Normal reference values for the adult right ventricle by magnetic resonance imaging

The purpose of this study was to establish reference ranges for magnetic resonance imaging (MRI) measurements of the adult right ventricle stratified by gender. Cardiovascular MRI is increasingly used for evaluating the right ventricle in congenital and acquired heart disease, but gender-specific normative values are currently unavailable. Study participants included 500 subjects free of clinical cardiovascular disease who were participants in the Multi-Ethnic Study of Atherosclerosis (MESA). All subjects underwent MRI according to a standard protocol. The endocardial margins of the right ventricle were manually contoured on short-axis images, and right ventricular (RV) volumes were calculated using a summation-of-disks method. RV dimensions were measured on 4-chamber gradient-echo images and in the short-axis plane. Except for the ejection fraction, all unadjusted RV parameters were significantly greater in men than in women (p <0.001). In the entire study population, RV volumes and linear dimensions each correlated significantly with height (r = 0.38 to 0.64, p = 0.001 for all) and body surface area (r = 0.41 to 0.64, p = 0.001 for all). Gender differences persisted after adjustment for subject height. After adjustment for body surface area, volumetric variables remained significantly greater (p = 0.001) in men than in women. Even after adjusting for body surface area and height, Chinese participants had significantly lower RV volumes compared with Caucasians. In conclusion, gender-specific normal values for the adult right ventricle by MRI are presented. Cardiovascular MRI measures of RV volumes and linear dimensions differ significantly according to gender and body size. These values will be useful to differentiate RV health from diseases that result in abnormal RV structure and function.     

Effects of surgical and endoscopic electrocautery on modern-day permanent pacemaker and implantable cardioverter-defibrillator systems

Background: Current guidelines recommend that all implanted pacemakers (PPM) and defibrillators (ICD) be interrogated before and after every invasive procedure. The ability of newer devices to withstand system malfunction or failure during surgery/endoscopy remains unknown.
Objective: To determine the frequency of PPM or ICD malfunction from periprocedural electrocautery.
Methods: Ninety-two consecutive individuals referred for evaluation of a PPM or ICD system prior to noncardiac surgery/endoscopy were enrolled. Devices were preoperatively programmed to a "monitor only" zone to allow for detection of electromagnetic interferences (EMIs). Pacing parameters were maintained without disabling rate responsiveness. The devices were fully interrogated again after surgery. Correlations of inappropriate EMI sensing were made with reference to the distance from the site of electrocautery application to the device system.
Results: All devices withstood periprocedural EMI exposure without malfunction or changes in programming. Minor changes in lead parameters were noted. Three device systems demonstrated brief atrial mode switching episodes, one of which was likely secondary to inappropriate sensing of atrial noise . Two pacemaker devices demonstrated inappropriate sensing of ventricular noise, both of which occurred when the application of electrocautery was within close proximity to the pacemaker generator (<8 cm). No ventricular sensed events were noted in any ICD system.
Conclusions: EMIs during noncardiac surgical/endoscopic procedures pose little threat to current device systems. Rare occasions of inappropriate sensing by devices can be seen in situations where the application of unipolar electrocautery is in close proximity of the system. Routine postsurgical interrogation of PPM or ICDs may not be necessary.     

Evolving role of multidetector computed tomography in evaluation of arrhythmogenic right ventricular dysplasia/cardiomyopathy

The purpose of this study was to report 1 center's experience with multidetector computed tomography (MDCT) in the evaluation of patients suspected to have arrhythmogenic right ventricular (RV) dysplasia/cardiomyopathy (ARVD/C). RV dilatation/dysfunction is 1 of the most important criteria for establishing the diagnosis of ARVD/C. Cardiac magnetic resonance imaging (MRI) is the most preferred imaging modality for the diagnosis of ARVD/C. However, many patients with suspected ARVD/C have implantable cardioverter-defibrillators, prohibiting the use of MRI. Thirty-one patients (19 men; mean age 41 +/- 12 years) referred for evaluation of known or suspected ARVD/C had a complete reevaluation including contrast-enhanced cardiac MDCT at the center. Two patients underwent both cardiac MRI and MDCT. Seventeen of 31 patients met Task Force criteria for ARVD/C and were confirmed to have ARVD/C. Multidetector computed tomographic images were analyzed for qualitative and quantitative characteristic findings of ARVD/C. Increased RV trabeculation (p <0.001), RV intramyocardial fat (p <0.001), and scalloping (p <0.001) were significantly associated with the final diagnosis of ARVD/C. RV volumes, RV inlet dimensions, and RV outflow tract surface area were increased in patients with ARVD/C compared with patients who did not meet the criteria. RV and left ventricular functional analysis was performed in 2 patients. In conclusion, cardiac MDCT has a strong potential to detect many qualitative and quantitative abnormalities of the right ventricle in patients with ARVD/C. Limitations include implantable cardioverter-defibrillators and motion artifacts, along with well-known radiation and contrast-induced reaction.     

Endoplasmic reticulum stress enhances fibrotic remodeling in the lungs

Evidence of endoplasmic reticulum (ER) stress has been found in lungs of patients with familial and sporadic idiopathic pulmonary fibrosis. We tested whether ER stress causes or exacerbates lung fibrosis by (i) conditional expression of a mutant form of surfactant protein C (L188Q SFTPC) found in familial interstitial pneumonia and (ii) intratracheal treatment with the protein misfolding agent tunicamycin. We developed transgenic mice expressing L188Q SFTPC exclusively in type II alveolar epithelium by using the Tet-On system. Expression of L188Q SFTPC induced ER stress, as determined by increased expression of heavy-chain Ig binding protein (BiP) and splicing of X-box binding protein 1 (XBP1) mRNA, but no lung fibrosis was identified in the absence of a second profibrotic stimulus. After intratracheal bleomycin, L188Q SFTPC-expressing mice developed exaggerated lung fibrosis and reduced static lung compliance compared with controls. Bleomycin-treated L188Q SFTPC mice also demonstrated increased apoptosis of alveolar epithelial cells and greater numbers of fibroblasts in the lungs. With a complementary model, intratracheal tunicamycin treatment failed to induce lung remodeling yet resulted in augmentation of bleomycin-induced fibrosis. These data support the concept that ER stress produces a dysfunctional epithelial cell phenotype that facilitates fibrotic remodeling. ER stress pathways may serve as important therapeutic targets in idiopathic pulmonary fibrosis.     

Meta-analysis of randomized trials of angioedema as an adverse event of renin-angiotensin system inhibitors

Angioedema is a rare, potentially life-threatening adverse event of renin-angiotensin system inhibitors. The objective of the present study was to determine the risk of angioedema from randomized clinical trials. A PubMed/CENTRAL/EMBASE search was made for randomized clinical trials from 1980 to October 2011 in patients on angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), or direct renin inhibitor (DRI). Trials with a total number of patients ≥100 and a duration of ≥8 weeks were included for analysis. Incidence of angioedema was pooled by weighing the incident rate of each trial by the inverse of the variance. Twenty-six trials with 74,857 patients in the ACE inhibitor arm with 232,523 person-years of follow-up, 19 trials with 35,479 patients on ARB with 122,293 person-years of follow-up, and 2 trials with 5,141 patients on DRI with 1,735 person-years of follow-up met the inclusion criteria and were included in the analysis. In head-to-head comparison in 7 trials, risk of angioedema with ACE inhibitors was 2.2 times higher than with ARBs (95% confidence interval [CI] 1.5 to 3.3). With ACE inhibitors and ARBs, incidence of angioedema was higher in heart failure trials compared to hypertension or coronary artery disease trials without heart failure (p <0.0001). Weighted incidence of angioedema with ACE inhibitors was 0.30% (95% CI 0.28 to 0.32) compared to 0.11% (95% CI 0.09 to 0.13) with ARBs, 0.13% (95% CI 0.08 to 0.19) with DRIs, and 0.07% with placebo (95% CI 0.05 to 0.09). In conclusion, incidence of angioedema with ARBs and DRI was <1/2 than that with ACE inhibitors and not significantly different from placebo. Incidence of angioedema was higher in patients with heart failure compared to those without heart failure with ACE inhibitors and ARBs.     

Absence of a Primary Role for <Emphasis Type="Italic">SCN10A</Emphasis> Mutations in Arrhythmogenic Right Ventricular Dysplasia/Cardiomyopathy

Prior reports have identified associations between SCN10A and cardiac disorders, such as atrial fibrillation and Brugada syndrome. We evaluated SCN10A in 151 probands with ARVD/C. In this cohort, 10 putatively pathogenic SCN10A variants were identified, including a novel frameshift insertion. Despite a known role for the encoded protein in peripheral nerve function, the proband with the frameshift variant had no discernible neurological abnormalities. Arrhythmic phenotypes were not different between those with a rare variant in SCN10A and those without. The prevalence of rare variants in SCN10A was similar among ARVD/C probands with and without a desmosome mutation and similar among healthy Caucasian controls. These results indicate the absence of a primary role for SCN10A mutations in ARVD/C.     

Initial validation of a novel ECGI system for localization of premature ventricular contractions and ventricular tachycardia in structurally normal and abnormal hearts

Background

View into Ventricular Onset (VIVO) is a novel ECGI system that uses 3D body surface imaging, myocardial CT/MRI, and 12?lead ECG to localize earliest ventricular activation through analysis of simulated and clinical vector cardiograms.