Coronary Artery Remodeling Research Articles

Adverse remodeling of the obtuse marginal artery in compensatory hypertrophied myocardium from spontaneously hypertensive rats.

Spontaneously hypertensive rats (SHR) serve as a model of genetic hypertension. Adverse remodeling of a coronary artery has been reported in SHR. This model is used to study new therapies in regression vascular remodeling. However, no data are available that show remodeling of the intramyocardial branch of the obtuse marginal artery in 10-month-old SHR. This study was designed to assess remodeling (changes in vascular structure and fibrosis) of this coronary artery. The study was performed on 10-month-old male SHR (n=7) and normotensive control Wistar Kyoto rats (WKY) (n=7). Using histology, we show that the external diameter, lumen diameter, wall width, and cross-sectional area of the intramyocardial artery were significantly greater in SHR than in WKY. The wall-to-lumen ratio was similar in SHR and WKY. The collagen volume density of the intramyocardial artery in SHR was significantly greater than in WKY. Our results show hypertrophic outward remodeling in the intramyocardial branch of the obtuse marginal artery of the left ventricle in SHR. This artery can serve as a new vascular bed from adult SHR to study novel therapies in regression coronary artery remodeling.

TCT-424 One-Year Clinical, Angiographic and OCT Follow-up after Absorb BVS Implantation in Long Coronary Artery Lesions: mechanisms of coronary artery remodeling

TCT-424 One-Year Clinical, Angiographic and OCT Follow-up after Absorb BVS Implantation in Long Coronary Artery Lesions: mechanisms of coronary artery remodeling

Short-term esmolol attenuates remodeling of the thoracic aorta in hypertensive rats by decreasing concentrations of ADMA down-regulated by oxidative stress

Esmolol produces early regression of left ventricular hypertrophy and improves coronary artery remodeling, although the impact of short-term treatment with this beta-blocker on remodeling in large arteries has not yet been studied. We hypothesized that even a short (48h) course of esmolol might alter remodeling of the aorta in the spontaneously hypertensive rat (SHR). Fourteen-month-old male SHRs were treated intravenously with vehicle (SHR, n=8) or esmolol (SHR-E, n=8) (300μg/kg/min). Age-matched, vehicle-treated male Wistar-Kyoto rats (WKY, n=8) served as controls. After 48h, we studied the structure, volume density of elastic fibers, and passive mechanical properties of the aorta. Determination of asymmetrical dimethylarginine concentrations and total protein carbonyls in the aorta were analyzed. Esmolol significantly attenuated abnormal aortic wall thickness, cross-sectional area, wall-to-lumen ratio, volume density of elastic fibers, and wall stiffness. The protective effect of esmolol could be related to a decrease in asymmetrical dimethylarginine levels after down-regulation by oxidative stress. These findings could play a key role in the selection of antihypertensive therapy in patients with hypertension and aortic remodeling.

Multi-Layer Mechanical Model of Glagov Remodeling in Coronary Arteries: Differences between In-Vivo and Ex-Vivo Measurements.

When blood vessels undergo remodeling because of the buildup of atherosclerotic plaque, it is thought that they first undergo compensatory or outward remodeling, followed by inward remodeling: the lumen area stays roughly constant or increases slightly and then decreases rapidly. The second phase of remodeling is supposed to start after the plaque burden exceeds about 40%. These changes in the vessel were first observed by S. Glagov who examined cross-sections of coronary arteries at different stages of the disease. In this paper, we use a mathematical model based on growth and elasticity theory to verify the main aspects of Glagov’s result. However, both our model and curve-fitting to the data suggest that the critical stenosis is around 20% rather than 40%. Our model and data from the PROSPECT trial also show that Glagov remodeling is qualitatively different depending on whether measurements are taken ex-vivo or in-vivo. Our results suggest that the first outward phase of “Glagov remodeling” is largely absent for in-vivo measurements: that is, the lumen area always decreases as plaque builds up. We advocate that care must be taken when infering how in-vivo vessels remodel from ex-vivo data.

Estrogen therapy may counterbalance eutrophic remodeling of coronary arteries and increase bradykinin relaxation in a rat model of menopausal hypertension.

Objective:Hypertension causes adverse remodeling and vasomotor alterations in coronaries. Hormones such as estrogen may help counterbalance some of these effects. The aim of this study was to analyze the effects of ovariectomy and estrogen therapy in a rat model of menopausal hypertension induced by angiotensin II (AII).Methods:We investigated diameter, tone, and mechanics of intramural coronaries taken from ovariectomized female rats (n = 11) that received chronic AII treatment to induce hypertension, and compared the results with those found in female rats that were also given estrogen therapy (n = 11). The “hypertensive control” group (n = 11) underwent an abdominal sham operation, and received AII. After 4 weeks of AII treatment, side branches of left anterior descendent coronary (approximately 200 μm in diameter) were isolated, cannulated with plastic microcannulas at both ends, and studied in vitro in a vessel chamber. The inner and outer diameter of the arteries were measured by microangiometry, and spontenuous tone, wall thickness, wall cross-sectional area, tangential stress, incremental distensibility, circumferential incremental elastic modulus, thromboxane agonist-induced tone, and bradykinin-induced dilation were calculated.Results:In hypertension, intramural small coronaries show inward eutrophic remodeling after ovariectomy comparing with hypertensive controls. Estrogen therapy had an opposite effect on vessel diameter. Hormone therapy led to an increase in spontaneous tone, allowing for greater dilatative capacity.Conclusions:Estrogen may therefore be considered to counterbalance some of the adverse changes seen in the wall of intramural coronaries in the early stages of chronic hypertension.

Early regression of coronary artery remodeling with esmolol and DDAH/ADMA pathway in hypertensive rats.

Our preclinical study demonstrated that esmolol produces early regression of left ventricular hypertrophy in arterial hypertension. The aim of this study was to assess the effects of short-term esmolol therapy on the regression of left anterior descending artery remodeling in spontaneously hypertensive rats (SHRs), and to determine whether the asymmetric dimethylarginine (ADMA)/dimethylarginine dimethylaminohydrolase (DDAH) pathway, a regulator of nitric oxide (NO) bioavailability, accounted for this regression. Fourteen-month-old male SHRs were treated intravenously with vehicle (SHR, n=15) or esmolol (SHR-E, n=20) (300 μg kg-1 min-1). Age-matched, vehicle-treated male Wistar-Kyoto rats (WKY, n=15) served as controls. SHRs were also treated with nitroglycerin (SHR-N, n=5). After 48 h, the left anterior descending artery structure and morphology were assessed, and dose-response curves for 5-hydroxytryptamine (5-HT, 10-9-3 × 10-5 mol l-1) were constructed. ADMA concentrations in plasma and left ventricle and DDAH activity in tissue were analyzed. Wall thickness and cross-sectional area were significantly lower after treatment with esmolol in SHR-E than in SHR. Media thickness and smooth muscle cell count were lower in SHR-E than in SHR. Esmolol induced a significant reduction in adventitial cell count in SHR-E. The area under the concentration-response curves was significantly higher in SHR than in SHR-E, as were the esmolol normalized coronary artery contracting responses to 5-HT. We found significantly lower ADMA levels and significantly higher DDAH activity in the ventricle in SHR-E than in SHR. The protective effect of esmolol on the regression of left anterior descending artery remodeling may be related to the reduction in ADMA levels.

Vitamin D and conjugated equine estrogen: the association with coronary artery atherosclerosis in cynomolgus monkeys.

To analyze vitamin D3 plasma concentrations among monkeys randomized to oral conjugated equine estrogen (CEE) versus control and the association with coronary artery atherosclerosis (CAA). Surgically postmenopausal monkeys (N = 50) were fed an atherogenic diet containing a woman's equivalent of 1000 IU/day of vitamin D3. The monkeys were randomized at baseline to receive CEE (equivalent of 0.45 mg/d, n = 25) or placebo (n = 25). 25-hydroxyvitamin D3 (25OHD3) was measured at baseline and 20 months later. At 20 months, CAA evidence of coronary artery remodeling, and American Heart Association (AHA) severity scores were assessed. The percent change in 25OHD3 concentrations from baseline to 20 months postrandomization was inversely correlated with plaque area of the right coronary artery (P = 0.048), left circumflex artery (P = 0.039), left anterior descending artery (P = 0.017), and AHA severity score (AHA LADmax) (P = 0.016). Those with increased 25OHD3 concentrations who were taking CEE also had significantly lower AHA scores compared with those who were not taking CEE and did not have an increase in 25OHD3 (P = 0.01). Monkeys with increases in 25OHD3 concentrations had significantly less severe CAA. Those with increases in 25OHD3 with CEE were associated with significantly decreased AHA lesion scores, decreased plaque, and greater coronary artery remodeling. If these findings are present in women, achieving higher 25OHD3 concentrations (or being a vitamin D supplementation "responder") may be associated with cardioprotection, and further studies to evaluate a synergistic effect with CEE and vitamin D on cardiovascular health are needed.

Sex-Specific Genetic Variants are Associated With Coronary Endothelial Dysfunction.

BackgroundEndothelial dysfunction is an early stage of atherosclerosis. Single‐nucleotide polymorphisms (SNPs) have been associated with vascular dysfunction, cardiac events, and coronary artery remodeling. We aimed to detect SNPs associated with endothelial dysfunction and determine whether these associations are sex specific.Methods and ResultsSix hundred forty‐three subjects without significant obstructive coronary artery disease underwent invasive coronary endothelial function assessment. We collected data from 1536 SNPs that had previously been associated with vasoreactivity, angiogenesis, inflammation, artery calcification, atherosclerotic risk factors, insulin resistance, hormone levels, blood coagulability, or with coronary heart disease. Coronary vascular reactivity was assessed by the percent change in coronary artery diameter ≤ −20% after an intracoronary bolus injection of acetylcholine on invasive coronary physiology study. SNPs significantly associated with coronary epicardial endothelial dysfunction were ADORA1,KCNQ1, and DNAJC4 in the whole cohort, LPA, MYBPH, ADORA3, and PON1 in women and KIF6 and NFKB1 in men (P<0.01).ConclusionsWe have identified several significant SNPs that are associated with an increased risk of coronary endothelial dysfunction. These associations appear to be sex specific and may explain gender‐related differences in development of atherosclerosis.

Endothelial dysfunction and outward remodeling in coronary and mesenteric arteries in response to high fat diet in mice

It is well established that vascular endothelial dysfunction is an underlying mechanism in the pathophysiology of hypertension, atherosclerosis, diabetes and other cardiovascular diseases (CVD). Additionally, this cardiovascular pathophysiology is accentuated in aged population. We hypothesize that intake of high fat diet would exacerbate age‐related vascular endothelial dysfunction, promoting the onset and propagation of CVD. To test this hypothesis twelve‐week‐old male mice with C57BL6/J background were randomly divided into four groups and fed normal chow (NC) or HFS (42% fat) for a period of 3 or 12 months. We isolated the left coronary artery (LCA) and 2nd‐order mesenteric artery (MA) and mounted them in the wire‐ and pressure myograph. Both young and aged HFS mice had impaired glucose tolerance as well as an increase in cholesterol levels and weight gain compared to both groups of mice on NC. Aged HFS did have a significant increase in body weight (BW) when compared to young HFS. There was no difference in BW between young and aged mice on NC. Endothelium‐dependent ACh‐induced relaxing responses were blunted in MA and LCA from young HFS compared to young NC mice. Strikingly, this endothelial dysfunction was similar compared to aged NC mice. In addition, endothelial dysfunction in LCA and MA was worsened in aged HFS mice. MA from aged HFS mice developed outward hypertrophic remodeling compared to their younger counterparts and aged‐matched NC mice. These findings suggest that high fat diet in aged individuals can accelerate endothelial dysfunction and increase the risk of CVD.Support or Funding InformationThe work presented here is supported by NIH grant R01HL107885 and R01HL107885‐05S1

Expansive arterial remodeling of the carotid arteries and its effect on atherosclerotic plaque composition and vulnerability: an in-vivo black-blood 3T CMR study in symptomatic stroke patients.

BackgroundBased on intravascular ultrasound of the coronary arteries expansive arterial remodeling is supposed to be a feature of the vulnerable atheroslerotic plaque. However, till now little is known regarding the clinical impact of expansive remodeling of carotid lesions. Therefore, we sought to evaluate the correlation of expansive arterial remodeling of the carotid arteries with atherosclerotic plaque composition and vulnerability using in-vivo Cardiovascular Magnetic Resonance (CMR).MethodsOne hundred eleven symptomatic patients (74 male/71.8 ± 10.3y) with acute unilateral ischemic stroke and carotid plaques of at least 2 mm thickness were included. All patients received a dedicated multi-sequence black-blood carotid CMR (3Tesla) of the proximal internal carotid arteries (ICA). Measurements of lumen, wall, outer wall, hemorrhage, calcification and necrotic core were determined. Each vessel-segment was classified according to American Heart Association (AHA) criteria for vulnerable plaque. A modified remodeling index (mRI) was established by dividing the average outer vessel area of the ICA segments by the lumen area measured on TOF images in a not affected reference segment at the distal ipsilateral ICA. Correlations of mRI and clinical symptoms as well as plaque morphology/vessel dimensions were evaluated.ResultsSeventy-eight percent (157/202) of all internal carotid arteries showed atherosclerotic disease with AHA Lesion-Type (LT) III or higher. The mRI of the ICA was significantly different in normal artery segments (AHA LT I; mRI 1.9) compared to atherosclerotic segments (AHA LT III-VII; mRI 2.5; p < 0.0001). Between AHA LT III-VII there was no significant difference of mRI. Significant correlations (p < 0.05) of the mRI with lumen-area (LA), wall-area (WA), vessel-area (VA) and wall-thickness (WT), necrotic-core area (NC), and ulcer-area were observed. With respect to clinical presentation (symptomatic/asymptomatic side) and luminal narrowing (stenotic/non-stenotic) no relevant correlations or significant differences regarding the mRI were found.ConclusionExpansive arterial remodeling exists in the ICA. However, no significant association between expansive arterial remodeling, stroke symptoms, complicated AHA VI plaque, and luminal stenosis could be established. Hence, results of our study suggest that expansive arterial remodeling is not a very practical marker for plaque vulnerability in the carotid arteries.

Histopathological Characteristics of Post-inflamed Coronary Arteries in Kawasaki Disease-like Vasculitis of Rabbits.

Kawasaki disease (KD) is a systemic vasculitis in infants that develops predominantly in the coronary arteries. Despite the clinically transient nature of active inflammation in childhood albeit rare complications (e.g., coronary artery aneurysm), KD has recently been suggested to increase the incidence of ischemic heart diseases in young adulthood. However, little is known about the histopathology of the coronary artery long after development of the acute KD vasculitis. To address this, we conducted histological studies of rabbit coronary arteries in adolescent phase after induction of the KD-like vasculitis induced by horse serum administration. After a transmural infiltration of inflammatory cells in acute phase at day 7, the artery exhibited a gradual decrease in the number of inflammatory cells and thickening of the intima during the chronic phase up to day 90, where proteoglycans were distinctly accumulated in the intima with abundant involvement of α-smooth muscle actin (α-SMA)-positive cells, most of which accompanied expression of VCAM-1 and NF-κB. Distinct from classical atherosclerosis, inflammatory cells, e.g., macrophages, were barely detected during the chronic phase. These observations indicate that the KD-like coronary arteritis is followed by intimal thickening via accumulation of proteoglycans and proliferation of α-SMA-positive cells, reflecting aberrant coronary artery remodeling.

Advances of evaluating coronary artery remodeling by intravascular ultrasound

Advances of evaluating coronary artery remodeling by intravascular ultrasound

Abstract 12063: High-risk Plaque Co-localizes With Low Endothelial Shear Stress and Expansive Remodeling in Human Coronary Arteries: A 3D Optical Coherence Tomography Study

Background: High risk plaque accounts for the majority of acute coronary events. Low endothelial shear stress (ESS) is a key factor of the natural history of atherosclerosis. The role of ESS in high risk plaque formation is not well studied in man. Hypothesis: To explore the association of low ESS with high risk plaque and to identify the ESS milieu and vascular remodeling response in high risk vs. non high risk plaque. Methods: 35 coronary arteries from 30 patients were 3D reconstructed with fusion of coronary angiography and optical coherence tomography (Fig A-D) . ESS was calculated in the 3D reconstructed arteries using computational fluid dynamics (Fig E) and classified into low, moderate and high in 3 mm long segments. In each segment: i) fibroatheromas were classified into high risk and non high risk based on fibrous cap thickness and lipid pool size ii) vascular remodeling was classified into constrictive, compensatory and expansive. Results: Fibroatheromas in low ESS segments had significantly thinner fibrous cap compared to high ESS segments (89±84 vs.138±83 μm, p&lt;0.05). Lipid pool size was comparable across all ESS categories. The majority of low ESS segments co-localized with high risk plaques (29 vs. 9%, p&lt;0.05), whereas the majority of high ESS co-localized with non high risk plaques (24 vs. 9%, p&lt;0.05, Fig F ). Compensatory and expansive remodeling was the predominant remodeling response in low ESS segments containing high risk plaques. In non-stenotic fibroatheromas (expansive or compensatory remodeling) low ESS was predominantly associated with high risk plaques (29 vs. 3%, p&lt;0.05) whereas high ESS was associated with non high risk plaques (Fig F) . Conclusions: Novel combined anatomic and functional imaging with 3D OCT showed that low ESS and non-constrictive remodeling are associated with high risk plaque in man. Further studies are needed to assess the role of ESS and vascular remodeling in high risk plaque rupture and precipitation of clinical outcomes.

GW26-e0743 Impact of Plaque Characteristics on Serial Coronary Artery Remodeling Response to Changes in Plaque Size: OCT and IVUS findings

GW26-e0743 Impact of Plaque Characteristics on Serial Coronary Artery Remodeling Response to Changes in Plaque Size: OCT and IVUS findings

Coronary Plaque Characteristics Affect No-Reflow During Primary Percutaneous Coronary Intervention: A Pooled Analysis of 14 Observational Studies Using Intravascular Ultrasound.

The association between coronary plaque composition and no-reflow during percutaneous coronary intervention (PCI) is still debated. We performed a systematic literature search using MEDLINE, Embase, Cochrane, and Ovid databases for intravascular ultrasound (IVUS) studies evaluating the relationship between coronary plaque characteristics and no-reflow after PCI. Fourteen observational trials were included in the meta-analysis, including 1457 patients (237 in the no-reflow group, 1220 in the normal reflow group). Pooled analysis indicated that the no-reflow group had a significantly higher absolute volume of fibrofatty plaque (weighted mean differences [WMD], 4.94 mm(3); 95% confidence interval [CI], 1.83-l8.06; P = .002), external elastic membrane cross-sectional area (EEM-CSA) (WMD, 3.40 mm2; 95% CI, 2.22-4.58; P = .00001), plaque area (WMD, 4.06 mm(2); 95% CI, 2.24-5.89; P = .0001), and artery remodeling index (WMD, 0.09; 95% CI, 0.06-0.13; P = .00001), and a smaller percentage of fibrous plaque (WMD, -5.89 %; 95% CI, -0.66 to -11.12; P = .03) than in the normal reflow group. There were no significant differences in the other plaque components between the two groups. This meta-analysis confirmed that high absolute volume of fibrofatty plaque, EEM-CSA, plaque area, and coronary artery remodeling index, and a decreased percentage of fibrous plaque as detected by IVUS in culprit lesions, are linked with the development of the no-reflow phenomenon after PCI.

Remodeling of left circumflex coronary arterial tree in pacing-induced heart failure.

Congestive heart failure (CHF) is a very serious heart disease that manifests an imbalance between left ventricle supply and demand. Although the mechanical demand of the failing heart has been well characterized, the systematic remodeling of the entire coronary arterial tree that constitutes the supply of the myocardium is lacking. We hypothesize that the well-known increase in ventricle wall stress during CHF causes coronary vascular rarefaction to increase the vascular flow resistance, which in turn compromises the perfusion of the heart. Morphometric (diameters, length, and numbers) data of the swine left circumflex (LCx) arterial tree were measured in both CHF (n = 6) and control (n = 6) groups, from which a computer reconstruction of the entire LCx tree was implemented down to the capillary level to enable a hemodynamic analysis of coronary circulation. The vascular flow resistance was increased by ∼75% due to a significant decrease of vessel numbers (∼45%) and diameters in the first capillary segments (∼10%) of the LCx arterial tree after 3-4 wk of pacing. The structural remodeling significantly changed the wall shear stress in vessel segments of the entire LCx arterial tree of CHF animals. This study enhances our knowledge of coronary arterial tree remodeling in heart failure, which provides a deeper understanding of the deterioration of supply-demand relation in left ventricle.

HIV and coronary arterial remodeling from the Multicenter AIDS Cohort Study (MACS).

Positive remodeling (PR), a coronary artery characteristic associated with risk for myocardial infarction (MI), may be more prevalent in HIV-infected (HIV+) people. We evaluated the prevalence of PR using coronary CT angiography (CCTA) in HIV+ and HIV-uninfected (HIV-) men. Men enrolled in the Multicenter AIDS Cohort Study underwent CCTA if they were 40-70 years, had normal kidney function and no history of coronary revascularization. Multivariable logistic regression models were used to estimate the odds ratio (OR) of PR by HIV serostatus, adjusting for demographics and coronary artery disease (CAD) risk factors. Analysis of PR among atherosclerotic segments further adjusted for plaque type and stenosis. The prevalence of PR was 8.4% versus 12.1% (p=0.10) for HIV- and HIV+men, respectively. After demographic adjustment, HIV+men had twice the odds of PR [OR 2.01(95% CI 1.20-3.38)], which persisted after CAD risk factor adjustment [1.76(1.00-3.10)]. Higher systolic blood pressure, total cholesterol, diabetes medication use, older age, segment number with plaque present, mixed and non-calcified plaque, and stenosis>50%, were associated with increased odds of PR, while higher HDL cholesterol, higher nadir CD4 count, and black race were associated with lower PR odds. Among atherosclerotic segments, the association between HIV infection and PR persisted, but was not statistically significantly. HIV+men have more positively remodeled arterial segments, which may be due to more coronary segments with atherosclerosis or HIV-related immunosuppression. Further studies are needed to evaluate whether PR contributes to higher rates of MI in HIV+individuals.

Association of insulin resistance and coronary artery remodeling: an intravascular ultrasound study.

BackgroundThere are few studies that investigated the correlation between insulin resistance (IR) and the coronary artery remodeling. The aim of the study is to investigate the association of IR measured by homeostasis model assessment of insulin resistance (HOMA-IR) and coronary artery remodeling evaluated by intravascular ultrasound (IVUS).MethodsA total of 298 consecutive patients who received percutaneous coronary interventions under IVUS guidance were retrospectively enrolled. The value of HOMA-IR more than 2.5 was considered as IR positive. Metabolic syndrome was classified according to NCEP ATP III guidelines. The remodeling index was defined as the ratio of the external elastic membrane (EEM) area at the lesion site to the EEM area at the proximal reference site.ResultsA total of 369 lesions were analyzed (161 lesions in HOMA-IR positive and 208 lesions in HOMA-IR negative). Remodeling index was significantly higher in the HOMA-IR positive group compared with the negative group (HOMA-IR positive vs. negative: 1.074 ± 0.109 vs. 1.042 ± 0.131, p = 0.013). There was a significant positive correlation between remodeling index and HOMA-IR (p = 0.010). Analysis of HOMA-IR according to remodeling groups showed increasing tendency of HOMA-IR, and it was statistically significant (p = 0.045). Multivariate analysis revealed that only HOMA-IR was an independent predictor of remodeling index (r = 0.166, p = 0.018).ConclusionIncreased IR estimated by HOMA-IR was significantly associated with a higher remodeling index and positive coronary artery remodeling.

Intravascular Ultrasonic Imaging of Coronary Arterial Remodeling in Heart Transplant Recipients

The purpose of this study was to evaluate long-term changes of transplant coronary arteries, including vessel, plaque, and lumen areas. There are limited long-term data on vessel remodeling after heart transplantation. We analyzed serial intravascular ultrasound images of the left anterior descending coronary artery (LAD) in 54 heart transplantation recipients. Nine patients (16.7%) had a history of rejection. Proximal left anterior descending artery segments were matched among time points, a ≥20-mm long segment was analyzed every 1mm, and results were normalized for analysis length and reported asmm(3)/mm. During follow-up, vessel area decreased (-0.48 ± 1.3mm(3)/mm/year), and plaque area did not change (-0.01 ± 0.47mm(3)/mm/year). As a result, lumen area decreased (-0.52 ± 1.34mm(3)/mm/year). The change in mean lumen area was well correlated to the change in mean vessel area (r= 0.94, p <0.01) but not to the change in mean plaque area (r=-0.27, p= 0.05). In conclusion, lumen loss occurred during long-term follow-up of patients who underwent heart transplantation, primarily secondary to negative remodeling (decrease in vessel dimensions).

Noncalcified Plaque in Cardiac CT: Quantification and Clinical Implications

Coronary computed tomography angiography (CTA) is being increasingly used for direct, noninvasive evaluation of the coronary arteries. Beyond stenosis, coronary CTA also permits assessment of atherosclerotic plaque (including total and noncalcified plaque burden) and coronary artery remodeling, previously only measurable through invasive techniques. It has been shown that coronary plaque volume for noncalcified and mixed plaques and the arterial remodeling index correlate closely with corresponding measures from invasive intravascular ultrasound. Several studies have also shown a strong relationship between adverse plaque features imaged by coronary CTA and acute coronary syndrome, major adverse cardiovascular events, and ischemia. The aim of this review is to summarize current methods for quantitative measurement of atherosclerotic plaque features from coronary CTA and to discuss the clinical implications of noncalcified plaque as detected by CTA and reported in the current literature.