JACC. Cardiovascular imaging最新文献

Background: Hemodynamically obstructive coronary plaques may contain more vulnerable plaque characteristics than nonobstructive lesions.

Objectives: The authors aimed to assess whether pressure-wire-based physiologic indices in nonculprit lesions are associated with vulnerable plaque characteristics.

Methods: In the PROSPECT II study, patients with recent myocardial infarction underwent coronary angiography and culprit lesion percutaneous coronary intervention plus combined near-infrared spectroscopy and intravascular ultrasound assessment of all 3 coronary arteries. Instantaneous wave-free ratio (iFR) or fractional flow reserve (FFR) measurements were performed in intermediate lesions with angiographic stenosis >40%.

Results: Among 898 patients, 319 angiographically intermediate lesions in 275 patients had matched intravascular ultrasound/near-infrared spectroscopy and FFR/iFR measurements; 96 (30.1%) lesions were physiologically significant (FFR ≤0.80 or iFR ≤0.89) and 223 (69.9%) were not. Physiologically significant lesions, compared with those that were not, more likely had a minimal lumen area ≤4.0 mm² (96.9% vs 83.9%), plaque burden ≥70% (92.7% vs 71.3%) and maximum lipid core burden index in any 4 mm segment of the lesion ≥324.7 (57.0% vs 45.4%). By multivariable analysis, lesion location in the left anterior descending artery, small minimal lumen area, and larger plaque burden were independently associated with physiologic significance, whereas maximum lipid core burden index in any 4 mm segment of the lesion was not.

Conclusions: In patients with recent myocardial infarction, angiographically intermediate but physiologically significant coronary lesions were more likely to have high-risk vulnerable plaque features compared with nonphysiologically significant stenoses. However, coronary lesions without physiological significance also had a moderate-to-high prevalence of high-risk plaque characteristics, which may explain the residual risk associated with conservative noninterventional management of these lesions. (Providing Regional Observations to Study Predictors of Events in the Coronary Tree II [PROSPECT II]; NCT02171065).

Background: The 2018 ACC (American College of Cardiology)/AHA (American Heart Association) and 2021 ESC (European Society of Cardiology)/EAS (European Atherosclerosis Society) guidelines recommend coronary artery calcium (CAC) score for risk refinement in primary prevention of atherosclerotic cardiovascular disease (ASCVD).

Objectives: The study sought to compare CAC utility as a risk-refining tool following the ACC/AHA guideline using pooled cohort equations (PCE) or PREVENT (Predicting Risk of cardiovascular disease EVENTs) equations and ESC/EAS guideline using SCORE2 (Systematic COronary Risk Evaluation 2).

Methods: A total of 1,903 statin-naive participants 55 to 75 years of age, free of ASCVD and diabetes, with low-density lipoprotein cholesterol <190 mg/dL from the prospective population-based Rotterdam Study were included. Per the guidelines, we determined proportions of CAC scan-eligible and reclassified men and women, ASCVD incidence rates, and numbers needed to treat for 10 years (NNT_10y).

Results: By the ACC/AHA (PCE), 18.3% of men and 11.9% of women, and by ACC/AHA (PREVENT), 13.4% of men and 3.4% of women were eligible for a CAC scan. By the ESC/EAS, 46.6% of men and 44.9% of women were CAC eligible. Proportions of uprisked and derisked individuals varied per guideline. Among ACC/AHA and ESC/EAS CAC-eligible individuals, incidence rates ranged from 9.3 to 23.8 per 1,000 person-years, and the estimated NNT_10y to prevent 1 ASCVD event, based on high-intensity statin use, varied from 11 to 26.

Conclusions: The ACC/AHA and ESC/EAS guidelines differ in the selection and application of the CAC score for primary prevention of ASCVD. Guideline-directed application of CAC score in a middle-aged apparently healthy population improved risk stratification at an acceptable NNT_10y for both guidelines.

Light chain amyloidosis and transthyretin amyloidosis are rare protein misfolding disorders characterized by amyloid deposition in organs, varied clinical manifestations, and poor outcomes. Amyloid fibrils trigger various signaling pathways that initiate cellular, metabolic, structural, and functional changes in the heart and other organs. Imaging modalities have advanced to enable detection of amyloid deposits in involved organs and to assess organ dysfunction, disease stage, prognosis, and treatment response. The Amyloidosis Forum hosted a hybrid meeting to focus on the use of imaging endpoints in clinical trials for systemic immunoglobulin light chain amyloidosis and transthyretin amyloidosis. Stakeholders from academia and industry, together with representatives from multiple regulatory agencies reviewed the use of imaging biomarkers with a focus on cardiac amyloidosis, described applications and limitations of imaging in clinical trials, and discussed qualification of imaging as a surrogate clinical outcome. Survey results provided important patient perspectives. This review summarizes the proceedings of the Amyloidosis Forum.

The concept of high-risk plaque emerged from pathologic and epidemiologic studies 3 decades ago that demonstrated plaque rupture with thrombosis as the predominant mechanism of acute coronary syndrome and sudden cardiac death. Thin-cap fibroatheroma, a plaque with a large lipidic core covered by a thin fibrous cap, is the prototype of the rupture-prone plaque and has been traditionally defined as "vulnerable plaque." Although knowledge on the pathophysiology of plaque instability continues to grow, the risk profile of our patients has shifted and the character of atherosclerotic disease has evolved, partly because of widespread use of lipid-lowering therapies and other preventive measures. In vivo intracoronary imaging studies indicate that superficial erosion causes up to 40% of acute coronary syndromes. This changing landscape calls for broader perspective, expanding the concept of high-risk plaque to the precursors of all major substrates of coronary thrombosis beyond plaque rupture. Other factors to take into consideration include dynamic changes in plaque composition, the importance of plaque burden, inflammatory activation (both local and systemic), healing mechanisms, regional hemodynamic pattern, properties of the fluid phase of blood, and the amount of myocardium at risk subtended by a lesion. Rather than the traditional focus limited to the thin-cap fibroatheroma, the authors advocate a more comprehensive approach that considers both morphologic features and biological activity of plaques and blood. This position paper highlights the challenges to the usual concept of high-risk plaque, proposes a broader definition, and analyzes its key morphologic features, the technological progress of plaque imaging (particularly using intracoronary imaging techniques), advances in pharmacologic therapies for plaque regression and stabilization, and the feasibility and efficacy of focal interventional treatments including preemptive plaque sealing.

Background: Clinical guidelines do not recommend coronary computed tomographic angiography (CTA) in elderly patients or in the presence of heavy coronary calcification. Photon-counting coronary computed tomographic angiography (PCCTA) introduces ultrahigh in-plane resolution and multienergy imaging, but the ability of this technology to overcome these limitations is unclear.

Objectives: The authors evaluate the ability of PCCTA to quantitatively assess coronary luminal stenosis in the presence and absence of calcification, comparing both the ultrahigh-resolution (UHR)-PCCTA and the multienergy standard-resolution (SR)-PCCTA with the criterion-standard 3-dimensional invasive quantitative coronary angiography (3D QCA).

Methods: The authors included 100 patients who had both PCCTA and invasive coronary angiography (ICA). They comparatively evaluated luminal diameter stenosis with PCCTA and 3D QCA, anatomic disease severity (according to CAD-RADS [Coronary Artery Disease-Reporting and Data System]) and the diagnostic performance of PCCTA in identifying coronary arteries with ≥50% diameter stenosis on 3D QCA requiring invasive hemodynamic severity evaluation and/or revascularization.

Results: The authors analyzed 257 vessels and 343 plaques. UHR-PCCTA luminal evaluation relative to 3D QCA was more precise than SR-PCCTA (median difference: 3% [Q1-Q3: 1%-6%] vs 6% [Q1-Q3: 2%-11%]; P < 0.001), particularly in severely calcified arteries (median difference 3% [Q1-Q3: 1%-6%] vs 6% [Q1-Q3: 3%-13%]; P = 0.002). Per-vessel agreement for CAD-RADS between UHR-PCCTA and 3D QCA was near-perfect (κ = 0.90 [Q1-Q3: 0.84-0.95]; P < 0.001), and it was substantial for SR-PCCTA (κ = 0.63 [Q1-Q3: 0.54-0.71]; P < 0.001), especially in severely calcified arteries: κ = 0.90 (Q1-Q3: 0.83-0.97; P < 0.001) and κ = 0.67 (Q1-Q3: 0.56-0.77; P < 0.001), respectively. Per-vessel diagnostic performance of SR- and UHR-PCCTA was excellent: AUC: 0.94 (95% CI: 0.91-0.98; P < 0.001) and 0.99 (95% CI: 0.98-1.00; P < 0.001), respectively. UHR-PCCTA diagnostically outperformed SR-PCCTA: ΔAUC: 0.05 (95% CI: 0.01-0.08; P = 0.01).

Conclusions: PCCTA compares favorably with ICA for lumen assessment and anatomic disease severity classification in patients presenting with acute coronary syndrome or patients referred for ICA. UHR-PCCTA luminal evaluation is superior to SR-PCCTA, especially in patients with heavy coronary calcification. UHR-PCCTA has excellent diagnostic performance in identifying coronary arteries with ≥50% luminal stenosis on 3D QCA, outperforming standard-resolution imaging.