The OCT-NIRF imaging with a clinical dose of ICG was feasible to accurately assess plaque inflammation and DES-related inflammation in a beating coronary artery. This highly translatable dual-modal molecular-structural imaging strategy could be relevant for clinical intracoronary estimation of high-risk plaques and DES biology.

Comprehensive imaging of both the structural and biochemical characteristics of atherosclerotic plaque is essential for the diagnosis and study of coronary artery disease because both a plaque’s morphology and its biochemical composition affect the level of risk it poses. Optical coherence tomography (OCT) and fluorescence lifetime imaging (FLIm) are promising optical imaging methods for characterizing coronary artery plaques morphologically and biochemically, respectively. In this study, we present a hybrid intravascular imaging device, including a custom-built OCT/FLIm system, a hybrid optical rotary joint, and an imaging catheter, to visualize the structure and biochemical composition of the plaque in an atherosclerotic rabbit artery in vivo. Especially, the autofluorescence lifetime of the endogenous tissue molecules can be used to characterize the biochemical composition; thus no exogenous contrast agent is required. Also, the physical properties of the imaging catheter and the imaging procedures are similar to those already used clinically, facilitating rapid translation into clinical use. This new intravascular imaging catheter can open up new opportunities for clinicians and researchers to investigate and diagnose coronary artery disease by simultaneously providing tissue microstructure and biochemical composition data in vivo without the use of exogenous contrast agent.

The phase-segregated NiPx@FePyOz core@shell NPs act as a colloidally stable, ready-to-use, and excellent OER active transition metal phosphide-based catalyst.

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Rationale: Inflammation plays a pivotal role in the pathogenesis of the acute coronary syndrome. Detecting plaques with high inflammatory activity and specifically treating those lesions can be crucial to prevent life-threatening cardiovascular events. Methods: Here, we developed a macrophage mannose receptor (MMR)-targeted theranostic nanodrug (mannose-polyethylene glycol-glycol chitosan-deoxycholic acid-cyanine 7-lobeglitazone; MMR-Lobe-Cy) designed to identify inflammatory activity as well as to deliver peroxisome proliferator-activated gamma (PPARγ) agonist, lobeglitazone, specifically to high-risk plaques based on the high mannose receptor specificity. The MMR-Lobe-Cy was intravenously injected into balloon-injured atheromatous rabbits and serial in vivo optical coherence tomography (OCT)-near-infrared fluorescence (NIRF) structural-molecular imaging was performed. Results: One week after MMR-Lobe-Cy administration, the inflammatory NIRF signals in the plaques notably decreased compared to the baseline whereas the signals in saline controls even increased over time. In accordance with in vivo imaging findings, ex vivo NIRF signals on fluorescence reflectance imaging (FRI) and plaque inflammation by immunostainings significantly decreased compared to oral lobeglitazone group or saline controls. The anti-inflammatory effect of MMR-Lobe-Cy was mediated by inhibition of TLR4/NF-κB pathway. Furthermore, acute resolution of inflammation altered the inflamed plaque into a stable phenotype with less macrophages and collagen-rich matrix. Conclusion: Macrophage targeted PPARγ activator labeled with NIRF rapidly stabilized the inflamed plaques in coronary sized artery, which could be quantitatively assessed using intravascular OCT-NIRF imaging. This novel theranostic approach provides a promising theranostic strategy for high-risk coronary plaques.

BackgroundSubclinical left ventricular (LV) diastolic dysfunction in type 2 diabetes (T2D) is a common finding and represents an early sign of diabetic cardiomyopathy. However, the relationship between LV diastolic dysfunction and the incident T2D has not been previously studied.MethodsA total of 1817 non-diabetic participants (mean age, 54 years; 48% men) from the Korean Genome and Epidemiology Study who were free of cardiovascular disease were studied. LV structure and function were assessed by conventional echocardiography and tissue Doppler imaging. Subclinical LV diastolic dysfunction was defined using age-specific cutoff limits for early diastolic (Em) velocity, mitral E/Em ratio, and left atrial volume index.ResultsDuring the 6-year follow-up period, 273 participants (15%) developed T2D. Participants with incident T2D had greater LV mass index (86.7 ± 16.4 vs. 91.2 ± 17.0 g/m2), worse diastolic function, reflected by lower Em velocity (7.67 ± 1.80 vs. 7.47 ± 1.70) and higher E/Em ratio (9.19 ± 2.55 vs. 10.23 ± 3.00), and higher prevalence of LV diastolic dysfunction (34.6 vs. 54.2%), compared with those who did not develop T2D (all P < 0.001). In a multivariate logistic regression model, lower Em velocity (odd ratio [OR], 0.867; 95% confidence interval [CI] 0.786–0.957) and the presence of LV diastolic dysfunction (OR, 1.617; 95% CI 1.191–2.196) were associated with the development of T2D, after adjusting for potential confounding factors.ConclusionsIn a community-based cohort, the presence of subclinical LV diastolic dysfunction was a predictor of the progression to T2D. These data suggest that the echocardiographic assessment of LV diastolic function may be helpful in identifying non-diabetic subjects at risk of incident T2D.

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Background Apart from nondippers’ impact on cardiovascular events, the prevalence of isolated nocturnal hypertension (INH) and its consequences on both the heart and brain were not clearly investigated in the general population. Methods and Results The participants underwent ambulatory blood pressure monitoring evaluations for arterial stiffness, echocardiography, and brain magnetic resonance imaging. They were grouped into normotension, INH, and overt diurnal hypertension, based on ambulatory blood pressure monitoring and history of antihypertensive treatment. White matter hyperintensity, arterial stiffness, and echocardiographic parameters were compared. Of the 1734 participants, there were 475 (27.4%) subjects with normotension, 314 with INH (18.1%), and 945 with overt diurnal hypertension (54.5%). Prevalence of INH was not different between sex or age. Of INH, 71.3% (n=224) was caused by elevated diastolic blood pressure. After multivariable adjustment, INH showed higher pulse wave velocity ( P <0.001) and central systolic blood pressure ( P <0.001), left ventricular mass index ( P =0.026), and worse left ventricular diastolic function (early diastolic mitral annular velocity) ( P <0.001) than normotension. Mean white matter hyperintensity scores of INH were not different from normotension ( P =0.321), but the odds for white matter hyperintensity presence were higher in INH than normotension (odds ratio, 1.504 [95% CI, 1.097–2.062]; P =0.011). Conclusions INH was common in the general population and associated with increased arterial stiffness, left ventricular hypertrophy, and diastolic dysfunction. White matter hyperintensity was more likely to be present in the INH group than in the normotension group. The use of ambulatory blood pressure monitoring should be encouraged to identify masked INH and prevent the occurrence of cardiovascular events.