Heart failure with preserved ejection fraction or non-cardiac dyspnea in paroxysmal atrial fibrillation: The role of left atrial strain.

BACKGROUND: Diagnosis of heart failure with preserved ejection fraction (HFpEF) in patients with dyspnea and paroxysmal atrial fibrillation (AF) is challenging. Speckle tracking-derived left atrial strain (LAS) provides an accurate estimate of left ventricular (LV) filling pressures and left atrial (LA) phasic function. However, data on clinical utility of LAS in patients with dyspnea and AF are scarce. OBJECTIVE: To assess relationship between the LAS and the probability of HFpEF in patients with dyspnea and paroxysmal AF. METHODS: The study included 205 consecutive patients (62 ± 10 years, 58% males) with dyspnea (NYHA≥II), paroxysmal AF and preserved LV ejection fraction (≥50%), who underwent speckle tracking echocardiography during sinus rhythm. Probability of HFpEF was estimated using H2FPEF and HFA-PEFF scores, which combine clinical characteristics, echocardiographic parameters and natriuretic peptides. RESULTS: Patients with high probability of HFpEF were significantly older, had higher body mass index, NT-proBNP, E/e', pulmonary artery pressure and larger LA volume index than patients in low-to-intermediate probability groups (all p < 0.05). All components of LAS and LA strain rate showed proportional impairment with increasing probability of HFpEF (all p < 0.05). Out of the speckle tracking-derived parameters, reservoir LAS showed the largest area under the curve (AUC = 0.78, p < 0.001) and the strongest independent predictive value (OR: 1.22, 95% CI 1.08-1.38) to identify patients with high probability of HFpEF. CONCLUSIONS: Reservoir LAS shows a high diagnostic performance to distinguish HFpEF from non-cardiac causes of dyspnea in symptomatic patients with paroxysmal AF.

VT Recurrence After Ablation: Incomplete Ablation or Disease Progression? A Multicentric European Study.

AIM: To determine whether ventricular tachycardia (VT) recurrences in arrhythmogenic RV cardiomyopathy (ARVC) and nonischemic cardiomyopathy (NICM) are related to incomplete ablation or disease progression. METHODS: ARVC and NICM patients with two substrate maps of the same diseased ventricle with an interprocedural delay of ≥12 months were included. Disease progression was defined as ≥1 factor: scar area progression (PROG, +5%), ventricular remodeling (dilatation [+25 mL] or decreased ejection fraction [-5%EF]). Incomplete ablation was defined as index VT recurrence or ablation in previously unablated regions inside index scar without PROG. RESULTS: Twenty patients from nine centers were included (80% male 55 ± 16 years, 7 ARVC and 13 NICM, LVEF 43 ± 14%). Mean delay was 28 ± 18 months. Disease progression occurred in 75% with ventricular remodeling in 70%: ventricular dilation in 45% (ARVC [71%]; NICM [38%]), decreased EF in 60% [RVEF in ARVC (71%); LVEF in NICM (54%)], and scar progression in 50% (in ARVC [57%] and NICM [46%]). Index VT recurrence was observed in 40%. Redo ablation sites were located in previously unablated regions inside the index scar in 70% of patients. VT recurrence following the second procedure was seen in 25%. Fifteen percent died during a follow-up of 17 ± 17 months. CONCLUSION: Disease progression is the rule in ARVC and NICM while scar progression occurs in half. However, even if disease progression is frequently observed, incomplete index ablation is the most common finding, strongly suggesting the need for more extensive ablation.

Global and right ventricular end-diastolic volumes correlate better with preload after correction for ejection fraction.

BACKGROUND: Volumetric monitoring with right ventricular end-diastolic volume indexed (RVEDVi) and global end-diastolic volume indexed (GEDVi) is increasingly being suggested as a superior preload indicator compared with the filling pressures central venous pressure (CVP) or the pulmonary capillary wedge pressure (PCWP). However, static monitoring of these volumetric parameters has not consistently been shown to be able to predict changes in cardiac index (CI). The aim of this study was to evaluate whether a correction of RVEDVi and GEDVi with a measure of the individual contractile reserve, assessed by right ventricular ejection fraction (RVEF) and global ejection fraction, improves the ability of RVEDVi and GEDVi to monitor changes in preload over time in critically ill patients. METHODS: Hemodynamic measurements, both by pulmonary artery and by transcardiopulmonary thermodilution, were performed in 11 mechanically ventilated medical ICU patients. Correction of volumes was achieved by normalization to EF deviation from normal EF values in an exponential fashion. Data before and after fluid administration were obtained in eight patients, while data before and after diuretics were obtained in seven patients. RESULTS: No correlation was found between the change in cardiac filling pressures (DeltaCVP, DeltaPCWP) and DeltaCI (R(2) 0.01 and 0.00, respectively). Further, no correlation was found between DeltaRVEDVi or DeltaGEDVi and DeltaCI (R(2) 0.10 and 0.13, respectively). In contrast, a significant correlation was found between DeltaRVEDVi corrected to RVEF (DeltacRVEDVi) and DeltaCI (R(2) 0.64), as well as between DeltacGEDVi and DeltaCI (R(2) 0.59). An increase in the net fluid balance with +844 + or - 495 ml/m(2) resulted in a significant increase in CI of 0.5 + or - 0.3 l/min/m(2); however, only DeltacRVEDVi (R(2) 0.58) and DeltacGEDVi (R(2) 0.36) correlated significantly with DeltaCI. Administration of diuretics resulting in a net fluid balance of -942 + or - 658 ml/m(2) caused a significant decrease in CI with 0.7 + or - 0.5 l/min/m(2); however, only DeltacRVEDVi (R(2) 0.80) and DeltacGEDVi (R(2) 0.61) correlated significantly with DeltaCI. CONCLUSION: Correction of volumetric preload parameters by measures of ejection fraction improved the ability of these parameters to assess changes in preload over time in this heterogeneous group of critically ill patients.

Whole-body PET with FDG for the diagnosis of recurrent gastric cancer.

This retrospective study was designed to assess the accuracy of fluorine-18 fluorodeoxyglucose positron emission tomography (FDG-PET) in diagnosing recurrence of gastric cancer. Thirty-three patients who had received surgical treatment for gastric cancer with curative intent and who had subsequently undergone FDG-PET for suspected recurrence were retrieved from the PET database. All patients were reviewed with full knowledge of prior conventional diagnostic work-up. Results were compared with a gold standard, consisting of histological confirmation or radiological and clinical follow-up. The gold standard established disease recurrence in 20/33 patients (prevalence 61%). Sensitivity and specificity of FDG-PET for the diagnosis of recurrence were 70% (14/20) and 69% (9/13), respectively. Positive and negative predictive values were 78% (14/18) and 60% (9/15), respectively. Of the six false-negative cases, all had intra-abdominal lesions (three had generalised abdominal metastases, one liver metastasis, one local recurrence and one ovarian metastasis). In the subgroup with previous signet cell differentiation of the primary tumour ( n=13, disease prevalence 62%), sensitivity was 62% (5/8) and specificity, 60% (3/5). Survival analysis for the entire patient group using Kaplan-Meier statistics yielded a longer survival in the PET-negative group (mean+/-SD, 21.9+/-19.0 months) than in the PET-positive group (mean+/-SD, 9.2+/-8.2 months) ( P=0.01). In the patient group with proven recurrence ( n=20), the mean survival for the PET-negative group was 18.5 (+/-12.5) months, as compared with 6.9 (+/-6.5) months for the PET-positive group ( P=0.05). Because of its poor sensitivity and low negative predictive value, FDG-PET is not suited for screening purposes in the follow-up of treated gastric cancer. However, FDG-PET appears to provide important additional information concerning the prognosis of recurrent gastric cancer.