Multimodality imaging of aortitis is useful for identification of acute and chronic mural changes due to inflammation, edema, and fibrosis, as well as characterization of structural luminal changes including aneurysm and stenosis or occlusion. Identification of related complications such as dissection, hematoma, ulceration, rupture, and thrombosis is also important. Imaging is often vital for obtaining specific diagnoses (i.e., Takayasu arteritis) or is used adjunctively in atypical cases (i.e., giant cell arteritis). The extent of disease is established at baseline, with associated therapeutic and prognostic implications. Imaging of aortitis may be useful for screening, routine follow up, and evaluation of treatment response in certain clinical settings. Localization of disease activity and structural abnormality is useful for guiding biopsy or surgical revascularization or repair. In this review, we discuss the available imaging modalities for diagnosis and management of the spectrum of aortitis disorders that cardiovascular physicians should be familiar with for facilitating optimal patient care.

BackgroundSignificant paravalvular leak (PVL) after transcatheter aortic valve replacement (TAVR) confers a worse prognosis. Symptoms related to significant PVL may be difficult to differentiate from those related to other causes of heart failure. Cardiovascular magnetic resonance (CMR) directly quantifies valvular regurgitation, but has not been extensively studied in symptomatic post-TAVR patients.MethodsCMR was compared to qualitative (QE) and semi-quantitative echocardiography (SQE) for classifying PVL and prognostic value at one year post-imaging in 23 symptomatic post-TAVR patients. The primary outcome was a composite of all-cause death, heart failure hospitalization, and intractable symptoms necessitating repeat invasive therapy; the secondary outcome was a composite of all-cause death and heart failure hospitalization. The difference in event-free survival according to greater than mild PVL versus mild or less PVL by QE, SQE, and CMR were evaluated by Kaplan-Meier survival analysis.ResultsCompared to QE, CMR reclassified PVL severity in 48% of patients, with most patients (31%) reclassified to at least one grade higher. Compared to SQE, CMR reclassified PVL severity in 57% of patients, all being reclassified to at least one grade lower; SQE overestimated PVL severity (mean grade 2.5 versus 1.7, p = 0.001). The primary and secondary outcomes occurred in 48% and 35% of patients, respectively. Greater than mild PVL by CMR was associated with reduced event-free survival for the primary outcome (p < 0.0001), however greater than mild PVL by QE and SQE were not (p = 0.83 and p = 0.068). Greater than mild PVL by CMR was associated with reduced event-free survival for the secondary outcome, as well (p = 0.012).ConclusionIn symptomatic post-TAVR patients, CMR commonly reclassifies PVL grade compared with QE and SQE. CMR provides superior prognostic value compared to QE and SQE, as patients with greater than mild PVL by CMR (RF > 20%) had a higher incidence of adverse events.

Speckle-tracking left ventricular global longitudinal strain (GLS) assessment may provide substantial prognostic information for hypertrophic cardiomyopathy (HCM) patients. Reference values for GLS have been recently published. We aimed to evaluate the prognostic value of standardized reference values for GLS in HCM patients. An analysis of HCM clinic patients who underwent GLS was performed. GLS was defined as normal (more negative or equal to -16%) and abnormal (less negative than -16%) based on recently published reference values. Patients were followed for a composite of events including heart failure hospitalization, sustained ventricular arrhythmia, and all-cause death. The power of GLS to predict outcomes was assessed relative to traditional clinical and echocardiographic variables present in HCM. 79 HCM patients were followed for a median of 22 months (interquartile range 9-30 months) after imaging. During follow-up, 15 patients (19%) met the primary outcome. Abnormal GLS was the only echocardiographic variable independently predictive of the primary outcome [multivariate Hazard ratio 5.05 (95% confidence interval 1.09-23.4, p = 0.038)]. When combined with traditional clinical variables, abnormal GLS remained independently predictive of the primary outcome [multivariate Hazard ratio 5.31 (95 % confidence interval 1.18-24, p = 0.030)]. In a model including the strongest clinical and echocardiographic predictors of the primary outcome, abnormal GLS demonstrated significant incremental benefit for risk stratification [net reclassification improvement 0.75 (95 % confidence interval 0.21-1.23, p < 0.0001)]. Abnormal GLS is an independent predictor of adverse outcomes in HCM patients. Standardized use of GLS may provide significant incremental value over traditional variables for risk stratification.

Summary:The vast majority of left ventricular aneurysms (LVA) are secondary to coronary artery disease. The natural history of LVA is now better understood. The increasing use of noninvasive techniques has allowed earlier recognition and better appreciation of LVA genesis and pathophysiology . Improvements in surgical anesthesia and techniques have resulted in more successful LVA surgery. This article reviews the pathogenesis, natural history, and complications of LVA. Surgical indications and available treatment options in the management of patients with LVA and severe symptoms are presented. Left ventricular pseudoaneurysm (false aneurysm) will also be discussed.Key words: noninvasive techniques, ventricular amhythmias, congestive heart failure, endocardial resection, left ventricular aneurysmectomy DefinitionsThe marked variability in the definition of LVA is partly responsible for difficulties encountered in studying different reports regarding the natural history and treatment of the entity. Definitions vary across different disciplines and technologies. To the pathologist, LVA usually refers to a thin and stretched area of the ventricle where mature scar tissue has replaced most of the myocardium. T o the physiologist and clinician, LVA is best defined as a portion of the ventricle that manifests systolic expansion ir- respective of histologic structure. The surgeon's definition essentially agrees with the pathologist's.For the purpose of this discussion, LVA is defined as a localized protrusion of the left ventricular (LV) cavity during systole and diastole with akinetic or dyskinetic walls. EtiologyLeft ventricular aneurysm most commonly results from acute myocardial infarction (MI). An incidence varying from 3.5 to 5% has been reported in autopsy studies.',2 Angiographically defined LVA has been reported in 7.6% of patients with coronary arteIy disease referred for coronary angi~graphy.~ On the other hand, in selected patients undergoing radionuclide angiography soon after MI, 35 % had LVA.4 Greater than 80% of left ventricular aneurysms involve the anterior wall and/or apex and are associated with high-grade stenosis or complete occlusion of the proximal or mid-left anterior descending coronary artery (LAD).3-5 The presence of only three muscle layers at the apex (compared with four layers at the base) explains the predeliction of the apex to LVA formation. Myocardial infarction is usually transmural and is associated with high peak levels of the enzyme creatine k i n a~e .~.~ Approximately 50% of left ventricular aneurysms occumng after acute MI appear within 48 h from the onset of chest pain. The remainder appear within two weeks.4 Once formed, LVA rarely resolves. Myocardial infarction and LVA may result from coronary arterial emboli or anomalous origin of the left coronary artery from the pulmonary artery.Not all patients with coronary atherosclerosis have scar tissue in the area of LVA. Transient occlusion of a coronary artery may result in reversible dyskinesis (physiologic LVA).' Patients with i...