Quantitative cardiovascular magnetic resonance perfusion imaging identifies reduced flow reserve in microvascular coronary artery disease.
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ABSTRACT:
SUBMITTER: Zorach B
PROVIDER: S-EPMC5822618 | BioStudies | 2018-01-01
REPOSITORIES: biostudies
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Project description:Non-invasive assessment of myocardial ischaemia is a cornerstone of the diagnosis of coronary artery disease. Measurement of myocardial blood flow (MBF) using positron emission tomography (PET) is the current reference standard for non-invasive quantification of myocardial ischaemia. Dynamic myocardial perfusion cardiovascular magnetic resonance (CMR) offers an alternative to PET and a recently developed method with automated inline perfusion mapping has shown good correlation of MBF values between CMR and PET. This study assessed the repeatability of myocardial perfusion mapping by CMR in healthy subjects.Forty-two healthy subjects were recruited and underwent adenosine stress and rest perfusion CMR on two visits. Scans were repeated with a minimum interval of 7 days. Intrastudy rest and stress MBF repeatability were assessed with a 15-min interval between acquisitions. Interstudy rest and stress MBF and myocardial perfusion reserve (MPR) were measured for global myocardium and regionally for coronary territories and slices.There was no significant difference in intrastudy repeated global rest MBF (0.65?±?0.13 ml/g/min vs 0.62?±?0.12 ml/g/min, p?=?0.24, repeatability coefficient (RC) =24%) or stress (2.89?±?0.56 ml/g/min vs 2.83?±?0.64 ml/g/min, p?=?0.41, RC?=?29%) MBF. No significant difference was seen in interstudy repeatability for global rest MBF (0.64?±?0.13 ml/g/min vs 0.64?±?0.15 ml/g/min, p?=?0.80, RC?=?32%), stress MBF (2.71?±?0.61 ml/g/min vs 2.55?±?0.57 ml/g/min, p?=?0.12, RC?=?33%) or MPR (4.24?±?0.69 vs 3.73?±?0.76, p?=?0.25, RC?=?36%). Regional repeatability was good for stress (RC?=?30-37%) and rest MBF (RC?=?32-36%) but poorer for MPR (RC?=?35-43%). Within subject coefficient of variation was 8% for rest and 11% for stress within the same study, and 11% for rest and 12% for stress between studies.Fully automated, inline, myocardial perfusion mapping by CMR shows good repeatability that is similar to the published PET literature. Both rest and stress MBF show better repeatability than MPR, particularly in regional analysis.
1000-01-01 | S-EPMC6036695 | BioStudies
Project description:Even in absence of obstructive coronary artery disease women with angina pectoris have a poor prognosis possibly due to coronary microvascular disease. Coronary microvascular disease can be assessed by transthoracic Doppler echocardiography measuring coronary flow velocity reserve (CFVR) and by positron emission tomography measuring myocardial blood flow reserve (MBFR). Diffuse myocardial fibrosis can be assessed by cardiovascular magnetic resonance (CMR) T1 mapping. We hypothesized that coronary microvascular disease is associated with diffuse myocardial fibrosis.Women with angina, a clinically indicated coronary angiogram with <50 % stenosis and no diabetes were included. CFVR was measured using dipyridamole (0.84 mg/kg) and MBFR using adenosine (0.84 mg/kg). Focal fibrosis was assessed by 1.5 T CMR late gadolinium enhancement (0.1 mmol/kg) and diffuse myocardial fibrosis by T1 mapping using a modified Look-Locker pulse sequence measuring T1 and extracellular volume fraction (ECV).CFVR and CMR were performed in 64 women, mean (SD) age 62.5 (8.3) years. MBFR was performed in a subgroup of 54 (84 %) of these women. Mean native T1 was 1023 (86) and ECV (%) was 33.7 (3.5); none had focal fibrosis. Median (IQR) CFVR was 2.3 (1.9; 2.7), 23 (36 %) had CFVR < 2 indicating coronary microvascular disease, and median MBFR was 2.7 (2.2; 3.0) and 19 (35 %) had a MBFR value below 2.5. No significant correlations were found between CFVR and ECV or native T1 (R (2) = 0.02; p = 0.27 and R (2) = 0.004; p = 0.61, respectively). There were also no correlations between MBFR and ECV or native T1 (R (2) = 0.1; p = 0.13 and R (2) = 0.004, p = 0.64, respectively). CFVR and MBFR were correlated to hypertension and heart rate.In women with angina and no obstructive coronary artery disease we found no association between measures of coronary microvascular disease and myocardial fibrosis, suggesting that myocardial ischemia induced by coronary microvascular disease does not elicit myocardial fibrosis in this population. The examined parameters seem to provide independent information about myocardial and coronary disease.
2016-01-01 | S-EPMC5096323 | BioStudies
Project description:BACKGROUND:In patients with angina and nonobstructive coronary artery disease (NOCAD), confirming symptoms due to coronary microvascular dysfunction (CMD) remains challenging. Cardiac magnetic resonance (CMR) assesses myocardial perfusion with high spatial resolution and is widely used for diagnosing obstructive coronary artery disease (CAD). OBJECTIVES:The goal of this study was to validate CMR for diagnosing microvascular angina in patients with NOCAD, compared with patients with obstructive CAD and correlated to the index of microcirculatory resistance (IMR) during invasive coronary angiography. METHODS:Fifty patients with angina (65 ± 9 years of age) and 20 age-matched healthy control subjects underwent adenosine stress CMR (1.5- and 3-T) to assess left ventricular function, inducible ischemia (myocardial perfusion reserve index [MPRI]; myocardial blood flow [MBF]), and infarction (late gadolinium enhancement). During subsequent angiography within 7 days, 28 patients had obstructive CAD (fractional flow reserve [FFR] ?0.8) and 22 patients had NOCAD (FFR >0.8) who underwent 3-vessel IMR measurements. RESULTS:In patients with NOCAD, myocardium with IMR <25 U had normal MPRI (1.9 ± 0.4 vs. controls 2.0 ± 0.3; p = 0.49); myocardium with IMR ?25 U had significantly impaired MPRI, similar to ischemic myocardium downstream of obstructive CAD (1.2 ± 0.3 vs. 1.2 ± 0.4; p = 0.61). An MPRI of 1.4 accurately detected impaired perfusion related to CMD (IMR ?25 U; FFR >0.8) (area under the curve: 0.90; specificity: 95%; sensitivity: 89%; p < 0.001). Impaired MPRI in patients with NOCAD was driven by impaired augmentation of MBF during stress, with normal resting MBF. Myocardium with FFR >0.8 and normal IMR (<25 U) still had blunted stress MBF, suggesting mild CMD, which was distinguishable from control subjects by using a stress MBF threshold of 2.3 ml/min/g with 100% positive predictive value. CONCLUSIONS:In angina patients with NOCAD, CMR can objectively and noninvasively assess microvascular angina. A CMR-based combined diagnostic pathway for both epicardial and microvascular CAD deserves further clinical validation.
2018-01-01 | S-EPMC5835222 | BioStudies
Project description:Knowledge on sex differences in myocardial perfusion, blood volume (MBV), and extracellular volume (ECV) in healthy individuals is scarce and conflicting. Therefore, this was investigated quantitatively by cardiovascular magnetic resonance (CMR). Healthy volunteers (n?=?41, 51% female) underwent CMR at 1.5?T. Quantitative MBV [%] and perfusion [ml/min/g] maps were acquired during adenosine stress and at rest following an intravenous contrast bolus (0.05?mmol/kg, gadobutrol). Native T1 maps were acquired before and during adenosine stress, and after contrast (0.2?mmol/kg) at rest and during adenosine stress, rendering rest and stress ECV maps. Compared to males, females had higher perfusion, ECV, and MBV at stress, and perfusion and ECV at rest (p?<?0.01 for all). Multivariate linear regression revealed that sex and MBV were associated with perfusion (sex beta -0.31, p?=?0.03; MBV beta -0.37, p?=?0.01, model R2?=?0.29, p?<?0.01) while sex and hematocrit were associated with ECV (sex beta -0.33, p?=?0.03; hematocrit beta -0.48, p?<?0.01, model R2?=?0.54, p?<?0.001). Myocardial perfusion, MBV, and ECV are higher in female healthy volunteers compared to males. Sex is an independent contributor to perfusion and ECV, beyond other physiological factors that differ between the sexes. These findings provide mechanistic insight into sex differences in myocardial physiology.
2020-01-01 | S-EPMC7316834 | BioStudies
Project description:BACKGROUND:Both ischemic and non-ischemic heart disease can cause disturbances in the myocardial blood volume (MBV), myocardial perfusion and the myocardial extracellular volume fraction (ECV). Recent studies suggest that native myocardial T1 mapping can detect changes in MBV during adenosine stress without the use of contrast agents. Furthermore, native T2 mapping could also potentially be used to quantify changes in myocardial perfusion and/or MBV. Therefore, the aim of this study was to explore the relative contributions of myocardial perfusion, MBV and ECV to native T1 and native T2 at rest and during adenosine stress in normal physiology. METHODS:Healthy subjects (n?=?41, 26?±?5?years, 51% females) underwent 1.5?T cardiovascular magnetic resonance (CMR) scanning. Quantitative myocardial perfusion [ml/min/g] and MBV [%] maps were computed from first pass perfusion imaging at adenosine stress (140 microg/kg/min infusion) and rest following an intravenous contrast bolus (0.05?mmol/kg, gadobutrol). Native T1 and T2 maps were acquired before and during adenosine stress. T1 maps at rest and stress were also acquired following a 0.2?mmol/kg cumulative intravenous contrast dose, rendering rest and stress ECV maps [%]. Myocardial T1, T2, perfusion, MBV and ECV values were measured by delineating a region of interest in the midmural third of the myocardium. RESULTS:During adenosine stress, there was an increase in myocardial native T1, native T2, perfusion, MBV, and ECV (p???0.001 for all). Myocardial perfusion, MBV and ECV all correlated with both native T1 and native T2, respectively (R2?=?0.35 to 0.61, p?<?0.001 for all). Multivariate linear regression revealed that ECV and perfusion together best explained the change in native T2 (ECV beta 0.21, p?=?0.02, perfusion beta 0.66, p?<?0.001, model R2?=?0.64, p?<?0.001), and native T1 (ECV beta 0.50, p?<?0.001, perfusion beta 0.43, p?<?0.001, model R2?=?0.69, p?<?0.001). CONCLUSIONS:Myocardial native T1, native T2, perfusion, MBV, and ECV all increase during adenosine stress. Changes in myocardial native T1 and T2 during adenosine stress in normal physiology can largely be explained by the combined changes in myocardial perfusion and ECV. TRIAL REGISTRATION:Clinicaltrials.gov identifier NCT02723747. Registered March 16, 2016.
2019-01-01 | S-EPMC6876099 | BioStudies
Project description:Microvascular ischemia is one of the hallmarks of hypertrophic cardiomyopathy (HCM) and has been associated with poor outcome. However, myocardial fibrosis, seen on cardiovascular magnetic resonance (CMR) as late gadolinium enhancement (LGE), can be responsible for rest perfusion defects in up to 30% of patients with HCM, potentially leading to an overestimation of the ischemic burden. We investigated the effect of left ventricle (LV) scar on the total LV ischemic burden using novel high-resolution perfusion analysis techniques in conjunction with LGE quantification.30 patients with HCM and unobstructed epicardial coronary arteries underwent CMR with Fermi constrained quantitative perfusion analysis on segmental and high-resolution data. The latter were corrected for the presence of fibrosis on a pixel-by-pixel basis.High-resolution quantification proved more sensitive for the detection of microvascular ischemia in comparison to segmental analysis. Areas of LGE were associated with significant reduction of myocardial perfusion reserve (MPR) leading to an overestimation of the total ischemic burden on non-corrected perfusion maps. Using a threshold MPR of 1.5, the presence of LGE caused an overestimation of the ischemic burden of 28%. The ischemic burden was more severe in patients with fibrosis, also after correction of the perfusion maps, in keeping with more severe disease in this subgroup.LGE is an important confounder in the assessment of the ischemic burden in patients with HCM. High-resolution quantitative analysis with LGE correction enables the independent evaluation of microvascular ischemia and fibrosis and should be used when evaluating patients with HCM.
2016-01-01 | S-EPMC4714488 | BioStudies
Project description:BACKGROUND:Novel cardiac magnetic resonance (CMR) stress T1 mapping can detect ischemia and myocardial blood volume changes without contrast agents and may be a more comprehensive ischemia biomarker than myocardial blood flow. OBJECTIVES:This study describes the performance of the first prospective validation of stress T1 mapping against invasive coronary measurements for detecting obstructive epicardial coronary artery disease (CAD), defined by fractional flow reserve (FFR <0.8), and coronary microvascular dysfunction, defined by FFR ?0.8 and the index of microcirculatory resistance (IMR ?25 U), compared with first-pass perfusion imaging. METHODS:Ninety subjects (60 patients with angina; 30 healthy control subjects) underwent CMR (1.5- and 3-T) to assess left ventricular function (cine), ischemia (adenosine stress/rest T1 mapping and perfusion), and infarction (late gadolinium enhancement). FFR and IMR were assessed ?7 days post-CMR. Stress and rest images were analyzed blinded to other information. RESULTS:Normal myocardial T1 reactivity (?T1) was 6.2 ± 0.4% (1.5-T) and 6.2 ± 1.3% (3-T). Ischemic viable myocardium downstream of obstructive CAD showed near-abolished T1 reactivity (?T1 = 0.7 ± 0.7%). Myocardium downstream of nonobstructive coronary arteries with microvascular dysfunction showed less-blunted T1 reactivity (?T1 = 3.0 ± 0.9%). Stress T1 mapping significantly outperformed gadolinium-based first-pass perfusion, including absolute quantification of myocardial blood flow, for detecting obstructive CAD (area under the receiver-operating characteristic curve: 0.97 ± 0.02 vs. 0.91 ± 0.03, respectively; p < 0.001). A ?T1 of 1.5% accurately detected obstructive CAD (sensitivity: 93%; specificity: 95%; p < 0.001), whereas a less-blunted ?T1 of 4.0% accurately detected microvascular dysfunction (area under the receiver-operating characteristic curve: 0.95 ± 0.03; sensitivity: 94%; specificity: 94%: p < 0.001). CONCLUSIONS:CMR stress T1 mapping accurately detected and differentiated between obstructive epicardial CAD and microvascular dysfunction, without contrast agents or radiation.
2018-01-01 | S-EPMC5835225 | BioStudies
Project description:To evaluate the interstudy repeatability of multislice quantitative cardiovascular magnetic resonance myocardial blood flow (MBF), myocardial perfusion reserve (MPR), and extracellular volume (ECV). A unique saturation recovery self-gated acquisition was used for the perfusion scans.An ungated golden angle radial turboFLASH pulse sequence was used to scan 10 subjects on two separate days on a 3T scanner. A single saturation pulse was followed by a set of four slices. Rest and hyperemia scans were acquired during free breathing. The images were reconstructed using an iterative algorithm with spatiotemporal constraints. The ungated images were retrospectively binned (self-gated) into near-systole and near-diastole. Deformable registration was performed to adjust for respiratory and residual cardiac motion, and the data were fit with a Fermi model to estimate the interstudy repeatability of quantitative self-gated MBF and MPR.The coefficient of variation (CoV) of the territorial MPR using the self-gated near-systole data was 18.6%. The self-gated near-diastole data gave less good CoV of MPR, equal to 46.2%. For MBFs, and using smaller (segmental) regions, the CoVs were 20.1% and 22.7% for the estimation of myocardial blood flow at stress and rest, respectively, using the self-gated near-systole data. The self-gated near-diastole data gave CoV?=?48.6% and 44.9% for stress and rest.The self-gated free-breathing technique for quantification of myocardial blood flow showed good repeatability for near-systole, with results comparable to published studies on interstudy repeatability of quantitative myocardial perfusion MRI using ECG-gating and breath-holds. Self-gated near-diastole data results were less repeatable. J. Magn. Reson. Imaging 2016;43:1369-1378.
1000-01-01 | S-EPMC4865416 | BioStudies
Project description:Perfusion-cardiovascular magnetic resonance (CMR) is generally accepted as an alternative to SPECT to assess myocardial ischemia non-invasively. However its performance vs gated-SPECT and in sub-populations is not fully established. The goal was to compare in a multicenter setting the diagnostic performance of perfusion-CMR and gated-SPECT for the detection of CAD in various populations using conventional x-ray coronary angiography (CXA) as the standard of reference.In 33 centers (in US and Europe) 533 patients, eligible for CXA or SPECT, were enrolled in this multivendor trial. SPECT and CXA were performed within 4 weeks before or after CMR in all patients. Prevalence of CAD in the sample was 49% and 515 patients received MR contrast medium. Drop-out rates for CMR and SPECT were 5.6% and 3.7%, respectively (ns). The study was powered for the primary endpoint of non-inferiority of CMR vs SPECT for both, sensitivity and specificity for the detection of CAD (using a single-threshold reading), the results for the primary endpoint were reported elsewhere. In this article secondary endpoints are presented, i.e. the diagnostic performance of CMR versus SPECT in subpopulations such as multi-vessel disease (MVD), in men, in women, and in patients without prior myocardial infarction (MI). For diagnostic performance assessment the area under the receiver-operator-characteristics-curve (AUC) was calculated. Readers were blinded versus clinical data, CXA, and imaging results.The diagnostic performance (= area under ROC = AUC) of CMR was superior to SPECT (p = 0.0004, n = 425) and to gated-SPECT (p = 0.018, n = 253). CMR performed better than SPECT in MVD (p = 0.003 vs all SPECT, p = 0.04 vs gated-SPECT), in men (p = 0.004, n = 313) and in women (p = 0.03, n = 112) as well as in the non-infarct patients (p = 0.005, n = 186 in 1-3 vessel disease and p = 0.015, n = 140 in MVD).In this large multicenter, multivendor study the diagnostic performance of perfusion-CMR to detect CAD was superior to perfusion SPECT in the entire population and in sub-groups. Perfusion-CMR can be recommended as an alternative for SPECT imaging.ClinicalTrials.gov, Identifier: NCT00977093.
2012-01-01 | S-EPMC3443449 | BioStudies
Project description:Aims:To determine the clinical impact of lipoprotein apheresis in patients with refractory angina and raised lipoprotein(a)?>?500?mg/L on the primary end point of quantitative myocardial perfusion, as well as secondary end points including atheroma burden, exercise capacity, symptoms, and quality of life. Methods:We conducted a single-blinded randomized controlled trial in 20 patients with refractory angina and raised lipoprotein(a)?>?500?mg/L, with 3?months of blinded weekly lipoprotein apheresis or sham, followed by crossover. The primary endpoint was change in quantitative myocardial perfusion reserve (MPR) assessed by cardiovascular magnetic resonance. Secondary endpoints included measures of atheroma burden, exercise capacity, symptoms and quality of life. Results:The primary endpoint, namely MPR, increased following apheresis (0.47; 95% CI 0.31-0.63) compared with sham (-0.16; 95% CI?-?0.33-0.02) yielding a net treatment increase of 0.63 (95% CI 0.37-0.89; P?<?0.001 between groups). Improvements with apheresis compared with sham also occurred in atherosclerotic burden as assessed by total carotid wall volume (P?<?0.001), exercise capacity by the 6?min walk test (P?=?0.001), 4 of 5 domains of the Seattle angina questionnaire (all P?<?0.02) and quality of life physical component summary by the short form 36 survey (P?=?0.001). Conclusion:Lipoprotein apheresis may represent an effective novel treatment for patients with refractory angina and raised lipoprotein(a) improving myocardial perfusion, atheroma burden, exercise capacity and symptoms.
2017-01-01 | S-EPMC6075617 | BioStudies