS) and with genetically determined hypertrophic cardiomyopathy (HCM). Methods: 44 patients with symptomatic valvular AS (n = 22) and HCM (n = 22) were studied. Cine images were acquired with fast imaging with steady-state precession (trueFISP) on a 1.5 T scanner (Sonata, Siemens Medical Solutions). Gadolinium contrast-enhanced MRI was performed with a segmented inversion-recovery sequence. The location, extent and enhancement pattern of hyperenhanced myocardium was analysed in a 12-segment model. Results: Mean LV mass was 238.6 (SD 75.3) g in AS and 205.4 (SD 80.5) g in HCM (p = 0.17). Hyperenhancement was observed in 27% of patients with AS and in 73% of patients with HCM (p , 0.01). In AS, hyperenhancement was observed in 60% of patients with a maximum diastolic wall thickness > 18 mm, whereas no patient with a maximum diastolic wall thickness , 18 mm had hyperenhancement (p , 0.05). Patients with hyperenhancement had more severe AS than patients without hyperenhancement (aortic valve area 0.80 (0.09) cm 2 v 0.99 (0.3) cm 2 , p , 0.05; maximum gradient 98 (22) mm Hg v 74 (24) mm Hg, p , 0.05). In HCM, hyperenhancement was predominant in the anteroseptal regions and patients with hyperenhancement had higher end diastolic (125.4 (36.9) ml v 98.8 (16.9) ml, p , 0.05) and end systolic volumes (38.9 (18.2) ml v 25.2 (1.7) ml, p , 0.05). The volume of hyperenhancement (percentage of total LV myocardium), where present, was lower in AS than in HCM (4.3 (1.9)% v 8.6 (7.4)%, p, 0.05). Hyperenhancement was observed in 4.5 (3.1) and 4.6 (2.7) segments in AS and HCM, respectively (p = 0.93), and the enhancement pattern was mostly patchy with multiple foci. Conclusions: Focal scarring can be observed in severe LV hypertrophy caused by AS and HCM, and correlates with the severity of LV remodelling. However, focal scarring is significantly less prevalent in adaptive LV hypertrophy caused by AS than in genetically determined HCM. R emodelling in left ventricular (LV) hypertrophy is accompanied by several structural changes. Interstitial and replacement fibrosis are among the morphological alterations that have been observed in LV hypertrophy caused by pressure overload and in genetically determined hypertrophic cardiomyopathy (HCM).

The aim of this study was to test whether an improvement of left ventricular ejection fraction (EF) in the early phase after acute myocardial infarction is associated with a reduction of the severity of central and obstructive sleep apnoea.40 consecutive patients with acute myocardial infarction underwent polysomnography and cardiovascular magnetic resonance imaging within 5 days and 12 weeks after the event to assess sleep apnoea and cardiac function. We stratified the sample in patients who improved their left ventricular EF within 12 weeks by o5% (improved EF group, DEF 9¡1%, n516) and in those who did not (unchanged EF group, DEF -1¡1%, n524).Prevalence of sleep apnoea (o15 apnoea and hypopnoea events?h -1 ) within f5 days after myocardial infarction was 55%. Apnoea and hypopnoea events?h -1 were significantly more reduced in the improved EF group compared with the unchanged EF group (-10¡3 versus 1¡3 events?h -1 ; p50.036). This reduction was based on a significant alleviation of obstructive events (-7¡2 versus 4¡3 events?h -1 ; p50.009), while the reduction of central events was similar between groups (p50.906).An improvement of cardiac function early after myocardial infarction is associated with an alleviation of sleep apnoea. This finding suggests that re-evaluation of treatment indication for sleep apnoea is needed when a change in cardiac function occurs.