CT pulmonary angiography-based scoring system to predict the prognosis of acute pulmonary embolism.

Background: The purpose is to develop a comprehensive risk-scoring system based on CT findings for predicting 30-day mortality after acute pulmonary embolism (PE), and to compare it with PE Severity Index (PESI).

Materials And Methods: The study included consecutive 1698 CT pulmonary angiograms (CTPA) positive for acute PE performed at a single institution (2003-2010). Two radiologists independently assessed each study regarding clinically relevant findings and then performed adjudication.

Normal ventricular diameter ratio on CT provides adequate assessment for critical right ventricular strain among patients with acute pulmonary embolism.

There is variability in guideline recommendations for assessment of the right ventricle (RV) with imaging as prognostic information after acute pulmonary embolism (PE). The objective of this study is to identify a clinical scenario for which normal CT-derived right-to-left ventricular (RV/LV) ratio is sufficient to exclude RV strain or PE-related short-term death. This retrospective cohort study included 579 consecutive subjects (08/2003-03/2010) diagnosed with acute PE with normal CT-RV/LV ratio (<0.

Smad3 Signaling Promotes Fibrosis While Preserving Cardiac and Aortic Geometry in Obese Diabetic Mice.

Background: Heart failure in diabetics is associated with cardiac hypertrophy, fibrosis and diastolic dysfunction. Activation of transforming growth factor-β/Smad3 signaling in the diabetic myocardium may mediate fibrosis and diastolic heart failure, while preserving matrix homeostasis. We hypothesized that Smad3 may play a key role in the pathogenesis of cardiovascular remodeling associated with diabetes mellitus and obesity.

Selecting an oral anticoagulant for patients with nonvalvular atrial fibrillation.

While the use of warfarin has been the cornerstone of thromboembolism prevention in patients with atrial fibrillation (AF), its limitations have led to the introduction of a new generation of direct-acting oral anticoagulants. Evidence from large phase III clinical trials, observational studies and pharmacokinetic analyses can guide clinicians to select the most effective and safest form of anticoagulation for patients with nonvalvular AF. This manuscript describes the main pharmacologic, clinical and epidemiological characteristics of each new oral anticoagulant and their use in selected clinical scenarios, including patients with: advanced age; at low or high risk of stroke; potential drug-drug interactions; on concomitant antiplatelet therapy; at high risk for acute coronary syndrome; with recent gastrointestinal bleeding; with renal impairment; and with hepatic dysfunction.

CXCR3-independent actions of the CXC chemokine CXCL10 in the infarcted myocardium and in isolated cardiac fibroblasts are mediated through proteoglycans.

Aims: The CXC chemokine CXCL10 is up-regulated in the infarcted myocardium and limits cardiac fibrosis by inhibiting growth factor-mediated fibroblast migration. CXCL10 signals by binding to its receptor CXCR3; however, recently CXCR3-independent CXCL10 actions have been suggested. Our study explores the role of CXCR3 signalling in myocardial infarction and investigates its involvement in mediating the anti-fibrotic effects of CXCL10.

Comparison of the phase III clinical trial designs of novel oral anticoagulants versus warfarin for the treatment of nonvalvular atrial fibrillation: implications for clinical practice.

Although vitamin K antagonists (VKAs) have been the backbone of thromboprophylaxis in nonvalvular atrial fibrillation, their limitations have encouraged the development of a new generation of oral anticoagulants. This review compares the different designs and procedures used to conduct four phase III trials that tested dabigatran, rivaroxaban, apixaban, and edoxaban versus VKAs. Although pharmacologic characteristics and results of the main trials are briefly discussed, this review mainly focuses on study designs, enrollment criteria, populations studied, quality metrics, and transition strategies between oral anticoagulants.

Computed tomography and echocardiography in patients with acute pulmonary embolism: part 2: prognostic value.

Purpose: The aim of the study was to compare the prognostic value of right ventricular (RV) dysfunction detected on computed tomography pulmonary angiography (CTPA) and transthoracic echocardiography (TTE) in patients with acute pulmonary embolism (PE).

Materials And Methods: From all consecutive CTPAs performed between August 2003 and May 2010 that were positive for acute PE (n=1744), those with TTE performed within 48 hours of CTPA (n=785) were selected as the study cohort. Multivariate logistic regression analysis was performed to assess the association of CTPA RV/left ventricular (LV) diameter ratio and TTE RV strain with PE-related 30-day mortality, including other associated factors as covariates.

Computed tomography and echocardiography in patients with acute pulmonary embolism: part 1: correlation of findings of right ventricular enlargement.

Purpose: To evaluate the correlation between the computed tomography (CT)-derived right ventricle (RV) to left ventricle (LV) diameter ratio and the RV size determined by echocardiography in patients with acute pulmonary embolism.

Materials And Methods: Consecutive CT pulmonary angiography examinations (August 2003 to May 2010) from a single, large, urban teaching hospital were retrospectively reviewed. For a cohort of 777 subjects who underwent echocardiography within 48 hours of the CT acquisition, the qualitative RV size (divided into 5 categories) extracted from the echocardiography report was correlated with the CT-derived RV/LV diameter ratio.

Thrombospondin-1 induction in the diabetic myocardium stabilizes the cardiac matrix in addition to promoting vascular rarefaction through angiopoietin-2 upregulation.

Rationale: Diabetes mellitus is associated with cardiac fibrosis. Matricellular proteins are induced in fibrotic conditions and modulate fibrogenic and angiogenic responses by regulating growth factor signaling.

Objective: Our aim was to test the hypothesis that the prototypical matricellular protein thrombospondin (TSP)-1, a potent angiostatic molecule and crucial activator of transforming growth factor-β, may play a key role in remodeling of the diabetic heart.

Thrombospondin-1 regulates adiposity and metabolic dysfunction in diet-induced obesity enhancing adipose inflammation and stimulating adipocyte proliferation.

As a typical matricellular protein, thrombospondin (TSP)-1, binds to the structural matrix and regulates cellular behavior by modulating growth factor and cytokine signaling. Obesity and diabetes are associated with marked upregulation of TSP-1 in adipose tissue. We hypothesized that endogenous TSP-1 may play an important role in the pathogenesis of diet-induced obesity and metabolic dysfunction.

Systematic characterization of myocardial inflammation, repair, and remodeling in a mouse model of reperfused myocardial infarction.

Mouse models of myocardial infarction are essential tools for the study of cardiac injury, repair, and remodeling. Our current investigation establishes a systematic approach for quantitative evaluation of the inflammatory and reparative response, cardiac function, and geometry in a mouse model of reperfused myocardial infarction. Reperfused mouse infarcts exhibited marked induction of inflammatory cytokines that peaked after 6 hr of reperfusion.

Endogenous thrombospondin 1 protects the pressure-overloaded myocardium by modulating fibroblast phenotype and matrix metabolism.

The matricellular protein thrombospondin (TSP) 1 is induced after tissue injury and may regulate reparative responses by activating transforming growth factor-β, by suppressing angiogenesis and by modulating inflammation and matrix metabolism. We hypothesized that endogenous TSP-1 may be involved in the pathogenesis of cardiac remodeling in the pressure-overloaded heart. Myocardial TSP-1 expression was increased in a mouse model of pressure overload because of transverse aortic constriction.

Smad3 signaling critically regulates fibroblast phenotype and function in healing myocardial infarction.

Rationale: Cardiac fibroblasts are key effector cells in the pathogenesis of cardiac fibrosis. Transforming growth factor (TGF)-beta/Smad3 signaling is activated in the border zone of healing infarcts and induces fibrotic remodeling of the infarcted ventricle contributing to the development of diastolic dysfunction.

Objective: The present study explores the mechanisms responsible for the fibrogenic effects of Smad3 by dissecting its role in modulating cardiac fibroblast phenotype and function.

CCR5 signaling suppresses inflammation and reduces adverse remodeling of the infarcted heart, mediating recruitment of regulatory T cells.

Myocardial infarction triggers an inflammatory reaction that is involved in cardiac remodeling. Cardiac repair is dependent on regulatory mechanisms that suppress inflammation and prevent excessive matrix degradation. Chemokine induction in the infarcted heart mediates recruitment of leukocyte subsets with distinct properties.

Induction of the CXC chemokine interferon-gamma-inducible protein 10 regulates the reparative response following myocardial infarction.

Rationale: Interferon-gamma-inducible protein (IP)-10/CXCL10, an angiostatic and antifibrotic chemokine with an important role in T-cell trafficking, is markedly induced in myocardial infarcts, and may regulate the reparative response.

Objective: To study the role of IP-10 in cardiac repair and remodeling.

Methods And Results: We studied cardiac repair in IP-10-null and wild-type (WT) mice undergoing reperfused infarction protocols and examined the effects of IP-10 on cardiac fibroblast function.

The extracellular matrix as a modulator of the inflammatory and reparative response following myocardial infarction.

The dynamic alterations in the cardiac extracellular matrix following myocardial infarction not only determine the mechanical properties of the infarcted heart, but also directly modulate the inflammatory and reparative response. During the inflammatory phase of healing, rapid activation of Matrix Metalloproteinases (MMP) causes degradation of the cardiac extracellular matrix. Matrix fragments exert potent pro-inflammatory actions, while MMPs process cytokines and chemokines altering their biological activity.

Monocyte chemoattractant protein-1/CCL2 as a biomarker in acute coronary syndromes.

The CC chemokine monocyte chemoattractant protein (MCP)-1/CCL2 is involved in the formation, progression, and destabilization of atheromatous plaques and plays an essential role in postinfarction remodeling. These properties generated significant interest in the potential significance of MCP-1 as a biomarker in acute coronary syndromes (ACS). Emerging evidence suggests that MCP-1 plasma levels have prognostic value in the acute and chronic phase following ACS, providing information independent of standard clinical variables.

Left main coronary artery stenosis treatment with two paclitaxel-eluting stents in a patient with cardiac allograft vasculopathy.

Cardiac transplantation is a well defined therapy for end stage heart failure. After the first year of transplantation, allograft coronary artery disease (ACAD) is the second main cause of death. The ACAD is defined as a diffuse process affecting the entire length of epicardial vessels.

No association found between the insertion/deletion of a 287-bp alu repeat sequence within intron 16 of the angiotensin-I-converting enzyme (ACE) gene in Mexican patients and binary restenosis after coronary stenting.

Background: It has been suggested that the incidence of coronary restenosis after a percutaneous coronary intervention is much higher in patients with a 287-bp alu repeat sequence within intron 16 of the angiotensin-I-converting enzyme (ACE) gene (deletion allele) than in others, but published studies are conflicting.

Methods: The presence (insertion) or absence (deletion) of a 287-bp alu repeat sequence within intron 16 of the ACE gene (I/D polymorphism) was analyzed by polymerase chain reaction in a group of 168 patients with coronary artery disease who underwent coronary artery stenting. Basal and procedure coronary angiographies were analyzed searching for angiographic predictors of restenosis and follow-up angiography was analyzed looking for binary restenosis.

The interleukin 1B-511 polymorphism is associated with the risk of developing restenosis after coronary stenting in Mexican patients.

Inflammation is the primary response to vessel wall injury caused by stent placement in coronary arteries. Cytokines of the interleukin-1 family are central regulators in immunoinflammatory mechanisms. The objective of this study was to test for association between IL-1 family gene polymorphisms and risk for restenosis after coronary stent placement.

Predictors of mortality and adverse outcome in elderly high-risk patients undergoing percutaneous coronary intervention.

Objectives: We sought to identify predictors of in-hospital and long-term (> 1 year) mortality and major adverse cardiac events (MACE) in elderly patients referred for percutaneous coronary intervention (PCI).

Methods: Seventy-three patients (> or = 80 years) were included. Clinical and interventional characteristics were collected retrospectively.