Bois, John P.

Diagnosis of the inflammatory aortopathies and importantly, their distinction in the later stages of disease from genetically mediated or acquired (degenerative) aortopathy remains a challenging clinical problem. Historically, the diagnosis of inflammatory aortopathy has required tissue sampling and pathological assessment. Although histological diagnosis remains an important diagnostic criterion, the ability to obtain sufficient tissue samples is problematic and requires invasive approaches that pose important risk. Continuing refinement in the capabilities of multimodality imaging, including ultrasound, computed tomography, magnetic resonance imaging, and positron emission tomography provides important insights into the broad spectrum of disease which comprise the inflammatory aortopathies. This review examines the current and emerging role of multimodality imaging in the evaluation of aortitis.

Left ventricular hypertrophy (LVH), or an increase in cardiac mass, usually reflects pathologic adaptation to chronic pressure or volume loads. Physiologic adaptation in athletes as well as genetic, metabolic, and infiltrative disorders may also result in increased cardiac mass. Given vast differences in prognosis and therapeutic options associated with different underlying conditions, the evaluation of patients with LVH necessitates a modern, comprehensive evaluation incorporating multimodality imaging. Herein we present a systematic approach to patients with incidental LVH.

Among patients undergoing cardioversion for atrial fibrillation, the presence of left ventricular thrombus is a relatively uncommon and challenging clinical dilemma. While left atrial appendage thrombus is a contraindication to cardioversion, there is paucity of data regarding the safety of cardioversion in with the presence of left ventricular apical thrombus. Also, thrombus characteristics such as protrusion and mobility on echocardiography are known risk factors for systemic embolism. In this article, we present a case highlighting the management of atrial fibrillation in the setting of left ventricular dysfunction, acute heart failure, and echocardiographic evidence of acute left ventricular apical thrombus.

ObjectiveValvular heart disease is common in patients with rheumatoid arthritis (RA). However, there is uncertainty about how often to perform echocardiographic surveillance in this population. The objective of this study was to assess the progression rate of mild and moderate aortic stenosis (AS) in patients with RA.MethodsA population‐based cohort of patients with RA and either mild (2.0–2.9 m/second) or moderate (3.0–3.9 m/second) AS was identified. Demographic, clinical, and echocardiographic data were collected. Annual progression rate of AS was then calculated for the study cohort and the impact of pertinent RA variables on progression rate determined.ResultsSixty‐eight patients with RA and mild or moderate AS met the inclusion requirements. Peak aortic valve (AV) velocity and mean AV gradient increased during the study period, whereas AV area decreased, consistent with progression of AS (P<.001). Mean (SD) annual increase in peak AV jet velocity was 0.05 m/second (0.01) and in mean AV gradient was 1.0 mm Hg (0.18). Mean annual decrease in AV area was 0.04 (0.01) cm2. The progression rate of AS was higher in patients with increased erythrocyte sedimentation rates (ESR) (P=.001).ConclusionsThe rate of AS progression in the RA population was higher in patients with increased ESR but less than that of the reported rate of AS progression in the general population. Although the cause for this finding is uncertain, these results suggest that patients with RA who have mild or moderate AS should undergo echocardiographic surveillance for disease progression similar to that of the general population.

Background Atrial fibrillation (AF) is the most common sustained atrial arrhythmia. One potential target for ablation is left atrial (LA) scar (LAS) regions that may be the substrate for re-entry within the atria, thereby sustaining AF. Identification of LAS through LA delayed gadolinium enhancement (LADE) with MRI has been proposed. Objectives We sought to evaluate LADE in patients referred for catheter ablation of AF. Methods Prospective analysis was conducted of consecutive patients who underwent pulmonary vein antrum isolation (PVAI) ablation for AF at a single institution. Patients underwent LADE with MRI to determine LAS regions before ablation. MRI data were analysed independently in accordance with prespecified institutional protocol by two staff cardiac radiologists to whom patient outcomes were masked, and reports of LADE were documented. Where no initial consensus occurred regarding delayed enhancement (DE), a third staff cardiac radiologist independently reviewed the case and had the deciding vote. Results Of the 149 consecutive patients (mean (SD) age, 59 (9) years), AF was persistent in 64 (43%) and paroxysmal in 85 (57%); 45 (30%) had prior ablation. Only five patients (3%) had identifiable DE in LA walls (persistent AF, n=1; paroxysmal AF, n=4). LADE was present in two (4%) of the 45 patients with previous left PVAI. The presence of LADE was not associated with a higher recurrence rate of AF. Conclusions In contrast to previous studies, the finding of DE within LA walls was uncommon and, when present, did not correlate with AF type or risk of AF recurrence. It therefore is of unclear clinical significance.

ObjectivesPrior analysis at our institution found that patients with hypertrophic cardiomyopathy (HCM) who experience postprandial symptoms (PPS) are more likely to have resting left ventricular outflow tract (LVOT) obstruction and reduced quality of life. Our objective was to determine whether PPS in patients with HCM vs healthy subjects occur as a result of measurable hemodynamic alterations in the postprandial hemodynamic response.MethodsWe conducted a prospective cross‐sectional study examining 45 patients with HCM and 10 controls who underwent fasting and postprandial 2‐dimensional Doppler echocardiography. Postprandial echocardiographic measurements were obtained at symptom onset or 30 minutes after consumption of a standardized meal, whichever occurred first.ResultsThe HCM population included 18 (40%) patients with PPS and 27 (60%) without PPS. Compared to controls, mean resting peak LVOT gradient was 23.4 ± 17.6 mmHg in HCM patients with PPS and 25.1 ± 33.1 mmHg in those without PPS (P = 0.10). The mean change in peak LVOT gradient after a meal was 0.7 ± 1.1 mmHg for controls, 5.0 ± 8.3 mmHg for HCM patients with PPS, and 1.5 ± 18.2 mmHg for HCM patients without PPS (P = 0.64).ConclusionAlthough the ability to provoke an increased LVOT gradient with a postprandial, upright exercise study protocol was recently reported, the current study suggests that a resting, supine, postprandial protocol does not elicit evidence of LVOT obstruction. Therefore, future investigations should consider whether simply performing an upright postprandial study in HCM patients with PPS will provide evidence of dynamic LVOT or if the addition of an exercise component is necessary.