Background: Aortic atherosclerosis and coronary artery disease (CAD) are closely linked. Early detection of aortic atherosclerosis with the adoption of appropriate preventive measures may therefore help to reduce mortality and morbidity related to CAD. Arterial remodeling, by which the wall adapts to physiological or pathological insults by a change in vessel size, is being increasingly recognized as an important aspect of atherosclerosis. In this prospective longitudinal study we used cardiovascular magnetic resonance (CMR) to detect aortic plaque and to study aortic wall remodeling in asymptomatic subjects.
Methods: We recruited 175 healthy volunteers (49 years, 110 men) and documented their cardiovascular risk profile. Each subject underwent echocardiogram (ECG)-gated T1-weighted spin-echo imaging of the infrarenal abdominal aorta at baseline and after 2 years.
Findings: Of the 175 subjects who volunteered at baseline, CMR was successful in 174 (99%), with one (0.6%) failure due to claustrophobia. At 2 years, follow-up scanning was performed in 169 subjects (97%). Infrarenal aortic plaque was identified at baseline in nine (5.2%) subjects. This was reconfirmed in all nine (100%) cases at 2-year follow-up. No new cases of infrarenal plaque were identified at follow-up. The signal characteristics of the plaque on the subtracted images of the Dixon method indicate that all plaques were fibrous. In the nine subjects with infrarenal plaque, the total plaque burden increased as assessed by the total wall volume (561 to 677 mm3, p = 0.0063). The total vessel volume also increased (1737 to 1835 mm3, p = 0.031) but there was no change in the total luminal volume (1175 to 1157 mm3, p = 0.29).
Conclusions: Cardiovascular magnetic resonance detects subclinical aortic atherosclerosis, can follow plaque burden over time, and confirms the presence of Glagov remodeling with preservation of the lumen despite progression of plaque. Cardiovascular magnetic resonance is well suited for the longitudinal follow-up of the general population with atherosclerosis, may help in the understanding of the natural history of atherosclerosis, and in particular may help determine factors to retard disease progression at an early stage.
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http://dx.doi.org/10.1081/jcmr-120030576 | DOI Listing |
BMC Cardiovasc Disord
January 2025
Department of Cardiology, The Affiliated Hospital of Xuzhou Medical University, 99#, Huaihai West Road, Xuzhou, 221002, China.
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Methods: This was a single-centre, retrospective study.
Clin Neuroradiol
January 2025
Neurosciences Research Center (NSRC), Tabriz University of Medical Sciences, Tabriz, Iran.
Background: Hypertension (HTN) is a prevalent cardiovascular condition associated with cognitive impairments, including memory deficits and attention lapses. Understanding the neural mechanisms underlying HTN-related cognitive dysfunction is crucial for optimizing treatment strategies.
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J Vis Exp
January 2025
Department of Bioengineering, Imperial College London; The Francis Crick Institute;
Mechanical forces continuously provide feedback to heart valve morphogenetic programs. In zebrafish, cardiac valve development relies on heart contraction and physical stimuli generated by the beating heart. Intracardiac hemodynamics, driven by blood flow, emerge as fundamental information shaping the development of the embryonic heart.
View Article and Find Full Text PDFJ Magn Reson Imaging
January 2025
Clinical Physiology, Department of Clinical Sciences Lund, Lund University, Skåne University Hospital, Lund, Sweden.
Background: Real-time (RT) phase contrast (PC) flow MRI can potentially be used to measure blood flow in arrhythmic patients. Undersampled RT PC has been combined with online compressed sensing (CS) reconstruction (CS RT) enabling clinical use. However, CS RT flow has not been validated in a clinical setting.
View Article and Find Full Text PDFZh Nevrol Psikhiatr Im S S Korsakova
January 2025
Pirogov Russian National Research Medical University (Pirogov University), Moscow, Russia.
Hemorrhagic transformation (HT) is a serious complication that worsens outcomes and increases mortality in patients with ischemic stroke (IS). HT can occur both spontaneously and after reperfusion therapy. Severe ischemic injury in IS is not sufficient in itself to cause HT; one of the key elements in its development is reperfusion.
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