Comparison of wall thickening and ejection fraction by cardiovascular magnetic resonance and echocardiography in acute myocardial infarction

<p>Abstract</p> <p>Objectives</p> <p>The purpose of this study was to compare cardiovascular magnetic resonance (CMR) and echocardiography (echo) in patients treated with primary percutaneous coronary intervention (PCI) for acute myocardial infarction (AMI) with emphasis on the analysis of left ventricular function and left ventricular wall motion characteristics.</p> <p>Methods</p> <p>We performed CMR and echo in 52 patients with first AMI shortly after primary angioplasty and four months thereafter. CMR included cine-MR and T1-weighted first-pass and late-gadolinium enhancement (LGE) sequences. Global ejection fraction (EF_CMR, %) and regional left ventricular function (systolic wall thickening %, [SWT]) were determined from cine-MR images. In echo the global left ventricular function (EF_echo, %) and regional wall motion abnormalities were determined. A segment in echo was scored as "infarcted" if it was visually > 50% hypokinetic.</p> <p>Results</p> <p>EF_echorevealed a poor significant agreement with EF_CMRat baseline (r: 0.326; p < 0.01) but higher correlation at follow-up (r: 0.479; p < 0.001). The number of infarcted segments in echocardiography correlated best with the number of segments which showed systolic wall thickening < 30% (r: 0.498; p < 0.001) at baseline and (r: 0.474; p < 0.001) at follow-up. Improvement of EF was detected in both CMR and echocardiography increasing from 44.2 ± 11.6% to 49.2 ± 11% (p < 0.001) by CMR and from 51.2 ± 8.1% to 54.5 ± 8.3% (p < 0.001) by echocardiography.</p> <p>Conclusion</p> <p>Wall motion and EF by CMR and echocardiography correlate poorly in the acute stage of myocardial infarction. Correlation improves after four months. Systolic wall thickening by CMR < 30% indicates an infarcted segment with influence on the left ventricular function.</p

QFR predicts the incidence of long-term adverse events in patients with suspected CAD : feasibility and reproducibility of the method

AIMS: We evaluate feasibility and reproducibility of post hoc quantitative flow ratio (QFR) measurements and their prognostic predictive power during long-term follow-up. METHODS AND RESULTS: Between 2010 and 2012, 167 patients without angiographic evidence of significant stenoses were enrolled in a prospective registry. Of these patients, 96% presented 7 years follow-up data. QFR was measured post hoc by three certified investigators. QFR analysis was feasible in 71% of left anterior descending (LAD), 72% of left circumflex (LCX), and 61% of right (RCA) coronaries for a total of 350 measurements repeated in triplicate. Coefficients of variation were 2.1% for RCA and LCX, and 2.8% for the LAD (quartile coefficients of dispersion respectively 1.5, 1.4, and 1.3). QFR ≤0.80 was recorded in 25 patients (27 vessels, in 74% of the cases LAD). A total of 86 major adverse cardiovascular and cerebrovascular events were observed in 76 patients. QFR ≤0.80 in at least one of the three vessels was the strongest predictor of events (HR 3.14, 95%CI 1.78–5.54, p = 0.0001). This association was maintained in several sensitivity analyses. CONCLUSIONS: QFR reproducibility is acceptable, even when analysis is performed post hoc. A pathological QFR is not rare in patients without angiographic evidence of significant stenosis and is a predictor of incident events during long-term follow-up. Condensed Abstract: In a post hoc analysis of 167 patients without evidence of angiographic significant stenosis, the presence of QFR value ≤0.80 in at least one of the three coronary vessels showed to be the strongest predictor of major adverse cardiovascular and cerebrovascular events during long-term follow-up. QFR reproducibility have been shown to be acceptable among experienced operators. Keywords: fractional flow reserve; coronary artery disease; coronary interventions; Quantitative flow reserv

Single-Beat Noninvasive Imaging of Ventricular Endocardial and Epicardial Activation in Patients Undergoing CRT

BACKGROUND: Little is known about the effect of cardiac resynchronization therapy (CRT) on endo- and epicardial ventricular activation. Noninvasive imaging of cardiac electrophysiology (NICE) is a novel imaging tool for visualization of both epi- and endocardial ventricular electrical activation. METHODOLOGY/PRINCIPAL FINDINGS: NICE was performed in ten patients with congestive heart failure (CHF) undergoing CRT and in ten patients without structural heart disease (control group). NICE is a fusion of data from high-resolution ECG mapping with a model of the patient's individual cardiothoracic anatomy created from magnetic resonance imaging. Beat-to-beat endocardial and epicardial ventricular activation sequences were computed during native rhythm as well as during ventricular pacing using a bidomain theory-based heart model to solve the related inverse problem. During right ventricular (RV) pacing control patients showed a deterioration of the ventricular activation sequence similar to the intrinsic activation pattern of CHF patients. Left ventricular propagation velocities were significantly decreased in CHF patients as compared to the control group (1.6±0.4 versus 2.1±0.5 m/sec; p<0.05). CHF patients showed right-to-left septal activation with the latest activation epicardially in the lateral wall of the left ventricle. Biventricular pacing resulted in a resynchronization of the ventricular activation sequence and in a marked decrease of total LV activation duration as compared to intrinsic conduction and RV pacing (129±16 versus 157±28 and 173±25 ms; both p<0.05). CONCLUSIONS/SIGNIFICANCE: Endocardial and epicardial ventricular activation can be visualized noninvasively by NICE. Identification of individual ventricular activation properties may help identify responders to CRT and to further improve response to CRT by facilitating a patient-specific lead placement and device programming

HDL-related biomarkers are robust predictors of survival in patients with chronic liver failure

Abstract Background & Aims The occurrence of acute decompensation (AD) worsens the prognosis of advanced chronic liver disease (ACLD). Various insults leading to increased systemic inflammation trigger acute-on-chronic liver failure (ACLF) with dramatically increased short-term mortality. During acute conditions such as sepsis, high-density lipoprotein cholesterol (HDL-C) levels decrease rapidly and HDL particles undergo profound changes in their composition and function. Indices of HDL quantity and quality may therefore associate with progression and survival in patients with advanced liver disease. Methods We studied levels of HDL-cholesterol (HDL-C), its subclasses HDL2-C and HDL3-C, and apolipoprotein(apo)A-I as indices of HDL quantity and HDL cholesterol efflux capacity as a metric of HDL functionality in 508 patients with compensated or decompensated cirrhosis including ACLF and 40 age- and gender-matched controls. Results Baseline levels of HDL-C and apoA-I were significantly lower in stable cirrhosis compared to control and further decreased in AD and ACLF . In stable cirrhosis (n=228), both HDL-C and apoA-I predicted the development of liver-related complications independently of MELD. In patients with AD with or without ACLF (n=280) both HDL-C and apoA-I were MELD-independent predictors of 90-day mortality. On ROC analysis, high diagnostic accuracies for 90-day mortality in AD patients were found for HDL-C (AUROC 0.79 ) and apoA-I (AUROC 0.80 ), very similar to that of MELD (AUROC 0.81 ). On Kaplan-Meier analysis, HDL-C 17 mg/dl and apoA-I 50 mg/dl indicated poor short-term survival. The prognostic accuracy of HDL-C was validated in a large external validation cohort of 985 patients with portal hypertension due to ACLD (AUROCs HDL-C: 0.81 vs. MELD: 0.77). Conclusion HDL-related biomarkers are robust predictors of disease progression and survival in chronic liver failure

HDL-related biomarkers are robust predictors of survival in patients with chronic liver failure

Background & Aims: High-density lipoprotein cholesterol (HDL-C) levels are reduced in patients with chronic liver disease and inversely correlate with disease severity. During acute conditions such as sepsis, HDL-C levels decrease rapidly and HDL particles undergo profound changes in their composition and function. We aimed to determine whether indices of HDL quantity and quality associate with progression and survival in patients with advanced liver disease. Methods: HDL-related biomarkers were studied in 508 patients with compensated or decompensated cirrhosis (including acute-on-chronic liver failure [ACLF]) and 40 age- and gender-matched controls. Specifically, we studied levels of HDL-C, its subclasses HDL2-C and HDL3-C, and apolipoprotein A1 (apoA-I), as well as HDL cholesterol efflux capacity as a metric of HDL functionality. Results: Baseline levels of HDL-C and apoA-I were significantly lower in patients with stable cirrhosis compared to controls and were further decreased in patients with acute decompensation (AD) and ACLF. In stable cirrhosis (n = 228), both HDL-C and apoA-I predicted the development of liver-related complications independently of model for end-stage liver disease (MELD) score. In patients with AD, with or without ACLF (n = 280), both HDL-C and apoA-I were MELD-independent predictors of 90-day mortality. On ROC analysis, both HDL-C and apoA-I had high diagnostic accuracy for 90-day mortality in patients with AD (AUROCs of 0.79 and 0.80, respectively, similar to that of MELD 0.81). On Kaplan-Meier analysis, HDL-C <17 mg/dl and apoA-I <50 mg/dl indicated poor short-term survival. The prognostic accuracy of HDL-C was validated in a large external validation cohort of 985 patients with portal hypertension due to advanced chronic liver disease (AUROCs HDL-C: 0.81 vs. MELD: 0.77). Conclusion: HDL-related biomarkers are robust predictors of disease progression and survival in chronic liver failure

Modern Interpretation of Giant Cell Tumor of Bone: Predominantly Osteoclastogenic Stromal Tumor

Owing to striking features of numerous multinucleated cells and bone destruction, giant cell tumor (GCT) of bone, often called as osteoclastoma, has drawn major attractions from orthopaedic surgeons, pathologists, and radiologists. The name GCT or osteoclastoma gives a false impression of a tumor comprising of proliferating osteoclasts or osteoclast precursors. The underlying mechanisms for excessive osteoclastogenesis are intriguing and GCT has served as an exciting disease model representing a paradigm of osteoclastogenesis for bone biologists. The modern interpretation of GCT is predominantly osteoclastogenic stromal cell tumors of mesenchymal origin. A diverse array of inflammatory cytokines and chemokines disrupts osteoblastic differentiation and promotes the formation of excessive multi-nucleated osteoclastic cells. Pro-osteoclastogenic cytokines such as receptor activator of nuclear factor kappa-B ligand (RANKL), interleukin (IL)-6, and tumor necrosis factor (TNF) as well as monocyte-recruiting chemokines such as stromal cell-derived factor-1 (SDF-1) and monocyte chemoattractant protein (MCP)-1 participate in unfavorable osteoclastogenesis and bone destruction. This model represents a self-sufficient osteoclastogenic paracrine loop in a localized area. Consistent with this paradigm, a recombinant RANK-Fc protein and bisphosphonates are currently being tried for GCT treatment in addition to surgical excision and conventional topical adjuvant therapies