Circulation: Cardiovascular Imaging最新文献

Background: Coronary artery calcium (CAC) is heterogeneous in older age and is incompletely explained by traditional atherosclerotic cardiovascular disease risk factors. The extremes of subclinical atherosclerosis burden are strongly associated with either a low or high 10-year risk of incident atherosclerotic cardiovascular disease, respectively. However, the genetic underpinnings of differences in arterial aging remain unclear. We sought to determine the independent association of 2 polygenic scores for coronary heart disease (CHD) with CAC in adults ≥75 years of age.

Methods: There were 1865 ARIC (Atherosclerosis Risk in Communities) participants who underwent genetic testing at visit 1 (1987-1989) and CAC scans at visit 7 (2018-2019). In the primary analysis, an externally derived multi-ancestry polygenic CHD risk score was calculated for both White and Black participants. Results were confirmed using a separate ARIC-derived polygenic CHD risk score, including ≥6 million variants computed for White participants. We used multivariable logistic regression models to assess the association of polygenic CHD risk with CAC, after adjusting for baseline, time-averaged lifestyle, traditional risk factors, and local ancestry principal components.

Results: In the primary analysis, the average age was 80.6 years old, 61.6% were women, and the median CAC score was 246 (189 participants with CAC=0, 364 participants with CAC≥1000). Compared with persons below the 20th percentile of polygenic CHD risk, persons with polygenic-CHD risk above the 80th percentile had 82% lower odds of having CAC=0 (odds ratio, 0.18 [95% CI, 0.09-0.37]) and had >4-fold higher odds of CAC≥1000 (odds ratio, 4.77 [95% CI, 2.88-7.88]). On a continuous scale, each SD increment increase in the polygenic risk score was associated with a 78% higher CAC score. Results were nearly identical using a second confirmatory polygenic CHD risk score in White participants.

Conclusions: Polygenic CHD risk is robustly associated with a lower prevalence of CAC=0 and a higher prevalence of CAC≥1000 in adults ≥75 years of age, beyond lifestyle and traditional risk factors. These results suggest a heritable contribution to distinct healthy and unhealthy arterial aging phenotypes that persist throughout the life course.

Background: Coronary flow capacity (CFC) is a measure that integrates hyperemic myocardial blood flow and myocardial flow reserve to quantify the pathophysiological impact of coronary artery disease on vasodilator capacity. We assessed the prognostic value of CFC derived from ⁸²Rb positron emission tomography/computed tomography in patients with suspected coronary artery disease and normal myocardial perfusion imaging.

Methods: We studied 1967 patients with suspected coronary artery disease and normal myocardial perfusion at the semiquantitative analysis of stress/rest cardiac ⁸²Rb positron emission tomography/computed tomography imaging. Coronary artery calcium scores were calculated and categorized into 3 groups: 0, 0.1 to 99.9, and ≥100. Patients were classified as having myocardial steal, severely reduced CFC, moderately reduced CFC, mildly reduced CFC, minimally reduced CFC, or normal flow using previously defined thresholds. The outcome end points were myocardial infarction and cardiac death, whichever occurred first.

Results: During a mean time of 41±27 months, 49 events occurred (2.5% cumulative event rate, with an annualized event rate of 0.5% person-years). At multivariable Cox analysis, coronary artery calcium score categories and impaired CFC resulted as independent predictors of events (both P<0.001). The annualized event rate was higher in patients with impaired CFC compared with those with normal CFC (P<0.05). Kaplan-Meier analysis showed that patients with impaired CFC were at the highest risk of events.

Conclusions: In patients with suspected coronary artery disease and normal myocardial perfusion, impaired CFC is associated with a higher risk of cardiac events. Evaluating CFC can help identify patients' candidates for additional therapies to prevent future events.

Background: Elevated Lp(a) (lipoprotein[a]) is a risk marker for atherosclerotic disease, but the underlying mechanisms remain elusive. We examined the association of Lp(a) with changes in coronary atherosclerosis following intensive lipid-lowering therapy.

Methods: In the PACMAN-AMI trial (Effects of the PCSK9 Antibody Alirocumab on Coronary Atherosclerosis in Patients With Acute Myocardial Infarction), 300 patients with acute myocardial infarction were randomized to receive biweekly alirocumab 150 mg or placebo in addition to high-intensity statins. Patients underwent serial 2-vessel intravascular ultrasound, optical coherence tomography, and near-infrared spectroscopy in the non-infarct-related arteries at baseline and after 52 weeks. The main end points were percent atheroma volume by intravascular ultrasound, minimum fibrous cap thickness by optical coherence tomography, and maximum lipid core burden index within 4 mm (maxLCBI_4mm) by near-infrared spectroscopy.

Results: A total of 265 patients had serial intravascular ultrasound data (mean age, 58±9 years; 16% women). Alirocumab resulted in greater reductions in percent atheroma volume and maxLCBI_4mm, as well as a greater increase in minimum fibrous cap thickness, compared with placebo. In the alirocumab group, the reduction in maxLCBI_4mm was smaller in patients with higher baseline Lp(a), defined by the highest quartile (Q4, ≥98 nmol/L; n=30), than in those with lower baseline Lp(a) (Q1-Q3, <98 nmol/L; n=99; -40.2 [-91.1 to 10.7] versus -91.4 [-113.9 to -68.9], respectively; P=0.01 after adjustment for clinically relevant baseline variables), and was comparable to the maxLBI_4mm reduction in the placebo group (-37.60 [-57.40 to -17.80]; n=134). These findings were consistent when higher baseline Lp(a) was defined by cut-off values of ≥75 versus <75 nmol/L (n=35 versus 94, respectively, in the alirocumab group) and ≥125 versus <125 nmol/L (n=23 versus 106, respectively). Changes in percent atheroma volume and minimum fibrous cap thickness did not differ in relation to baseline Lp(a).

Conclusions: In patients with acute myocardial infarction, elevated Lp(a) at baseline is associated with attenuation of plaque lipid regression despite intensive treatment with alirocumab plus high-intensity statin. This finding may explain the residual cardiovascular risk associated with high Lp(a) despite optimal control of lipid levels.

Registration: URL: https://www.clinicaltrials.gov; Unique identifier: NCT03067844.

Background: Accumulation of CXCR4 (C-X-C motif chemokine receptor 4)-positive immune cells after acute myocardial infarction (AMI) can be visualized by positron emission tomography. For a broader clinical application, there is a need for CXCR4-directed radiotracers labeled with isotopes that can be used with single-photon emission computed tomography (SPECT). We report on the detection of CXCR4 expression after AMI in humans using the novel tracer [^99mTc]-PentixaTec.

Methods: In this retrospective analysis, 9 patients with AMI after mechanical revascularization underwent myocardial inflammation imaging with [^99mTc]-PentixaTec SPECT/computed tomography and rest perfusion SPECT imaging. Tracer uptake in the infarcted area, spleen, bone marrow, and blood pool were used for semiquantitative analysis and calculation of signal-to-background ratios. The extent and intensity of SPECT-derived inflammatory changes were compared with serological markers and perfusion defects.

Results: CXCR4-directed SPECT was positive in all patients. Increased CXCR4 expression was only detected in areas with diminished perfusion corresponding to the affected vessel in coronary angiography, with a signal-to-background ratio (infarcted area-to-blood pool) of 2.36±0.74. Uptake in bone marrow and spleen showed a significant correlation with CXCR4 expression in the infarcted areas (r=0.73 and P=0.03 for spleen and r=0.81 and P=0.008 for bone marrow, respectively). The extent and intensity of SPECT-derived inflammatory changes showed no significant association with serum troponin, CK (creatine kinase), leukocyte, or CRP (C-reactive protein) levels.

Conclusions: This is the first report of in vivo CXCR4 imaging after AMI using a ^99mTc-labeled tracer. Increased CXCR4 expression was observed locally in the infarcted region and was related to a systemic inflammatory response in the reticuloendothelial system. This proof-of-concept investigation demonstrates the general feasibility of evaluating the inflammation-related CXCR4 expression in the myocardium after AMI using conventional scintigraphy or SPECT and might, thus, broaden its worldwide application in clinical practice.

Background: Accurate assessment of left ventricular filling pressure in patients with atrial fibrillation or flutter (AF) remains difficult. A novel 2-dimensional scoring system, visually assessing time difference between mitral valve and tricuspid valve opening (VMT) score, based on temporal analysis of early diastolic valve opening, could be applied to these patients. We aimed to determine the usefulness of the VMT score in patients with AF.

Methods: We analyzed 119 consecutive patients with AF who underwent cardiac catheterization as a derivation cohort. The diagnostic performance of the VMT score was further evaluated in an external data set containing 189 patients with AF. Elevated left ventricular filling pressure was defined as a mean pulmonary arterial wedge pressure ≥15 mm Hg. The time sequence of atrioventricular valve opening was visually assessed and scored (0, tricuspid valve first; 1, simultaneous; 2, mitral valve first). When the inferior vena cava was dilated, 1 point was added, and the VMT score was finally graded as 0 to 3. Conventional Doppler parameters to estimate left ventricular filling pressure were also measured.

Results: Pulmonary arterial wedge pressure was elevated with an increase in the VMT score (0: 10±3, 1: 13±5, 2: 22±7, 3: 27±6 mm Hg; P<0.001), resulting in a significant rise in pulmonary arterial wedge pressure from VMT score 1 to 2. VMT≥2 predicted elevated pulmonary arterial wedge pressure with an accuracy of 87%, and the diagnostic accuracy of the VMT score was significantly higher than that of conventional Doppler parameters (C index, 0.88 versus 0.54-0.68; P<0.001). In addition, VMT ≥2 showed an incremental predictive value over plasma brain natriuretic peptide levels (C index, 0.79-0.93; P<0.001). In the external validation cohort, VMT≥2 demonstrated acceptable accuracy of 72%.

Conclusions: VMT scoring was a useful echocardiographic marker of elevated left ventricular filling pressure and had an incremental benefit over practical biomarkers in patients with AF.

Large vessel vasculitides (LVV) comprise a group of inflammatory disorders that involve the large arteries, such as the aorta and its primary branches. The cause of LVV is often rheumatologic and includes giant cell arteritis and Takayasu arteritis. Giant cell arteritis is the most common form of LVV affecting people >50 years of age with a slight female predominance. Takayasu arteritis is more frequently seen in younger populations and is significantly more common in women. Prompt identification of LVV is crucial as it can lead to debilitating complications if left untreated, including blindness in the case of giant cell arteritis and large artery stenosis and aneurysms in the case of all forms of LVV. Noninvasive imaging methods have greatly changed the approach to managing LVV. Today, imaging (with ultrasound, magnetic resonance imaging, computed tomography, and positron emission tomography) is routinely used in the diagnosis of LVV. In patients with giant cell arteritis, imaging often spares the use of invasive procedures such as temporal artery biopsy. In addition, vascular imaging is also crucial for longitudinal surveillance of arterial damage. Finally, imaging is currently being studied for its role in assessing treatment response and ongoing disease activity and its potential value in determining the presence of vascular wall remodeling (eg, scarring). This review explores the current uses of noninvasive vascular imaging in LVV.