PurposeParametric imaging of absolute myocardial blood flow (MBF) using [15O]H2O enables determination of MBF with high spatial resolution. The aim of this study was to develop a method for generating reproducible, high-quality and quantitative parametric MBF images with minimal user intervention.MethodsNineteen patients referred for evaluation of MBF underwent rest and adenosine stress [15O]H2O positron emission tomography (PET) scans. Ascending aorta and right ventricular (RV) cavity volumes of interest (VOIs) were used as input functions. Implementation of a basis function method (BFM) of the single-tissue model with an additional correction for RV spillover was used to generate parametric images. The average segmental MBF derived from parametric images was compared with MBF obtained using nonlinear least-squares regression (NLR) of VOI data. Four segmentation algorithms were evaluated for automatic extraction of input functions. Segmental MBF obtained using these input functions was compared with MBF obtained using manually defined input functions.ResultsThe average parametric MBF showed a high agreement with NLR-derived MBF [intraclass correlation coefficient (ICC) = 0.984]. For each segmentation algorithm there was at least one implementation that yielded high agreement (ICC > 0.9) with manually obtained input functions, although MBF calculated using each algorithm was at least 10% higher. Cluster analysis with six clusters yielded the highest agreement (ICC = 0.977), together with good segmentation reproducibility (coefficient of variation of MBF <5%).ConclusionParametric MBF images of diagnostic quality can be generated automatically using cluster analysis and a implementation of a BFM of the single-tissue model with additional RV spillover correction.Electronic supplementary materialThe online version of this article (doi:10.1007/s00259-011-1730-3) contains supplementary material, which is available to authorized users.

LGE-CMR-derived scar tissue characteristics are of predictive value for the occurrence of ventricular tachyarrhythmias in patients with ischaemic cardiomyopathy. Additional estimation of scar core size and/or peri-infarct zone does not appear to increase the diagnostic accuracy over total scar size alone.

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Objective-Individuals with familial hypobetalipoproteinemia (FHBL) have been reported to be prone to fatty liver disease (FLD). Conversely, the profound reduction of low-density lipoprotein (LDL) cholesterol in this disorder might decrease cardiovascular risk. In the present study, we assessed hepatic steatosis as well as noninvasive surrogate markers for cardiovascular disease (CVD) in subjects with FHBL and in matched controls. Methods and Results-Hepatic steatosis was assessed by abdominal ultrasonography. Carotid intima-media thickness (IMT) and distal common carotid arterial wall stiffness as surrogate markers for CVD risk were measured using high-resolution B-mode ultrasonography. Whereas transaminase levels were only modestly elevated, both prevalence (54% versus 29%; Pϭ0.01) and severity of steatosis were significantly higher in FHBL individuals compared with controls. Despite similar IMT measurements, arterial stiffness was significantly lower in FHBL (Pϭ0.04) compared with controls. Additionally, the increase in arterial stiffness as seen in the presence of traditional risk factors was attenuated, suggesting that very low levels of apoB-containing lipoproteins can negate the adverse effects of other risk factors on the vasculature. Conclusions-FHBL is characterized by an increased prevalence and severity of fatty liver disease. The observed decreased level of arterial wall stiffness, most pronounced in the presence of nonlipid risk factors, is indicative of cardiovascular protection in these subjects. Key Words: apolipoprotein B Ⅲ arterial stiffness Ⅲ cardiovascular risk Ⅲ familial hypobetalipoproteinemia Ⅲ fatty liver disease F amilial hypobetalipoproteinemia (FHBL) is a hereditary disorder of lipoprotein metabolism characterized by very low levels of apolipoprotein (apo) B-100. Plasma levels below the fifth percentile are distinctive for this condition that inherits as an autosomal dominant trait. The prevalence in the general population is estimated to vary from 0.1% to 1.9%. 1,2 Genetic causes of hypobetalipoproteinemia include FHBL, abetalipoproteinemia, and chylomicron remnant disease (OMIM numbers 601519, 246700, and 200100, respectively). A small percentage of FHBL can be explained by mutations in the gene-encoding apolipoprotein B-100 (APOB). These include nonsense, frame-shift, and splicing mutations. Recently, it was reported that a missense mutation in the APOB gene can also lead to FHBL. 3 APOB gene mutations lead to truncated forms of apolipoprotein B (apoB) and are characterized by slower hepatic secretion, as well as more rapid plasma clearance compared with wild-type apoB-100 particles. 4,5 Because apoB is the main constituent of such lipoproteins, including very low-density lipoprotein (VLDL), intermediate-density lipoprotein, and low-density lipoprotein (LDL), FHBL subjects are characterized by exceptionally low levels of these proatherogenic particles from birth onwards.Whereas subjects with heterozygous FHBL are generally asymptomatic, 2 potential implications have been attribute...

BackgroundThere has been increasing interest in quantitative myocardial blood flow (MBF) imaging over the last years and it is expected to become a routinely used technique in clinical practice. Positron emission tomography (PET) using [15O]H2O is the established gold standard for quantification of MBF in vivo. A fundamental issue when performing quantitative MBF imaging is to define the limits of MBF in a clinically suitable population. The aims of the present study were to determine the limits of MBF and to determine the relationship among coronary artery disease (CAD) risk factors, gender and MBF in a predominantly symptomatic patient cohort without significant CAD.MethodsA total of 128 patients (mean age 54 ± 10 years, 50 men) with a low to intermediate pretest likelihood of CAD were referred for noninvasive evaluation of CAD using a hybrid PET/computed tomography (PET/CT) scanner. MBF was quantified with [15O]H2O at rest and during adenosine-induced hyperaemia. Obstructive CAD was excluded in these patients by means of invasive or CT-based coronary angiography.ResultsGlobal average baseline MBF values were 0.91 ± 0.34 and 1.09 ± 0.30  ml·min−1·g−1 (range 0.54–2.35  and 0.59–2.75 ml·min−1·g−1) in men and women, respectively (p < 0.01). However, no gender-dependent difference in baseline MBF was seen following correction for rate–pressure product (0.98 ± 0.45 and 1.09 ± 0.30 ml·min−1·g−1 in men and women, respectively; p = 0.08). Global average hyperaemic MBF values were 3.44 ± 1.20 ml·min−1·g−1 in the whole study population, and 2.90 ± 0.85 and 3.78 ± 1.27 ml·min−1·g−1 (range 1.52–5.22 and 1.72–8.15 ml·min−1·g−1) in men and women, respectively (p < 0.001). Multivariate analysis identified male gender, age and body mass index as having an independently negative impact on hyperaemic MBF.ConclusionGender, age and body mass index substantially influence reference values and should be corrected for when interpreting hyperaemic MBF values.