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Pressure overload and heart failure electrophysiological remodeling (HF-ER) in pigs are associated with decreased conduction velocity (CV) and dispersion of repolarization, which lead to higher risk of ventricular arrhythmia. This work aimed to establish the correlation between QRS complex duration and underlying changes in CV during increased intraventricular pressure (IVP) and/or HF-ER ex-vivo, and to determine whether QRS duration could be sensitive to an acute increase in left ventricular (LV) afterload in-vivo. HF-ER was induced in 7 pigs by high-rate ventricular pacing. Seven weight-matched animals were used as controls. Isolated Langendorff-perfused hearts underwent programmed ventricular stimulation to study QRS complex duration and CV under low/high IVP, using volume-conducted ECG and epicardial optical mapping, respectively. Four additional pigs underwent open-chest surgery to increase LV afterload by partially clamping the ascending aorta, while measuring QRS complex duration during sinus rhythm (SR). In 13 hearts included for analysis, both HF-ER and increased IVP showed significantly slower epicardial CV (-40% and -15%, p < 0.001 and p = 0.004, respectively), which correlated with similar widening of the QRS complex (+41% and +17%, p = 0.005 and p < 0.001, respectively). HF-ER hearts shower larger prolongation of the QRS complex than controls upon increasing the IVP (+21% vs. +12%, respectively. HF-ER*IVP interaction: p = 0.004). QRS complex widened after increasing LV afterload in-vivo (n=3), with correlation between QRS duration and aortic diastolic pressures (R = 0.58, p < 0.001). In conclusion, high IVP and/or HF-ER significantly decrease CV, which correlates with QRS widening on the ECG during ventricular pacing. Increased myocardial wall stress also widens the QRS complex during SR in-vivo., (Copyright © 2017 Elsevier Ltd. All rights reserved.)

Background: The Killip classification categorizes heart failure (HF) in acute myocardial infarction, and has a prognostic value. Although non-ST-elevation myocardial infarction (NSTEMI) is increasing steadily, little information is available about the prognostic value of low Killip class in this scenario. Our aim was to assess the prognostic value of mild HF in NSTEMI., Methods: 835 patients with NSTEMI between 2005 and 2007 were prospectively recruited. Patients in Killip-1 (K1=684) or Killip-2 class (K2=113) were selected (38, with K>2, excluded). Clinical, angiographic, treatment strategies, and 30-day all-cause mortality, together with other cardiovascular outcomes were recorded., Results: K2 patients were mostly women (K1 27.9% vs K2 48.0%, p<0.001) and older (K1 66.6years vs K2 73.8years, p<0.001) with a higher frequency of diabetes mellitus (p<0.001) and hypertension (p<0.001). Smoking was less frequent in the K2-group (p=0.003). A previous infarction/revascularization history was similar in both groups. The infarction size, assessed by Troponin I/Creatin kinase, did not differ between groups (p=0.378 and p=0.855). Multivessel coronary disease and revascularization procedures were less common in group K2 (p=0.015 and p=0.005 vs group K1, respectively). Patients in K2 had a worse prognosis in terms of maximum Killip class, death and major adverse cardiovascular events (p<0.001). After multivariate analysis, mild HF at presentation was an independent risk factor for mortality (OR=6.50; IC 95%: 2.48-16.95; p<0.001)., Conclusion: Mild HF at presentation in NSTEMI is linked to a poor prognosis, with increased short-term mortality. Thus, a more aggressive approach including early cardiac catheterization and revascularization should be considered., (Copyright (c) 2010 European Federation of Internal Medicine. Published by Elsevier B.V. All rights reserved.)