Non-invasive assessment of ventriculo-arterial coupling using aortic wave intensity analysis combining central blood pressure and phase-contrast cardiovascular magnetic resonance.

BACKGROUND: Wave intensity analysis (WIA) in the aorta offers important clinical and mechanistic insight into ventriculo-arterial coupling, but is difficult to measure non-invasively. We performed WIA by combining standard cardiovascular magnetic resonance (CMR) flow-velocity and non-invasive central blood pressure (cBP) waveforms. METHODS AND RESULTS: Two hundred and six healthy volunteers (age range 21-73 years, 47% male) underwent sequential phase contrast CMR (Siemens Aera 1.5 T, 1.97 × 1.77 mm2, 9.2 ms temporal resolution) and supra-systolic oscillometric cBP measurement (200 Hz). Velocity (U) and central pressure (P) waveforms were aligned using the waveform foot, and local wave speed was calculated both from the PU-loop (c) and the sum of squares method (cSS). These were compared with CMR transit time derived aortic arch pulse wave velocity (PWVtt). Associations were examined using multivariable regression. The peak intensity of the initial compression wave, backward compression wave, and forward decompression wave were 69.5 ± 28, -6.6 ± 4.2, and 6.2 ± 2.5 × 104 W/m2/cycle2, respectively; reflection index was 0.10 ± 0.06. PWVtt correlated with c or cSS (r = 0.60 and 0.68, respectively, P < 0.01 for both). Increasing age decade and female sex were independently associated with decreased forward compression wave (-8.6 and -20.7 W/m2/cycle2, respectively, P < 0.01) and greater wave reflection index (0.02 and 0.03, respectively, P < 0.001). CONCLUSION: This novel non-invasive technique permits straightforward measurement of wave intensity at scale. Local wave speed showed good agreement with PWVtt, and correlation was stronger using the cSS than the PU-loop. Ageing and female sex were associated with poorer ventriculo-arterial coupling in healthy individuals.

Making MRI available for patients with cardiac implantable electronic devices: growing need and barriers to change.

More than half of us will need a magnetic resonance imaging (MRI) scan in our lifetimes. MRI is an unmatched diagnostic test for an expanding range of indications including neurological and musculoskeletal disorders, cancer diagnosis, and treatment planning. Unfortunately, patients with cardiac pacemakers or defibrillators have historically been prevented from having MRI because of safety concerns. This results in delayed diagnoses, more invasive investigations, and increased cost. Major developments have addressed this-newer devices are designed to be safe in MRI machines under specific conditions, and older legacy devices can be scanned provided strict protocols are followed. This service however remains difficult to deliver sustainably worldwide: MRI provision remains grossly inadequate because patients are less likely to be referred, and face difficulties accessing services even when referred. Barriers still exist but are no longer technical. These include logistical hurdles (poor cardiology and radiology interaction at physician and technician levels), financial incentives (re-imbursement is either absent or fails to acknowledge the complexity), and education (physicians self-censor MRI requests). This article therefore highlights the recent changes in the clinical, logistical, and regulatory landscape. The aim of the article is to enable and encourage healthcare providers and local champions to build MRI services urgently for cardiac device patients, so that they may benefit from the same access to MRI as everyone else. KEY POINTS: • There is now considerable evidence that MRI can be provided safely to patients with cardiac implantable electronic devices (CIEDs). However, the volume of MRI scans delivered to patients with CIEDs is fifty times lower than that of the estimated need, and patients are approximately fifty times less likely to be referred. • Because scans for this patient group are frequently for cancer diagnosis and treatment planning, MRI services need to develop rapidly, but the barriers are no longer technical. • New services face logistical, educational, and financial hurdles which can be addressed effectively to establish a sustainable service at scale.

Texture analysis of cardiovascular magnetic resonance cine images differentiates aetiologies of left ventricular hypertrophy.

AIM: To investigate whether unenhanced cardiovascular magnetic resonance (CMR) balanced steady state free precession (bSSFP) cine images could be analysed using textural analysis (TA) software to differentiate different aetiologies of disease causing increased myocardial wall thickness (left ventricular hypertrophy [LVH]) and indicate the severity of myocardial tissue abnormality. MATERIALS AND METHODS: A mid short axis unenhanced cine frame of 216 patients comprising 50 cases of hypertrophic cardiomyopathy (HCM; predominantly Left ventricular outflow tract obstruction [LVOTO] subtype), 52 cases of cardiac amyloid (CA; predominantly AL: light chain subtype), 68 cases of aortic stenosis (AS), 15 hypertensive patients with LVH (HTN+LVH), and 31 healthy volunteers (HV) underwent TA of the CMR cine images (CMRTA) using TexRAD (TexRAD Ltd, Cambridge, UK). Among the HV, 16/31 were scanned twice to form a test-retest reproducibility cohort. CMRTA comprised a filtration-histogram technique to extract and quantify features using six parameters. RESULTS: Test-retest analysis in the HV showed a medium filter (3 mm) was the most reproducible (intra-class correlation of 0.9 for kurtosis and skewness and 0.8 for mean and SD). Disease cohorts were statistically different (p<0.001) to HV for all parameters. Pairwise comparisons of CMRTA parameters showed kurtosis and skewness was consistently significant in ranking the degree of difference from HV (greatest to least): CA, HCM, LVH+HTN, AS (p<0.001). Similarly, mean, standard deviation, entropy, and mean positive pixel (MPP) were consistent in ranking degree of difference from HV: HCM, CA, AS and HTN+LVH. CONCLUSION: Radiomic features of bSSFP CMR data sets derived using TA show promise in discriminating between the aetiologies of LVH.

The risk of cardiac failure following metal-on-metal hip arthroplasty.

AIMS: The aim of this study was to determine whether patients with metal-on-metal (MoM) arthroplasties of the hip have an increased risk of cardiac failure compared with those with alternative types of arthroplasties (non-MoM). PATIENTS AND METHODS: A linkage study between the National Joint Registry, Hospital Episodes Statistics and records of the Office for National Statistics on deaths was undertaken. Patients who underwent elective total hip arthroplasty between January 2003 and December 2014 with no past history of cardiac failure were included and stratified as having either a MoM (n = 53 529) or a non-MoM (n = 482 247) arthroplasty. The primary outcome measure was the time to an admission to hospital for cardiac failure or death. Analysis was carried out using data from all patients and from those matched by propensity score. RESULTS: The risk of cardiac failure was lower in the MoM cohort compared with the non-MoM cohort (adjusted hazard ratio (aHR) 0.901; 95% confidence interval (CI) 0.853 to 0.953). The risk of cardiac failure was similar following matching (aHR 0.909; 95% CI 0.838 to 0.987) and the findings were consistent in subgroup analysis. CONCLUSION: The risk of cardiac failure following total hip arthroplasty was not increased in those in whom MoM implants were used, compared with those in whom other types of prostheses were used, in the first seven years after surgery. Cite this article: Bone Joint J 2018;100-B:20-7.

Quantifying the paradoxical effect of higher systolic blood pressure on mortality in chronic heart failure.

BACKGROUND: Although higher blood pressures are generally recognised to be an adverse prognostic marker in risk assessment of cardiology patients, its relationship to risk in chronic heart failure (CHF) may be different. OBJECTIVE: To examine systematically published reports on the relationship between blood pressure and mortality in CHF. METHODS: Medline and Embase were used to identify studies that gave a hazard or relative risk ratio for systolic blood pressure in a stable population with CHF. Included studies were analysed to obtain a unified hazard ratio and quantify the degree of confidence. RESULTS: 10 studies met the inclusion criteria, giving a total population of 8088, with 29 222 person-years of follow-up. All studies showed that a higher systolic blood pressure (SBP) was a favourable prognostic marker in CHF, in contrast to the general population where it is an indicator of poorer prognosis. The decrease in mortality rates associated with a 10 mm Hg higher SBP was 13.0% (95% CI 10.6% to 15.4%) in the heart failure population. This was not related to aetiology, ACE inhibitor or beta blocker use. CONCLUSION: SBP is an easily measured, continuous variable that has a remarkably consistent relationship with mortality within the CHF population. The potential of this simple variable in outpatient assessment of patients with CHF should not be neglected. One possible application of this information is in the optimisation of cardiac resynchronisation devices.

Haemodynamic effects of changes in atrioventricular and interventricular delay in cardiac resynchronisation therapy show a consistent pattern: analysis of shape, magnitude and relative importance of atrioventricular and interventricular delay.

OBJECTIVE: To assess the haemodynamic effect of simultaneously adjusting atrioventricular (AV) and interventricular (VV) delays. METHOD: 35 different combinations of AV and VV delay were tested by using digital photoplethysmography (Finometer) with repeated alternations to measure relative change in systolic blood pressure (SBP(rel)) in 15 patients with cardiac resynchronisation devices for heart failure. RESULTS: Changing AV delay had a larger effect than changing VV delay (range of SBP(rel) 21 v 4.2 mm Hg, p < 0.001). Each had a curvilinear effect. The curve of response to AV delay fitted extremely closely to a parabola (average R2 = 0.99, average residual variance 0.8 mm Hg2). The response to VV delay was significantly less curved (quadratic coefficient 67 v 1194 mm Hg/s2, p = 0.003) and therefore, although the residual variance was equally small (0.8 mm Hg2), the R2 value was 0.7. Reproducibility at two months was good, with the SD of the difference between two measurements of SBP(rel) being 2.5 mm Hg for AV delay (2% of mean systolic blood pressure) and 1.5 mm Hg for VV delay (1% of mean systolic blood pressure). CONCLUSIONS: Changing AV and VV delays results in a curvilinear acute blood pressure response. This shape fits very closely to a parabola, which may be valuable information in developing a streamlined clinical protocol. VV delay adjustment provides an additional, albeit smaller, haemodynamic benefit to AV optimisation.