Circulation: Cardiovascular Imaging最新文献

Percutaneous coronary intervention outcomes rely heavily on accurate lesion assessment and procedural planning. Invasive tools, such as fractional flow reserve, nonhyperemic pressure ratios, intravascular ultrasound, and optical coherence tomography, provide essential physiological and anatomic insights but are resource-intensive, prolong procedures, and increase contrast and radiation exposure. Coronary computed tomography (CT) angiography has emerged as a noninvasive modality with high diagnostic accuracy for coronary artery disease, capable of detailing plaque composition, lesion length, and vessel geometry. With the integration of CT-derived fractional flow reserve and CT myocardial perfusion imaging, coronary CT angiography now offers both anatomic and functional evaluation, bridging diagnostic and interventional decision-making. Despite guideline endorsement for coronary artery disease diagnosis, its role in guiding percutaneous coronary intervention strategies remains underutilized and absent from revascularization recommendations. This review outlines a practical, step-by-step framework for integrating coronary CT angiography into contemporary percutaneous coronary intervention planning, covering acquisition protocols, software platforms, lesion assessment, and stent strategy optimization. It also explores emerging intraprocedural applications, including fusion imaging, augmented and virtual reality, and holographic visualization. By synthesizing current evidence and identifying gaps, this review positions coronary CT angiography as a promising adjunct in precision-based percutaneous coronary intervention.

Background: Fibrosis, with accumulation of type I collagen, is a hallmark of postthrombotic change after deep vein thrombosis (DVT), but tools for its direct detection are lacking. Here, we investigate whether molecular magnetic resonance imaging (MRI) using a collagen-specific gadolinium-based probe can detect and measure changes in collagen during thrombus resolution and in response to treatment in a mouse model of DVT.

Methods: Venous thrombus was induced in the inferior vena cava of BALB/c mice (n=45), and MRI was performed at day 2 (n=3) and weeks 1, 2, and 3 post-surgery using the collagen-specific probe, EP-3533 (10 μmol/kg; n=11-13/group). A subgroup of mice with DVT (n=7) was treated with pravastatin in drinking water (40 mg/kg per day) for 3 weeks post-DVT. Pre- and post-EP-3533 MRI scans were performed. Magnetic resonance venography was used to measure thrombus volume. Inversion recovery T1-weighted images and T1 maps, pre- and post-contrast, were used to calculate the percent change (%) in Δ contrast-to-noise ratio, Δ signal-to-noise ratio, and Δ relaxation rate. Tissues were used for ex vivo analyses.

Results: EP-3533 uptake increased during thrombus organization and resolution, resulting in MRI signal enhancement, with % Δ contrast-to-noise ratio, % Δ signal-to-noise ratio, and % Δ relaxation rate peaking at 3 weeks after DVT. MRI measurements of collagen accumulation quantified as an increase in % Δ contrast-to-noise ratio (ρ=0.89; P=0.012) and % Δ relaxation rate (ρ=0.80; P=0.029) correlated positively with collagen histology. The spatial distribution of gadolinium in the tissue colocalized with collagen type I based on immunohistochemistry (ρ=0.95; P<0.001). Statin treatment decreased both collagen accumulation and vein wall thickness, without affecting thrombus size.

Conclusions: Molecular MRI using a collagen-targeting probe made collagenous thrombus visible on MRI and detected changes in collagen content during thrombus resolution.

Background: Chronic aortic regurgitation (AR) is associated with significant cardiac remodeling, but the prevalence and prognostic impact of extravalvular cardiac damage remain unexplored.

Methods: Adults with moderate or greater chronic AR identified on echocardiogram between January 2008 and July 2024 were included. Exclusion criteria were acute AR, hypertrophic and infiltrative cardiomyopathies, prior cardiac surgery, and valve stenosis. Cardiac damage was classified into hierarchical stages: no cardiac damage (stage 0), left ventricular damage (stage 1), moderate or greater mitral regurgitation or left atrial enlargement or atrial fibrillation (stage 2), pulmonary hypertension or moderate or greater tricuspid regurgitation (stage 3), and significant right ventricular dysfunction (stage 4). The primary outcome was the association between cardiac damage stages and all-cause mortality under medical surveillance.

Results: Of 4026 patients (median age, 72 [61-80] years), 78% had moderate AR, 11% had moderate-severe, and 11% had severe AR. Cardiac damage was present in 87% of patients: 14% in stage 1, 53% in stage 2, 18% in stage 3, and 2% in stage 4. In a multivariable model, including age, sex, AR severity, and Charlson Comorbidity Index, cardiac damage stages were associated with mortality. Adjusted hazard ratios were 1.42 (95% CI, 1.04-1.96) for stage 1, 1.58 (95% CI, 1.21-2.06) for stage 2, 2.78 (95% CI, 2.10-3.67) for stage 3, and 5.34 (95% CI, 3.67-7.76) for stage 4. Adding cardiac damage staging to multivariable models improved predictive accuracy for mortality, increasing the concordance statistics from 0.73 (95% CI, 0.71-0.75) to 0.76 (95% CI, 0.74-0.77).

Conclusions: Cardiac damage is present in nearly 90% of patients with moderate or greater AR and is associated with increased mortality, highlighting the need for a more comprehensive evaluation of cardiac structure and function beyond the aortic valve and left ventricle.

Background: Guidelines recommend 3-hour cardiac amyloid radionuclide imaging (CARI) for transthyretin amyloid cardiomyopathy. Citing rapid blood clearance of ^99mTc-hydroxymethylene-diphosphonate (HMDP) and efficient laboratory throughput, 1-hour imaging is increasingly practiced despite limited supporting evidence. We sought to compare diagnostic performance and interpreter experience of 1-hour versus 3-hour HMDP-CARI.

Methods: Consecutive patients with suspected transthyretin amyloid cardiomyopathy (n=114) underwent both 1-hour and 3-hour HMDP single photon emission computed tomography (CT)/CT. Two cardiologist-radiologist reader teams, blinded to imaging timepoint (1 versus 3 hours), assessed overall interpretation, single photon emission CT-based Perugini grade, interpretation difficulty, interpreter confidence, and need for CT-fused images for anatomic localization. Discordant, equivocal, and difficult cases were arbitrated by a third tie-breaking team. The myocardial-to-blood-pool radiotracer uptake ratio (3-dimensional Score) was measured as a surrogate of contrast resolution.

Results: Interinterpreter agreement was high at both time points (κ≥0.81), with more cases requiring arbitration at 3 hours versus 1 hour (22% versus 13%; P=0.049). Overall interpretation and Perugini grades were concordant between time points in 111/114 (97%) and 106/114 (93%) patients, respectively. Three patients (3%) were negative at 1 hour but equivocal at 3 hours, all of which were clinically ruled out for transthyretin amyloid cardiomyopathy. Interpreter confidence was comparable at both timepoints (97% versus 95%; P=0.317). Compared with 3-hour imaging, contrast resolution was inferior (lower 3-dimensional score, P<0.001) and CT fusion was more frequently needed (57% versus 31%, P<0.001) at 1-hour imaging.

Conclusions: In a prospective, blinded comparison of 1-hour versus 3-hour HMDP-CARI, diagnostic performance and interpreter experience were similar, with readers requesting CT fusion more frequently at 1 hour to optimize myocardial-to-blood pool discrimination.

Background: A formal prognostic staging system in wild-type transthyretin amyloid cardiomyopathy (ATTRwt-CM), based on echocardiographic imaging, is lacking. We evaluated the prognostic performance of global longitudinal strain (GLS) staging in a large cohort of patients with ATTRwt-CM, including under tafamidis treatment and relative to National Amyloidosis Center (NAC) biomarker staging.

Methods: A multicentric, international ATTRwt-CM patient cohort with baseline GLS (distribution quartiles), evaluated by echocardiography, was studied, related to all-cause mortality.

Results: The study comprised 816 patients with ATTRwt-CM, median age of 81.5 years, 83% males, and 72% tafamidis initiated. During a 2.2-year median follow-up, 29.7% of patients died. GLS worsened with increasing NAC disease stage (I: -14.3%, II: -11.6%, III: -11.4%; P<0.001). Median survival per baseline GLS quartile stage 1 (<-15.8%), 2 (-15.8 to -12.9%), 3 (-12.8 to -10.0%), and 4 (GLS >-10.0%) was not met, 6.7, 4.6, and 3.4 years, respectively (P<0.001). The median GLS -12.8% cutoff predicted 1-year mortality with 74% sensitivity, 52% specificity (area under the curve, 0.73 [95% CI, 0.66-0.80]; P<0.001). GLS was the only independent echocardiographic and strong mortality predictor, independent of other predictors, including age, New York Heart Association class symptoms, NAC stage, and tafamidis treatment (hazard ratio, 1.08 [95% CI, 1.04-1.12]; P<0.001), also when restricted to 591 tafamidis-treated subjects (hazard ratio, 1.15 [95% CI, 1.08-1.22]; P<0.001). Baseline GLS -12.8% cutoff value provided further prognostic discriminative ability for mortality within each NAC disease stage stratum (all P<0.050). Likelihood ratio test indicated incremental prognostic value of GLS (staging) over baseline NAC staging (P<0.001).

Conclusions: GLS is a strong, independent mortality predictor in ATTRwt-CM, irrespective of tafamidis treatment, that may be an adjunct or complementary to biomarker staging.