Background-There are currently no guidelines advising long-term surveillance of patients following an acute pulmonary embolism (PE), because long-term outcome studies are rare. We investigated the long-term cardiovascular and all-cause mortality of a large patient cohort with confirmed PE in relation to baseline cardiovascular disease (CVD). Methods and Results-Clinical details of all patients presenting with acute PE to a tertiary hospital were retrieved from medical records, and their survival tracked from a statewide death registry. There were 1023 (45% males) patients admitted with confirmed PE from 2000 to 2007. During a mean follow-up of 3.8Ϯ2.6 years, 363 patients died (35.5%), of whom only 31 (3.0%) died in-hospital during the index PE admission. The 3-month, 6-month, 1-year, 3-year, and 5-year cumulative mortality rates were 8.3%, 11.1%, 16.3%, 26.7%, and 31.6% respectively. Annual mortality did not improve over the 7-year period. The postdischarge mortality of 8.5%/patient-year was 2.5-fold that of an age-and sex-matched general population, being 12.6-fold in the youngest quintile (Ͻ55 years) and 1.9-fold in the oldest quintile (Ն83 years). Patients with known CVD at baseline had 2.2-fold greater all-cause mortality than those without CVD, and this effect, although at a lower level of risk, remained significant after multivariate analysis. Of the 332 deaths occurring postdischarge, 40% were attributed to cardiovascular causes. Conclusions-In a contemporary adult population, PE is associated with a substantially increased long-term mortality, of which nearly half is cardiovascular. Our study highlights the urgent need to develop long-term surveillance strategies in this population. (Circ Cardiovasc Qual Outcomes. 2011;4:122-128.)Key Words: pulmonary embolism Ⅲ long-term Ⅲ mortality Ⅲ predictors Ⅲ cardiovascular Ⅲ heart disease Ⅲ thrombosis V enous thromboembolic disease is a worldwide problem, with acute pulmonary embolism (PE) its most severe manifestation. 1 The outcome of patients with acute PE is only partly (and to a small extent) determined by the size and extent of thrombus burden, and much more by the presence and extent of right ventricular dysfunction. 2 Symptomatic PE can cause death within 1 hour of onset in up to 10% of cases 3 ; it is the third largest cause of cardiovascular death after coronary artery disease and stroke, 4 occurring in up to 7% to 30% of all autopsy series. 1 Predictors of acute mortality following acute PE include: age Ͼ70 years, coexistent malignancy, heart failure, pulmonary disease, systemic hypotension, right ventricular dysfunction, and biomarkers such as cardiac troponins and B-type natriuretic peptide. [5][6][7][8] In contrast to the abundant data regarding acute outcome, predictors of long-term mortality remain poorly defined because of the rarity of large cohort studies. The few studies extending beyond 6 months have indicated an increased 1-year mortality rate after PE, which may be as high as 25%. 9 -11 Increased long-term risk of recurrent PE, cancer, and c...

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The accuracy of QCA in predicting functionally significant FFR is limited and is dependent on FFR cut-off used and lesion severity. Where FFR is not available or contraindicated, 3D-QCA may assist in the evaluation of coronary lesions of intermediate severity.

Background Current understanding of metabolic heart disease consists of a myriad of different pathophysiological mechanisms. Epicardial adipose tissue (EAT) is increasingly recognized as metabolically active and associated with adverse cardiovascular outcomes. The present study aimed to investigate the effect of increased EAT volume index on left ventricular (LV) myocardial fat content and burden of interstitial myocardial fibrosis and their subsequent effects on LV myocardial contractile function. Methods and Results A total of 40 volunteers (mean age, 35±10 years; 26 males) of varying body mass index (25.0±4.1 kg/m 2 ; range, 19.3–36.3 kg/m 2 ) and without diabetes mellitus or hypertension were prospectively recruited. EAT volume index, LV myocardial fat content, and extracellular volume were quantified by magnetic resonance imaging. LV myocardial contractile function was quantified by speckle tracking echocardiography global longitudinal strain on the same day as magnetic resonance imaging examination. Mean total EAT volume index, LV myocardial fat content, and extracellular volume were 30.0±19.6 cm 3 /m 2 , 5.06%±1.18%, and 27.5%±0.5%, respectively. On multivariable analyses, increased EAT volume index and insulin resistance were independently associated with both increased LV myocardial fat content content and higher burden of interstitial myocardial fibrosis. Furthermore, increased EAT volume index was independently associated with LV global longitudinal strain. Conclusions Increased EAT volume index and insulin resistance were independently associated with increased myocardial fat accumulation and interstitial myocardial fibrosis. Increased EAT volume index was associated with detrimental effects on myocardial contractile function as evidenced by a reduction in LV global longitudinal strain.

We demonstrate, for the first time, marked exercise impairment and cardiac compression in patients with a large HH and normal respiratory function. After HH repair, exercise capacity improves significantly and correlates with resolution of LA compression.

Objectives: It was the aim of this study to determine the prognostic significance of the Charlson Comorbidity Index (CCI) following acute pulmonary embolism (PE) and assess the prognosis of patients without comorbidities (defined as a CCI score of 0). Methods: Outcomes of 1,023 consecutive patients admitted with confirmed PE were tracked after a median of 3.7 years (25-75th interquartile range 1.5-6.1 years). All were assigned a non-age-adjusted CCI score. Results: The median CCI score was 1.0 (interquartile range 0.0-3.0). Three hundred and fifty-one (34%) patients had a CCI score of 0. Only 1 (0.3%) of 31 in-hospital deaths occurred in patients with a CCI score of 0. Long-term mortality for these patients was similar to the population-derived age- and sex-matched mortality rate, and was significantly better than for those with a CCI score ≥1 (12.5 vs. 47.5%; p < 0.0001 adjusted for age and sex). In multivariate analysis, CCI (per 1-score increase) independently predicted in-hospital (hazard ratio 1.27, 95% confidence interval 1.09-1.49; p = 0.003) and post-discharge (hazard ratio 1.35, 95% confidence interval 1.29-1.42; p < 0.0001) death. The c statistics for the multivariate prediction models for in-hospital (incorporating CCI score and serum sodium level) and post-discharge death (age, CCI score, hyperlipidemia, serum sodium and hemoglobin) were 0.738 and 0.788, respectively (both p < 0.0001). Conclusion: The CCI can be incorporated into risk models, with good discriminatory power, for predicting in-hospital and long-term outcomes following acute PE. Patients with a CCI score of 0 have a favorable long-term outcome following acute PE.

Rodents, mice and rats in particular, are the species of choice for evaluating chemical carcinogenesis. However, different species and strains often respond very differently, undermining the logic of extrapolation of animal results to humans and complicating risk assessment. Intracisternal A particles (IAPs), endogenous retroviral sequences, are an important class of transposable elements that induce genomic mutations and cell transformation by disrupting gene expression. Several lines of evidence support a role of IAPs as mouse-specific genetic factors in responses to toxicity and expression of disease phenotypes. Since multiple subtypes and copies of IAPs are present in the mouse genome, their activity and locations relative to functional genes are of critical importance. This study identified the major "active" subtypes of IAPs (subtype 1/1a) that are responsible for newly transposed IAP insertions described in the literature, and confirmed that (1) polymorphisms for IAP insertions exist among different mouse strains and (2) promoter activity of the LTRs can be modulated by chemicals. This study further identified all the genes in the C57BL/6 mouse genome with IAP subtype 1 and 1a sequences inserted in their proximity, and the major biofunctional categories and cellular signaling networks of those genes. Since many "IAP-associated genes" play important roles in the regulation of cell proliferation, cell cycle, and cell death, the associated IAPs, upon activation, can affect cellular responses to xenobiotics and disease processes, especially carcinogenesis. This systemic analysis provides a solid foundation for further investigations of the role of IAPs as species- and strain-specific disease susceptibility factors.

The clinical and histological features of 13 malignant melanomas in children less than 13 years of age in New South Wales, Australia, were compared with those in a control group of children with 15 Spitz nevi, 4 of which were considered atypical, and 2 unusual compound nevocellular nevi. Six of the controls had been previously diagnosed histologically as malignant melanoma. The objective observations made by one or more histopathologists experienced in reporting melanocytic lesions, and the clinical details, mainly from the Sydney Melanoma Unit files, were entered on a detailed protocol. Evaluation was assisted by the use of SPSS-X software on a mainframe VAX computer. Six of the 13 children with malignant melanoma died with their disease. The most frequent clinical features found in the malignant melanomas were bleeding, ulceration, itching, and black or variegated color. Recent enlargement and darkening were noted in the majority of both the malignant melanomas and the Spitz nevi. Histological features favoring malignancy in this series were mitoses within 0.25 mm of the dermal margin of the melanoma, a dermal mitotic rate exceeding 2/mm2, ulceration, surface exudate, large pigment granules, and clear-cell differentiation. The median thickness of the malignant melanomas was 1.3 mm but in the 4 children who died with melanoma the median thickness was 2.9 mm. Absence of mitoses, predominance of spindle cells, and diffuse maturation favored Spitz nevus. The median thickness of the Spitz nevi was 0.7 mm.