Atrial Wall Thickening Research Articles

Multimodality evaluation of pseudo-tumoural atrial wall thickening.

Multimodality evaluation of pseudo-tumoural atrial wall thickening.

Unusual Localization of Pennella Sp. in Swordfish (Xiphias gladius) Hearts.

Simple SummaryCopepods of the genus Pennella are parasites of marine aquatic organisms (e.g., cephalopods, pelagic fish, cetaceans). They can infest fish of economic interest, including tuna and swordfish. The infestation of Pennella sp. in fish creates problems of food safety and fish marketing. Generally, these copepods penetrate the host’s muscle, without damaging internal organs. Here, we report on Pennella sp. infestation in swordfish heart muscle. The severity of the cardiac lesions we observed suggests that parasites of the genus Pennella pose a concern for food safety as well as animal health.The genus Pennella comprises hematophagous parasites of marine aquatic species, including cephalopods, marine mammals, and pelagic fish. Nine species have been officially included in the genus Pennella plus another six species inquirendae. They are most often found in the host’s musculature, without penetrating internal organs. For the present study, 83 hearts from swordfish (Xiphias gladius) caught in the Mediterranean Sea were sampled and immediately fixed in formalin for histopathological analysis. In total, 10 (12.05%) hearts were found to be parasitized by copepods of the genus Pennella. Macroscopically, there was mild-to-severe fibrinous pericarditis with atrial wall thickening and multiple parasitic nodules. Histologically, the parasitic nodules were surrounded by an inflammatory-necrotizing reaction. Parasitic infestation by Pennella spp. is common in pelagic fish and in swordfish, in particular. Here, however, we report atypical cardiac localization. A future area of focus is the evaluation of cardiac Pennella spp. infestation by histopathology and genetic identification of the parasites.

Atrial wall thickening, fevers, and atrial fibrillation caused by immunoglobulin G4-related biatrial cardiomyopathy.

Atrial wall thickening, fevers, and atrial fibrillation caused by immunoglobulin G4-related biatrial cardiomyopathy.

Dietary Inflammatory Index in Relation to Carotid Intima Media Thickness among Overweight or Obese Children and Adolescents

Background: Low-grade systematic inflammation triggers atrial wall thickening, which predisposes to several cardiovascular events. Since diet is a strong moderator of systematic inflammation, the literature review-based dietary inflammatory index (DII®) score has been recently introduced for evaluating inflammatory properties of an individual’s diet. The aim of the present study was to assess the association of DII, with carotid intima media thickness (cIMT) among overweight or obese children and adolescents. Methods: A total of 339 children and adolescents (48% girls) aged from 6 to 13 years, with WHO body mass index z-score >1 were enrolled in this cross-sectional study. A valid and reliable semi-quantitative food frequency questionnaire was used to collect dietary intakes and calculate DII score. cIMT was measured in the common carotid artery with high-resolution ultrasonography. Results: In this cross-sectional study, the mean ± SD age of participants was 9.3 ± 1.7 years. Among participants, 68% were obese and 83% were in the pubertal stage. DII ranged from –5.43 to 4.42, with the mean of –2.83 in the lowest, and 1.25 in the highest tertile of DII. When fit as a continuous variable, DII score had no significant association with cIMT after adjusting for potential confounders. However, the participants in the highest DII score tertile compared to the lowest had 2.46-fold increased risk of high cIMT in the multivariable adjusted model (p for trend = 0.02). Discussion/Conclusion: Higher DII scores were associated with increased risk of high cIMT.

Cardiovascular magnetic resonance imaging of scar development following pulmonary vein isolation: a prospective study.

AimsCardiovascular magnetic resonance (MR) provides non-invasive assessment of early (24-hour) edema and injury following pulmonary vein isolation (by ablation) and subsequent scar formation. We hypothesize that 24-hours after ablation, cardiovascular MR would demonstrate a pattern of edema and injury due to ablation and the severity would correlate with subsequent scar.MethodsFifteen atrial fibrillation patients underwent cardiovascular MR prior to pulmonary vein isolation, 24-hours post (N = 11) and 30-days post (N = 7) ablation, with T2-weighted (T2W) and late gadolinium enhancement (LGE) imaging. Left atrial wall thickness, edema enhancement ratio and LGE enhancement were assessed at each time point. Volumes of LGE and edema enhancement were measured, and the circumferential presence of injury was assessed at 24-hours, including comparison with LGE enhancement at 30 days.ResultsLeft atrial wall thickness was increased 24-hours post-ablation (10.7±4.1 mm vs. 7.0±1.8 mm pre-PVI, p<0.05). T2W enhancement at 24-hours showed increased edema enhancement ratio (1.5±0.4 for post-ablation, vs. 0.9±0.2 pre-ablation, p<0.001). Edema and LGE volumes at 24-hours were correlated with 30-day LGE volume (R = 0.76, p = 0.04, and R = 0.74, p = 0.09, respectively). Using a 16 segment model for assessment, 24-hour T2W had sensitivity, specificity, and accuracy of 82%, 63%, and 79% respectively, for predicting 30-day LGE. 24-hour LGE had sensitivity, specificity, and accuracy of 91%, 47%, and 84%.ConclusionsIncreased left atrial wall thickening and edema were characterized on cardiovascular MR early post-ablation, and found to correlate with 30-day LGE scar.

Atrial Giant Cell Myocarditis

Background— Giant cell myocarditis (GCM) typically causes fulminant heart failure, arrhythmias, or heart block, necessitating aggressive immunosuppression, ventricular assist device insertion, or cardiac transplantation. We describe a novel variant of GCM, primarily involving the atria, that displays distinctive clinical features and follows a more benign course than ventricular GCM. Methods and Results— We identified 6 patients (median age 67.5 years, 4 male) with atrial GCM in our pathology consultation practices from 2010 to 2012. Clinical history, imaging, and pathology materials were reviewed. Clinically, 4 patients had atrial fibrillation, 1 had acute heart failure, and 1 had incidental disease at autopsy. Among the 5 living patients, echocardiography revealed severe atrial dilatation (5 cases), mitral/tricuspid regurgitation (5), atrial mural thrombus (3), atrial wall thickening (2), and atrial hypokinesis (2). Ventricular function was preserved in all 5. Histological review of surgically resected atria showed giant cell and lymphocytic infiltrates, lymphocytic myocarditis-like foci, cardiomyocyte necrosis, and cardiomyocyte hypertrophy in all cases. Other features included interstitial fibrosis (5), poorly-formed granulomas (4), eosinophils (4), neutrophils (1), and vasculitis (1). Treatment consisted of steroids and cyclosporine (1), pacemaker placement for sick sinus syndrome (1), and supportive care (3). All 5 living patients returned to baseline exercise tolerance after 6 to 16 weeks of follow-up. Conclusions— Atrial GCM represents a distinct clinicopathologic entity with a more favorable prognosis than classic ventricular GCM. This disorder should be included in the differential diagnosis of atrial dilatation, particularly when associated with atrial wall thickening. The utility of immunomodulatory therapy for this condition remains unknown.

Circulation: Clinical Summaries

<i>Circulation:</i> Clinical Summaries

A patient with Wegener's granulomatosis in apparent remission presenting with complete atrioventricular block

Wegener's granulomatosis is a systemic necrotizing granulomatous vasculitis of small- to medium-sized vessels typically affecting upper and lower airways, lungs, and kidneys. Cardiac involvement is less common and conducting tissue involvement is extremely rare. Cardiac manifestations are often not clinically apparent, but are associated with increased mortality. We report the case of a 36-year-old female with Wegener's thought to be in remission, presenting in complete atrioventricular (AV) block, with echocardiographic evidence of basal interatrial septum and basal lateral left atrial wall thickening. Despite immunosuppression therapy a permanent pacemaker was required for recurring complete AV block. Although rare, this case emphasizes the need for careful and regular screening for cardiac involvement in this multi-system condition.

Pacing-induced ventricular remodeling in the chick embryonic heart.

Chronic ectopic pacing in the adult heart induces myocardial hypotrophy close to the pacing site. We have recently described a similar localized decrease of compact myocardium thickness in the chick embryonic heart after 48 h of intermittent apical ventricular pacing. Here we analyze the cellular mechanisms underlying the response of the embryonic heart to pacing. Because the developing heart had been found to adjust its morphology according to functional demands by undergoing cellular hyperplasia or hypoplasia, we hypothesized that the stimulation should result in hypoplasia of the apical ventricular compartment. Morphologic analysis of hearts submitted to 18 h of effective pacing during 48 h showed a mild to moderate ventricular dilatation, a 28% decrease in the apical compact layer thickness with no changes in other ventricular locations, and atrial wall thickening. These modifications were caused by changes in the number of cell layers, whereas cell size was similar between paced and control hearts. Analysis of proliferative activity after 24 h of pacing showed a decrease of 32% in the rate of cell proliferation limited to the apical compact layer exposed to stimulation. No ultrastructural injury or increased cell death was found. These changes were accompanied by down-regulation of the myocardial growth factor fibroblast growth factor-2 but no differences were found in the expression of platelet-derived growth factor. Thus, chronic intermittent ventricular pacing induces myocardial remodeling in the chick embryonic heart, on the basis of locally regulated rates of cell proliferation.