Left ventricular stiffness predicts outcome in patients with severe aortic stenosis undergoing transcatheter aortic valve implantation.

OBJECTIVES: Assessment of the prognostic role of left ventricular stiffness (LVS) in patients with aortic stenosis (AS) undergoing transcatheter aortic valve implantation (TAVI). METHODS: We performed a complete two-dimensional transthoracic echocardiographic study before and after TAVI in patients with severe AS at high surgical risk. In order to assess LVS, we measured LV end-diastolic pressure (EDP) invasively during TAVI and LV end-diastolic volume (EDV) by means of echocardiography. We defined LVS as the EDV indexed by body surface area at an EDP of 20 mm Hg (EDVI20 ). Our aim was to assess the impact of LVS on one-year all-cause mortality after TAVI. RESULTS: One hundred sixty-six patients undergoing TAVI (64% female; mean age 82.7 ± 5.1 years) were enrolled. Seven patients died within the first 30 days after TAVI and 21 within 1 year. Overall follow-up duration was 580 ± 478 days. At multivariate analysis, independent predictors of 1-year all-cause mortality were moderate-to-severe paravalvular leak (PVL; HR 4.7, 95% confidence interval [CI] 1.9-11, P=.0003), female gender (HR 3.5, 95% CI 1.0-12, P=.045), and EDVI20 (HR 0.94, 95% CI 0.90-0.98, P=.015). In particular, patients with higher LVS (EDVI20 ≤48 mL/m2 ) had a 1-year mortality of 26.9% vs 7.4% in patients with lower LVS (EDVI20 >48 mL/m2 ; HR 4.2, 95% CI 1.6-10.6, P=.0007). Patients with higher LVS who developed moderate-to-severe PVL had the worst outcome (incremental chi-square test, P=.014). CONCLUSION: In patients with AS, an increased LVS has a negative prognostic impact. Development of significant PVL in patients with higher LVS had an incremental adverse effect.

Bedside diagnosis and follow-up of patients with pleural effusion by a hand-carried ultrasound device early after cardiac surgery.

OBJECTIVES: The aim of this study was to assess the potential value of hand-carried ultrasound (HCU) devices in the diagnosis and follow-up of patients with pleural effusion (PE) after cardiac surgery. METHODS: Seventy consecutive patients were evaluated at bedside early after cardiac surgery, in the upright sitting position, using an HCU device on hospital admission and every 3 days until hospital discharge. The posterior chest wall was scanned along the paravertebral, scapular, and posterior axillary lines. For each hemithorax, an effusion index was derived as the sum of the intercostal spaces between the lower and upper limits of the PE along the lines of scanning, divided by 3. A standard chest radiograph was performed in all patients on hospital admission and at hospital discharge, and was qualitatively scored (0, absent; 1, small; 2, large PE). The findings of the HCU device and radiograph were compared using kappa statistics and the Kruskal-Wallis test. RESULTS: A chest ultrasound was feasible in all patients (mean [+/- SD] time, 5 +/- 2 min). Compared with the chest ultrasound, a physical examination showed a sensitivity of 69% and a specificity of 77%. On hospital admission, the HCU device detected a PE in 72 of 140 hemithoraxes. Agreement with the finding of the radiograph was 76% (kappa = 0.52). In 15 hemithoraxes, the HCU device revealed a PE that had not been diagnosed using the radiograph. Conversely, in 18 hemithoraxes a PE that had been diagnosed with a radiograph was not confirmed by the HCU device. The correlation between ultrasound and radiographic scores was statistically significant (p < 0.001). At hospital discharge, a PE was present in 31 of 140 hemithoraxes according to the findings of the HCU device, and in 38 of 140 hemithoraxes according to the findings of the radiograph (agreement, 78%; kappa = 0.44). CONCLUSIONS: In patients early after cardiac surgery, HCU devices allow rapid PE detection and improve the clinical diagnosis. Compared to a radiograph, this method offers the unique advantage of the bedside evaluation of patients without the need for radiation exposure.

The role of macrophage colony-stimulating factor in patients with acute myocardial infarction: a pilot study.

We assessed whether macrophage colony-stimulating factor (M-CSF) levels are associated with left ventricular systolic dysfunction (LVSD) in patients with acute myocardial infarction (AMI). We studied 56 patients with AMI (mean age: 67 ± 12 years) and identified those with clinical (Killip class >II) or echocardiographic signs (ejection fraction ≤45%) of LVSD. We evaluated the established cardiovascular risk factors and measured several cardiovascular biomarkers, including M-CSF. Serum M-CSF concentrations (pg/mL) were significantly increased in patients with both clinical and echocardiographic signs of LVSD (460 ± 265 vs 290 ± 210, P = .0103 and 493 ± 299 vs 287 ± 174, P = .0028, respectively). We found a significant inverse association between M-CSF and ejection fraction (r = -.351, P = .0079). Logistic regression analysis revealed that, among all evaluated clinical and biochemical parameters, the stronger predictor of LVSD was M-CSF (odds ratios 2.1, 95% confidence interval 1.1-2.9, P = .0168). This is the first study reporting plasma M-CSF levels as independent determinants of low LV ejection fraction and clinical LV dysfunction in patients with AMI.