Left ventricular extracellular volume fraction and atrioventricular interaction in hypertension.

OBJECTIVES: Left atrial enlargement (LAE) predicts cardiovascular morbidity and mortality. Impaired LA function also confers poor prognosis. This study aimed to determine whether left ventricular (LV) interstitial fibrosis is associated with LAE and LA impairment in systemic hypertension. METHODS: Following informed written consent, a prospective observational study of 86 hypertensive patients (49 ± 15 years, 53% male, office SBP 168 ± 30 mmHg, office DBP 97 ± 4 mmHg) and 20 normotensive controls (48 ± 13 years, 55% male, office SBP 130 ± 13 mmHg, office DBP 80 ± 11 mmHg) at 1.5-T cardiovascular magnetic resonance was conducted. Extracellular volume fraction (ECV) was calculated by T1-mapping. LA volume (LAV) was measured with biplane area-length method. LA reservoir, conduit and pump function were calculated with the phasic volumetric method. RESULTS: Indexed LAV correlated with indexed LV mass (R = 0.376, p < 0.0001) and ECV (R = 0.359, p = 0.001). However, ECV was the strongest significant predictor of LAE in multivariate regression analysis (odds ratio [95th confidence interval] 1.24 [1.04-1.48], p = 0.017). Indexed myocardial interstitial volume was associated with significant reductions in LA reservoir (R = -0.437, p < 0.0001) and conduit (R = -0.316, p = 0.003) but not pump (R = -0.167, p = 0.125) function. Multiple linear regression, correcting for age, gender, BMI, BP and diabetes, showed an independent decrease of 3.5% LA total emptying fraction for each 10 ml/m2 increase in myocardial interstitial volume (standard ß coefficient -3.54, p = 0.002). CONCLUSIONS: LV extracellular expansion is associated with LAE and impaired LA reservoir and conduit function. Future studies should identify if targeting diffuse LV fibrosis is beneficial in reverse remodelling of LA structural and functional pathological abnormalities in hypertension. KEY POINTS: • Left atrial enlargement (LAE) and impairment are markers of adverse prognosis in systemic hypertension but their pathophysiology is poorly understood. • Left ventricular extracellular volume fraction was the strongest independent multivariate predictor of LAE and was associated with impaired left atrial reservoir and conduit function. • LV interstitial expansion may play a central role in the pathophysiology of adverse atrioventricular interaction in systemic hypertension.

Repaired coarctation of the aorta, persistent arterial hypertension and the selfish brain.

BACKGROUND: It has been estimated that 20-30% of repaired aortic coarctation (CoA) patients develop hypertension, with significant cardiovascular morbidity and mortality. Vertebral artery hypoplasia (VAH) with an incomplete posterior circle of Willis (ipCoW; VAH + ipCoW) is associated with increased cerebrovascular resistance before the onset of increased sympathetic nerve activity in borderline hypertensive humans, suggesting brainstem hypoperfusion may evoke hypertension to maintain cerebral blood flow: the "selfish brain" hypothesis. We now assess the "selfish brain" in hypertension post-CoA repair. METHODS: Time-of-flight cardiovascular magnetic resonance angiography from 127 repaired CoA patients (34 ± 14 years, 61% male, systolic blood pressure (SBP) 138 ± 19 mmHg, diastolic blood pressure (DBP) 76 ± 11 mmHg) was compared with 33 normotensive controls (42 ± 14 years, 48% male, SBP 124 ± 10 mmHg, DBP 76 ± 8 mmHg). VAH was defined as < 2 mm and ipCoW as hypoplasia of one or both posterior communicating arteries. RESULTS: VAH + ipCoW was more prevalent in repaired CoA than controls (odds ratio: 5.8 [1.6-20.8], p = 0.007), after controlling for age, sex and body mass index (BMI). VAH + ipCoW was an independent predictor of hypertension (odds ratio: 2.5 [1.2-5.2], p = 0.017), after controlling for age, gender and BMI. Repaired CoA subjects with VAH + ipCoW were more likely to have difficult to treat hypertension (odds ratio: 3.3 [1.01-10.7], p = 0.049). Neither age at time of CoA repair nor any specific repair type were significant predictors of VAH + ipCoW in univariate regression analysis. CONCLUSIONS: VAH + ipCoW predicts arterial hypertension and difficult to treat hypertension in repaired CoA. It is unrelated to age at time of repair or repair type. CoA appears to be a marker of wider congenital cerebrovascular problems. Understanding the "selfish brain" in post-CoA repair may help guide management. JOURNAL SUBJECT CODES: High Blood Pressure; Hypertension; Magnetic Resonance Imaging (MRI); Cardiovascular Surgery; Cerebrovascular Malformations.

Cardiovascular Manifestations and Complications of Loeys-Dietz Syndrome: CT and MR Imaging Findings.

Loeys-Dietz syndrome (LDS) is a recently described genetic connective tissue disorder with a wide spectrum of multisystem involvement. LDS is characterized by rapidly progressive aortic and peripheral arterial aneurysmal disease. LDS and the other inherited aortopathies such as Marfan syndrome have overlapping phenotypic features. However, LDS is characterized by a more aggressive vascular course; patient morbidity and mortality occur at an early age, with complications developing at relatively smaller aortic dimensions. In addition, there is more diffuse arterial involvement in LDS, with a large proportion of patients developing aneurysms of the iliac, mesenteric, and intracranial arteries. Early diagnosis and careful follow-up are essential for ensuring timely intervention in patients with arterial disease. Cross-sectional angiography has an important role in the baseline assessment, follow-up, and evaluation of acute complications of LDS, the thresholds and considerations of which differ from those of other inherited aortopathies. In this article, LDS is compared with other genetic vascular connective tissue disorders. In addition, the genetic, histopathologic, and cardiovascular manifestations of this disease process are reviewed, with a focus on computed tomographic and magnetic resonance imaging findings. Online DICOM image stacks and supplemental material are available for this article. ©RSNA, 2018.

Hypertensive heart disease versus hypertrophic cardiomyopathy: multi-parametric cardiovascular magnetic resonance discriminators when end-diastolic wall thickness ≥ 15 mm.

OBJECTIVES: European guidelines state left ventricular (LV) end-diastolic wall thickness (EDWT) ≥15mm suggests hypertrophic cardiomyopathy (HCM), but distinguishing from hypertensive heart disease (HHD) is challenging. We identify cardiovascular magnetic resonance (CMR) predictors of HHD over HCM when EDWT ≥15mm. METHODS: 2481 consecutive clinical CMRs between 2014 and 2015 were reviewed. 464 segments from 29 HCM subjects with EDWT ≥15mm but without other cardiac abnormality, hypertension or renal impairment were analyzed. 432 segments from 27 HHD subjects with EDWT ≥15mm but without concomitant cardiac pathology were analyzed. Magnitude and location of maximal EDWT, presence of late gadolinium enhancement (LGE), LV asymmetry (>1.5-fold opposing segment) and systolic anterior motion of the mitral valve (SAM) were measured. Multivariate logistic regression was performed. Significance was defined as p<0.05. RESULTS: HHD and HCM cohorts were age-/gender-matched. HHD had significantly increased indexed LV mass (110±27g/m2 vs. 91±31g/m2, p=0.016) but no difference in site or magnitude of maximal EDWT. Mid-wall LGE was significantly more prevalent in HCM. Elevated indexed LVM, mid-wall LGE and absence of SAM were significant multivariate predictors of HHD, but LV asymmetry was not. CONCLUSIONS: Increased indexed LV mass, absence of mid-wall LGE and absence of SAM are better CMR discriminators of HHD from HCM than EDWT ≥15mm. KEY POINTS: • Hypertrophic cardiomyopathy (HCM) is often diagnosed with end-diastolic wall thickness ≥15mm. • Hypertensive heart disease (HHD) can be difficult to distinguish from HCM. • Retrospective case-control study showed that location and magnitude of EDWT are poor discriminators. • Increased left ventricular mass and midwall fibrosis are independent predictors of HHD. • Cardiovascular magnetic resonance parameters facilitate a better discrimination between HHD and HCM.

Endovascular closure of thoracic aortic pseudoaneurysms: A combined device occlusion and coil embolization technique in patients unsuitable for surgery or stenting.

OBJECTIVES: Our aim was to retrospectively evaluate non-stent graft closure of ascending aortic pseudoaneurysms at our center over a 10-year period, and describe a combined device occlusion and coil embolization technique. BACKGROUND: Aortic pseudoaneurysms (APAs) are a rare complication post cardiothoracic surgery, but can have fatal complications. There is increasing use of percutaneous interventional techniques for occlusion of aortic pseudoaneurysms in patients who are considered unsuitable for surgery. Stent graft deployment may not be possible depending on the specific anatomy and pathology. METHODS AND RESULTS: Retrospective evaluation of the catheter laboratory database was performed at our center and anonymized data was obtained for patients who had nonstent endovascular treatment of APAs. Twelve patients were identified with a mean age of 63 ± 16 years. Seven patients had the combined occlusion and embolization technique, only 1/7 (14.3%) died from complications related to APAs. Five patients had occlusion device only, 3/5 (60%) died of complications related to their APA. The mean survival for the patients who had a combination procedure was 33.2±.22.6 months (range, 1 - 60 months), compared to 2.7 ± 2.6 months with device closure only (note 2 patients had short follow up of <3 months). CONCLUSIONS: We evaluate non-stent graft percutaneous closure of APAs in a high-risk patient group and provide data on the use of a novel combined occlusion device and coil embolization technique. We feel this is a viable approach to APA closure in this population but this will require larger clinical studies in the future. © 2016 Wiley Periodicals, Inc.

Measurement of myocardium at risk with cardiovascular MR: comparison of techniques for edema imaging.

PURPOSE: To determine variability and agreement for detecting myocardial edema with T2-weighted short-tau inversion recovery (STIR), acquisition for cardiac unified T2 edema (ACUT2E), T2 mapping, and early gadolinium enhancement (EGE) after successfully reperfused ST-segment-elevation myocardial infarction (STEMI) and diagnostic accuracy of each sequence to predict infarct-related artery (IRA). MATERIALS AND METHODS: Local ethics committee approved the study, with patient informed written consent. On day 2 after successful primary angioplasty for STEMI, 53 patients were prospectively enrolled; 40 patients (mean age, 60 years) completed study. Two sets of cardiac magnetic resonance (MR) images were obtained on same day 6 hours apart. Basal, midcavity, and apical sections were obtained with each sequence. Interobserver, intraobserver, and interimage variability (1 minus intraclass correlation coefficient) and agreement (Bland-Altman method) were assessed. RESULTS: Size of myocardial edema significantly differed. Mean size of myocardium at risk was similar between T2-weighted STIR (18.2 g) and T2 mapping (17.3 g) (P = .54). Mean size differed between T2-weighted STIR (18.2 g) and ACUT2E (14.0 g) (P = .01) and between T2-weighted STIR (18.2 g) and EGE (14.2 g) (P = .003). T2 mapping and EGE had best agreement (interobserver bias: T2-weighted STIR, -0.9 [mean difference] ± 9.6 [standard deviation]; ACUT2E, -2.5 ± 6.9; T2 mapping, -3.8 ± 4.7; EGE, -5.3 ± 5.9; interimage bias: T2-weighted STIR, 1.5 ± 5.8; ACUT2E, -0.8 ± 4.9; T2 mapping, 3.1 ± 4.0; EGE, 1.1 ± 4.9; intraobserver bias: T2-weighted STIR, 1.4 ± 5.8; ACUT2E, 0.6 ± 4.7; T2 mapping, 2.2 ± 3.1; EGE, 1.7 ± 2.9). Variability was lowest for T2 mapping (intraobserver, 0.05; interobserver, 0.09; interimage, 0.1) followed by EGE (intraobserver, 0.03; interobserver, 0.14; interimage, 0.14), with improved detection of territory of IRA versus ACUT2E (intraobserver, 0.11; interobserver, 0.22; interimage, 0.12) and T2-weighted STIR (intraobserver, 0.1; interobserver, 0.32; interimage, 0.1). CONCLUSION: Cardiac MR methods to detect and quantify infarct myocardial edema are not interchangeable; T2 mapping is the most reproducible method, followed by EGE, ACUT2E, and T2-weighted STIR. Clinical trial registration no. NCT01468662

Adaptations of aortic and pulmonary artery flow parameters measured by phase-contrast magnetic resonance angiography during supine aerobic exercise.

PURPOSE: Increased oxygen uptake and utilisation during exercise depend on adequate adaptations of systemic and pulmonary vasculature. Recent advances in magnetic resonance imaging techniques allow for direct quantification of aortic and pulmonary blood flow using phase-contrast magnetic resonance angiography (PCMRA). This pilot study tested quantification of aortic and pulmonary haemodynamic adaptations to moderate aerobic supine leg exercise using PCMRA. METHODS: Nine adult healthy volunteers underwent pulse gated free breathing PCMRA while performing heart rate targeted aerobic lower limb exercise. Flow was assessed in mid ascending and mid descending thoracic aorta (AO) and main pulmonary artery (MPA) during exercise at 180 % of individual resting heart rate. Flow sequence analysis was performed by experienced operators using commercial offline software (Argus, Siemens Medical Systems). RESULTS: Exercise related increase in HR (rest: 69 ± 10 b min(-1), exercise: 120 ± 13 b min(-1)) resulted in cardiac output increase (from 6.5 ± 1.4 to 12.5 ± 1.8 L min(-1)). At exercise, ascending aorta systolic peak velocity increased from 89 ± 14 to 122 ± 34 cm s(-1) (p = 0.016), descending thoracic aorta systolic peak velocity increased from 104 ± 14 to 144 ± 33 cm s(-1) (p = 0.004), MPA systolic peak velocity from 86 ± 18 to 140 ± 48 cm s(-1) (p = 0.007), ascending aorta systolic peak flow rate from 415 ± 83 to 550 ± 135 mL s(-1) (p = 0.002), descending thoracic aorta systolic peak flow rate from 264 ± 70 to 351 ± 82 mL s(-1) (p = 0.004) and MPA systolic peak flow rate from 410 ± 80 to 577 ± 180 mL s(-1) (p = 0.006). CONCLUSION: Quantitative blood flow and velocity analysis during exercise using PCMRA is feasible and detected a steep exercise flow and velocity increase in the aorta and MPA. Exercise PCMRA can serve as a research and clinical tool to help quantify exercise blood flow adaptations in health and disease and investigate patho-physiological mechanisms in cardio-pulmonary disease.

Computed tomographic coronary angiography - is it ready as a screening tool for coronary artery disease?

Currently, there are no formal screening programmes for coronary artery disease (CAD). Computed tomographic coronary angiography (CTCA) has been suggested as a non-invasive and reliable method of atherosclerotic plaque assessment, with the potential for use in screening programmes. In this article, we briefly present the current understanding of atherosclerotic plaque formation, explain key technological aspects of CTCA and critique this method in the light of World Health Organisation (WHO) criteria for devising a screening programme. Current evolving and future insights are also considered. Overall, in our view, there is currently insufficient evidence to support the formal use of CTCA in a screening programme for CAD, although this viewpoint will undoubtedly evolve.

Feasibility of Wave Intensity Analysis from 4D Cardiovascular Magnetic Resonance Imaging Data.

Congenital heart defects (CHD) introduce haemodynamic changes; e.g., bicuspid aortic valve (BAV) presents a turbulent helical flow, which activates aortic pathological processes. Flow quantification is crucial for diagnostics and to plan corrective strategies. Multiple imaging modalities exist, with phase contrast magnetic resonance imaging (PC-MRI) being the current gold standard; however, multiple predetermined site measurements may be required, while 4D MRI allows for measurements of area (A) and velocity (U) in all spatial dimensions, acquiring a single volume and enabling a retrospective analysis at multiple locations. We assessed the feasibility of gathering hemodynamic insight into aortic hemodynamics by means of wave intensity analysis (WIA) derived from 4D MRI. Data were collected in n = 12 BAV patients and n = 7 healthy controls. Following data acquisition, WIA was successfully derived at three planes (ascending, thoracic and descending aorta) in all cases. The values of wave speed were physiological and, while the small sample limited any clinical interpretation of the results, the study shows the possibility of studying wave travel and wave reflection based on 4D MRI. Below, we demonstrate for the first time the feasibility of deriving wave intensity analysis from 4D flow data and open the door to research applications in different cardiovascular scenarios.

The sinister course of an intramural right coronary artery.

We report the case of an adolescent who was presented with long-standing exertional symptoms, and was diagnosed with an anomalous right coronary arterial origin arising above the commissural junction between the left and right aortic sinus, with inter-arterial and intramural compression. The precise origin of this lesion outside the aortic sinuses is unusual, and multi-detector computed tomography gave excellent definition and spatial resolution of the anomalous origin and course. It is crucial to have a high index of suspicion of exertional symptoms, as sudden death may be the first manifestation of an anomalous coronary artery.

A Segmental Approach from Molecular Profiling to Medical Imaging to Study Bicuspid Aortic Valve Aortopathy.

Bicuspid aortic valve (BAV) patients develop ascending aortic (AAo) dilation. The pathogenesis of BAV aortopathy (genetic vs. haemodynamic) remains unclear. This study aims to identify regional changes around the AAo wall in BAV patients with aortopathy, integrating molecular data and clinical imaging. BAV patients with aortopathy (n = 15) were prospectively recruited to surgically collect aortic tissue and measure molecular markers across the AAo circumference. Dilated (anterior/right) vs. non-dilated (posterior/left) circumferential segments were profiled for whole-genomic microRNAs (next-generation RNA sequencing, miRCURY LNA PCR), protein content (tandem mass spectrometry), and elastin fragmentation and degeneration (histomorphometric analysis). Integrated bioinformatic analyses of RNA sequencing and proteomic datasets identified five microRNAs (miR-128-3p, miR-210-3p, miR-150-5p, miR-199b-5p, and miR-21-5p) differentially expressed across the AAo circumference. Among them, three miRNAs (miR-128-3p, miR-150-5p, and miR-199b-5p) were predicted to have an effect on eight common target genes, whose expression was dysregulated, according to proteomic analyses, and involved in the vascular-endothelial growth-factor signalling, Hippo signalling, and arachidonic acid pathways. Decreased elastic fibre levels and elastic layer thickness were observed in the dilated segments. Additionally, in a subset of patients n = 6/15, a four-dimensional cardiac magnetic resonance (CMR) scan was performed. Interestingly, an increase in wall shear stress (WSS) was observed at the anterior/right wall segments, concomitantly with the differentially expressed miRNAs and decreased elastic fibres. This study identified new miRNAs involved in the BAV aortic wall and revealed the concomitant expressional dysregulation of miRNAs, proteins, and elastic fibres on the anterior/right wall in dilated BAV patients, corresponding to regions of elevated WSS.

Cerebral Blood Flow Response to Simulated Hypovolemia in Essential Hypertension: A Magnetic Resonance Imaging Study.

Hypertension is associated with raised cerebral vascular resistance and cerebrovascular remodeling. It is currently unclear whether the cerebral circulation can maintain cerebral blood flow (CBF) during reductions in cardiac output (CO) in hypertensive patients thereby avoiding hypoperfusion of the brain. We hypothesized that hypertension would impair the ability to effectively regulate CBF during simulated hypovolemia. In the present study, 39 participants (13 normotensive, 13 controlled, and 13 uncontrolled hypertensives; mean age±SD, 55±10 years) underwent lower body negative pressure (LBNP) at -20, -40, and -50 mmHg to decrease central blood volume. Phase-contrast MR angiography was used to measure flow in the basilar and internal carotid arteries, as well as the ascending aorta. CBF and CO decreased during LBNP (P<0.0001). Heart rate increased during LBNP, reaching significance at -50 mmHg (P<0.0001). There was no change in mean arterial pressure during LBNP (P=0.3). All participants showed similar reductions in CBF (P=0.3, between groups) and CO (P=0.7, between groups) during LBNP. There was no difference in resting CBF between the groups (P=0.36). In summary, during reductions in CO induced by hypovolemic stress, mean arterial pressure is maintained but CBF declines indicating that CBF is dependent on CO in middle-aged normotensive and hypertensive volunteers. Hypertension is not associated with impairments in the CBF response to reduced CO.

Noctural dipping status and left ventricular hypertrophy: A cardiac magnetic resonance imaging study.

We investigate the impact of dipper status on cardiac structure with cardiovascular magnetic resonance (CMR). Ambulatory blood pressure monitoring and 1.5T CMR were performed in 99 tertiary hypertension clinic patients. Subgroup analysis by extreme dipper (n = 9), dipper (n = 39), non-dipper (n = 35) and reverse dipper (n = 16) status was performed, matched in age, gender and BMI. Left ventricular (LV) mass was significantly higher for extreme dippers than dippers after correction for covariates (100 ± 6 g/m2 vs 79 ± 3 g/m2 , P = .004). Amongst extreme dippers and dippers (n = 48), indexed LV mass correlated positively with the extent of nocturnal blood pressure dipping (R = .403, P = .005). On post-hoc ANCOVA, the percentage of nocturnal dip had significant effect on indexed LV mass (P = .008), but overall SBP did not (P = .348). In the tertiary setting, we found a larger nocturnal BP drop was associated with more LV hypertrophy. If confirmed in larger studies, this may have implications on nocturnal dosing of anti-hypertensive medications.

The In Vivo Morphology of Post-Infarct Ventricular Septal Defect and the Implications for Closure.

OBJECTIVES: The aim of this study was to define the dynamic in vivo morphology of post-infarct ventricular septal defect (PIVSD), which has not been previously described in living patients. BACKGROUND: PIVSD is a devastating complication of acute myocardial infarction. METHODS: The anatomic features of PIVSD, as demonstrated by computed tomography or magnetic resonance imaging, were retrospectively reviewed. RESULTS: Thirty-two PIVSDs were assessed, 16 left coronary artery and 16 right coronary artery PIVSDs. PIVSDs were large (mean maximum dimension 26.5 ± 11.5 mm, mean area 5.2 ± 4.2 cm2) and oval (mean eccentricity index 1.7 ± 0.5), with thin margins (diastolic mean thickness 5 mm from the edge of the PIVSD 6.4 ± 3.0mm), and only 22% of PIVSDs were entirely confined to the septum. The defects could be larger in diastole or systole. The stem of the largest available Amplatzer occluder stem (St. Jude Medical, St. Paul, Minnesota) filled only 50% of defects. Patients with small defects may survive without closure. Without closure, those with large defects die. If accepted for closure, PIVSD size and coronary territory did not predict survival >1 year (overall 60%). CONCLUSIONS: This is the first detailed anatomic description of PIVSD in living patients. Defects may be larger in systole or diastole, meaning that single-phase measurement is unsuitable. Its complex nature means that the most commonly available occluder device is frequently unsuitable. Successful closure leads to prolonged survival and should be attempted where possible. This study may lead to improved patient selection, closure techniques, and device design.

ECG strain pattern in hypertension is associated with myocardial cellular expansion and diffuse interstitial fibrosis: a multi-parametric cardiac magnetic resonance study.

AIMS: In hypertension, the presence of left ventricular (LV) strain pattern on 12-lead electrocardiogram (ECG) carries adverse cardiovascular prognosis. The underlying mechanisms are poorly understood. We investigated whether hypertensive ECG strain is associated with myocardial interstitial fibrosis and impaired myocardial strain, assessed by multi-parametric cardiac magnetic resonance (CMR). METHODS AND RESULTS: A total of 100 hypertensive patients [50 ± 14 years, male: 58%, office systolic blood pressure (SBP): 170 ± 30 mmHg, office diastolic blood pressure (DBP): 97 ± 14 mmHg) underwent ECG and 1.5T CMR and were compared with 25 normotensive controls (46 ± 14 years, 60% male, SBP: 124 ± 8 mmHg, DBP: 76 ± 7 mmHg). Native T1 and extracellular volume fraction (ECV) were calculated with the modified look-locker inversion-recovery sequence. Myocardial strain values were estimated with voxel-tracking software. ECG strain (n = 20) was associated with significantly higher indexed LV mass (LVM) (119 ± 32 vs. 80 ± 17 g/m2, P < 0.05) and ECV (30 ± 4 vs. 27 ± 3%, P < 0.05) compared with hypertensive subjects without ECG strain (n = 80). ECG strain subjects had significantly impaired circumferential strain compared with hypertensive subjects without ECG strain and controls (-15.2 ± 4.7 vs. -17.0 ± 3.3 vs. -17.3 ± 2.4%, P < 0.05, respectively). In subgroup analysis, comparing ECG strain subjects to hypertensive subjects with elevated LVM but no ECG strain, a significantly higher ECV (30 ± 4 vs. 28 ± 3%, P < 0.05) was still observed. Indexed LVM was the only variable independently associated with ECG strain in multivariate logistic regression analysis [odds ratio (95th confidence interval): 1.07 (1.02-1.12), P < 0.05). CONCLUSION: In hypertension, ECG strain is a marker of advanced LVH associated with increased interstitial fibrosis and associated with significant myocardial circumferential strain impairment.

Registration and Modeling From Spaced and Misaligned Image Volumes.

We address the problem of object modeling from 3D and 3D+T data made up of images, which contain different parts of an object of interest, are separated by large spaces, and are misaligned with respect to each other. These images have only a limited number of intersections, hence making their registration particularly challenging. Furthermore, such data may result from various medical imaging modalities and can, therefore, present very diverse spatial configurations. Previous methods perform registration and object modeling (segmentation and interpolation) sequentially. However, sequential registration is ill-suited for the case of images with few intersections. We propose a new methodology, which, regardless of the spatial configuration of the data, performs the three stages of registration, segmentation, and shape interpolation from spaced and misaligned images simultaneously. We integrate these three processes in a level set framework, in order to benefit from their synergistic interactions. We also propose a new registration method that exploits segmentation information rather than pixel intensities, and that accounts for the global shape of the object of interest, for increased robustness and accuracy. The accuracy of registration is compared against traditional mutual information based methods, and the total modeling framework is assessed against traditional sequential processing and validated on artificial, CT, and MRI data.

The Relationship Between Left Ventricular Wall Thickness, Myocardial Shortening, and Ejection Fraction in Hypertensive Heart Disease: Insights From Cardiac Magnetic Resonance Imaging.

Hypertensive heart disease is often associated with a preserved left ventricular ejection fraction despite impaired myocardial shortening. The authors investigated this paradox in 55 hypertensive patients (52±13 years, 58% male) and 32 age- and sex-matched normotensive control patients (49±11 years, 56% male) who underwent cardiac magnetic resonance imaging at 1.5T. Long-axis shortening (R=0.62), midwall fractional shortening (R=0.68), and radial strain (R=0.48) all decreased (P<.001) as end-diastolic wall thickness increased. However, absolute wall thickening (defined as end-systolic minus end-diastolic wall thickness) was maintained, despite the reduced myocardial shortening. Absolute wall thickening correlated with ejection fraction (R=0.70, P<.0001). In multiple linear regression analysis, increasing wall thickness by 1 mm independently increased ejection fraction by 3.43 percentage points (adjusted ß-coefficient: 3.43 [2.60-4.26], P<.0001). Increasing end-diastolic wall thickness augments ejection fraction through preservation of absolute wall thickening. Left ventricular ejection fraction should not be used in patients with hypertensive heart disease without correction for degree of hypertrophy.

Comprehensive characterisation of hypertensive heart disease left ventricular phenotypes.

OBJECTIVE: Myocardial intracellular/extracellular structure and aortic function were assessed among hypertensive left ventricular (LV) phenotypes using cardiovascular magnetic resonance (CMR). METHODS: An observational study from consecutive tertiary hypertension clinic patients referred for CMR (1.5 T) was performed. Four LV phenotypes were defined: (1) normal with normal indexed LV mass (LVM) and LVM to volume ratio (M/V), (2) concentric remodelling with normal LVM but elevated M/V, (3) concentric LV hypertrophy (LVH) with elevated LVM but normal indexed end-diastolic volume (EDV) or (4) eccentric LVH with elevated LVM and EDV. Extracellular volume fraction was measured using T1-mapping. Circumferential strain was calculated by voxel-tracking. Aortic distensibility was derived from high-resolution aortic cines and contemporaneous blood pressure measurements. RESULTS: 88 hypertensive patients (49±14 years, 57% men, systolic blood pressure (SBP): 167±30 mm Hg, diastolic blood pressure (DBP): 96±14 mm Hg) were compared with 29 age-matched/sex-matched controls (47±14 years, 59% men, SBP: 128±12 mm Hg, DBP: 79±10 mm Hg). LVH resulted from increased myocardial cell volume (eccentric LVH: 78±19 mL/m(2) vs concentric LVH: 73±15 mL/m(2) vs concentric remodelling: 55±9 mL/m(2), p<0.05, respectively) and interstitial fibrosis (eccentric LVH: 33±10 mL/m(2) vs concentric LVH: 30±10 mL/m(2) vs concentricremodelling: 19±2 mL/m(2), p<0.05, respectively). LVH had worst circumferential impairment (eccentric LVH: -12.8±4.6% vs concentric LVH: -15.5±3.1% vs concentric remodelling: -17.1±3.2%, p<0.05, respectively). Concentric remodelling was associated with reduced aortic distensibility, but not with large intracellular/interstitial expansion or myocardial dysfunction versus controls. CONCLUSIONS: Myocardial interstitial fibrosis varies across hypertensive LV phenotypes with functional consequences. Eccentric LVH has the most fibrosis and systolic impairment. Concentric remodelling is only associated with abnormal aortic function. Understanding these differences may help tailor future antihypertensive treatments.

Recommendations for accurate CT diagnosis of suspected acute aortic syndrome (AAS)--on behalf of the British Society of Cardiovascular Imaging (BSCI)/British Society of Cardiovascular CT (BSCCT).

Accurate and timely assessment of suspected acute aortic syndrome is crucial in this life-threatening condition. Imaging with CT plays a central role in the diagnosis to allow expedited management. Diagnosis can be made using locally available expertise with optimized scanning parameters, making full use of recent advances in CT technology. Each imaging centre must optimize their protocols to allow accurate diagnosis, to optimize radiation dose and in particular to reduce the risk of false-positive diagnosis that may simulate disease. This document outlines the principles for the acquisition of motion-free imaging of the aorta in this context.

Prevalence and predictors of asymmetric hypertensive heart disease: insights from cardiac and aortic function with cardiovascular magnetic resonance.

AIMS: We sought to determine the prevalence of asymmetric hypertensive heart disease (HHD) overlapping morphologically with hypertrophic cardiomyopathy (HCM) and to determine predictors of this pattern of hypertensive remodelling. METHODS AND RESULTS: One hundred and fifty hypertensive patients underwent 1.5 T cardiovascular magnetic resonance imaging. Twenty-one patients were excluded due to concomitant cardiac pathology that may confound the hypertrophic response, e.g. myocardial infarction, moderate-severe valvular disease, or other cardiomyopathy. Asymmetric HHD was defined as a segmental wall thickness of ≥15 mm and >1.5-fold the opposing wall in ≥1 myocardial segments, measured from short-axis cine stack at end-diastole. Ambulatory blood pressure, myocardial replacement fibrosis, aortic distensibility and aortoseptal angle were investigated as predictors of asymmetric HHD by multivariate logistic regression. Out of 129 hypertensive subjects (age: 51 ± 15 years, 50% male, systolic blood pressure: 170 ± 30 mmHg, diastolic blood pressure: 97 ± 16 mmHg), asymmetric HHD occurred in 21%. Where present, maximal end-diastolic wall thickness (EDWT) was 17.8 ± 1.9 mm and located exclusively in the basal or mid septum. In asymmetric HHD, aortoseptal angle (114 ± 10° vs. 125 ± 9° vs. 123 ± 12°, P < 0.05, respectively) was significantly reduced compared to concentric left ventricular hypertrophy (LVH) and compared to no LVH, respectively. Aortic distensibility in asymmetric HHD (1.01 ± 0.60 vs. 1.83 ± 1.65 mm2/mmHg × 103, P < 0.05, respectively) was significantly reduced compared to subjects with no LVH. Age (odds ratio [95th confidence interval]: 1.10 [1.02-1.18], P < 0.05) and indexed LV mass (1.09 [0.98-1.28], P < 0.0001) were significant, independent predictors of asymmetric HDD. CONCLUSIONS: Asymmetric HHD morphologically overlapping with HCM, according to the current ESC guidelines, is common. Postulating a diagnosis of HCM on the basis of EDWT of ≥15 mm should be made with caution in the presence of arterial hypertension particular in male subjects with elevated LV mass.