ABSTRACT
By convention, the ascending aorta is measured by echo from leading edge to leading edge. "Leading edge" connotes the edge of the aortic wall that is closest to the probe (at the top of the inverted "V" of the ultrasound image). By transthoracic echo (TTE), the leading edges are the outer anterior wall and inner posterior wall. By transesophageal echo (TEE), the leading edges are the outer posterior wall and inner anterior wall. Aortic measurements should be taken (by convention) in diastole (when the aorta is moving least). Simple TTE is 70 to 85% sensitive in diagnosing ascending aortic dissection. TEE sensitivity approaches 100%, though the tracheal carina imposes a blind spot on TEE, impeding visualization of distal ascending aorta and proximal aortic arch. While computed tomography angiography may be superior for defining full anatomic extent of aortic dissection, echocardiography is superior in assessing functional consequences such as mechanism and severity of aortic regurgitation, evidence of myocardial ischemia when complicated by coronary dissection, or evidence of tamponade physiology when pericardial effusion is present. Reverberation artifact can mimic a dissection flap. A true flap moves independently of the outer aortic wall which can be confirmed by M-mode. Color flow respects a true flap but does not respect a reverberation artifact. Assessment for bicuspid aortic valve (BAV) morphology should be done in systole, not diastole. In diastole, when the valve is closed, the raphé can make a bicuspid valve appear trileaflet. Doming in the parasternal long axis (PLAX) view and an eccentric closure line on PLAX M-mode should also raise suspicion for BAV.
ABSTRACT
Infective endocarditis is a common and treatable condition that carries a high mortality rate. Currently the workup of infective endocarditis relies on the integration of clinical, microbiological and echocardiographic data through the use of the modified Duke criteria (MDC). However, in cases of prosthetic valve endocarditis (PVE) echocardiography can be normal or non-diagnostic in a high proportion of cases leading to decreased sensitivity for the MDC. Evolving multimodality imaging techniques including leukocyte scintigraphy (white blood cell imaging), 18F-fluorodeoxyglucose positron emission tomography (FDG-PET), multidetector computed tomographic angiography (MDCTA), and cardiac magnetic resonance imaging (CMRI) may each augment the standard workup of PVE and increase diagnostic accuracy. While further studies are necessary to clarify the ideal role for each of these imaging techniques, nevertheless, these modalities hold promise in determining the diagnosis, prognosis, and care of PVE. We start by presenting a clinical vignette, then evidence supporting various modality strategies, balanced by limitations, and review of formal guidelines, when available. The article ends with the authors' summary of future directions and case conclusion.
ABSTRACT
The Chk2-mediated deoxyribonucleic acid (DNA) damage checkpoint pathway is important for mitochondrial DNA (mtDNA) maintenance. We show in this paper that mtDNA itself affects cell cycle progression. Saccharomyces cerevisiae rho(0) cells, which lack mtDNA, were defective in G1- to S-phase progression. Deletion of subunit Va of cytochrome c oxidase, inhibition of F(1)F(0) adenosine triphosphatase, or replacement of all mtDNA-encoded genes with noncoding DNA did not affect G1- to S-phase progression. Thus, the cell cycle progression defect in rho(0) cells is caused by loss of DNA within mitochondria and not loss of respiratory activity or mtDNA-encoded genes. Rad53p, the yeast Chk2 homologue, was required for inhibition of G1- to S-phase progression in rho(0) cells. Pif1p, a DNA helicase and Rad53p target, underwent Rad53p-dependent phosphorylation in rho(0) cells. Thus, loss of mtDNA activated an established checkpoint kinase that inhibited G1- to S-phase progression. These findings support the existence of a Rad53p-regulated checkpoint that regulates G1- to S-phase progression in response to loss of mtDNA.
