Explore the vast range of titles available.

Background Arteriosclerosis (arterial stiffening) is associated with future cardiovascular events, with this effect postulated to be due to its effect on cardiac afterload, atherosclerosis (plaque formation) progression or both, but with limited evidence examining these early in disease formation. The aim of the current study is to examine the association between arteriosclerosis, atherosclerosis and ventricular remodelling in a population at low-intermediate cardiovascular risk. Methods One thousand six hundred fifty-one subjects free of clinical cardiovascular disease and with a < 20% 10 year cardiovascular risk score underwent a cardiovascular magnetic resonance (CMR) study and whole body CMR angiogram. Arteriosclerosis was measured using total arterial compliance (TAC) - calculated as the indexed stroke volume divided by the pulse pressure. Atherosclerosis was quantified using a standardised atheroma score (SAS) which was calculated by scoring 30 arterial segments within the body based on the degree of stenosis, summating these scores and normalising it to the number of assessable segments. Left ventricular remodelling was measured using left ventricular mass to volume ratio (LVMVR). Results One thousand five hundred fifteen (38% male, 53.8 ± 8.2 years old) completed the study. On univariate analysis TAC was associated with SAS but this was lost after accounting for cardiovascular risk factors in both males (B = − 0.001 (− 0.004–0.002), p  = 0.62) and females (B = 0.000(95%CI -0.002--0.002), p  = 0.78). In contrast compliance correlated with LVMVR after accounting for cardiovascular risk factors (B = − 0.12(95%CI -0.16--0.091), p  < 0.001 in males; B = − 0.12(95%CI -0.15--0.086), p  < 0.001 in females). Conclusion Systemic arteriosclerosis is associated with left ventricular remodelling but not atherosclerosis. Future efforts in cardiovascular risk prevention should thus seek to address both arteriosclerosis and atherosclerosis individually.

Background Carotid-femoral pulse wave velocity (cf-PWV) and aortic PWV measured using MRI (MRI-PWV) show good correlation, but with a significant and consistent bias across studies. The aim of the current study was to evaluate whether the differences between cf.-PWV and MRI-PWV can be accounted for by inaccuracies of currently used distance measurements. Methods One hundred fourteen study participants were recruited into one of 4 groups: Type 2 diabetes melltus (T2DM) with cardiovascular disease (CVD) ( n  = 23), T2DM without CVD ( n  = 41), CVD without T2DM ( n  = 25) and a control group ( n  = 25). All participants underwent cf.-PWV, cardiac MRI and whole body MR angiography(WB-MRA). 90 study participants also underwent aortic PWV using MRI. cf.-PWV EXT was performed using a SphygmoCor device (Atcor Medical, West Ryde, Australia). The true intra-arterial pathlength was measured using the WB-MRA and then used to recalculate the cf.-PWV EXT to give a cf.-PWV MRA . Results Distance measurements were significantly lower on WB-MRA than on external tape measure (mean diff = −85.4 ± 54.0 mm, p  < 0.001). MRI-PWV was significantly lower than cf.-PWV EXT (MRI-PWV = 8.1 ± 2.9 vs. cf.-PWV EXT  = 10.9 ± 2.7 ms −1 , p  < 0.001). When cf.-PWV was recalculated using the inter-arterial distance from WB-MRA, this difference was significantly reduced but not lost (MRI-PWV = 8.1 ± 2.9 ms −1 vs. cf.-PWV MRA 9.1 ± 2.1 ms −1 , mean diff = −0.96 ± 2.52 ms −1 , p  = 0.001). Recalculation of the PWV increased correlation with age and pulse pressure. Conclusion Differences in cf.-PWV and MRI PWV can be predominantly but not entirely explained by inaccuracies introduced by the use of simple surface measurements to represent the convoluted arterial path between the carotid and femoral arteries.

Common carotid intima media thickness (CIMT) and ankle brachial pressure index (ABPI) are used as surrogate marker of atherosclerosis, and have been shown to correlate with arterial stiffness, however their correlation with global atherosclerotic burden has not been previously assessed. We compare CIMT and ABPI with atheroma burden as measured by whole body magnetic resonance angiography (WB-MRA). 50 patients with symptomatic peripheral arterial disease were recruited. CIMT was measured using ultrasound while rest and exercise ABPI were performed. WB-MRA was performed in a 1.5T MRI scanner using 4 volume acquisitions with a divided dose of intravenous gadolinium gadoterate meglumine (Dotarem, Guerbet, FR). The WB-MRA data was divided into 31 anatomical arterial segments with each scored according to degree of luminal narrowing: 0 = normal, 1 = <50%, 2 = 50-70%, 3 = 70-99%, 4 = vessel occlusion. The segment scores were summed and from this a standardized atheroma score was calculated. The atherosclerotic burden was high with a standardised atheroma score of 39.5±11. Common CIMT showed a positive correlation with the whole body atheroma score (β 0.32, p = 0.045), however this was due to its strong correlation with the neck and thoracic segments (β 0.42 p = 0.01) with no correlation with the rest of the body. ABPI correlated with the whole body atheroma score (β -0.39, p = 0.012), which was due to a strong correlation with the ilio-femoral vessels with no correlation with the thoracic or neck vessels. On multiple linear regression, no correlation between CIMT and global atheroma burden was present (β 0.13 p = 0.45), while the correlation between ABPI and atheroma burden persisted (β -0.45 p = 0.005). ABPI but not CIMT correlates with global atheroma burden as measured by whole body contrast enhanced magnetic resonance angiography in a population with symptomatic peripheral arterial disease. However this is primarily due to a strong correlation with ilio-femoral atheroma burden.

Background Whole body cardiovascular MR (WB CVMR) combines whole body angiography and cardiac MR assessment. It is accepted that there is a high disease burden in patients with diabetes, however the quantification of the whole body atheroma burden in both arterial and cardiac disease has not been previously reported. In this study we compare the quantified atheroma burden in those individuals with and without diabetes by clinical cardiovascular disease (CVD) status. Methods 158 participants underwent WB CVMR, and were categorised into one of four groups: (1) type 2 diabetes mellitus (T2DM) with CVD; (2) T2DM without CVD; (3) CVD without T2DM; (4) healthy controls. The arterial tree was subdivided into 31 segments and each scored according to the degree of stenosis. From this a standardised atheroma score (SAS) was calculated. Cardiac MR and late gadolinium enhancement images of the left ventricle were obtained for assessment of mass, volume and myocardial scar assessment. Results 148 participants completed the study protocol—61 % male, with mean age of 64 ± 8.2 years. SAS was highest in those with cardiovascular disease without diabetes [10.1 (0–39.5)], followed by those with T2DM and CVD [4 (0–41.1)], then those with T2DM only [3.23 (0–19.4)] with healthy controls having the lowest atheroma score [2.4 (0–19.4)]. Both groups with a prior history of CVD had a higher SAS and left ventricular mass than those without (p < 0.001 for both). However after accounting for known cardiovascular risk factors, only the SAS in the group with CVD without T2DM remained significantly elevated. 6 % of the T2DM group had evidence of silent myocardial infarct, with this subcohort having a higher SAS than the remainder of the T2DM group [7.7 (4–19) vs. 2.8 (0–17), p = 0.024]. Conclusions Global atheroma burden was significantly higher in those with known cardiovascular disease and without diabetes but not in those with diabetes and cardiovascular disease suggesting that cardiovascular events may occur at a lower atheroma burden in diabetes.

Assess the feasibility of whole body magnetic resonance angiography (WB-MRA) for monitoring global atheroma burden in a population with peripheral arterial disease (PAD). 50 consecutive patients with symptomatic PAD referred for clinically indicated MRA were recruited. Whole body MRA (WB-MRA) was performed at baseline, 6 months and 3 years. The vasculature was split into 31 anatomical arterial segments. Each segment was scored according to degree of luminal narrowing: 0 = normal, 1 = <50 %, 2 = 50–70 %, 3 = 71–99 %, 4 = vessel occlusion. The score from all assessable segments was summed, and then normalised to the number of assessable vessels. This normalised score was divided by four (the maximum vessel score) and multiplied by 100 to give a final standardised atheroma score (SAS) with a score of 0–100. Progression was assessed with repeat measure ANOVA. 36 patients were scanned at 0 and 6 months, with 26 patients scanned at the 3 years follow up. Only those who completed all three visits were included in the final analysis. Baseline atherosclerotic burden was high with a mean SAS of 15.7 ± 10.3. No significant progression was present at 6 months (mean SAS 16.4 ± 10.5, p  = 0.67), however there was significant disease progression at 3 years (mean SAS 17.7 ± 11.5, p  = 0.01). Those with atheroma progression at follow-up were less likely to be on statin therapy (79 vs 100 %, p  = 0.04), and had significantly higher baseline SAS (17.6 ± 11.2 vs 10.7 ± 5.1, p  = 0.043). Follow up of atheroma burden is possible with WB-MRA, which can successfully quantify and monitor atherosclerosis progression at 3 years follow-up.

Background The aim of this study was to use whole body cardiovascular magnetic resonance imaging (WB CVMR) to assess the heart and arterial network in a single examination, so as to describe the burden of atherosclerosis and subclinical disease in participants with symptomatic single site vascular disease. Methods 64 patients with a history of symptomatic single site vascular disease (38 coronary artery disease (CAD), 9 cerebrovascular disease, 17 peripheral arterial disease (PAD)) underwent whole body angiogram and cardiac MR in a 3 T scanner. The arterial tree was subdivided into 31 segments and each scored according to the degree of stenosis. From this a standardised atheroma score (SAS) was calculated. Cine and late gadolinium enhancement images of the left ventricle were obtained. Results Asymptomatic atherosclerotic disease with greater than 50 % stenosis in arteries other than that responsible for their presenting complain was detected in 37 % of CAD, 33 % of cerebrovascular and 47 % of PAD patients. Unrecognised myocardial infarcts were observed in 29 % of PAD patients. SAS was significantly higher in PAD patients 24 (17.5-30.5) compared to CAD 4 (2–11.25) or cerebrovascular disease patients 6 (2-10) (ANCOVA p < 0.001). Standardised atheroma score positively correlated with age (β 0.36 p = 0.002), smoking status (β 0.34 p = 0.002), and LV mass (β -0.61 p = 0.001) on multiple linear regression. Conclusion WB CVMR is an effective method for the stratification of cardiovascular disease. The high prevalence of asymptomatic arterial disease, and silent myocardial infarctions, particularly in the peripheral arterial disease group, demonstrates the importance of a systematic approach to the assessment of cardiovascular disease.

Aim Quantitative MRI assessments of cardiac structure and function are possible and potentially useful for longitudinal clinical monitoring. The aim of this study was to compare the magnitude and repeatability of left ventricular (LV) ejection fraction (EF) and mass (LVM) measurements in patients with clinically distinct cardiac conditions. Materials and Methods Patients were recruited into four groups: (i) congestive heart failure (CHF), (ii) left ventricular hypertrophy (LVH), (iii) recent post myocardial infarct (PMI), and (iv) healthy normal volunteers (HNV). LV short-axis images were acquired on a 1.5T MRI scanner and analysed on a satellite workstation. EF and LVM (at ED) values were derived from myocardial segmentations, and intra-observer test-retest coefficients of repeatability (CoR) were determined for each cohort. Results The mean EF for the CHF patients (30.3%) was lower than for the other cohorts (LVH 72.7%, PMI 53.0%, HNV 67.0%; P  < 0.0002). As expected, the mean LVM for the CHF patients (143 g) was greater than for the other cohorts (LVH 122 g, PMI 124 g, HNV 107 g), but only significant when compared to the HNV cohort ( P  = 0.004). The intra-observer CoR values for EF were 1.5% (LVH), 1.6% (HNV), 2.6% (PMI) and 5.5% (CHF), and 4.6 g (HNV), 6.7 g (PMI), 8.3 g (CHF) and 9.8 g (LVH) for LVM. Conclusion The EF, LVM and associated repeatability parameters are variable and dependent upon the clinical condition under investigation. It is important that reproducibility data for EF and LVM are acquired individually and specifically on a per-cohort basis if the parameters are to form reliable endpoints for longitudinal clinical follow-up assessments.

IntroductionArteriosclerosis (arterial stiffening) and atherosclerosis (plaque formation) are pathophysiological processes afflicting the vasculature, both of which are associated with future cardiovascular events. However the degree to which they overlap or simply co-exist is poorly understood. The aim of the current study is to determine if these two processes are significantly associated with one another.Methods1651 volunteers with no clinical manifestation of cardiovascular disease and <20% 10-year cardiovascular risk underwent a cardiac MRI and whole body MR angiogram as part of the TASCFORCE study. Systemic arterial stiffness was measured using total arterial compliance (TAC) – calculated as the indexed stroke volume divided by the pulse pressure. Systemic atheroma burden (AB) was calculated by scoring 30 arterial segments within the body based on the degree of stenosis, summating these scores and normalising it to the number of assessable segments.Results1515 (574 male, 53.8±8.2 years-old) completed the study.?On multiple linear regression age (B=–0.001 (95%CI –?0.002–−0.000), p=0.004), heart rate (B=–0.003 (95%CI –?0.003–−0.002), p<0.001) and blood pressure (B=–0.008 (95%CI –0.009–−0.008), p<0.001) were independently associated with TAC, while age (B=0.061 (95%CI 0.04–0.08), p<0.001), and smoking pack-year history (B=0.003 (95%CI 0.005), p=0.022) were independently associated with AB. TAC and AB?demonstrated a significant correlation with each other (Spearman rho=–0.12, p<0.001), however on multivariable analysis accounting for age, blood pressure, sex, BMI, smoking status and cholesterol no significant association persisted (B=–?0.001 (95%CI –0.004–0.002), p=0.62).ConclusionSystemic arteriosclerosis and atherosclerosis are separate entities with each determined by different risk factors. Future efforts in cardiovascular risk prevention should seek to address both of these pathophysiological entities.

IntroductionSouth Asians (SAs) have a higher risk of cardiovascular disease (CVD) and stroke, but paradoxically lower prevalence of peripheral arterial disease (PAD) than Western Europeans (WEs). The aim of this study was to determine early changes in systemic atherosclerotic burden and cardiac remodelling as measured using whole body cardiovascular MRI (WB-CVMR).Methods19 SA and 38 age, gender and BMI matched WE were recruited. All were ≥40 years, free from CVD and with a 10-year risk of CVD <20%. WB-CVMR was performed which comprised a whole body angiogram (WBA) and cardiac magnetic resonance (CMR). These were performed on a 3T MRI scanner following dual phase injection of gadoteric acid. A standardised atherosclerotic score (SAS) was calculated from the WBA, while indexed left ventricular mass and volumes were calculated from the CMR.ResultsSAs exhibited a significantly lower iliofemoral atheroma burden (regional SAS 0.0 ± 0.0 vs 1.9 ± 6.9, p = 0.048) and a trend towards lower overall atheroma burden (WB SAS 0.7 ± 0.8 vs 1.8 ± 2.3, p = 0.1). They had significantly lower indexed left ventricular mass (46.9 ± 11.8 vs 56.9 ± 13.4ml/m2, p = 0.008), end diastolic volume (63.9 ± 10.4 vs 75.2 ± 11.4ml/m2, p = 0.001), end systolic volume (20.5 ± 6.1 vs 24.6 ± 6.8ml/m2, p = 0.03) and stroke volume (43.4 ± 6.6 vs 50.6 ± 7.9ml/m2, p = 0.001), but with no significant difference in functional indices.ConclusionSouth Asians have a lower peripheral atherosclerotic burden and smaller hearts than Western Europeans even in a healthy population. Thus the paradoxical high risk of CVD compared with PVD risk may be due to an adverse cardiac haemodynamic status incurred by the smaller heart rather than atherosclerosis.

IntroductionUnrecognised myocardial infarctions (UMIs) have been described in 19–30% of the population using late gadolinium enhancement (LGE). However these studies have focussed on unselected cohorts including those with known cardiovascular disease. The aim of the current study was to ascertain the prevalence of UMIs in a non-high risk population and their physiological significance.Methods5,000 volunteers >40 years with no history of cardiovascular disease (CVD) and a 10 year risk of CVD of less than 20% were recruited to the Tayside Screening for Cardiac Events (TASCFORCE) study. Those with a BNP level greater than their gender-specific median were invited for a whole-body MR angiogram and cardiac MR including LGE. LGE was classed as absent, UMI, or non-specific.Results1,529 completed the imaging study with 53 (3.6%) excluded due to missing data or inadequate LGE image quality. 10 of the remaining 1476 (0.67%) displayed LGE. Of these, 3 (0.2%) were consistent with UMI, while 7 were non-specific occurring in the mid-myocardium (n = 4), epicardium (n = 1) or right ventricular insertion points (n = 2). Those with UMI had significantly higher BNP(median 116 (range 31–133) vs 22.6 (5–175) pg/ml, p = 0.015), lower ejection fraction (54.6 (36–62) vs 68.9 (38–89) %, p = 0.007) and larger end systolic volume (36.3 (27–61) vs 21.7 (5–65) ml/m2, p = 0.014). Those with non-specific LGE had lower diastolic blood pressure (68 (54–70) vs 72 (46–98) mmHg, p = 0.013), but no differences in their cardiac function.ConclusionDespite previous reports describing high prevalence of UMI, those who are of low-intermediate cardiovascular risk have a very low prevalence of UMI. LGE typical of UMI is associated with significantly impaired cardiac function, while LGE atypical of UMI has no adverse effect on function.