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Diagnostics
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Cardiovascular Imaging
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Cardiovascular Imaging

A special issue of Diagnostics (ISSN 2075-4418). This special issue belongs to the section "Medical Imaging and Theranostics".

Deadline for manuscript submissions: 31 March 2025 | Viewed by 1657

Special Issue Editors

Prof. Dr. Lars C. Gormsen

E-Mail Website
Guest Editor
Department of Nuclear Medicine & PET Center, Aarhus University Hospital, Palle Juul-Jensens Boulevard 165, DK 8200 Aarhus, Denmark
Interests: PET; nuclear cardiology; inflammatory diseases
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Riemer H.J.A. Slart

E-Mail Website
Guest Editor
Medical Imaging Center, Department of Nuclear Medicine & Molecular Imaging, University Medical Center Groningen, University of Groningen, P.O. Box 30.001, 9700 RB Groningen, The Netherlands
Interests: cardiovascular diseases; PET/CT; SPECT/CT; (hybrid) imaging; multimodality imaging
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue aims to present the role of noninvasive imaging modalities in the diagnosis and imaged-based therapeutic management of cardiovascular diseases, with particular attention being paid not only to the standard of care but also to the relevant developments for the near future. We encourage authors to submit both preclinical and clinical studies in this field. Clinical studies may include systematic reviews/meta-analyses, retrospective studies, and prospective studies emphasizing the role of and need for imaging techniques in primary diagnosis, treatment response, and disease relapse.

Prof. Dr. Lars C. Gormsen
Prof. Dr. Riemer H.J.A. Slart
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Diagnostics is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • cardiovascular imaging
  • noninvasive imaging
  • diagnosis
  • prognosis
  • marker

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Further information on MDPI's Special Issue polices can be found here.

Published Papers (2 papers)

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3 pages, 1811 KiB  
Interesting Images
Cardiac Hemangioma Mimicking Infective Endocarditis
by Ching-Mao Yang and Yu-Ning Hu
Diagnostics 2024, 14(19), 2109; https://doi.org/10.3390/diagnostics14192109 - 24 Sep 2024
Viewed by 601
Abstract
Cardiac hemangiomas are rare and often misdiagnosed due to their nonspecific clinical presentations. We report a case of a 70-year-old man presenting with chills and cold sweats, initially suspected of having infective endocarditis based on echocardiographic findings of a mobile mass on the [...] Read more.
Cardiac hemangiomas are rare and often misdiagnosed due to their nonspecific clinical presentations. We report a case of a 70-year-old man presenting with chills and cold sweats, initially suspected of having infective endocarditis based on echocardiographic findings of a mobile mass on the mitral valve. Laboratory results showed leukocytosis and elevated C-reactive protein, but blood cultures were negative. Transesophageal echocardiography later revealed a well-defined mass with characteristics suggestive of a tumor. Surgical excision confirmed the diagnosis of hemangioma. Postoperative recovery was uneventful, with no mitral regurgitation. This case highlights the importance of considering cardiac tumors in the differential diagnosis of intracardiac masses. Full article
(This article belongs to the Special Issue Cardiovascular Imaging)
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Figure 1

Figure 1
<p>(<b>A</b>) Four-chamber transthoracic echocardiography view showing a mobile mass (white arrow) on the posterior leaflet of the mitral valve. (<b>B</b>) Parasternal long-axis transthoracic echocardiography view showing a mobile mass (white arrow) on the posterior leaflet of the mitral valve (<a href="#app1-diagnostics-14-02109" class="html-app">Video S1</a>). (<b>C</b>) Transesophageal echocardiography showing a 1.9 × 1.4 cm polypoid mass with a pedicle attached to the annulus near the P2 segment. The mass partially protruded into the left ventricle during diastole (<a href="#app1-diagnostics-14-02109" class="html-app">Video S2</a>). (<b>D</b>) Transesophageal echocardiography showing a polypoid mass with a pedicle attached to the annulus near the P2 segment. Color Doppler indicated mild mitral regurgitation. Grading of the mitral regurgitation may have been underestimated due to the mitral mass obstacle (<a href="#app1-diagnostics-14-02109" class="html-app">Video S3</a>). Preoperative coronary artery angiography showed no obvious feeding arteries (<a href="#app1-diagnostics-14-02109" class="html-app">Videos S4–S6</a>).</p> Full article ">Figure 2
<p>(<b>A</b>) A round 1.5 × 1.5 × 1.5 cm tumor at the mitral annulus between P1 and P2. (<b>B</b>) A tumor on the posterior mitral annulus connected to underlying mitral annulus calcification. (<b>C</b>) Pathology showed hemangioma with dense lymphocyte infiltration (5× magnification). (<b>D</b>) CD34 stain revealed a capillary–cavernous hemangioma with dense lymphocyte infiltration (10× magnification).</p> Full article ">
5 pages, 2333 KiB  
Interesting Images
The Aortic Prosthesis and Aortic Valve Bioprosthesis Trombosis as a Late Complication in Patients after the Bentall Procedure Followed by a Valve-in-Valve Transcatheter Aortic Valve Implantation
by Paweł Muszyński, Oliwia Grunwald, Maciej Południewski, Paweł Kralisz, Szymon Kocańda, Tomasz Hirnle, Sławomir Dobrzycki and Marcin Kożuch
Diagnostics 2024, 14(18), 2070; https://doi.org/10.3390/diagnostics14182070 - 19 Sep 2024
Viewed by 802
Abstract
Background: Valve-in-Valve (ViV) transcatheter aortic valve implantation (TAVI) has emerged as a viable therapeutic option for structural valve degeneration following surgical aortic valve replacement (SAVR) or prior TAVI. However, the understanding of long-term complications and their management remains limited. Case presentation: We present [...] Read more.
Background: Valve-in-Valve (ViV) transcatheter aortic valve implantation (TAVI) has emerged as a viable therapeutic option for structural valve degeneration following surgical aortic valve replacement (SAVR) or prior TAVI. However, the understanding of long-term complications and their management remains limited. Case presentation: We present the case of a 69-year-old male with a history of ViV-TAVI, who presented with symptoms of non-ST elevation myocardial infarction (NSTEMI) and transient ischemic attack (TIA). Computed tomography (CT) revealed thrombosis of the ascending aortic graft and aortic valve prosthesis. Transthoracic echocardiography (TTE) further confirmed new valve dysfunction, indicated by an increase in the aortic valve mean gradient. Treatment with low-molecular-weight heparin (LMWH) resulted in partial thrombus resolution. The multidisciplinary Heart Team opted against coronary angiography and recommended the long-term administration of vitamin K antagonists (VKAs). Follow-up CT showed the complete resolution of the thrombus. Conclusions: Thrombosis of the aortic graft and aortic valve following ViV-TAVI may be attributed to alterations in blood flow or mechanical manipulations during the TAVI procedure, yet it can be effectively managed with VKA therapy. CT is a valuable tool in coronary assessment in patients with NSTEMI and aortic valve and/or aortic graft thrombosis. Full article
(This article belongs to the Special Issue Cardiovascular Imaging)
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Figure 1

Figure 1
<p>A 69-year-old male complaining of recurring chest pain, episodes of syncope and visual distortion was admitted to the hospital. His past medical history included the replacement of the ascending aorta with surgical aortic valve replacement (SAVR) in 2011 due to aortic aneurysm and aortic stenosis (Bentall procedure). He underwent transcatheter aortic valve implantation (TAVI) in 2021 due to the degeneration of aortic valve bioprosthesis, using a 26 mm balloon-expandable Sapien 3 Ultra (Edwards Lifesciences, Irvine, CA, USA). The treatment course after TAVI involved longitudinal single antiplatelet therapy (SAPT)—aspirin. In addition, he reported reduced exercise tolerance since the TAVI procedure. The coronarography in 2011 and angio-CT in 2021 excluded the significant coronary artery disease before operations. The angio-CT, including the aorta and head, at the current hospitalization found the thrombosis of the ascending aorta graft causing 80% stenosis (<b>A</b>–<b>C</b>; black arrow). Furthermore, due to the resolution of the neurological dysfunction, the patient was diagnosed with a transient ischemic attack (TIA). The transthoracic echocardiography revealed an increase in gradient through aortic valve bioprosthesis—a mean gradient of 24 mm Hg. The low-molecular-weight heparin (LMWH) in therapeutic dose was initiated. Despite the increase in cardiac enzymes, the chest pain and the diagnosis of non-ST elevation myocardial infarction (NSTEMI), the coronarography was not performed due to the risk involving the dislocation of the thrombi. After three days, the control CT displayed a significant reduction in the thrombus. The patient consulted with the Heart Team and was transferred to a higher reference clinical hospital with the availability of the cardiac surgery department.</p> Full article ">Figure 2
<p>After the consultation with the cardiac radiologist, the third ECG-gated cardiac CT was performed on the eighth day after the initial CT to access both the aorta and coronary arteries. To increase the quality of the image, an additional beta-blocker and nitroglycerin were administered before examination. The CT revealed aortic valve prosthesis thrombosis (<b>A</b>; red arrow) and a reduction in aortic thrombosis (<b>B</b>; orange arrow). The previous thrombus site was localized to originate within the ascending aorta graft, which was covered by soft tissue that resembled an ulcer. The probable dissection of the neointima along the prosthesis was the suspected cause of the initial aortic thrombosis (<b>C</b>,<b>D</b>; black arrow).</p> Full article ">Figure 3
<p>The CT discluded significant coronary artery stenosis (Cx—circumflex artery, RCA—right coronary artery, LAD—left anterior descending artery)<b>.</b> The myocardial infarction was treated conservatively with anticoagulation due to the presence of aortic graft and valve thrombosis, and it led to the resolution of the chest pain. The clinically insignificant lesions in the coronary arteries on CT were suggestive of the fact that NSTEMI could be caused by the occlusion of the ostium of the arteries by the aortic valve thrombus.</p> Full article ">Figure 4
<p>The transthoracic echocardiography showed a reduction in the gradients through the aortic valve prosthesis with parameters similar to that after the TAVI (on left: post-TAVI; on right: post-LMWH treatment). According to the 2021 ESC/EACTS Guidelines, in patients after TAVI, lifelong SAPT is recommended in the lack of indications for oral anticoagulants (OACs) [<a href="#B1-diagnostics-14-02070" class="html-bibr">1</a>]. However, despite similar recommendations for aspirin, the 2020 ACC/AHA Guidelines suggest that in patients with a low bleeding risk, it is worth acknowledging the antithrombotic prophylaxis with DAPT or VKA [<a href="#B2-diagnostics-14-02070" class="html-bibr">2</a>]. The direct-acting oral anticoagulants (DOACs) were not found to be superior to the administering antiplatelet or VKA, and in patients without indications for OAC, were linked to a higher incidence of all-cause mortality [<a href="#B3-diagnostics-14-02070" class="html-bibr">3</a>,<a href="#B4-diagnostics-14-02070" class="html-bibr">4</a>,<a href="#B5-diagnostics-14-02070" class="html-bibr">5</a>]. The 2021 ESC/EACTS and 2020 ACC/AHA Guidelines for managing valvular heart disease indicate that anticoagulation using VKAs or UFH is a first-line therapy for bioprosthetic valve thrombosis. Such an approach is highly effective in the normalization of valve function in 85% of the patients [<a href="#B6-diagnostics-14-02070" class="html-bibr">6</a>].</p> Full article ">Figure 5
<p>The transesophageal echocardiography failed to assess the aortic valve due to the artefacts. However, it confirmed the suspicion of the visible ruptured neointima within the aorta on the CT (<a href="#app1-diagnostics-14-02070" class="html-app">Video S1</a>—red circle). The patient again consulted with the Heart Team, and the decision about a conservative approach and administration of oral anticoagulation with vitamin K antagonists (VKAs) was sustained. At the 3-month follow-up, the patient was free from angina and syncope, and the control chest CT showed no sign of thrombus presence in the aortic region. The anatomical changes, such as the dimensions and shape of the aortic root, which occurred during TAVI, may have caused the dynamic switch in blood flow through the bioprosthetic valve, thus causing aortic remodelling. This contributes to the fact that the blood stagnates in the prosthetic sinuses, which complements Virchow’s triad and is attributed to thromboembolic events [<a href="#B7-diagnostics-14-02070" class="html-bibr">7</a>]. Furthermore, the ongoing structural bioprosthesis degeneration leading to fibrosis and calcification is often started by leaflet thickening and valve thrombosis [<a href="#B8-diagnostics-14-02070" class="html-bibr">8</a>]. The atherosclerotic plaque in the ascending aorta, or dissection of the neointima along the prosthesis, could also contribute to the thrombotic event. Aortic dissection was reported to be a rare TAVI procedure complication, occurring almost entirely as an acute condition. Regardless, there have been no previous reports of dissection of the neointima in the aortic prosthesis after ViV TAVI [<a href="#B9-diagnostics-14-02070" class="html-bibr">9</a>]. In our case, we suspect that a change in flow through the aorta or mechanical damage during the TAVI could have led to the dissection of the neointima and aortic thrombosis. Additionally, myocardial infarction in patients after TAVI can be the result of co-existing leaflet thrombosis and can cause difficulty in performing PCI procedures due to impaired coronary access [<a href="#B10-diagnostics-14-02070" class="html-bibr">10</a>]. In our case, the patient’s symptoms were most likely associated with the clinical presentation of ViV thrombosis and severe aortic graft thrombosis, in spite of the administration of SAPT—aspirin. The initial treatment with LMWH converted into VKA oral anticoagulants was sufficient to promote thrombus resolution and prevent recurrence at 3-month follow-up.</p> Full article ">
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