Left Ventricular Function and Volume with Coronary CT Angiography Improves Risk Stratification and Identification of Patients at Risk for Incident Mortality: Results from 7758 Patients in the Prospective Multinational CONFIRM Observational Cohort Study

Arsanjani, Reza; Berman, Daniel S.; Gransar, Heidi; Cheng, Victor; Dunning, Allison; Lin, Fay Y.; Achenbach, Stephan; Al-Mallah, Mouaz; Budoff, Matthew J.; Callister, Tracy Q.; Chang, Hyuk Jae; Cademartiri, Filippo; Chinnaiyan, Kavitha M.; Chow, Benjamin J.W.; Delago, Augustin; Hadamitzky, Martin; Hausleiter, Jöerg; Kaufmann, Philipp A.; LaBounty, Troy; Leipsic, Jonathon; Raff, Gilbert; Shaw, Leslee J.; Villines, Todd C.; Cury, Ricardo C.; Feuchtner, Gudrun; Min, James K.

doi:10.1148/radiol.14122816

Cited by 35 publications

(14 citation statements)

References 31 publications

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“…Despite the many causes of DCM, there are many similarities in the final structural and functional alterations, related to long-term stress and neurohormonal activation [5] , that eventually lead to systolic heart failure. Increased left ventricular end-diastolic volume and decreased left ventricular ejection fraction are risk factors for cardiac morbidity and mortality in the general population [6] . The mechanisms that determine the progression of DCM are not completely understood, but 30–48% are related to genetic mutations [1] , [2] , [3] , [4] ; DCM is also closely associated with hypertension [3] .…”

Section: Introductionmentioning

confidence: 99%

Over-expression of a cardiac-specific human dopamine D5 receptor mutation in mice causes a dilated cardiomyopathy through ROS over-generation by NADPH oxidase activation and Nrf2 degradation

Jiang

Liu

et al. 2018

Redox Biology

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Dilated cardiomyopathy (DCM) is a severe disorder caused by medications or genetic mutations. D5 dopamine receptor (D5R) gene knockout (D5-/-) mice have cardiac hypertrophy and high blood pressure. To investigate the role and mechanism by which the D5R regulates cardiac function, we generated cardiac-specific human D5R F173L(hD5F173L-TG) and cardiac-specific human D5R wild-type (hD5WT-TG) transgenic mice, and H9c2 cells stably expressing hD5F173L and hD5WT. We found that cardiac-specific hD5F173L-TG mice, relative to hD5WT-TG mice, presented with DCM and increased cardiac expression of cardiac injury markers, NADPH oxidase activity, Nrf2 degradation, and activated ERK1/2/JNK pathway. H9c2-hD5F173L cells also had an increase in NADPH oxidase activity, Nrf2 degradation, and phospho-JNK (p-JNK) expression. A Nrf2 inhibitor also increased p-JNK expression in H9c2-hD5F173L cells but not in H9c2-hD5WT cells. We suggest that the D5R may play an important role in the preservation of normal heart function by inhibiting the production of reactive oxygen species, via inhibition of NADPH oxidase, Nrf2 degradation, and ERK1/2/JNK pathways.

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Section: Introductionmentioning

confidence: 99%

Over-expression of a cardiac-specific human dopamine D5 receptor mutation in mice causes a dilated cardiomyopathy through ROS over-generation by NADPH oxidase activation and Nrf2 degradation

Jiang

Liu

et al. 2018

Redox Biology

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“…In 7758 patients from the Coronary CT Angiography Evaluation for Clinical Outcomes: An International Multicenter (CONFIRM) registry, worsening LV EF, and larger LV volumes predicted mortality and were associated with CAD. 62 In this registry, LV EF was classified as normal (≥55%), mildly reduced (55% but ≥45%), moderately reduced (45% but ≥35%), and severely reduced (<35%). Abnormal LV end-systolic volume (LVESV) was defined as ≥90 mL and abnormal LV end-diastolic volume (LVEDV) as ≥200 mL.…”

Section: Image Processing and Evaluationmentioning

confidence: 99%

“…Abnormal LV end-systolic volume (LVESV) was defined as ≥90 mL and abnormal LV end-diastolic volume (LVEDV) as ≥200 mL. 62 …”

Section: Image Processing and Evaluationmentioning

confidence: 99%

Analysis of ventricular function by CT

Rizvi

Deaño

Bachman

et al. 2015

Journal of Cardiovascular Computed Tomography

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The assessment of ventricular function, cardiac chamber dimensions and ventricular mass is fundamental for clinical diagnosis, risk assessment, therapeutic decisions, and prognosis in patients with cardiac disease. Although cardiac computed tomography (CT) is a noninvasive imaging technique often used for the assessment of coronary artery disease, it can also be utilized to obtain important data about left and right ventricular function and morphology. In this review, we will discuss the clinical indications for the use of cardiac CT for ventricular analysis, review the evidence on the assessment of ventricular function compared to existing imaging modalities such cardiac MRI and echocardiography, provide a typical cardiac CT protocol for image acquisition and post-processing for ventricular analysis, and provide step-by-step instructions to acquire multiplanar cardiac views for ventricular assessment from the standard axial, coronal, and sagittal planes. Furthermore, both qualitative and quantitative assessments of ventricular function as well as sample reporting are detailed.

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“…Evaluation of volumes and function – The quantification of ventricular volumes and function has been validated against other methods of great clinical applicability 38 , 39 , but recently the use of these measurements demonstrated a great potential for detection of cardiovascular risk and mortality 40 .…”

Section: Worldwide Impact Of the Latest Publications By Braziliansmentioning

confidence: 99%

Cardiovascular Computed Tomography and Magnetic Resonance: History and Growing Impact in Brazil and in the World

Nacif¹,

Rochitte²

2014

Arquivos Brasileiros De Cardiologia

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Left Ventricular Function and Volume with Coronary CT Angiography Improves Risk Stratification and Identification of Patients at Risk for Incident Mortality: Results from 7758 Patients in the Prospective Multinational CONFIRM Observational Cohort Study

Abstract: LV dysfunction and volumes measured with cardiac CT angiography augment risk prediction and discrimination for future mortality.

Cited by 35 publications

References 31 publications

Over-expression of a cardiac-specific human dopamine D5 receptor mutation in mice causes a dilated cardiomyopathy through ROS over-generation by NADPH oxidase activation and Nrf2 degradation

Over-expression of a cardiac-specific human dopamine D5 receptor mutation in mice causes a dilated cardiomyopathy through ROS over-generation by NADPH oxidase activation and Nrf2 degradation

Analysis of ventricular function by CT

Cardiovascular Computed Tomography and Magnetic Resonance: History and Growing Impact in Brazil and in the World

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