Thoracic Aortic Calcium Versus Coronary Artery Calcium for the Prediction of Coronary Heart Disease and Cardiovascular Disease Events

ObjectivesThis study compared the ability of coronary artery calcium (CAC) and thoracic aortic calcium (TAC) to predict coronary heart disease (CHD) and cardiovascular disease (CVD) events.BackgroundCoronary artery calcium has been shown to strongly predict CHD and CVD events, but it is unknown whether TAC, also measured within a single cardiac computed tomography (CT) scan, is of further value in predicting events.MethodsA total of 2,303 asymptomatic adults (mean age 55.7 years, 38% female) with CT scans were followed up for 4.4 years for CHD (myocardial infarction, cardiac death, or late revascularizations) and CVD (CHD plus stroke). Cox regression, adjusted for Framingham risk score (FRS), examined the relation of Agatston CAC and TAC categories, and log-transformed CAC and TAC with the incidence of CHD and CVD events and receiver-operator characteristic (ROC) curves tested whether TAC improved prediction of events over CAC and FRS.ResultsA total of 53% of subjects had Agatston CAC scores of 0; 8% 1 to 9; 19% 10 to 99; 12% 100 to 399; and 8% ≥400. For TAC, proportions were 69%, 5%, 12%, 8%, and 7%, respectively; 41 subjects (1.8%) experienced CHD and 47 (2.0%) CVD events. The FRS-adjusted hazard ratios (HR) across increasing CAC groups (relative to <10) ranged from 3.7 (p = 0.04) to 19.6 (p < 0.001) for CHD and from 2.8 (p = 0.07) to 13.1 (p < 0.001) for CVD events; only TAC scores of 100 to 399 predicted CHD and CVD (HR: 3.0, p = 0.008, and HR: 2.3, p = 0.04, respectively); these risks were attenuated after accounting for CAC. Findings were consistent when using log-transformed CAC and TAC Agatston and volume scores. The ROC curve analyses showed CAC predicted CHD and CVD events over FRS alone (p < 0.01); however, TAC did not further add to predicting events over FRS or CAC.ConclusionsThis study found that CAC, but not TAC, is strongly related to CHD and CVD events. Moreover, TAC does not further improve event prediction over CAC

Changing Drivers of Mortality Among Patients Referred for Cardiac Stress Testing

Objective: To identify temporal shifts in coronary artery disease (CAD) risk factor profiles, clinical parameters, and corresponding mortality rates among patients referred for radionuclide stress testing over 22 years. Patients and Methods: We assessed 39,750 patients with suspected CAD (“diagnostic” patients) and 10,982 patients with known CAD who underwent radionuclide stress testing between January 2, 1991, and December 31, 2012, and were followed up for at least 5 years (median, 12.7 years). Results: Among both diagnostic patients and those with known CAD, there was a marked temporal decline in typical angina and myocardial ischemia. However, several risk factors for disease progressively increased, including diabetes, obesity, and hypertension. In addition, the need to perform pharmacological testing in lieu of exercise increased markedly between the first and fourth epochs among both diagnostic patients (from 26.5% [1634 of 6176] to 53.0% [5781 of 10,908]; P<.001) and patients with known CAD (from 31.1% [999 of 3213] to 75.5% [1405 of 1860]; P<.001). The net effect of these competing positive and negative risk factor trends was no change in the adjusted annualized rate of mortality over the temporal span in our study, ranging from 1.57% per year in 1991-1995 to 1.76% per year in 2006-2012 among diagnostic patients and from 2.46% per year to 2.75% per year during the same intervals among patients with known CAD. Conclusion: Our findings suggest a marked contemporary shift in the drivers of all-cause mortality among patients undergoing cardiac stress tests away from such factors as typical angina and inducible myocardial ischemia, which are declining in prevalence, and toward such factors as diabetes and an inability to perform exercise, which are increasing in prevalence

Moving Beyond Binary Grading of Coronary Arterial Stenoses on Coronary Computed Tomographic Angiography Insights for the Imager and Referring Clinician

ObjectivesWe evaluated the technical and clinical utility of visual 5-point coronary stenosis grading on coronary computed tomographic angiography (CCTA).BackgroundThe binary approach used to assess coronary stenoses on CCTA does not adequately describe borderline obstructive lesions and limits full expression of clinically useful information.MethodsFrom 84 patients who underwent CCTA and invasive angiography, we identified 278 native coronary segments with ≥25% stenosis on CCTA after excluding all <25% stenotic, stented, and uninterpretable segments. Fifty <25% stenotic segments were randomly selected as controls. Segmental stenosis severity on CCTA was consensually graded using a 0 to 5 scale (grade 0 = none, grade 1 = 1% to 24%, grade 2 = 25% to 49%, grade 3 = 50% to 69%, grade 4 = 70% to 89%, grade 5 = 90% to 100%) by 2 readers, using visual inspection and computed tomography–based quantification (CTQCA). Invasive angiography–based stenosis quantification (IQCA) was performed for all segments, using the same 0 to 5 scale to score stenosis severity.ResultsOn CCTA, 185 (56%) segments had intermediate stenoses (grade 2 or grade 3). Stenosis severity by IQCA increased significantly with each step-up in CCTA grade (p < 0.001). CTQCA did not perform better than visual inspection. Visual CCTA stenosis grading differed from IQCA by >1 grade in only 4% of grade 2 to grade 5 segments (10 of 278; 2% of CCTA grade 2 segments, 4% of grade 3, 8% of grade 4, 2% of grade 5). Overall quantitative correlation was strong (r = 0.82) with high variability in agreement between CTQCA and IQCA for individual segments (95% of differences between 27.2% and 34.6%).ConclusionsWith current CCTA technology, experienced readers should consider adopting a visually based, multitiered grading approach to evaluate coronary stenoses. A ≤49% lesion on CCTA can be considered virtually exclusive of ≥70% stenosis by invasive angiography

Aortic Size Assessment by Noncontrast Cardiac Computed Tomography: Normal Limits by Age, Gender, and Body Surface Area

ObjectivesTo determine normal limits for ascending and descending thoracic aorta diameters in a large population of asymptomatic, low-risk adult subjects.BackgroundAssessment of aortic size is possible from gated noncontrast computed tomography (CT) scans obtained for coronary calcium measurements. However, normal limits for aortic size by these studies have yet to be defined.MethodsIn 4,039 adult patients undergoing coronary artery calcium (CAC) scanning, systematic measurements of the ascending and descending thoracic aorta diameters were made at the level of the pulmonary artery bifurcation. Multiple linear regression analysis was used to detect risk factors independently associated with ascending and descending thoracic aorta diameter and exclude subjects with these parameters from the final analysis. The final analysis groups for ascending and descending thoracic aorta included 2,952 and 1,931 subjects, respectively. Subjects were then regrouped by gender, age, and body surface area (BSA) for ascending and descending aorta, separately, and for each group, the mean, standard deviation, and upper normal limit were calculated for aortic diameter as well as for the calculated cross-sectional aortic area. Also, linear regression models were used to create BSA versus aortic diameter nomograms by age groups, and a formula for calculating predicted aortic size by age, gender, and BSA was created.ResultsAge, BSA, gender, and hypertension were directly associated with thoracic aorta dimensions. Additionally, diabetes was associated with ascending aorta diameter, and smoking was associated with descending aorta diameter. The mean diameters for the final analysis group were 33 ± 4 mm for the ascending and 24 ± 3 mm for the descending thoracic aorta, respectively. The corresponding upper limits of normal diameters were 41 and 30 mm, respectively.ConclusionsNormal limits of ascending and descending aortic dimensions by noncontrast gated cardiac CT have been defined by age, gender, and BSA in a large, low-risk population of subjects undergoing CAC scanning

A randomized, placebo-controlled trial of late Na current inhibition (ranolazine) in coronary microvascular dysfunction (CMD): impact on angina and myocardial perfusion reserve

AIMS: The mechanistic basis of the symptoms and signs of myocardial ischaemia in patients without obstructive coronary artery disease (CAD) and evidence of coronary microvascular dysfunction (CMD) is unclear. The aim of this study was to mechanistically test short-term late sodium current inhibition (ranolazine) in such subjects on angina, myocardial perfusion reserve index, and diastolic filling. MATERIALS AND RESULTS: Randomized, double-blind, placebo-controlled, crossover, mechanistic trial in subjects with evidence of CMD [invasive coronary reactivity testing or non-invasive cardiac magnetic resonance imaging myocardial perfusion reserve index (MPRI)]. Short-term oral ranolazine 500–1000 mg twice daily for 2 weeks vs. placebo. Angina measured by Seattle Angina Questionnaire (SAQ) and SAQ-7 (co-primaries), diary angina (secondary), stress MPRI, diastolic filling, quality of life (QoL). Of 128 (96% women) subjects, no treatment differences in the outcomes were observed. Peak heart rate was lower during pharmacological stress during ranolazine (−3.55 b.p.m., P < 0.001). The change in SAQ-7 directly correlated with the change in MPRI (correlation 0.25, P = 0.005). The change in MPRI predicted the change in SAQ QoL, adjusted for body mass index (BMI), prior myocardial infarction, and site (P = 0.0032). Low coronary flow reserve (CFR <2.5) subjects improved MPRI (P < 0.0137), SAQ angina frequency (P = 0.027), and SAQ-7 (P = 0.041). CONCLUSIONS: In this mechanistic trial among symptomatic subjects, no obstructive CAD, short-term late sodium current inhibition was not generally effective for SAQ angina. Angina and myocardial perfusion reserve changes were related, supporting the notion that strategies to improve ischaemia should be tested in these subjects. TRIAL REGISTRATION: clinicaltrials.gov Identifier: NCT01342029