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Objectives: In patients with arterial hypertension (AH), hypertension-mediated organ damage may be manifested by cardiac chamber enlargement and/or remodeling. Cardiac computed tomography imaging has emerged as an important method for morphological assessment of cardiac chambers. We tested the hypothesis that prevalence of cardiac chamber abnormalities is specifically related to clinical categories of AH in the general population., Methods: We studied 4747 individuals, mean age was 60 years (range: 40-93), 46% were men, undergoing 320-detector computed tomography in the Copenhagen General Population Study. Clinical categories of AH were: normotensive (n = 2484), untreated hypertensive (n = 1301), treated controlled hypertensive (n = 412) and treated uncontrolled hypertensive (n = 550). Chamber abnormalities in the form of left ventricular (LV) concentric remodeling, LV eccentric hypertrophy, LV concentric hypertrophy or left atrial enlargement were assessed, in addition to LV or right ventricular enlargement., Results: Chamber abnormalities were present in 23% of all individuals. Combined LV and left atrial abnormalities were rare (<2%). LV concentric remodeling (10%) was the most prevalent abnormality, and most commonly found in individuals with treated hypertension. LV and right ventricular enlargements were unrelated to hypertension. The highest frequencies of chamber abnormalities were found in individuals of elevated blood pressure (BP) with (40%) or without (32%) treatment, as opposed to individuals of normal BP with (27%) or without (14%) treatment, P less than 0.0001., Conclusion: In a general population cohort, untreated or inadequately treated AH was associated with the highest prevalence of cardiac chamber enlargement and remodeling. These observations suggest a strong link between elevated BPs and development of hypertension-mediated organ damage., (Copyright © 2020 Wolters Kluwer Health, Inc. All rights reserved.)

Objectives: Before cardiac resynchronization therapy (CRT) implantation, cardiac computed tomography (CT) can provide assessment of cardiac venous anatomy and visualize left ventricular (LV) myocardial scar. We hypothesized that localization and burden of transmural myocardial scar verified by cardiac CT are associated with echocardiographic and clinical response to CRT., Methods: We prospectively included 140 CRT recipients undergoing preimplant cardiac CT. We assessed transmural scar, defined as hypoperfusion involving more than one-half of the myocardial wall in each LV segment using a 17-segment model. Echocardiographic nonresponse was defined as less than 5% absolute improvement in LV ejection fraction at 6 months' follow-up. Clinical nonresponse was defined as 1 or more of the following at 6 months' follow-up: death, heart failure hospitalization, or no improvement in New York Heart Association class and less than 10% increase in 6-minute walk-test distance., Results: Higher burden of myocardial scar was associated with echocardiographic nonresponse (adjusted odds ratio, 3.02; 95% confidence interval, 1.03-8.91; P = 0.045). Scar concordant or adjacent to LV pacing site was associated with echocardiographic nonresponse (adjusted odds ratio, 8.2; 95% confidence interval, 1.51-44.27; P = 0.015). No association between scar and clinical nonresponse was demonstrated., Conclusions: Higher scar burden and scar in proximity to the LV pacing site assessed by cardiac CT are associated with echocardiographic nonresponse to CRT. Burden and location of scar were not associated with clinical nonresponse. Further large-scale studies are needed to assess the potential association between myocardial scar detected by cardiac CT and clinical CRT outcome.

Aims: Atrial fibrillation (AF) is a common cardiac arrhythmia that is associated with substantial morbidity and mortality. AF is associated with enlargement of the left atrium (LA), and the LA volume has important prognostic implications for the disease. The objective of the study was to determine how measurements of LA volume and function obtained by transthoracic echocardiography (TTE), cardiac magnetic resonance (CMR), and 320-slice multi-detector computed tomography (MDCT) correlate in patients with permanent AF., Methods and Results: Thirty-four patients with permanent AF participated in the study. TTE, CMR, and 320-slice MDCT imaging procedures were performed within 7 ± 4 days. 320-slice MDCT overestimated maximal LA volume (LAmax) and minimal LA volume (LAmin) compared with CMR (LAmax: 80 vs. 73 mL/m(2), P = 0.0017; LAmin: 69 vs. 64 mL/m(2), P = 0.0217), whereas TTE underestimated these parameters compared with CMR (LAmax: 60 vs. 73 mL/m(2), P < 0.0001; LAmin: 50 vs. 64 mL/m(2), P < 0.0001), and also compared with MDCT (LAmax: 60 vs. 80 mL/m(2), P < 0.0001; LAmin: 50 vs. 69 mL/m(2), P < 0.0001). Measurements of LA volumes by MDCT and CMR closely correlated, and both MDCT and CMR had excellent intra- and inter-observer agreement with correlation coefficients of >0.90. The correlation between TTE-derived measurements and CMR/MDCT was fair to moderate. Intra- and inter-observer agreement for LA volume measurements by TTE were inferior to CMR and MDCT., Conclusion: Measurements of LA volumes by CMR and 320-slice MDCT correlate closely in patients with permanent AF, and both modalities improve the reproducibility of measurements of LA volumes and function compared with 2D TTE.

Measurement of left atrial (LA) maximal volume (LA(max)) using two-dimensional transthoracic echocardiography (TTE) provides prognostic information in several cardiac diseases. However, the relationship between LA(max) and LA function is poorly understood and TTE is less well suited for measuring dynamic LA volume changes. Conversely, cardiac magnetic resonance imaging (CMR) and multi-slice computed tomography (MSCT) appears more appropriate for such measures. We sought to determine the relationship between LA size assessed with TTE and LA size and function assessed with CMR and MSCT. Fifty-four patients were examined 3 months post myocardial infarction with echocardiography, CMR and MSCT. Left atrial volumes and LA reservoir function were assessed by TTE. LA time-volume curves were determined and LA reservoir function (cyclic change and fractional change), passive emptying function (reservoir volume) and pump function (left atrial ejection fraction-LAEF) were derived using CMR and MSCT. Left atrial fractional change and left atrial ejection fraction (LAEF) determined with CMR and MSCT were unrelated to LA(max) enlargement by echocardiography (P = NS). There was an overall good agreement between CMR and MSCT, with a small to moderate bias in LA(max) (4.9 ± 10.4 ml), CC (3.1 ± 9.1 ml) and reservoir volume (3.4 ± 9.1 ml). TTE underestimates LA(max) with up to 32% compared with CMR and MSCT (P < 0.001). Left atrial function assessed with MSCT and CMR as LA fractional change and LAEF is not significantly related to LA(max) measured by TTE. TTE systematically underestimated LA volumes, whereas there are good agreements between MSCT and CMR for volumetric and functional properties.

Aims: The third isotype of beta adrenergic receptors (β3 ARs) has distinctly different effects on cardiomyocytes compared with β1 and β2 ARs. Stimulation of β3 ARs may reduce cardiomyocyte Na+ overload and reduce oxidative stress in heart failure (HF). We examined if treatment with the β3 AR agonist mirabegron increases LVEF in patients with HF.Methods and Results: In a double-blind trial we randomly assigned 70 patients with NYHA class II-III HF and LVEF <40% at screening-echocardiography to receive mirabegron or placebo for 6 months as add-on to optimized standard therapy. The primary endpoint was an increase in LVEF after 6 months as measured by computed tomography (CT). Changes in LVEF after 6 months between treatment groups were not significantly different (0.4%, -3.5 to 3.8%, P = 0.82). In an exploratory analysis, based on an expectation that the pathophysiological substrate targeted with treatment is dependent on the baseline LVEF, patients with LVEF <40% by CT given mirabegron had a significant increase in LVEF while no increase was seen in patients given placebo. The changes were significantly different between groups (5.5%, 0.6-10.4%, P < 0.03). Additionally, there was interaction between baseline LVEF and change in LVEF in the entire group of patients treated with mirabegron (R2  = 0.40, β  = -0.63, P < 0.001), but not in the placebo group (R2  = 0.00, β  = -0.01, P = 0.95). Treatment was generally well tolerated. Three patients in each group had fatal or life-threatening events.Conclusions: The primary endpoint was not reached. Exploratory analysis indicated that β3 AR stimulation by mirabegron increased LVEF in patients with severe HF. Treatment appeared safe. Additional studies in severe HF are needed.Trial Registration: NCT01876433. [ABSTRACT FROM AUTHOR]

Background: Left atrial volume (LAV) estimation with 3D echocardiography has been shown to be more accurate than 2D volume calculation. However, little is known about the possible effect of respiratory movements on the accuracy of the measurement.Methods: 100 consecutive patients admitted with chest pain were examined with 3D echocardiography and LAV was quantified during inspiratory breath hold, expiratory breath hold and during free breathing.Results: Of the 100 patients, only 65 had an echocardiographic window that allowed for 3D echocardiography in the entire respiratory cycle. Mean atrial end diastolic volume was 45.4 ± 14.5 during inspiratory breath hold, 46.4 ± 14.8 during expiratory breath hold and 45.6 ± 14.3 during free respiration. Mean end systolic volume was 17.6 ± 7.8 during inspiratory breath hold, 18.8 ± 8.0 during expiratory breath hold and 18.3 ± 8.0 during free respiration. No significant differences were seen in any of the measured parameters.Conclusions: The present study adds to the feasibility of 3D LAV quantitation. LAV estimation by 3D echocardiography may be performed during either end-expiratory or end-inspiratory breath-hold without any significant difference in the calculated volume. Also, the LAV estimation may be performed during free breathing. [ABSTRACT FROM AUTHOR]

Objective: There is a lack of disease-modifying treatments in hypertrophic cardiomyopathy (HCM). The aim of this randomised, placebo-controlled study was to assess if losartan could improve or ameliorate deterioration of cardiac function and exercise capacity.Methods: Echocardiography, exercise test and MRI or CT were performed at baseline and after 12 months in 133 patients (52±13 years, 35% female) randomly allocated to losartan (100 mg/day) or placebo.Results: Losartan had no effect on systolic function compared with placebo (mean difference for left ventricular ejection fraction (LVEF) 0% (95% CI -3% to 4%), p=0.84 or global longitudinal strain 0.7% (95% CI -0.2% to 1.6%), p=0.13). Neither Doppler measures of diastolic function, left atrial volume (mean difference 2 mL/m(2) (95% CI -4 to 8 mL/m(2)) p=0.53) nor exercise capacity (mean difference -0.3 metabolic equivalents (METS) (95% CI -1.0 to 0.3 METS), p=0.28) differed between the treatment groups. At follow-up, there was further progression of disease, with the most prominent impairment being an increase in left atrial volume of 6 mL/m(2) (95% CI 3 to 9 mL/m(2), p<0.0001) in both groups combined. LVEF decreased (mean change -2%, (95% CI -3% to -1%), p=0.037) and 4% of patients had end-stage HCM with a LVEF of less than 50% at the end of the study.Conclusion: Treatment with losartan had no effect on cardiac function or exercise capacity compared with placebo. Losartan fail to improve myocardial performance and failed to alter the progression of the disease. These findings do not support the use of angiotensin II receptor blockers as disease modifiers in adult patients with overt HCM.Trial Registration Number: NCT01447654-results. [ABSTRACT FROM AUTHOR]

Aims Atrial fibrillation (AF) is a common cardiac arrhythmia that is associated with substantial morbidity and mortality. AF is associated with enlargement of the left atrium (LA), and the LA volume has important prognostic implications for the disease. The objective of the study was to determine how measurements of LA volume and function obtained by transthoracic echocardiography (TTE), cardiac magnetic resonance (CMR), and 320-slice multi-detector computed tomography (MDCT) correlate in patients with permanent AF. Methods and results Thirty-four patients with permanent AF participated in the study. TTE, CMR, and 320-slice MDCT imaging procedures were performed within 7 ± 4 days. 320-slice MDCT overestimated maximal LA volume (LAmax) and minimal LA volume (LAmin) compared with CMR (LAmax: 80 vs. 73 mL/m2, P = 0.0017; LAmin: 69 vs. 64 mL/m2, P = 0.0217), whereas TTE underestimated these parameters compared with CMR (LAmax: 60 vs. 73 mL/m2, P < 0.0001; LAmin: 50 vs. 64 mL/m2, P < 0.0001), and also compared with MDCT (LAmax: 60 vs. 80 mL/m2, P < 0.0001; LAmin: 50 vs. 69 mL/m2, P < 0.0001). Measurements of LA volumes by MDCT and CMR closely correlated, and both MDCT and CMR had excellent intra- and inter-observer agreement with correlation coefficients of >0.90. The correlation between TTE-derived measurements and CMR/MDCT was fair to moderate. Intra- and inter-observer agreement for LA volume measurements by TTE were inferior to CMR and MDCT. Conclusion Measurements of LA volumes by CMR and 320-slice MDCT correlate closely in patients with permanent AF, and both modalities improve the reproducibility of measurements of LA volumes and function compared with 2D TTE. [ABSTRACT FROM PUBLISHER]

Background. Atrial fibrillation (AF) is associated with significant morbidity and mortality. To test the effect of interventions, knowledge of cardiac output (CO) is important. However, the irregular heart rate might cause some methods for determination of CO to have inherent weaknesses. Objective. To assess the validity of these methods in AF, a new inert gas rebreathing device and impedance cardiography was tested with echocardiography as reference. Methods. Using a cross-sectional design, 127 patients with AF and 24 in SR were consecutively recruited. Resting CO was measured using inert gas rebreathing ( n == 62) or impedance measurement of intrathoracic blood flow ( n == 89) in separate studies with echocardiographic measurement as reference. Results. CO determined with impedance cardiography was mean 4.77 L/min ±± 2.24(SD) compared to 4.93 L/min ±± 1.17 by echocardiography ( n == 89, n.s.) in patients with AF. CO by inert gas rebreathing was 4.98 L/min ±± 2.49(SD) compared to 5.70 L/min ±± 2.49 by echocardiography ( n == 62, n.s.) in patients with AF and SR (AF 5.42 ±± 2.9 vs. 6.27, n.s. and SR 4.09 ±± 1.08 vs. 4.35 ±± 0.86, n.s.). Mean bias between impedance cardiography and echocardiography was 0.14 ±± 0.95 L/min and −−0.13 ±± 0.98 L/min between inert gas rebreathing and echocardiography. Inert gas rebreathing showed larger intra-patient variation than impedance cardiography (0.11 vs. 0.054). Correlation between inert gas rebreathing and echocardiography was r == −−0.060 and between impedance cardiography and echocardiography was r == 0.128. Impedance cardiography and inert gas rebreathing both underestimated CO compared to echocardiography. Conclusion. Variation between the inert gas rebreathing and the reference method for AF patients was less than desired. Impedance cardiography was superior to inert gas rebreathing and showed acceptable agreement with echocardiography and variability similar to echocardiography. [ABSTRACT FROM AUTHOR]

Background: Mitral regurgitation (MR) secondary to ischemic heart disease (IHD) increases during exercise. We tested the hypothesis that the same is also true for MR due to mitral valve prolapse (MVP). Methods: Consecutive patients with asymptomatic MR of varying severity underwent exercise test on a supine bicycle with workload up to a maximum of 100 W. Echocardiographic measurements were performed at rest and at peak exercise. The study was designed to detect an effective regurgitant orifice (ERO) change of at least 10 mm during exercise. Results: Twenty-six patients (21 male, age 56 ± 12 years (mean ± SD)) were included. Patients had an ERO of 35 ± 23 mm (mean ± SD) and regurgitation volume of 48 ± 38 mL (mean ± SD). In these patients, ERO remained unchanged (an increase of 2 ± 15 mm during exercise, P = 0.6). The regurgitation volume (RVol) decreased with 11 ± 16 mL (mean ± SD), P = 0.003. When calculated for 1 minute, RVol increased during exercise (P = 0.01), but in relation to the total cardiac output it decreased significantly (P = 0.02). Conclusion: Exercise does not increase the severity of MR due to MVP, in contrast to MR secondary to IHD. Different disease mechanisms behind these two types of MR could explain this difference. (Echocardiography 2010;27:1031-1037) [ABSTRACT FROM AUTHOR]

Abstract: Background: Multidetector computed tomography (MDCT) of the heart provides both anatomical and functional information. The objective of this study was to evaluate the accuracy of quantitative assessment of left ventricular contractile function in relation to two-dimensional transthoracic echocardiography (TTE). Materials and methods: Sixty-four patients with known or suspected coronary artery disease underwent ECG-gated 64-slice MDCT and TTE. Regional left ventricular contractile function was measured by percent systolic wall thickening (SWT) in 16 myocardial segments using MDCT, and compared with visual evaluation of wall motion score (WMS) by TTE. Global SWT by MDCT was calculated as the mean SWT of all myocardial segments and compared with wall motion index (WMI) by TTE. Results: Eight hundred and eleven segments (81%) were classified as normokinetic, 142 (14%) as hypokinetic, 41 (4%) as akinetic and 5 (0.5%) as dyskinetic by TTE. A significant inverse linear trend was found between regional SWT by MDCT and WMS by TTE (p <0.001). Sensitivity and specificity for the identification of regional abnormalities of contractile function were 76% and 78%, respectively. A linear correlation between global SWT by MDCT and WMI by TTE was found (r =−0.8, p <0.001). Sensitivity and specificity for the identification of WMI>1.5 using global SWT was 91% and 94%, respectively. Conclusion: Quantification of systolic wall thickening by MDCT provides functional information, which is well correlated to visual assessment of global left ventricular contractile function by TTE. [Copyright &y& Elsevier]

Background: Subclinical leaflet thrombosis of bioprosthetic aortic valves after transcatheter valve replacement (TAVR) and surgical aortic valve replacement (SAVR) has been found with CT imaging. The objective of this study was to report the prevalence of subclinical leaflet thrombosis in surgical and transcatheter aortic valves and the effect of novel oral anticoagulants (NOACs) on the subclinical leaflet thrombosis and subsequent valve haemodynamics and clinical outcomes on the basis of two registries of patients who had CT imaging done after TAVR or SAVR.Methods: Patients enrolled between Dec 22, 2014, and Jan 18, 2017, in the RESOLVE registry, and between June 2, 2014, and Sept 28, 2016, in the SAVORY registry, had CT imaging done with a dedicated four-dimensional volume-rendered imaging protocol at varying intervals after TAVR and SAVR. We defined subclinical leaflet thrombosis as the presence of reduced leaflet motion, along with corresponding hypoattenuating lesions shown with CT. We collected data for baseline demographics, antithrombotic therapy, and clinical outcomes. We analysed all CT scans, echocardiograms, and neurological events in a masked fashion.Findings: Of the 931 patients who had CT imaging done (657 [71%] in the RESOLVE registry and 274 [29%] in the SAVORY registry), 890 [96%] had interpretable CT scans (626 [70%] in the RESOLVE registry and 264 [30%] in the SAVORY registry). 106 (12%) of 890 patients had subclinical leaflet thrombosis, including five (4%) of 138 with thrombosis of surgical valves versus 101 (13%) of 752 with thrombosis of transcatheter valves (p=0·001). The median time from aortic valve replacement to CT for the entire cohort was 83 days (IQR 33-281). Subclinical leaflet thrombosis was less frequent among patients receiving anticoagulants (eight [4%] of 224) than among those receiving dual antiplatelet therapy (31 [15%] of 208; p<0·0001); NOACs were equally as effective as warfarin (three [3%] of 107 vs five [4%] of 117; p=0·72). Subclinical leaflet thrombosis resolved in 36 (100%) of 36 patients (warfarin 24 [67%]; NOACs 12 [33%]) receiving anticoagulants, whereas it persisted in 20 (91%) of 22 patients not receiving anticoagulants (p<0·0001). A greater proportion of patients with subclinical leaflet thrombosis had aortic valve gradients of more than 20 mm Hg and increases in aortic valve gradients of more than 10 mm Hg (12 [14%] of 88) than did those with normal leaflet motion (seven [1%] of 632; p<0·0001). Although stroke rates were not different between those with (4·12 strokes per 100 person-years) or without (1·92 strokes per 100 person-years) reduced leaflet motion (p=0·10), subclinical leaflet thrombosis was associated with increased rates of transient ischaemic attacks (TIAs; 4·18 TIAs per 100 person-years vs 0·60 TIAs per 100 person-years; p=0·0005) and all strokes or TIAs (7·85 vs 2·36 per 100 person-years; p=0·001).Interpretation: Subclinical leaflet thrombosis occurred frequently in bioprosthetic aortic valves, more commonly in transcatheter than in surgical valves. Anticoagulation (both NOACs and warfarin), but not dual antiplatelet therapy, was effective in prevention or treatment of subclinical leaflet thrombosis. Subclinical leaflet thrombosis was associated with increased rates of TIAs and strokes or TIAs. Despite excellent outcomes after TAVR with the new-generation valves, prevention and treatment of subclinical leaflet thrombosis might offer a potential opportunity for further improvement in valve haemodynamics and clinical outcomes.Funding: RESOLVE (Cedars-Sinai Heart Institute) and SAVORY (Rigshospitalet). [ABSTRACT FROM AUTHOR]