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. The anti-VCAM-1 nanobody (Nb) (cAbVCAM-1–5) was radiolabelled with Fluorine-18 (¹⁸F), 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 [¹⁸F]-FB-cAbVCAM-1–5 or ¹⁸F-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 [¹⁸F]-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 [¹⁸F]-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 r² = 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). The [¹⁸F]-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.

Valvular heart disease (VHD), inducing valvular regurgitation, has been described in carcinoid heart disease and recently in Parkinson’s patients treated with pergolide. The aim of this study was to develop an in vivo model of drug-induced valvulopathy with pergolide in rats. Thirty male Wistar rats were given daily injections of either pergolide (0.5 mg/kg intraperitoneally) (n = 8), serotonin (20 mg/kg subcutaneously) (n = 8), or the vehicle only (n = 14) for 5 months. At 20 weeks, echocardiography demonstrated the presence of aortic regurgitation (AR) and/or mitral regurgitation (MR) in serotonin (86% AR, P = 0.0001; 57% MR, P = 0.006) and in pergolide animals (67% AR, P = 0.003; 67% MR, P = 0.003) compared with none in placebo. Pulmonary regurgitation (PR) and tricuspid regurgitation (TR) were found in the serotonin (71% PR, P = 0.19; 100% TR, P = 0.06 vs. placebo), pergolide (100% PR, P = 0.014; 83% TR, P = 0.35 vs. placebo), and placebo groups (36% PR; 57% TR). Tricuspid regurgitant area ratio (jet/atrium), however, was more severe in the serotonin [median 26.5 (range 17–42)%; P = 0.02] and pergolide animals [32 (17–39) %; P = 0.03] compared with placebo [12.5 (5–33)%]. We found a good correlation between valvular regurgitation and histologically assessed valvular thickness. Histological examination revealed the presence of diffusely thickened and myxoid aortic, mitral, and tricuspid valves in serotonin and pergolide animals as seen in VHD. We demonstrated, for the first time, that long-term pergolide administration led to VHD in rats. This small animal model will permit further in vivo investigation of drug-induced valvulopathies.

Atrial fibrillation (AF) ablation is increasingly being performed in electrophysiology laboratories. Pericardial effusion (PE) is certainly one of the most frequently observed complications during AF ablation. The aim of our study was to investigate the incidence and outcome of PE following cryothermal energy balloon ablation (CBA) in comparison with conventional circumferential pulmonary vein isolation with a focal radiofrequency (RF) catheter. A total of 133 consecutive patients (105 males) with paroxysmal AF were included in this study. Forty-six patients (36 males) underwent CBA (Arctic Front, Medtronic, USA) and 87 (69 males) point-by-point RF ablation guided by electroanatomical mapping (Carto, Biosense Webster, Diamond Bar, CA, USA). Ablation was performed under general anaesthesia with both techniques. All patients underwent a 2D transthoracic echocardiogram within 24 h before and after the procedure as routinely performed in our centre. Pericardial effusion was detected in 19 (14.2%) of 133 patients. Sixteen patients presented mild effusion, one moderate effusion, and two pericardial tamponades. There was no significant difference in the incidence of PE between the cryoballoon and the RF group (11 vs. 16%). A longer procedural time, coronary artery disease, and arterial hypertension were found to be independent predictors of PE during AF ablation. Pericardial effusion occurred in a similar proportion following CBA and RF ablation for AF. Pericardial effusion was mostly mild and asymptomatic, with benign clinical outcome not requiring additional hospitalization days.

Drug-induced valvular heart disease (DIVHD) was first described in the 1960s. Initially, associations with ergot derivatives used for migraine prevention, or with anorectic drugs, were described. Drugs used for the treatment of Parkinson’s disease and endocrine diseases, like hyperprolactinemia, may also induce VHD. More recently, the use of 3,4-methylendioxymetamphetamine (MDMA, ‘Ecstasy’) and benfluorexhave been found to be associated with DIVHD. Although some of these drugs were withdrawn from the market, several cases of patients requiring valve surgery even years after the cessation of therapy have been reported. DIVHD is not infrequent, may be severe, and has been described in association with several drugs. Even after drug cessation, long-term implications of this type of VHD may persist. The present review underlines the need for a careful evaluation of the associated clinical and echocardiographic risk factors to allow early recognition so as not to delay appropriate management.