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Key Points Contrast-enhanced MRI is a noninvasive, clinically useful technique for accurate quantification and localization of myocardial fibrotic burden Late-gadolinium enhancement imaging can be used to identify the presence, pattern, and size of replacement or focal fibrosis, and has proven prognostic capacity T1 mapping allows for the accurate quantitation of diffuse and infiltrative interstitial fibrosis, and has tremendous prognostic potential in a wide variety of ischaemic and nonischaemic diseases Additional studies are needed to further define the prognostic relevance of late-gadolinium enhancement, T1 mapping, or both techniques used simultaneously, across different pathologies Cardiac MRI is a noninvasive phenotyping tool that allows for accurate and easy detection and quantification of myocardial fibrosis in myocardial tissue. In this Review, Ambale-Venkatesh and Lima focus on late-gadolinium enhancement and T1 mapping strategies, and explore the different prognostic applications of this technique. Fibrotic remodelling of the extracellular matrix is a healing mechanism necessary immediately after myocardial injury. However, prolonged increase in myocardial fibrotic activity results in stiffening of the myocardium and heralds adverse outcomes related to systolic and diastolic dysfunction, as well as arrhythmogenesis. Cardiac MRI provides a noninvasive phenotyping tool for accurate and easy detection and quantification of myocardial fibrosis by probing the retention of gadolinium-contrast agent in myocardial tissue. Late-gadolinium enhancement (LGE) cardiac MRI has been used extensively in a large number of studies for measurement of myocardial scarring. T1 mapping, a fairly new technique that can be used to identify the exact T1 value of the tissue, provides a direct measurement of the extracellular volume fraction of the myocardium. In contrast to LGE, T1 mapping can be used to measure diffuse myocardial fibrosis and differentiate between disease processes. In this Review, we describe the basic principles of imaging myocardial fibrosis using contrast-enhanced MRI and summarize its use for prognostic purposes.

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 . . .

Sudden emotional distress, such as that caused by an unexpected death, can sometimes produce severe transient left ventricular dysfunction. This stress-induced cardiomyopathy appears to be a form of myocardial stunning associated with marked sympathetic stimulation. Sudden emotional distress, such as that caused by an unexpected death, can sometimes produce severe transient left ventricular dysfunction. The potentially lethal consequences of emotional stress are deeply rooted in folk wisdom, as reflected by phrases such as “scared to death” and “a broken heart.” In the past decade, cardiac contractile abnormalities and heart failure have been reported after acute emotional stress, 1 – 6 but the mechanism remains unknown. We evaluated 19 patients with “stress cardiomyopathy,” a syndrome of profound myocardial stunning precipitated by acute emotional stress, in an effort to identify the clinical features that distinguish this syndrome from acute myocardial infarction and the cause of transient stress-induced myocardial dysfunction. Methods Study Patients Nineteen previously healthy patients were admitted . . .

Despite the low sensitivity of the electrocardiogram (ECG) in detecting left ventricular hypertrophy (LVH), ECG-LVH is known to be a strong predictor of cardiovascular risk. Understanding reasons for the discrepancies in detection of LVH by ECG versus imaging could help improve the diagnostic ability of ECG. We examined factors associated with false-positive and false-negative ECG-LVH, using cardiac magnetic resonance imaging (MRI) as the gold standard. We also compared the prognostic significance of ECG-LVH and MRI-LVH as predictors of cardiovascular events. This analysis included 4,748 participants (mean age 61.9 years, 53.5% females, 61.7% nonwhites). Logistic regression with stepwise selection was used to identify factors associated with false-positive (n = 208) and false-negative (n = 387), compared with true-positive (n = 208) and true-negative (n = 4,041) ECG-LVH, respectively. A false-negative ECG-LVH status was associated with increased odds of Hispanic race/ethnicity, current smoking, hypertension, increased systolic blood pressure, prolongation of QRS duration, and higher body mass index and with lower odds of increased ejection fraction (model-generalized R2 = 0.20). A false-positive ECG-LVH status was associated with lower odds of black race, Hispanic race/ethnicity, minor ST-T abnormalities, increased systolic blood pressure, and presence of any major electrocardiographic abnormalities (model-generalized R2 = 0.29). Both ECG-LVH and MRI-LVH were associated with an increased risk of cardiovascular disease events (hazard ratio 1.51, 95% confidence interval 1.03 to 2.20 and hazard ratio 1.81, 95% confidence interval 1.33 to 2.46, respectively). In conclusion, discrepancy in LVH detection by ECG and MRI can be relatively improved by considering certain participant characteristics. Discrepancy in diagnostic performance, yet agreement on predictive ability, suggests that LVH by ECG and LVH by imaging are likely to be two distinct but somehow related phenotypes.

Aims Resistin is a circulating inflammatory biomarker that is associated with cardiovascular disease. We investigated the associations of resistin and incident heart failure (HF) and its subtypes, as well as specific measures of subclinical HF (myocardial fibrosis and relevant biomarkers). Methods We analysed data from 1968 participants in the Multi‐Ethnic Study of Atherosclerosis with measurements of plasma resistin levels at clinic visits from 2002 to 2005. Participants were subsequently followed for a median of 10.5 years for HF events. The associations between resistin levels and incident HF, HF with reduced ejection fraction (HFrEF), and HF with preserved ejection fraction (HFpEF) were examined using multivariable Cox proportional hazards models. Linear regression models assessed the associations between resistin levels and myocardial fibrosis from cardiac magnetic resonance imaging, as well as hs‐cTnT and NT‐proBNP. Results The mean age of the cohort was 64.7 years, and 50.0% were female. Seventy‐four participants (4%) developed incident HF during follow‐up. In a Cox proportional hazards model adjusted for age, gender, education level, race/ethnicity, and traditional risk factors, higher resistin levels were significantly associated with incident HF (HR 1.44, CI 1.18–1.75, P = 0.001) and HFrEF (HR 1.47, CI 1.07–2.02, P = 0.016), but not with HFpEF (HR 1.25, CI 0.89–1.75, P = 0.195). Resistin levels showed no significant associations with myocardial fibrosis, NT‐proBNP, or hs‐cTnT levels. Conclusions In a multi‐ethnic cohort free of cardiovascular disease at baseline, elevated resistin levels were associated with incident HF, more prominently with incident HFrEF than HFpEF, but not with subclinical myocardial fibrosis or biomarkers of HF.

Atrial fibrillation (AF) occurs frequently in patients with chronic obstructive pulmonary disease. Epidemiologic studies have found inconsistent associations between lung function and AF, and none have studied pulmonary emphysema, which overlaps only partially with chronic obstructive pulmonary disease in the general population. The aim of this study was to assess the relation among lung function measured by spirometry, the percentage of emphysema-like lung on computed tomography, and incident AF. The Multi-Ethnic Study of Atherosclerosis (MESA) is a multicenter cohort study following 6,814 subjects free of clinical cardiovascular disease, including AF, at baseline. Spirometry was performed in a subset of 3,965 participants. Percentage emphysema was defined on baseline computed tomographic scans as lung regions <950 Hounsfield units. Incident AF was identified from hospital discharge diagnosis and Medicare claims data. Cox proportional hazards models were used to assess independent associations of lung volumes and percentage emphysema with AF. A total of 3,811 participants with valid spirometric results were included in this study. The mean age was 64.5 ± 9.8 years, and 49.4% were men. AF developed in 149 subjects (3.8%) over a mean follow-up period of 4.1 years after spirometry. Lower levels of forced expiratory volume at 1 second and forced vital capacity were associated with a higher risk for AF (hazard ratios 1.21 and 1.19 per 500 ml, respectively, p <0.001) after adjustment for demographic and cardiovascular risk factors. Percentage emphysema was not significantly related to AF. In conclusion, in a multiethnic community-based sample of subjects free of cardiovascular disease at baseline, functional airflow limitation was related to a higher risk for AF.

Aims Proteomic profiling offers an expansive approach to biomarker discovery and mechanistic hypothesis generation for LV remodelling, a critical component of heart failure (HF). We sought to identify plasma proteins cross‐sectionally associated with left ventricular (LV) size and geometry in a diverse population‐based cohort without known cardiovascular disease (CVD). Methods and results Among participants of the Multi‐Ethnic Study of Atherosclerosis (MESA), we quantified plasma abundances of 1305 proteins using an aptamer‐based platform at exam 1 (2000–2002) and exam 5 (2010–2011) and assessed LV structure by cardiac magnetic resonance (CMR) at the same time points. We used multivariable linear regression with robust variance to assess cross‐sectional associations between plasma protein abundances and LV structural characteristics at exam 1, reproduced findings in later‐life at exam 5, and explored relationships of associated proteins using annotated enrichment analysis. We studied 763 participants (mean age 60 ± 10 years at exam 1; 53% female; 19% Black race; 31% Hispanic ethnicity). Following adjustment for renal function and traditional CVD risk factors, plasma levels of 3 proteins were associated with LV mass index at both time points with the same directionality (FDR < 0.05): leptin (LEP), renin (REN), and cathepsin‐D (CTSD); 20 with LV end‐diastolic volume index: LEP, NT‐proBNP, histone‐lysine N‐methyltransferase (EHMT2), chordin‐like protein 1 (CHRDL1), tumour necrosis factor‐inducible gene 6 protein (TNFAIP6), NT‐3 growth factor receptor (NTRK3), c5a anaphylatoxin (C5), neurogenic locus notch homologue protein 3 (NOTCH3), ephrin‐B2 (EFNB2), osteomodulin (OMD), contactin‐4 (CNTN4), gelsolin (GSN), stromal cell‐derived factor 1 (CXCL12), calcineurin subunit B type 1 (PPP3R1), insulin‐like growth factor 1 receptor (IGF1R), bone sialoprotein 2 (IBSP), interleukin‐11 (IL‐11), follistatin‐related protein 1 (FSTL1), periostin (POSTN), and biglycan (BGN); and 4 with LV mass‐to‐volume ratio: RGM domain family member B (RGMB), transforming growth factor beta receptor type 3 (TGFBR3), ephrin‐A2 (EFNA2), and cell adhesion molecule 3 (CADM3). Functional annotation implicated regulation of the PI3K‐Akt pathway, bone morphogenic protein signalling, and cGMP‐mediated signalling. Conclusions We report proteomic profiling of LV size and geometry, which identified novel associations and reinforced previous findings on biomarker candidates for LV remodelling and HF. If validated, these proteins may help refine risk prediction and identify novel therapeutic targets for HF.

The relation between glycemic index, glycemic load, and subclinical coronary atherosclerosis is unknown. The aim of the study was to evaluate the associations between energy-adjusted glycemic index, glycemic load, and coronary artery calcium (CAC). This study was cross-sectional analysis of 28,429 asymptomatic Korean men and women (mean age 41.4 years) without a history of diabetes or cardiovascular disease. All participants underwent a health screening examination between March 2011 and April 2013, and dietary intake over the preceding year was estimated using a validated food frequency questionnaire. Cardiac computed tomography was used for CAC scoring. The prevalence of detectable CAC (CAC score >0) was 12.4%. In multivariable-adjusted models, the CAC score ratios (95% confidence intervals) comparing the highest to the lowest quintile of glycemic index and glycemic load were 1.74 (1.08 to 2.81; p trend = 0.03) and 3.04 (1.43 to 6.46; p trend = 0.005), respectively. These associations did not differ by clinical subgroups, including the participants at low cardiovascular risk. In conclusion, these findings suggest that high dietary glycemic index and glycemic load were associated with a greater prevalence and degree of CAC, with glycemic load having a stronger association.

Aims The effects of inhibition of sodium glucose cotransporter (SGLT)‐1, as opposed to SGLT2, on cardiovascular structure and function are not well known. We assessed the associations of a missense genetic variant of SGLT1 with cardiac structure and function. Methods and results We evaluated associations of a functionally modifying variant of SLC5A1 (rs17683011 [p.Asn51Ser]), the gene that encodes SGLT1, with cardiac structure and function on echocardiography among middle‐aged adults in the Coronary Artery Risk Development in Young Adults Study. Of 1904 participants (55.3 ± 3.5 years, 57% female, 34% Black), 166 (13%) White participants and 18 (3%) Black participants had at least one copy of rs17683011. There were no significant differences in age, sex, body mass index, glucose, or diabetes status by the presence of the rs17683011 variant. In Black participants, the presence of at least one copy of the rs17683011 variant was significantly associated with better GLS compared with those without a copy of the variant after covariate adjustment (−15.8 ± 0.7% vs. −14.0 ± 0.1%, P = 0.02). Although the direction of effect was consistent, the association between the presence of at least one copy of rs17683011 and GLS was not statistically significant in White participants (−15.1 ± 0.2% vs. −14.8 ± 0.1%, P = 0.16). There were no significant associations between rs17683011 and other measures of LV structure, systolic function, or diastolic function. Conclusions The rs17683011 variant, a functionally modifying variant of the SGLT1 gene, was associated with higher GLS among middle‐age adults. These exploratory findings require further validation and suggest that SGLT1 inhibition may have beneficial effects upon LV systolic function.