Background—Cardiac sarcoidosis is associated with an increased risk of heart failure and sudden death, but its risk in patients with preserved left ventricular ejection fraction is unknown. Using cardiovascular magnetic resonance in patients with extracardiac sarcoidosis and preserved left ventricular ejection fraction, we sought to (1) determine the prevalence of cardiac sarcoidosis or associated myocardial damage, defined by the presence of late gadolinium enhancement (LGE), (2) quantify their risk of death/ventricular tachycardia (VT), and (3) identify imaging-based covariates that predict who is at greatest risk of death/VT.Methods and Results—Parameters of left and right ventricular function and LGE burden were measured in 205 patients with left ventricular ejection fraction >50% and extracardiac sarcoidosis who underwent cardiovascular magnetic resonance for LGE evaluation. The association between covariates and death/VT in the entire group and within the LGE+ group was determined using Cox proportional hazard models and time-dependent receiver–operator curves analysis. Forty-one of 205 patients (20%) had LGE; 12 of 205 (6%) died or had VT during follow-up; of these, 10 (83%) were in the LGE+ group. In the LGE+ group (1) the rate of death/VT per year was >20× higher than LGE− (4.9 versus 0.2%, P<0.01); (2) death/VT were associated with a greater burden of LGE (14±11 versus 5±5%, P<0.01) and right ventricular dysfunction (right ventricular EF 45±12 versus 53±28%, P=0.04). LGE burden was the best predictor of death/VT (area under the receiver-operating characteristics curve, 0.80); for every 1% increase of LGE burden, the hazard of death/VT increased by 8%.Conclusions—Sarcoidosis patients with LGE are at significant risk for death/VT, even with preserved left ventricular ejection fraction. Increased LGE burden and right ventricular dysfunction can identify LGE+ patients at highest risk of death/VT.
Introduction: Many of the deleterious effects associated with chronic kidney disease (CKD) are secondary to the resultant systemic inflammation. The gut microbial changes caused by CKD are thought to perpetuate systemic inflammation. Therefore, strategies aimed at modulating the gut microbiota may be helpful in reducing complications associated with CKD. We hypothesized that supplementation with high‐amylose maize resistant starch type 2 (HAM‐RS2) would beneficially alter the gut microbiome and lead to lower levels of systemic inflammation.
Methods: A double‐blind, parallel, randomized, placebo‐controlled trial was performed comparing dietary supplementation of HAM‐RS2 with placebo in patients with end‐stage CKD. Fecal microbial data were obtained from a subset of patients after DNA extraction and 16s sequencing.
Findings: Supplementation of HAM‐RS2 led to a decrease in serum urea, IL‐6, TNFα, and malondialdehyde (P < 0.05). The Faecalibacterium genus was significantly increased in relative abundance following HAM‐RS2 supplementation (HAM‐RS2‐Day 0: 0.40 ± 0.50 vs. HAM‐RS2‐Day 56: 3.21 ± 4.97 P = 0.03) and was unchanged by placebo (Control‐Day 0: 0.72 ± 0.72 vs. Control‐Day 56: 0.83 ± 1.57 P = 0.5).
Discussion: Supplementation of amylose resistant starch, HAM‐RS2, in patients with CKD led to an elevation in Faecalibacterium and decrease in systemic inflammation. Microbial manipulation in CKD patients by using the prebiotic fiber may exert an anti‐inflammatory effect through an elevation in the bacterial genera Faecalibacterium.
Background
Cardiac infiltration is an important cause of death in sarcoidosis. Tran-sthoracic echocardiography (TTE) has limited sensitivity for the detection of cardiac sarcoidosis (CS). Late gadolinium enhancement (LGE) cardiovascular magnetic resonance (CMR) is used to diagnose CS but has limitations of cost and availability. We sought to determine whether TTE- derived global longitudinal strain (GLS) may be used to identify individuals with CS, despite preserved left ventricular ejection fraction (LVEF), and whether abnormal GLS is associated with major cardiovascular events (MCE).
Methods
We studied 31 patients with biopsy- proven extra- cardiac sarcoidosis, LVEF>50% and LGE on CMR (CS+ group), and 31 patients without LGE (CS−group), matched by age, sex, and severity of lung disease. GLS was measured using vendor- independent speckle tracking software. Parameters of left and right ventricular systolic and diastolic function were also studied. Receiver- operating characteristic curves were used to identify GLS cutoff for CS detection, and Kaplan–Meier plots to determine the ability of GLS to predict MCE.
Results
LGE was associated with reduced GLS (−19.6±1.9% in CS− vs −14.7±2.4% in CS+, P<.01) and with reduced E/A ratio (1.1±0.3 vs 0.9±0.3, respectively, P =.01). No differences were noted in other TTE parameters. GLS magnitude inversely correlated with LGE burden (r=−.59). GLS cutoff of −17% showed sensitivity and specificity 94% for detecting CS. Patients who experienced MCE had worse GLS than those who did not (−13.4±0.9% vs −17.7±0.4%, P=.0003).
Conclusions
CS is associated with significantly reduced GLS in the presence of preserved LVEF. GLS measurements may become part of the TTE study performed to screen for CS.
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