QRS duration reflects underlying changes in conduction velocity during increased intraventricular pressure and heart failure.

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.

The COR trial: a randomized study with continuous rhythm monitoring to compare the efficacy of cryoenergy and radiofrequency for pulmonary vein isolation.

BACKGROUND: Results from randomized trials designed to compare cryoenergy with radiofrequency for pulmonary vein (PV) isolation are lacking. OBJECTIVE: To compare the efficacy of a simplified strategy for PV cryoablation (group C) vs PV isolation with open-irrigated radiofrequency catheters (group R). METHODS: Fifty patients with paroxysmal atrial fibrillation (AF) and 4 independent PVs received a Reveal XT implantable cardiac monitor and were randomized to group C or group R. In group C, PV ablation was done with a single Arctic Front balloon (23 or 28 mm) per patient and two 300-second applications per PV. No further applications were delivered to close residual conduction gaps. In group R, bidirectional PV conduction block was pursued with Lasso and Navistar ThermoCool catheters and the CARTO system. The primary end point was the proportion of patients remaining free from AF recurrences ≥2 minutes without taking antiarrhythmic drugs 12 months after ablation. RESULTS: The primary end point was met by 12 (48%) patients in group C and 25 (68%) patients in group R (odds ratio 0.43; P = .05). This difference disappeared after adjustment for acute procedural outcome. In patients for whom all 4 PVs were blocked at the end of the procedure, there was no difference between group C and group R in the primary end point (67% vs 68%; P = .94). CONCLUSIONS: The efficacy of the simplified strategy for PV cryoablation tested in this study is inferior to PV isolation using open-irrigated radiofrequency catheters with electrophysiological and electroanatomical guidance. Complete PV conduction block is critical to the success of AF ablation.

Mild heart failure is a mortality marker after a non-ST-segment acute myocardial infarction.

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.

Short-term and mid-term follow-up of sutureless surgery for postinfarction subacute free wall rupture.

We report our short-term and mid-term results with sutureless repair of postinfarction subacute left ventricular free wall rupture (LVFWR). For this purpose, we evaluated the short-term and mid-term postoperative results assessed by clinical examination and echocardiography of all patients who underwent surgery for subacute LVFWR between January 2004 and January 2009. Twenty-one patients were operated. Direct suture repair of LVFWR was carried out in only one patient. In all other cases we used a pericardial patch with biological glue. Early mortality was 19% (n=4). The median duration of follow-up was 17.3 months (interquartile range, 5-38.7), with a 13-month survival of 76%. Follow-up echocardiography showed no constriction associated with the rupture zone in any patient. According to our early experience, sutureless LVFWR repair is safe, effective and reproducible, and offers acceptable morbidity and mortality during follow-up.