Summary. Background: Recently, some prognostic models for acute pulmonary embolism (PE) have been proposed. We investigated whether the Pulmonary Embolism Severity Index (PESI) and the European Society of Cardiology (ESC) prognostic approaches result in different prognoses. Methods: Consecutive adult patients with acute PE were included. According to the ESC guidelines, high-risk patients were identified by the presence of shock/hypotension, intermediaterisk patients by elevated troponin I or right ventricular dysfunction as assessed by echocardiography, and low-risk patients by the absence of any of the above. In the PESI model, 11 clinical variables, easily accessible at the bedside, were used to generate three risk classes. The main outcomes were all-cause and PE-related in-hospital mortality. Results: Forty-one patients (8%, 95% confidence interval [CI] 5.8-10.8) of 510 died. According to the ESC model, 40% were at low risk of short-term mortality, 54% at intermediate risk, and 6% at high risk. The distribution according to the PESI model was 31% (P < 0.05 vs. ESC), 49% and 20% (P < 0.05 vs. ESC), respectively. Mortality increased through the risk classes (P < 0.01), without significant differences between the models. The ESC model identified with higher accuracy than the PESI model both high-risk and low-risk patients (P < 0.05 for both). When patients with shock/hypotension were excluded, the PESI model stratified patients into classes with increasing PE-related mortality (0.7%, 4.3%, and 11.6%, P < 0.05). Troponin I and right ventricular dysfunction added incremental prognostic value to the PESI model, particularly in normotensive patients at intermediate risk. Conclusions: The ESC model showed higher accuracy than the PESI model in identifying high-risk and low-risk patients. In normotensive patients, the PESI model could guide clinical management as well as troponin I and echocardiography testing.
During cardiac resynchronization therapy (CRT) device implantation, left ventricular (LV) lead placement is usually performed by means of a transvenous approach using the tributaries of the coronary sinus (CS). The feasibility of transvenous lead positioning depends on many factors, including venous anatomy, accessibility of the vein, pacing threshold, lead stability, and the absence of phrenic nerve stimulation. 1 Clinical Perspective on p 467Several authors have reported variable individual responses to CRT and have indicated the LV pacing site as a major determinant of the hemodynamic response.2-4 However, in patients receiving biventricular pacing, LV lead positioning varies randomly on account of contingencies, unpredictable anatomic conditions, or technical reasons.Transvenous LV endocardial pacing via transseptal puncture has been implemented in the rare circumstance in which neither the transvenous CS epicardial nor the surgical option is feasible. Indeed, this technique enables the limitations of CS venous anatomy to be overcome and may constitute an alternative method of optimizing lead positioning and improving outcome. Initial experience in early studies with transvenous LV endocardial pacing has yielded promising results. [5][6][7] In the present study, we evaluated the acute hemodynamic effects of CRT through transvenous LV endocardial pacing in heart failure patients by analyzing LV pressure-volume relationships. Methods Patient Selection and ProcedureWe enrolled 12 consecutive heart failure patients with indications for CRT. The Institutional Review Board approved the protocol, and all patients gave written informed consent.Exclusion criteria were the presence of a previously implanted device, valvular insufficiency, or stenosis. The atrial and right ventricular leads were placed in the right atrium and at the apex of the right ventricle, respectively, in patients who were lightly sedated. The LV lead was positioned in the CS and advanced into the lateral or posterolateral vein in accordance with standard procedure. Background-During cardiac resynchronization therapy (CRT) device implantation, the pacing lead is usually positioned in the coronary sinus (CS) to stimulate the left ventricular (LV) epicardium. Transvenous LV endocardial pacing via transseptal puncture has been proposed as an alternative method. In the present study, we evaluated the acute hemodynamic effects of CRT through LV endocardial pacing in heart failure patients by analyzing LV pressure-volume relationships. Methods and Results-LV pressure and volume data were determined via conductance catheter during CRT device implantation in 10 patients. In addition to the standard epicardial CS pacing, the following endocardial LV sites were systematically assessed: the site transmural to the CS lead, the LV apex, the septal midwall, the basal lateral free wall, and the midlateral free wall. Four atrioventricular delays were tested. There was a significant improvement of systolic function with CRT in all LV pacing configurations, wherea...
Background The gut-derived hormone ghrelin, especially its acylated form, plays a major role in the regulation of systemic metabolism and exerts also relevant cardioprotective effects, hence it has been proposed for the treatment of heart failure (HF). We tested the hypothesis that ghrelin can directly modulate cardiac energy substrate metabolism. Methods and Results We used chronically instrumented dogs, 8 with pacing-induced HF and 6 normal controls. 1.2 nmol/kg/hour of human des-acyl ghrelin was infused intravenously for 15 min, followed by washout (re-baseline) and infusion of acyl ghrelin at the same dose. 3H-oleate and 14C-glucose were co-infused and arterial and coronary sinus blood sampled to measure cardiac free fatty acids (FFA) and glucose oxidation and lactate uptake. As expected, cardiac substrate metabolism was profoundly altered in HF, since baseline FFA and glucose oxidation were, respectively, >70% lower and >160% higher compared to control. Neither des-acyl ghrelin nor acyl ghrelin affected significantly function and metabolism in normal hearts. However, in HF, des-acyl and acyl ghrelin enhanced MVO2 by 10.2±3.5 and 9.9±3.7%, respectively, (P<0.05), while cardiac mechanical efficiency was not significantly altered. This was associated, respectively, with a 41.3±6.7 and 32.5±10.9% increase in FFA oxidation and a 31.3±9.2 and 41.4±8.9% decrease in glucose oxidation (all P<0.05). Conclusions Acute increases in des-acyl ghrelin or acyl ghrelin do not interfere with cardiac metabolism in normal, while they enhance FFA oxidation and reduce glucose oxidation in HF, thus partially correcting its metabolic alterations. This novel mechanism might contribute to the cardioprotective effects of ghrelin in HF.
This new ablation protocol seems to be promising in reducing fluoroscopy exposure and number of catheters used during left-sided AP ablation in children.
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