Irrigated vs. Non-irrigated Catheters in the Ablation of Accessory Pathways.

There is a paucity of data comparing irrigated to non-irrigated catheters in the ablation of accessory pathways (AP) in adult patients. Retrospective analysis of first-time AP ablations performed at our institution from May 2010 to June 2017. A total of 69 AP ablations were studied; irrigated catheters were used in 78.3% cases. Mean age was 40.9 ± 14.3 years and 56.7% were male. Among APs, 63.8% were left sided and 56.5% were concealed. The total procedure time was 232.0 ± 89.0 min, ablation time was 3.1 ± 5.1 min, and fluoroscopy time was 13.9 ± 15.4 min. The overall acute success rate of ablation was 62/69 (89%). Success rates trended higher with irrigated catheters in both groups and were significant for the population as a whole (94.4% vs. 73.3%, p = 0.04). Analyzing the entire cohort, success rates were significantly higher in ablations using irrigated catheters.

Dynamics in insulin resistance and plasma levels of adipokines in patients with acute decompensated and chronic stable heart failure.

BACKGROUND: Patients with heart failure (HF) develop metabolic derangements including increased adipokine levels, insulin resistance, inflammation and progressive catabolism. It is not known whether metabolic dysfunction and adipocyte activation worsen in the setting of acute clinical decompensation, or conversely, improve with clinical recovery. METHODS AND RESULTS: We assessed insulin resistance using homeostasis model assessment of insulin resistance (HOMA-IR), and measured plasma levels of N-terminal pro-B-type natriuretic peptide (NT-proBNP), adiponectin, visfatin, resistin, leptin, and tumor necrosis factor (TNF) α in 44 patients with acute decompensated HF (ADHF) due to left ventricular (LV) systolic dysfunction and again early (<1 wk) and late (> 6 mo) after clinical recovery, in 26 patients with chronic stable HF, and in 21 patients without HF. NT-proBNP was not increased in control subjects, mildly elevated in patients with stable HF, markedly elevated in patients with ADHF, and decreased progressively early and late after treatment. Compared to control subjects, plasma adiponectin, visfatin, leptin, resistin, and TNF-α were elevated in patients with chronic stable HF and increased further in patients with ADHF. Likewise, HOMA-IR was increased in chronic stable HF and increased further during ADHF. Adiponectin, visfatin, and HOMA-IR remained elevated at the time of discharge from the hospital, but returned to chronic stable HF levels. Adipokine levels were not related to body mass index in HF patients. HOMA-IR correlated positively with adipokines and TNF-α in HF patients. CONCLUSIONS: ADHF is associated with worsening of insulin resistance and elevations of adipokines and TNF-α, indicative of adipocyte activation. These metabolic abnormalities are reversible, but they temporally lag behind the clinical resolution of decompensated HF.

Episodes of acute heart failure syndrome are associated with increased levels of troponin and extracellular matrix markers.

BACKGROUND: Increased myocyte loss and extracellular matrix (ECM) turnover are central mechanisms that contribute to pathological myocardial remodeling in chronic heart failure (HF). We tested the hypothesis that episodes of acute HF syndrome (AHFS) are associated with transient increases in markers of myocyte injury and ECM turnover beyond those observed in chronic stable HF. METHODS AND RESULTS: Markers of myocyte injury and ECM turnover were assessed in 80 patients prospectively divided into 3 groups: AHFS (n=39); chronic stable systolic HF (n=21); and control subjects without HF (n=20). Myocyte injury was assessed by measuring plasma troponin I. ECM turnover was assessed by measuring plasma matrix metalloproteinases, tissue inhibitors of matrix metalloproteinases, and procollagen N-terminal type I and procollagen type III N-terminal peptides. In the AHFS group, biomarkers were obtained (1) at the time of hospital admission for an episode of HF decompensation, (2) at the time of hospital discharge, and (3) several weeks after discharge in patients who had returned to a chronic stable compensated state. In patients with stable HF (versus non-HF controls), there was a small increase in troponin I and little or no difference in any marker of ECM turnover. In patients with AHFS, troponin I and 3 markers of ECM turnover (matrix metalloproteinases-2, tissue inhibitors of matrix metalloproteinases-1, and procollagen type III N-terminal peptides) were elevated (versus chronic stable HF), and all fell toward chronic HF levels in patients who returned to a compensated state. CONCLUSIONS: Episodes of AHFS are associated with transient increases in markers of myocyte injury and ECM turnover that may reflect an acceleration of pathological myocardial remodeling during AHFS.