Andrew G. Elkington

Accurate assessment of the arterial input function during high-dose myocardial perfusion cardiovascular magnetic resonance.

To develop a method for accurate measurement of the arterial input function (AIF) during high‐dose, single‐injection, quantitative T1‐weighted myocardial perfusion cardiovascular magnetic resonance (CMR).

Myocardial late gadolinium enhancement cardiovascular magnetic resonance in hypertrophic cardiomyopathy caused by mutations in troponin I

Objective: To examine the influence of genotype on late gadolinium enhancement (LGE) and the potential of cardiovascular magnetic resonance (CMR) to detect preclinical hypertrophic cardiomyopathy. Design: Prospective, blinded cohort study of myocardial LGE in a genetically homogeneous population. Patients: 30 patients with disease causing mutations in the recognised hypertrophic cardiomyopathy gene for cardiac troponin I (TNNI3): 15 with echocardiographically determined left ventricular hypertrophy (LVH+) and 15 without (LVH−). Main outcome measures: CMR measures of regional left ventricular function, wall thickness, and mass, and the extent and distribution of LGE. Results: LGE was found in 12 (80%) LVH+ patients but with variable extent (mean 15%, range 3–48%). LGE was also found in two (13%) LVH− patients but the extent was limited (3.6%) and both patients were found to have an abnormal ECG and regional hypertrophy by cine CMR. The extent of LGE was positively associated with clinical markers of sudden death risk (21% with ⩾ 2 risk factors v 7% with ⩽ 1 risk factor, p  =  0.02) and left ventricular mass (r  =  0.56, p < 0.001) and was inversely associated with ejection fraction (r  =  −0.58, p < 0.001). Segmental analysis showed that as regional wall thickness increased, LGE was more prevalent (p < 0.0001) and more extensive (r  =  0.98, p  =  0.001). Conclusion: In patients with disease causing mutations in TNNI3, focal fibrosis was not detected by LGE CMR before LVH and ECG abnormalities were present. Once LVH is present, LGE is common and the extent correlates with adverse clinical parameters. This suggests that focal fibrosis is closely linked to disease development.

Effects of oral testosterone treatment on myocardial perfusion and vascular function in men with low plasma testosterone and coronary heart disease.

Intracoronary testosterone infusions induce coronary vasodilatation and increase coronary blood flow. Longer term testosterone supplementation favorably affected signs of myocardial ischemia in men with low plasma testosterone and coronary heart disease. However, the effects on myocardial perfusion are unknown. Effects of longer term testosterone treatment on myocardial perfusion and vascular function were investigated in men with CHD and low plasma testosterone. Twenty-two men (mean age 57 ± 9 [SD] years) were randomly assigned to oral testosterone undecanoate (TU; 80 mg twice daily) or placebo in a crossover study design. After each 8-week period, subjects underwent at rest and adenosine-stress first-pass myocardial perfusion cardiovascular magnetic resonance, pulse-wave analysis, and endothelial function measurements using radial artery tonometry, blood sampling, anthropomorphic measurements, and quality-of-life assessment. Although no difference was found in global myocardial perfusion after TU compared with placebo, myocardium supplied by unobstructed coronary arteries showed increased perfusion (1.83 ± 0.9 vs 1.52 ± 0.65; p = 0.037). TU decreased basal radial and aortic augmentation indexes (p = 0.03 and p = 0.02, respectively), indicating decreased arterial stiffness, but there was no effect on endothelial function. TU significantly decreased high-density lipoprotein cholesterol and increased hip circumference, but had no effect on hemostatic factors, quality of life, and angina symptoms. In conclusion, oral TU had selective and modest enhancing effects on perfusion in myocardium supplied by unobstructed coronary arteries, in line with previous intracoronary findings. The TU-related decrease in basal arterial stiffness may partly explain previously shown effects of exogenous testosterone on signs of exercise-induced myocardial ischemia.

Interstudy Reproducibility of Quantitative Perfusion Cardiovascular Magnetic Resonance

PURPOSE To determine the interstudy reproducibility of quantitative first-pass perfusion cardiovascular magnetic resonance with comparison of 2 previously described analysis techniques. There is no published data on the interstudy reproducibility of perfusion cardiovascular magnetic resonance which can be used to determine the significance of longitudinal changes in myocardial perfusion after pharmacologic or therapeutic interventions with defined sample sizes. METHODS Sixteen subjects (7 normal volunteers, 9 patients with coronary artery disease) had rest and adenosine stress perfusion cardiovascular magnetic resonance studies on two separate visits. A short axis slice was studied on each visit using a fast low-angle shot sequence. The global and regional myocardial perfusion reserve indices were calculated using 2 methods: model based constrained deconvolution with the Fermi function, and normalized upslopes. Reproducibility was defined as the standard deviation of the measurement differences, divided by the mean (coefficient of variation). RESULTS The reproducibility of global myocardial perfusion reserve indices was 21% in normal volunteers, which was similar to that in patients with coronary artery disease (CAD) (23%, p = .88). The reproducibility of regional myocardial perfusion reserve indices was 28% (p = .45 vs. global analysis). The reproducibility of global MPRi was superior with Fermi deconvolution compared with normalized upslopes (21% vs. 41%, p = .02). CONCLUSION At this stage of clinical development, the reproducibility of quantitative perfusion cardiovascular magnetic resonance is good, and superior using Fermi deconvolution in preference to upslope analysis.

Optimization of the arterial input function for myocardial perfusion cardiovascular magnetic resonance

To determine how injection rate, cardiac function, and breathhold influence the arterial input function (AIF), in order to optimize the AIF in the clinical setting for quantitative myocardial perfusion cardiovascular magnetic resonance (CMR).

Myocardial late gadolinium enhancement in specific cardiomyopathies by cardiovascular magnetic resonance: a preliminary experience.

Late gadolinium enhancement cardiovascular magnetic resonance (CMR) can visualize myocardial interstitial abnormalities. The aim of this study was to assess whether regions of abnormal myocardium can also be visualized by late enhancement gadolinium CMR in the specific cardiomyopathies. A retrospective review of all referrals for gadolinium CMR with specific cardiomyopathy over 20 months. Nine patients with different specific cardiomyopathies were identified. Late enhancement was demonstrated in all patients, with a mean signal intensity of 390 ± 220% compared with normal regions. The distribution pattern of late enhancement was unlike the subendocardial late enhancement related to coronary territories found in myocardial infarction. The affected areas included papillary muscles (sarcoid), the mid-myocardium (Anderson–Fabry disease, glycogen storage disease, myocarditis, Becker muscular dystrophy) and the global sub-endocardium (systemic sclerosis, Loefflers endocarditis, amyloid, Churg–Strauss). Focal myocardial late gadolinium enhancement is found in the specific cardiomyopathies, and the pattern is distinct from that seen in infarction. Further systematic studies are warranted to assess whether the pattern and extent of late enhancement may aid diagnosis and prognostic assessment.

Combined Long‐ and Short‐Axis Myocardial Perfusion Cardiovascular Magnetic Resonance

PURPOSE To date, myocardial perfusion cardiovascular magnetic resonance (CMR) has been reported in single and multiple short-axis slices. Three short-axis planes can assess 16 segments of the standard 17-segment myocardial model, but this approach fails to assess the ventricular apex that requires at least one long-axis plane. We therefore evaluated the feasibility and benefit of combined long- and short-axis perfusion CMR to enable complete 17 segments coverage for comprehensive myocardial perfusion assessment. METHODS AND MATERIALS Using a hybrid echo planar imaging (EPI) sequence, we performed rest and adenosine stress first-pass perfusion CMR studies with 3 short-axis (basal, mid, apical) planes, and additional long-axis planes in the same cardiac cycle in a broad range of cardiology patients. RESULTS Perfusion CMR was performed in 53 consecutive patients using the combined short-long-axis imaging protocol. Twenty-nine of those studied had known or suspected coronary artery disease (CAD), 18 hypertrophic cardiomyopathy, and 6 suspected microvascular perfusion abnormalities. In 39 patients (70%), it was possible to acquire 5 slices at rest and stress including both the horizontal and vertical long axes. In 15 patients (27%), only one long-axis could be acquired, and in 2 patients (5%) only 3 slices (short axis) could be obtained. However, in none of the patients with known or suspected CAD was apical ischemia demonstrated by the long-axis views, despite apical ischemia having been demonstrated with recent SPECT studies in 8 of these patients. CONCLUSION Rest-stress myocardial perfusion CMR is able to achieve complete segmental coverage of the myocardium using the combined short-long axis approach using an EPI sequence in 97% of a long series of consecutive cardiology patients, while maintaining excellent spatial resolution. However, the long-axis views were not found to be able to demonstrate inducible perfusion defects in the apex.