AIMS Positron emission tomography-computed tomography (PET-CT) is a highly sensitive clinical molecular imaging modality to study atherosclerotic plaque biology. Therefore, we sought to develop a new PET tracer, targeting vascular cell adhesion molecule (VCAM)-1 and validate it in a murine atherosclerotic model as a potential agent to detect atherosclerotic plaque inflammation. METHODS AND RESULTS The anti-VCAM-1 nanobody (Nb) (cAbVCAM-1-5) was radiolabelled with Fluorine-18 ((18)F), with a radiochemical purity of >98%. In vitro cell-binding studies showed specific binding of the tracer to VCAM-1 expressing cells. In vivo PET/CT imaging of ApoE(-/-) mice fed a Western diet or control mice was performed at 2h30 post-injection of [(18)F]-FB-cAbVCAM-1-5 or (18)F-control Nb. Additionally, plaque uptake in different aorta segments was evaluated ex vivo based on extent of atherosclerosis. Atherosclerotic lesions in the aortic arch of ApoE(-/-) mice, injected with [(18)F]-FB-anti-VCAM-1 Nb, were successfully identified using PET/CT imaging, while background signal was observed in the control groups. These results were confirmed by ex vivo analyses where uptake of [(18)F]-FB-cAbVCAM-1-5 in atherosclerotic lesions was significantly higher compared with control groups. Moreover, uptake increased with the increasing extent of atherosclerosis (Score 0: 0.68 ± 0.10, Score 1: 1.18 ± 0.36, Score 2: 1.49 ± 0.37, Score 3: 1.48 ± 0.38%ID/g, Spearman's r(2) = 0.675, P < 0.0001). High lesion-to-heart, lesion-to-blood, and lesion-to-control vessel ratios were obtained (12.4 ± 0.4, 3.3 ± 0.4, and 3.1 ± 0.6, respectively). CONCLUSION The [(18)F]-FB-anti-VCAM-1 Nb, cross-reactive for both mouse and human VCAM-1, allows non-invasive PET/CT imaging of VCAM-1 expression in atherosclerotic plaques in a murine model and may represent an attractive tool for imaging vulnerable atherosclerotic plaques in patients.
We read with interest the recent article by Pyxaras et al .1 proposing corrected regression equations for improving the echocardiographic estimation of systolic pulmonary artery pressure (sPAP) and mean pulmonary artery pressure (mPAP) in patients with pulmonary hypertension (PH). The authors propose to slightly modify both the sPAP Bernouilli equation and the empirical mPAP equation (mPAP = 0.61 sPAP + 2 mmHg). Before accepting the authors' conclusion that their two corrected formulas may be more reliable than previous ones, we would like to make the …
Cardiac surgery is the second most frequent aetiology of left ventricular pseudoaneurysm (LVP). Left ventricular apical venting is a recognized cause of LVP. Prompt surgical treatment is usually needed since there is a high risk of rupture and spontaneous closure is very rare. We describe a case of spontaneous closure of a left ventricle pseudoaneurysm following apical venting.
This editorial refers to ‘Valvuloarterial impedance does not improve risk stratification in low-ejection fraction, low-gradient aortic stenosis: results from a multicentre study’ by F. Levy et al ., on page 358. The vast majority of patients with severe calcified aortic stenosis (AS) have normal left ventricular (LV) ejection fraction, even in the presence of symptoms.1 Nevertheless, ≈20% of patients with AS and undergoing valve surgery were found with reduced LV ejection fraction (<50%)1 in the last Euro Heart Survey. This characteristic is often the result of a concomitant coronary artery disease. In some patients, however, LV hypertrophy, due to the chronic pressure overload, is inadequate to normalize systolic wall stress, resulting in an afterload mismatch and a decrease in LV ejection fraction.2 Reduced LV function may lead to low-flow state and thus to low-gradient, despite the presence of severe AS. In fact, three main types of patients with severe AS, according to LV function and flow, are generally observed: (i) normal LV ejection fraction and normal flow, (ii) reduced LV ejection fraction and reduced flow, and (iii) normal LV ejection fraction and reduced flow. Low-ejection fraction/low-gradient severe AS represents a challenging clinical entity. The classification of patient in the so-called low-flow/low-gradient (LF/LG) severe AS subset may considerably vary from different studies and is generally based on the presence of the three following haemodynamic criteria: (i) an aortic valve area (AVA) <1 cm², (ii) a LV ejection fraction <30–45%, and (iii) a mean transvalvular pressure gradient (MPG) <30–40 mmHg.3–12 LF/LG severe AS is associated with a poor outcome under conservative management13 and a high operative mortality risk.14 Moreover, even after aortic valve replacement (AVR), the prognosis of such patients is worse than those with preserved LV function, and the improvement of symptoms remains limited. …
AIMSCardiac resynchronization therapy (CRT) can stop the vicious cycle resulting from dyssynchrony and generates left ventricular (LV) reverse remodelling. Our objective was to assess the time course and the relationship between improvement in LV dyssynchrony and reverse remodelling after CRT.METHODS AND RESULTSSixty-four consecutive patients were evaluated before, immediately after, and 3- and 6 months after CRT. We measured LV volumes, ejection fraction (EF), and sphericity index, and dyssynchrony was assessed using speckle-tracking radial strain. Response was defined as a >15% decrease in end-systolic volume (ESV) 6 months after CRT, and event-free survival was followed for 24 months. Responders and non-responders had similar baseline LV volumes and EF. During the first and the following 3 months after CRT, LV volumes gradually decreased (end-diastolic volume: 195±73 to 164±60* to 129±51 mL†, ESV: 141±70 to 110±47* to 82±40 mL†), and sphericity index and EF progressively increased (sphericity index: 1.52±0.20 to 1.75±0.31* to 1.94±0.34†, EF: 28±7 to 34±7* to 38±8%†, *†P<0.001) in responders. No such changes were observed in non-responders. Furthermore, dyssynchrony diminished progressively during the first and the following 3 months after CRT and patients with progressive resynchronization experienced fewer major cardiovascular events than those without (P<0.001).CONCLUSIONCRT can stop the vicious cycle of remodelling and dyssynchrony, and actually, turn it into the virtuous cycle of reverse remodelling and further resynchronization.
The introduction of 64-slice multi-detector computed tomography (CT) in 2005 made the non-invasive imaging of coronary arteries relatively easy to perform. Computed tomography coronary angiography (CTCA) has been shown to be highly accurate at detecting coronary artery disease (CAD), when compared with invasive X-ray coronary angiography and, in particular, has an excellent negative predictive value (NPV).1,2 There are also prognostic data confirming very low risk for patients with normal CTCA.3 One of the limitations of multidetector CT and despite very good temporal resolution of 150 ms, with half scan reconstruction, is the need for beta-Blockers to slow the heart rate to 65 bpm, for retrospective, and 60 bpm, for the low radiation dose, prospective gated acquisitions. This is to minimize coronary motion particularly of the right coronary artery. Dual-source CT, with twice the temporal resolution, can cope with faster heart rates, whereas the 320-slice CT can image the heart in one heart beat. The UK national institute of clinical excellence (NICE) have recently produced guidelines on the management of patients with chest pain of recent onset, endorsing the use of CTCA in their investigational algorithm. We discuss the radiation dose associated with …
A 61-year-old man with an uneventful medical history presented with two transient ischaemic attacks (TIA) with bulbar and peripheral deficit. Transthoracal and transoesophageal echocardiography revealed a patent foramen ovale (PFO) and a large, lobulated, pedunculated, non-calcified, and heterogenic mass attached to the septal tricuspid leaflet ( Panels 1–3 ) with important mobility. MRI suggested a myxoma, being isointense on T1-weighted turbo spin echo (TSE), iso-hyperintense on T2-weighted TSE, and hypointense on spoiled gradient echo. First-pass perfusion showed a heterogeneous and hypoperfused enhancement pattern, while contrast-enhanced inversion recovery images showed diffuse hyperenhancement ( Panels 4 and 5 ). Carotid echo-Doppler, Holter monitoring, and a …
Congenital aneurysms of the left ventricle (LV) are rare cardiac abnormalities and in most instances, are asymptomatic. However, some patients may present cardiac rupture, tamponade, ventricular arrhythmias, and eventually sudden death. Herein, we describe a case of a 64-year-old male patient who was hospitalized for critical limb ischaemia because of an acute embolic event. Transthoracic contrast echocardiography revealed a congenital aneurysm of the LV apex with a small thrombus and a reduced LV ejection fraction. Speckle tracking imaging showed an impaired myocardial torsion. Diagnosis was confirmed after surgical resection of the aneurysm. LV torsion and ejection fraction were normalized after surgery.
AIMSThe aim of this paper is to report clinical characteristics, consequences, echocardiographic features, and pathological findings encountered in patients suffering from valvular disease associated with benfluorex exposure in a multicentre French registry.METHODS AND RESULTSForty patients suffering from unexplained restrictive valvular disease with a previous exposition to benfluorex, a fenfluramine derivative, were identified from eight French university hospitals. Patients were mostly women (87.5%) with a mean age of 57 ± 9 years and high body mass index of 30 ± 7 kg/m²; 37.5% of them presented with severe heart failure symptoms (NYHA class III and IV). Benfluorex mean daily dose was 415 ± 131 mg with total therapy duration of 72 ± 53 months. Resulting cumulative dose was 910 ± 675 g. Common echocardiographic findings were leaflets and sub-valvular apparatus thickening and retraction. Aortic and mitral valve regurgitations resulting from leaflets loss of coaptation were the most frequent findings (87.5 and 82.5%) and were severe in 29 patients (72.5%). Multiple valve involvements were present in 31 cases (77.5%). Pulmonary arterial hypertension was identified in 20 cases (50%). Histopathological examination demonstrated abundant extra cellular matrix encasing the leaflets without modification of valve architecture. Fifteen patients (37.5%) underwent valvular surgery.CONCLUSIONBenfluorex-related valvulopathy shares numerous characteristics with other drug-induced valvular disease. Clinical consequences may be serious with severe heart failure symptoms that may lead to surgical treatment.
We report on the case of a 45-year-old lady with metastatic carcinoid tumour and carcinoid syndrome who develops severe valvulopathy involving the tricuspid and pulmonary valve. The use of three-dimensional transoesophageal echocardiography allowed more detailed morphological assessment of tricuspid and pulmonary valve pathology, sub-valvular apparatus and improved delineation of the relationship between these structures and surrounding cardiac chambers.
The introduction of devices for transcatheter aortic valve implantation, mitral repair, and closure of prosthetic paravalvular leaks has led to a greatly expanded armamentarium of catheter-based approaches to patients with regurgitant as well as stenotic valvular disease. Echocardiography plays an essential role in identifying patients suitable for these interventions and in providing intra-procedural monitoring. Moreover, echocardiography is the primary modality for post-procedure follow-up. The echocardiographic assessment of patients undergoing transcatheter interventions places demands on echocardiographers that differ from those of the routine evaluation of patients with native or prosthetic valvular disease. Consequently, the European Association of Echocardiography in partnership with the American Society of Echocardiography has developed the recommendations for the use of echocardiography in new transcatheter interventions for valvular heart disease. It is intended that this document will serve as a reference for echocardiographers participating in any or all stages of new transcatheter treatments for patients with valvular heart disease.
