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In an international study, the authors evaluated the diagnostic performance of coronary angiography by means of 64-row multidetector computed tomography (CT). The technique accurately identified obstructive coronary lesions, but the positive and negative predictive values were inadequate for this technology to replace conventional coronary angiography with the use of contrast medium. In this study, coronary angiography by means of 64-row multidetector computed tomography (CT) accurately identified obstructive coronary lesions, but the positive and negative predictive values were inadequate for this technology to replace conventional coronary angiography. Coronary artery disease is the leading cause of death in the United States. 1 In symptomatic patients, diagnosis of the presence and severity of coronary artery disease is critical for determining appropriate clinical management. 2 , 3 Indirect evaluation of coronary stenosis, such as through stress testing, has limited diagnostic ability as compared with direct conventional coronary angiography. 4 , 5 Conventional coronary angiography reveals the extent, location, and severity of coronary obstructive lesions, which are potent predictors of outcome, 2 , 3 , 6 , 7 and identifies high-risk patients who may benefit from revascularization. 3 , 6 , 8 – 11 Thus, invasive coronary angiography, despite the associated risks, remains the . . .

In a population-based study, emphysema was quantified by computed tomography, pulmonary function was assessed by spirometry, and cardiac volumes and function were measured by magnetic resonance imaging. Both percent emphysema and the severity of airflow obstruction were linearly related to reductions in left ventricular end-diastolic volume, stroke volume, and cardiac output. These effects were more pronounced among smokers. In a population-based study, emphysema and the severity of airflow obstruction were linearly related to reductions in left ventricular end-diastolic volume, stroke volume, and cardiac output. Chronic obstructive pulmonary disease (COPD), defined as airflow obstruction that is not fully reversible, 1 is currently the fourth leading cause of death in the United States. 2 COPD overlaps partially with emphysema, which is characterized by the destruction of alveolar walls and the permanent enlargement of air spaces distal to the terminal bronchioles. 1 , 3 Cor pulmonale, which can occur in very severe COPD, is characterized by elevated pulmonary vascular resistance and right heart failure, with associated reductions in left ventricular filling, left ventricular stroke volume, and cardiac output, although left ventricular ejection fraction is generally preserved. 4 – 7 This disorder may occur . . .

Our understanding of the specific aspects of vascular contributions to dementia remains unclear. We aim to identify the correlates of incident dementia in a multi-ethnic cardiovascular cohort. A total of 6806 participants with follow-up data for incident dementia were included. Probable dementia diagnoses were identified using hospitalization discharge diagnoses according to the International Classification of Diseases Codes (ICD). We used Random Forest analyses to identify the correlates of incident dementia and cognitive function from among 198 variables collected at the baseline MESA exam entailing demographic risk factors, medical history, anthropometry, lab biomarkers, electrocardiograms, cardiovascular magnetic resonance imaging, carotid ultrasonography, coronary artery calcium and liver fat content. Death and stroke were considered competing events. Over 14 years of follow-up, 326 dementia events were identified. Beyond age, the top correlates of dementia included coronary artery calcification, high sensitivity troponin, common carotid artery intima to media thickness, NT-proBNP, physical activity, pulse pressure, tumor necrosis factor-α, history of cancer, and liver to spleen attenuation ratio from computed tomography. Correlates of cognitive function included income and physical activity, body size, serum glucose, glomerular filtration rate, measures of carotid artery stiffness, alcohol use, and inflammation indexed as IL-2 and TNF soluble receptors and plasmin-antiplasmin complex. In a deeply phenotyped cardiovascular cohort we identified the key correlates of dementia beyond age as subclinical atherosclerosis and myocyte damage, vascular function, inflammation, physical activity, hepatic steatosis, and history of cancer.

Intense exercise in elite athletes is associated with increased left ventricular (LV) and right ventricular (RV) mass and volumes. However, the effect of physical activity on the RV in an older community-based population is unknown. We studied the association between levels of physical activity in adults and RV mass and volumes. The Multi-Ethnic Study of Atherosclerosis (MESA) performed cardiac magnetic resonance imaging on community-based participants without clinical cardiovascular disease. RV volumes were determined from manually contoured endocardial margins. RV mass was determined from the difference between epicardial and endocardial volumes multiplied by the specific gravity of myocardium. Metabolic equivalent-minutes/day were calculated from the self-reported frequency, duration, and intensity of physical activity. The study sample (n = 1,867) was aged 61.8 ± 10 years, 48% male, 44% white, 27% African American, 20% Hispanic, and 9% Chinese. Higher levels of moderate and vigorous physical activity were linearly associated with higher RV mass (P = 0.02) after adjusting for demographics, anthropometrics, smoking, cholesterol, diabetes mellitus, hypertension, and LV mass. Higher levels of intentional exercise (physical activity done for the sole purpose of conditioning or fitness) were nonlinearly associated with RV mass independent of LV mass (P = 0.03). There were similar associations between higher levels of physical activity and larger RV volumes. Higher levels of physical activity in adults were associated with greater RV mass independent of the associations with LV mass; similar results were found for RV volumes. Exercise-associated RV remodeling may have important clinical implications.

Cardiovascular magnetic resonance (CMR) is currently the gold standard for assessing both global and regional myocardial function. New tools for quantifying regional function have been recently developed to characterize early myocardial dysfunction in order to improve the identification and management of individuals at risk for heart failure. Of particular interest is CMR myocardial tagging, a non-invasive technique for assessing regional function that provides a detailed and comprehensive examination of intra-myocardial motion and deformation. Given the current advances in gradient technology, image reconstruction techniques, and data analysis algorithms, CMR myocardial tagging has become the reference modality for evaluating multidimensional strain evolution in the human heart. This review presents an in depth discussion on the current clinical applications of CMR myocardial tagging and the increasingly important role of this technique for assessing subclinical myocardial dysfunction in the setting of a wide variety of myocardial disease processes.

Subcellular localization of nitric oxide (NO) synthases with effector molecules is an important regulatory mechanism for NO signalling 1 . In the heart, NO inhibits L-type Ca 2+ channels 2 but stimulates sarcoplasmic reticulum (SR) Ca 2+ release 3 , 4 , 5 , leading to variable effects on myocardial contractility. Here we show that spatial confinement of specific NO synthase isoforms regulates this process. Endothelial NO synthase (NOS3) localizes to caveolae 6 , 7 , 8 , where compartmentalization with β-adrenergic receptors and L-type Ca 2+ channels 9 allows NO to inhibit β-adrenergic-induced inotropy 8 , 10 . Neuronal NO synthase (NOS1), however, is targeted to cardiac SR 11 . NO stimulation of SR Ca 2+ release via the ryanodine receptor (RyR) in vitro 3 , 4 suggests that NOS1 has an opposite, facilitative effect on contractility. We demonstrate that NOS1-deficient mice have suppressed inotropic response, whereas NOS3-deficient mice have enhanced contractility, owing to corresponding changes in SR Ca 2+ release. Both NOS1 −/− and NOS3 −/− mice develop age-related hypertrophy, although only NOS3 −/− mice are hypertensive. NOS1/3 −/− double knockout mice have suppressed β-adrenergic responses and an additive phenotype of marked ventricular remodelling. Thus, NOS1 and NOS3 mediate independent, and in some cases opposite, effects on cardiac structure and function.

Evidence suggests an association between autonomical nervous system (ANS) function and atrial fibrillation (AF) development. We sought to examine the association of baseline resting heart rate (RHR) and short-term heart rate variability (HRV) as surrogates of (ANS) with incident AF in individuals without previous cardiovascular disease. A total of 6,261 participants of the Multi-Ethnic Study of Atherosclerosis who were free of AF and diagnosed cardiovascular disease were enrolled. Three standard 10-second, 12-lead electrocardiograms (ECG) were used to measure RHR, the standard deviation of normal-to-normal intervals (SDNN) and the root mean square of successive differences in RR intervals (RMSSD). Cox proportional hazards models adjusted for demographics, atrioventricular nodal agents, and known cardiovascular risk factors were used to examine the association of baseline RHR, and log transformed SDNN and RMSDD with incident AF. Over a mean follow-up of 11.3 ± 3.7 years, 754 (12%) participants developed AF. Spline curve analysis revealed a nonlinear association between RHR, HRV, and incident AF. In fully adjusted models higher (but not lower) baseline RHR (RHR >76 beats/min) was associated with incident AF (hazard ratio 1.48 95% confidence interval 1.18 to 1.86). Additionally, lower values of RMSDD and SDNN and higher values of RMSDD were independently associated with incident AF. In conclusion, cardiac ANS dysregulation indicated as higher RHR and lower HRV is associated with incident AF independent of known cardiovascular risk factors.

Peripheral artery disease (PAD) is important to public health as a major contributor to cardiovascular morbidity and mortality. Recent developments in magnetic resonance imaging (MRI) techniques permit improved assessment of PAD anatomy and physiology, and may serve as surrogate end points after proangiogenic therapies. The PACE study is a randomized, double-blind, placebo-controlled clinical trial designed to assess the physiologic impact and potential clinical efficacy of autologous bone marrow–derived ALDHbr stem cells. The primary MRI end points of the study are as follows: (1) total collateral count, (2) calf muscle plasma volume (a measure of capillary perfusion) by dynamic contrast-enhanced MRI, and (3) peak hyperemic popliteal flow by phase-contrast MRI (PC-MRI). The interreader and intrareader and test-retest results demonstrated good-to-excellent reproducibility (interclass correlation coefficient range 0.61-0.98) for all magnetic resonance measures. The PAD participants (n=82) had lower capillary perfusion measured by calf muscle plasma volume (3.8% vs 5.6%) and peak hyperemic popliteal flow (4.1 vs 13.5mL/s) as compared with the healthy participants (n=16), with a significant level of collateralization. Reproducibility of the MRI primary end points in PACE was very good to excellent. The PAD participants exhibited decreased calf muscle capillary perfusion as well as arterial flow reserve when compared with healthy participants. The MRI tools used in PACE may advance PAD science by enabling accurate measurement of PAD microvascular anatomy and perfusion before and after stem cell or other PAD therapies.

Post-contrast myocardial T1 (T1 myo,c ) values have been shown to be sensitive to myocardial fibrosis. Recent studies have shown differences in results obtained from T1 myo,c and extracellular volume fraction (ECV) with respect to percentage fibrosis. By exploring the relationship between blood plasma volume and T1 myo,c , the underlying basis for the divergence can be explained. Furthermore, dose administration based on body mass index (BMI), age and gender can mitigate the divergence in results. Inter-subject comparison of T1 myo,c required adjustment for dose (in mmol/kg), time and glomerular filtration rate. Further adjustment for effective dose based on lean muscle mass reflected by blood/plasma volume was performed. A test case of 605 subjects from the MESA study who had undergone pre- and post-contrast T1 mapping was studied. T1 myo,c values were compared between subjects with and without metabolic syndrome (MetS), between smoking and non-smoking subjects, and subjects with and without impaired glucose tolerance, before and after dose adjustment based on plasma volume. Comparison with ECV (which is dose independent), pre-contrast myocardial T1 and blood normalized myocardial T1 values was also performed to validate the correction. There were significant differences in T1 myo,c (post plasma volume correction) and ECV between current and former smokers ( p value 0.017 and 0.01, respectively) but not T1 myo,c prior to correction ( p  = 0.12). Prior to dose adjustment for plasma volume, p value was <0.001 for T1 myo,c between MetS and non-MetS groups and was 0.13 between subjects with and without glucose intolerance; after adjustment for PV, p value was 0.63 and 0.99. Corresponding ECV p values were 0.44 and 0.99, respectively. Overall, ECV results showed the best agreement with PV corrected T1 myo,c (mean absolute difference in p values = 0.073) and pre-contrast myocardial T1 in comparison with other measures (T1 myo,c prior to correction, blood/plasma T1 value normalized myocardium). Weight-based contrast dosing administered in mmol/kg results in a bias in T1 values which can lead to erroneous conclusions. After adjustment for lean muscle mass based on plasma volume, results from T1 myo,c were in line with ECV derived results. Furthermore, the use of a modified equivalent dose adjusted for BMI, age, sex and hematocrit can be adopted for quantitative imaging.

Background While studies of the left atrium (LA) have demonstrated associations between volumes and emptying fraction with atrial fibrillation (AF), the contribution of right atrial (RA) abnormalities to incident AF remains poorly understood. Objectives Assess the association between RA structure and function with incident AF using feature-tracking cardiovascular magnetic resonance (CMR). Methods This is a prospective cohort study of all participants in the Multi-Ethnic Study of Atherosclerosis with baseline CMR, sinus rhythm, and free of clinical cardiovascular disease at study initiation. RA volume, strain, and emptying fraction in participants with incident AF ( n  = 368) were compared against AF-free ( n  = 2779). Cox proportional-hazards models assessed association between variables. Results Participants were aged 60 ± 10 yrs., 55% female, and followed an average 11.2 years. Individuals developing AF had higher baseline RA maximum volume index (mean ± standard deviation [SD]: 24 ± 9 vs 22 ± 8 mL/m 2 , p  = 0.002) and minimum volume index (13 ± 7 vs 12 ± 6 mL/m 2 , p  < 0.001), and lower baseline RA emptying fraction (45 ± 15% vs 47 ± 15%, p  = 0.02), peak global strain (34 ± 17% vs 36 ± 19%, p  < 0.001), and peak free-wall strain (40 ± 23% vs 42 ± 26%, p  = 0.049) compared with the AF-free population. After adjusting for traditional cardiovascular risk factors and LA volume and function, we found RA maximum volume index (hazards ratio [HR]: 1.13 per SD, p  = 0.041) and minimum volume index (HR: 1.12 per SD, p  = 0.037) were independently associated with incident AF. Conclusions In a large multiethnic population, higher RA volume indices were independently associated with incident AF after adjustment for conventional cardiovascular risk factors and LA parameters. It is unclear if this predictive value persists when additional adjustment is made for ventricular parameters.