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Quantitative stress cardiac magnetic resonance (CMR) can be performed using the dual-sequence (DS) technique or dual-bolus (DB) method. It is unknown if DS and DB produce similar results for myocardial blood flow (MBF) and myocardial perfusion reserve (MPR). The study objective is to investigate if there are any differences between DB- and DS-derived MBF and MPR.

Ischemic heart disease is a leading cause of death worldwide and comprises a large proportion of annual health care expenditure. Management of ischemic heart disease is now best guided by the physiologic significance of coronary artery stenosis. Invasive coronary angiography is the standard for diagnosing coronary artery stenosis. However, it is expensive and has risks including vascular access site complications and contrast material–induced nephropathy. Invasive coronary angiography requires fractional flow reserve (FFR) measurement to determine the physiologic significance of a coronary artery stenosis. Multiple noninvasive cardiac imaging modalities can also anatomically delineate or functionally assess for significant coronary artery stenosis, as well as detect the presence of myocardial infarction (MI). While coronary CT angiography can help assess the degree of anatomic stenosis, its inability to assess the physiologic significance of lesions limits its specificity. Physiologic significance of coronary artery stenosis can be determined by cardiac MR vasodilator or dobutamine stress imaging, CT stress perfusion imaging, FFR CT, PET myocardial perfusion imaging (MPI), SPECT MPI, and stress echocardiography. Clinically unrecognized MI, another clear indicator of physiologically significant coronary artery disease, is relatively common and is best evaluated with cardiac MRI. The authors illustrate the spectrum of imaging findings of ischemic heart disease (coronary artery disease, myocardial ischemia, and MI); highlight the advantages and disadvantages of the various noninvasive imaging methods used to assess ischemic heart disease, as illustrated by recent clinical trials; and summarize current indications and contraindications for noninvasive imaging techniques for detection of ischemic heart disease.Online supplemental material is available for this article.Published under a CC BY 4.0 license.

Congestive heart failure (CHF) results from cardiac dysfunction due to multiple causes; it is characterized by low cardiac output (insufficient pumping of blood) and congestion of blood and fluid throughout the body. Pulmonary symptoms are particularly important. Between two and three million people in the US are affected by CHF. A discussion is provided of recent developments in the treatment of one type of chronic CHF, which is caused by left ventricular myocardial dysfunction (impairment of function of the left ventricle, the chamber of the heart that pumps blood to the body). Abnormalities in both the pumping phase (systole) and the filling phase (diastole) are described; CHF can result from failure during either phase, but the two kinds of dysfunction require different treatment approaches. Many compensatory mechanisms of the circulatory system are ultimately detrimental to cardiac function. For instance, the levels of catecholamines (substances that cause blood vessel constriction) increase to compensate for heart failure, an adaptation that facilitates return of blood to the heart. Over prolonged periods, high concentrations of catecholamines can damage the heart muscle. CHF patients have a generally poor prognosis; one-year survival rates range between 34 and 70 percent. Therapy should begin with a diagnosis of the left ventricular dysfunction and should attempt to identify the effect of compensatory mechanisms. Some causes of CHF can be treated: these include noncompliance with medications or dietary recommendations, uncontrolled high blood pressure, and uncontrolled cardiac arrhythmias (irregularities in the heartbeat). Therapy with diuretics (drugs that increase salt and water excretion), digitalis (a drug to normalize cardiac rhythm), and vasodilating agents such as angiotensin-converting enzyme inhibitors, which dilate the blood vessels, are described and evaluated. Treatment for CHF is most effective if the disease is diagnosed early and the underlying causes are addressed. (Consumer Summary produced by Reliance Medical Information, Inc.)

IMPORTANCE: The role of stress cardiac magnetic resonance (CMR) imaging in clinical decision-making by reclassification of risk across American College of Cardiology/American Heart Association guideline–recommended categories has not been established. OBJECTIVE: To examine the utility of stress CMR imaging for risk reclassification in patients without a history of coronary artery disease (CAD) who presented with suspected myocardial ischemia. DESIGN, SETTING, AND PARTICIPANTS: A retrospective, multicenter cohort study with median follow-up of 5.4 years (interquartile range, 4.6-6.9) was conducted at 13 centers across 11 US states. Participants included 1698 consecutive patients aged 35 to 85 years with 2 or more coronary risk factors but no history of CAD who presented with suspected myocardial ischemia to undergo stress CMR imaging. The study was conducted from February 18, 2019, to March 1, 2020. MAIN OUTCOMES AND MEASURES: Cardiovascular (CV) death and nonfatal myocardial infarction (MI). Major adverse CV events (MACE) including CV death, nonfatal MI, hospitalization for heart failure or unstable angina, and late, unplanned coronary artery bypass graft surgery. RESULTS: Of the 1698 patients, 873 were men (51.4%); mean (SD) age was 62 (11) years, accounting for 67 CV death/nonfatal MIs and 190 MACE. Clinical models of pretest risk were constructed and patients were categorized using guideline-based categories of low (<1% per year), intermediate (1%-3% per year), and high (>3% year) risk. Stress CMR imaging provided risk reclassification across all baseline models. For CV death/nonfatal MI, adding stress CMR-assessed left ventricular ejection fraction, presence of ischemia, and late gadolinium enhancement to a model incorporating the validated CAD Consortium score, hypertension, smoking, and diabetes provided significant net reclassification improvement of 0.266 (95% CI, 0.091-0.441) and C statistic improvement of 0.086 (95% CI, 0.022-0.149). Stress CMR imaging reclassified 60.3% of patients in the intermediate pretest risk category (52.4% reclassified as low risk and 7.9% as high risk) with corresponding changes in the observed event rates of 0.6% per year for low posttest risk and 4.9% per year for high posttest risk. For MACE, stress CMR imaging further provided significant net reclassification improvement (0.361; 95% CI, 0.255-0.468) and C statistic improvement (0.092; 95% CI, 0.054-0.131), and reclassified 59.9% of patients in the intermediate pretest risk group (48.7% reclassified as low risk and 11.2% as high risk). CONCLUSIONS AND RELEVANCE: In this multicenter cohort of patients with no history of CAD presenting with suspected myocardial ischemia, stress CMR imaging reclassified patient risk across guideline-based risk categories, beyond clinical risk factors. The findings of this study support the value of stress CMR imaging for clinical decision-making, especially in patients at intermediate risk for CV death and nonfatal MI.

IMPORTANCE: It is uncertain whether unrecognized myocardial infarction (MI) is a risk factor for cerebral infarction. OBJECTIVE: To determine whether unrecognized MI detected by cardiac magnetic resonance imaging (MRI) is associated with cerebral infarction. DESIGN, SETTING, AND PARTICIPANTS: This is a cross-sectional study of ICELAND MI, a cohort substudy of the Age, Gene/Environment Susceptibility–Reykjavik Study conducted in Iceland. Enrollment occurred from January 2004 to January 2007 from a community-dwelling cohort of older Icelandic individuals. Participants aged 67 to 93 years who underwent both brain MRI and late gadolinium enhancement cardiac MRI were included. Data analysis was performed from September 2018 to March 2019. EXPOSURES: Unrecognized MI identified by cardiac MRI. MAIN OUTCOMES AND MEASURES: Unrecognized MI was defined as cardiac MRI evidence of MI without a history of clinically evident MI. Recognized MI was defined as cardiac MRI evidence of MI with a history of clinically evident MI. Cerebral infarctions on brain MRI were included regardless of associated symptoms. Multiple logistic regression was used to evaluate the association between MI status (no MI, unrecognized MI, or recognized MI) and cerebral infarction after adjustment for demographic factors and vascular risk factors. In addition, we evaluated the association between unrecognized MI and embolic infarcts of undetermined source. RESULTS: Five enrolled participants had nondiagnostic brain MRI studies and were excluded. Among 925 participants, 480 (51.9%) were women; the mean (SD) age was 75.9 (5.3) years. There were 221 participants (23.9%) with cardiac MRI evidence of MI, of whom 68 had recognized MI and 153 unrecognized MI. There were 308 participants (33.3%) with brain MRI evidence of cerebral infarction; 93 (10.0%) had embolic infarcts of undetermined source. After adjustment for demographic factors and vascular risk factors, the likelihood (odds ratio) of having cerebral infarction was 2.0 (95% CI, 1.2-3.4; P = .01) for recognized MI and 1.5 (95% CI, 1.02-2.2; P = .04) for unrecognized MI. After adjustment for demographics and vascular risk factors, unrecognized MI was also associated with embolic infarcts of undetermined source (odds ratio, 2.0 [95% CI, 1.1-3.5]; P = .02). CONCLUSIONS AND RELEVANCE: In a population-based sample, we found an association between unrecognized MI and cerebral infarction. These findings suggest that unrecognized MI may be a novel risk factor for cardiac embolism and cerebral infarction.

IMPORTANCE: Cardiac magnetic resonance (CMR) imaging can identify unrecognized myocardial infarction (UMI) in the general population. Unrecognized myocardial infarction by CMR portends poor prognosis in the short term but, to our knowledge, long-term outcomes are not known. OBJECTIVE: To determine the long-term outcomes of UMI by CMR compared with clinically recognized myocardial infarction (RMI) and no myocardial infarction (MI). DESIGN, SETTING, AND PARTICIPANTS: Participants of the population-based, prospectively enrolled ICELAND MI cohort study (aged 67-93 years) were characterized with CMR at baseline (from January 2004-January 2007) and followed up for up to 13.3 years. Kaplan-Meier time-to-event analyses and a Cox regression were used to assess the association of UMI at baseline with death and future cardiovascular events. MAIN OUTCOMES AND MEASURES: The primary outcome was all-cause mortality. Secondary outcomes were a composite of major adverse cardiac events (MACE: death, nonfatal MI, and heart failure). RESULTS: Of 935 participants, 452 (48.3%) were men; the mean (SD) age of participants with no MI, UMI, and RMI was 75.6 (5.3) years, 76.8 (5.2) years, and 76.8 (4.7) years, respectively. At 3 years, UMI and no MI mortality rates were similar (3%) and lower than RMI rates (9%). At 5 years, UMI mortality rates (13%) increased and were higher than no MI rates (8%) but still lower than RMI rates (19%). By 10 years, UMI and RMI mortality rates (49% and 51%, respectively) were not statistically different; both were significantly higher than no MI (30%) (P < .001). After adjusting for age, sex, and diabetes, UMI by CMR had an increased risk of death (hazard ratio [HR], 1.61; 95% CI, 1.27-2.04), MACE (HR, 1.56; 95% CI, 1.26-1.93), MI (HR, 2.09; 95% CI, 1.45-3.03), and heart failure (HR, 1.52; 95% CI, 1.09-2.14) compared with no MI and statistically nondifferent risk of death (HR, 0.99; 95% CI, 0.71-1.38) and MACE (HR, 1.23; 95% CI, 0.91-1.66) vs RMI. CONCLUSIONS AND RELEVANCE: In this study, all-cause mortality of UMI was higher than no MI, but within 10 years from baseline evaluation was equivalent with RMI. Unrecognized MI was also associated with an elevated risk of nonfatal MI and heart failure. Whether secondary prevention can alter the prognosis of UMI will require prospective testing.

Although mortality after ST-segment elevation myocardial infarction (MI) is on the decline, the number of patients developing heart failure as a result of MI is on the rise. Apart from timely reperfusion by primary percutaneous coronary intervention, there is currently no established therapy for reducing MI size. Thus, new cardioprotective therapies are required to improve clinical outcomes after ST-segment–elevation MI. Cardiovascular magnetic resonance has emerged as an important imaging modality for assessing the efficacy of novel therapies for reducing MI size and preventing subsequent adverse left ventricular remodeling. The recent availability of multiparametric mapping cardiovascular magnetic resonance imaging has provided new insights into the pathophysiology underlying myocardial edema, microvascular obstruction, intramyocardial hemorrhage, and changes in the remote myocardial interstitial space after ST-segment–elevation MI. In this article, we provide an overview of the recent advances in cardiovascular magnetic resonance imaging in reperfused patients with ST-segment–elevation MI, discuss the controversies surrounding its use, and explore future applications of cardiovascular magnetic resonance in this setting.

This multicenter study showed that the diagnostic performance of myocardial CT perfusion was similar to that of MR perfusion imaging in the detection of coronary artery disease.

Combined CT angiography and CT myocardial perfusion enables similar prediction of 2-year major adverse cardiovascular event–free survival, including the need for myocardial revascularization procedures, similar to that achieved with standard invasive coronary angiography and single photon emission CT perfusion imaging.

Supplemental Digital Content is available in the text.

Introduction:Quantitative myocardial blood flow (MBF) analysis using stress cardiac magnetic resonance (CMR) has been shown to detect obstructive coronary artery disease (CAD) and coronary microvascular dysfunction (CMD) in several mostly small, single-center studies. The AQUA-MBF (Assessment of QUAntitative MBF) study is a multicenter initiative involving 16 centers.Hypothesis:The goal of this sub-study is to determine if MBF can differentiate CAD, CMD, and normal volunteers in this multicenter setting.Methods:We present data from 53 subjects (15 with CAD, 20 at risk for CMD and 18 controls) who underwent vasodilator stress CMR (Figure) using 1.5T and 3.0T MR scanners (General Electric). At risk for CMD was defined as having diabetes and 2 other risk factors in absence of ≥50% stenosis based on coronary CT. CAD was defined as the presence of stenosis ≥70% based on invasive coronary angiography. Stress perfusion images were acquired using the dual sequence technique. Stress MBF was measured in each of the 16 AHA segments using Fermi deconvolution (Circle Cvi42). In the CAD group, each segment was further classified as having late gadolinium enhancement (LGE), supplied by CAD, or a normal remote territory. The means of the 5 groups were compared using one-way analysis of variance.Results:The segmental stress MBF (ml/g/min) for the 5 groups are shown in figure. Compared to the normal group, segmental stress MBF in 4 disease groups were significantly lower (p<0.001). Segmental MBF in those at risk for CMD was lower than normal segments and greater than CAD segments (p<0.001). LGE and CAD segments had the lowest stress MBF but similar to each other (p=0.9).Conclusions:In this multicenter study, we show that quantification of MBF using the dual sequence stress perfusion CMR technique can differentiate diseased from healthy myocardium and also between obstructive CAD and those at risk for CMD.

Context:The contiguous gene deletion syndrome (CAH-X) was described in a subset (7%) of congenital adrenal hyperplasia (CAH) patients with a TNXA/TNXBchimera, resulting in deletions of CYP21A2, encoding 21-hydroxylase necessary for cortisol biosynthesis, and TNXB, encoding the extracellular matrix glycoprotein tenascin-X (TNX). This TNXA/TNXBchimera is characterized by a 120-bp deletion in exon 35 and results in TNXBhaploinsufficiency, disrupted TGF-β signaling, and an Ehlers Danlos syndrome phenotype.Objective:The objective of the study was to determine the genetic status of TNXBand resulting protein defects in CAH patients with a CAH-X phenotype but not the previously described TNXA/TNXBchimera.Design, Settings, Participants, and Intervention:A total of 246 unrelated CAH patients were screened for TNXBdefects. Genetic defects were investigated by Southern blotting, multiplex ligation-dependent probe amplification, Sanger, and next-generation sequencing. Dermal fibroblasts and tissue were used for immunoblotting, immunohistochemical, and coimmunoprecipitation experiments.Main Outcome Measures:The genetic and protein status of tenascin-X in phenotypic CAH-X patients was measured.Results:Seven families harbor a novel TNXBmissense variant c.12174C>G (p.C4058W) and a clinical phenotype consistent with hypermobility-type Ehlers Danlos syndrome. Fourteen CAH probands carry previously described TNXA/TNXBchimeras, and seven unrelated patients carry the novel TNXBvariant, resulting in a CAH-X prevalence of 8.5%. This highly conserved pseudogene-derived variant in the TNX fibrinogen-like domain is predicted to be deleterious and disulfide bonded, results in reduced dermal elastin and fibrillin-1 staining and altered TGF-β1 binding, and represents a novel TNXA/TNXBchimera. Tenascin-X protein expression was normal in dermal fibroblasts, suggesting a dominant-negative effect.Conclusions:CAH-X syndrome is commonly found in CAH due to 21-hydroxylase deficiency and may result from various etiological mechanisms.

Late gadolinium enhancement MRI appears useful to identify patients who have dilated cardiomyopathy with left ventricular ejection fraction of 35% or higher and who are at risk for sudden cardiac death (SCD) or aborted SCD.

Congenital aortic valve fusion is associated with aortic dilation, aneurysm, and rupture in girls and women with Turner syndrome. Our objective was to characterize aortic valve structure in subjects with Turner syndrome and to determine the prevalence of aortic dilation and valve dysfunction associated with different types of aortic valves.

A high degree of noncompacted (trabeculated) myocardium in relationship to compact myocardium (trabeculated to compact myocardium TM ratio >2.3) has been associated with a diagnosis of left ventricular noncompaction (LVNC). The purpose of this study was to determine the normal range of the TM ratio in a large population-based study and to examine the relationship to demographic and clinical parameters.

Myocardial hemorrhage after myocardial infarction (MI) usually goes undetected. We investigated the diagnostic accuracy of bright-blood T2-weighted cardiac MRI for myocardial hemorrhage in experimental MI.

In hypertrophic cardiomyopathy (HCM), myocardial abnormalities are commonly heterogeneous. Two patterns of late gadolinium enhancement (LGE) have been reported: a bright “confluent” and an intermediate intensity abnormality termed “diffuse,” each representing different degrees of myocardial scarring. We used MRI to study the relation between intramural cardiac function and the extent of fibrosis in HCM. The aim of this study was to determine whether excess collagen or myocardial scarring, as determined by LGE MRI, are the primary mechanisms leading to heterogeneous regional contractile function in patients with HCM.

Using a resolution 1000-fold higher than prior studies, we studied (1) the degree to which late gadolinium-enhancement (LGE) cardiac magnetic resonance tracks fibrosis from chronic myocardial infarction and (2) the relationship between intermediate signal intensity and partial volume averaging at distinct “smooth” infarct borders versus disorganized mixtures of fibrosis and viable cardiomyocytes.

The area at risk (AAR) is a key determinant of myocardial infarction (MI) size. We investigated whether magnetic resonance imaging (MRI) measurement of AAR would be correlated with an angiographic AAR risk score in patients with acute MI.

Cripto-1 is a membrane-bound protein that is highly expressed in embryonic stem cells and in human tumors. In the present study, we investigated the effect of low levels of oxygen, which occurs naturally in rapidly growing tissues, on Cripto-1 expression in mouse embryonic stem (mES) cells and in human embryonal carcinoma cells. During hypoxia, Cripto-1 expression levels were significantly elevated in mES cells and in Ntera-2 or NCCIT human embryonal carcinoma cells, as compared with cells growing with normal oxygen levels. The transcription factor hypoxia-inducible factor-1α directly regulated Cripto-1 expression by binding to hypoxia-responsive elements within the promoter of mouse and human Cripto-1 genes in mES and NCCIT cells, respectively. Furthermore, hypoxia modulated differentiation of mES cells by enhancing formation of beating cardiomyocytes as compared with mES cells that were differentiated under normoxia. However, hypoxia failed to induce differentiation of mES cells into cardiomyocytes in the absence of Cripto-1 expression, demonstrating that Cripto-1 is required for hypoxia to fully differentiate mES cells into cardiomyocytes. Finally, cardiac tissue samples derived from patients who had suffered ischemic heart disease showed a dramatic increase in Cripto-1 expression as compared with nonischemic heart tissue samples, suggesting that hypoxia may also regulate Cripto-1 in vivo.

Current literature suggests that the incidence of cardiac involvement by lymphoma as identified by autopsy varies widely, ranging from 8.7% to 20%. Historically, many cases might have been clinically undetected; however, improved imaging techniques increasingly identify cardiac involvement incidentally. In addition, newer agents resulting in improved cancer therapy outcomes might alter the prevalence and location of metastatic deposits to include more unusual disease sites, including intracardiac locations. We present 2 cases and a review of the literature.

To determine whether in vivo T2-weighted cardiac magnetic resonance imaging (MRI) delineates the area at risk (AAR) in 2-day-old nonreperfused myocardial infarction (MI). AAR was defined as the size of the perfusion defect on day 0. MI and the residual ischemic viable border zone comprise the AAR.

Dominant, truncating mutations of eyes absent 4 (EYA4) on chromosome 6q23 can cause either nonsyndromic hearing loss DFNA10 or hearing loss with dilated cardiomyopathy (DCM). It has been proposed that truncations of the C‐terminal Eya domain cause DFNA10 whereas upstream truncations of the N‐terminal variable region cause hearing loss with DCM. Here we report an extended family co‐segregating autosomal dominant, postlingual‐onset, progressive, sensorineural hearing loss (SNHL) with a novel frameshift mutation, 1490insAA, of EYA4. The 1490insAA allele is predicted to encode a truncated protein with an intact N‐terminal variable region, but lacking the entire C‐terminal Eya domain. Clinical studies including electrocardiography, echocardiography, and magnetic resonance imaging (MRI) of the heart in nine affected family members revealed no DCM or associated abnormalities and confirmed their nonsyndromic phenotype. These are the first definitive cardiac evaluations of DFNA10 hearing loss to support a correlation of EYA4 mutation position with the presence or absence of DCM. These results will facilitate the counseling of patients with these phenotypes and EYA4 mutations. Published 2007 Wiley‐Liss, Inc.

Time‐series MRI data often suffers from image misalignment due to patient movement and respiratory and other physiologic motion during the acquisition process. It is necessary that this misalignment be corrected prior to any automated quantitative analysis. In this article a fast and automated technique for removing in‐plane misalignment from time‐series MRI data is presented. The method is computationally efficient, robust, and fine‐tuned for the clinical setting. The method was implemented and tested on data from 21 human subjects, including myocardial perfusion imaging, renal perfusion imaging, and blood‐oxygen level‐dependent cardiac T2*imaging. In these applications 10‐fold or better reduction in image misalignment is reported. The improvement after registration on representative time–intensity curves is shown. Although the method currently corrects translation motion using image center of mass, the mathematical framework of our approach may be extended to correct rotation and other higher‐order displacements. Magn Reson Med 49:506–514, 2003. © 2003 Wiley‐Liss, Inc.

Stem cells are being investigated for their potential use in regenerative medicine. A series of remarkable studies suggested that adult stem cells undergo novel patterns of development by a process referred to as transdifferentiation or plasticity. These observations fueled an exciting period of discovery and high expectations followed by controversy that emerged from data suggesting cell-cell fusion as an alternate interpretation for transdifferentiation. However, data supporting stem cell plasticity are extensive and cannot be easily dismissed. Myocardial regeneration is perhaps the most widely studied and debated example of stem cell plasticity. Early reports from animal and clinical investigations disagree on the extent of myocardial renewal in adults, but evidence indicates that cardiomyocytes are generated in what was previously considered a postmitotic organ. On the basis of postmortem microscopic analysis, it is proposed that renewal is achieved by stem cells that infiltrate normal and infarcted myocardium. To further understand the role of stem cells in regeneration, it is incumbent on us to develop instrumentation and technologies to monitor myocardial repair over time in large animal models. This may be achieved by tracking labeled stem cells as they migrate into myocardial infarctions. In addition, we must begin to identify the environmental cues that are needed for stem cell trafficking and we must define the genetic and cellular mechanisms that initiate transdifferentiation. Only then will we be able to regulate this process and begin to realize the full potential of stem cells in regenerative medicine.

The purpose of this study was to validate a first‐pass MRI method for imaging myocardial perfusion with multislice coverage and relatively small analyzable regions of interest (ROIs). A fast gradient‐echo (FGRE) sequence with an echo‐train (ET) readout was used to achieve multislice coverage, and a high dose of a contrast agent (CA) was used to achieve a high signal‐to‐noise ratio (SNR). Dogs (N= 6) were studied 1 day after reperfused myocardial infarction, and fluorescent microspheres were used as a standard for perfusion. First‐pass MRI correlated well vs. microsphere flow, achieving mean R values of 0.87 (range = 0.82–0.93), 0.71 (range = 0.46–0.85), and 0.72 (range = 0.49–0.95) for subendocardial ROIs, transmural ROIs, and the endocardial‐epicardial ratio, respectively. Additionally, analysis of myocardial time‐intensity curves (TICs) indicated that 15.8 ± 6.6° sectors, corresponding to 260 μl of endocardium, can be analyzed (R2> 0.95). Magn Reson Med 47:482–491, 2002. Published 2002 Wiley‐Liss, Inc.

After administration of gadolinium, infarcted myocardium exhibits delayed hyperenhancement and can be imaged using an inversion recovery (IR) sequence. The performance of such a method when using magnitude‐reconstructed images is highly sensitive to the inversion recovery time (TI) selected. Using phase‐sensitive reconstruction, it is possible to use a nominal value of TI, eliminate several breath‐holds otherwise needed to find the precise null time for normal myocardium, and achieve a consistent contrast. Phase‐sensitive detection is used to remove the background phase while preserving the sign of the desired magnetization during IR. Experimental results are presented which demonstrate the benefits of both phase‐sensitive IR image reconstruction and surface coil intensity normalization for detecting myocardial infarction (MI). The phase‐sensitive reconstruction method reduces the variation in apparent infarct size that is observed in the magnitude images as TI is changed. Phase‐sensitive detection also has the advantage of decreasing the sensitivity to changes in tissue T1with increasing delay from contrast agent injection. Magn Reson Med 47:372–383, 2002. Published 2002 Wiley‐Liss, Inc.

Inflammation contributes to atherosclerosis, but assessment in humans is largely restricted to measurement of markers in blood. We determined whether MRI properties of large arteries were associated with markers of inflammation in serum. Double inversion recovery, fast spin‐echo images of the common carotid arteries and infrarenal aorta were obtained at 1.5 T both before and after gadolinium‐DTPA (0.1 mmol/kg) in 52 subjects ≥40 years of age, 17 of whom had no risk factors for atherosclerosis and thus served as controls. Twenty‐two study participants had increases in wall thickness (14), T2‐weighted signal intensity (11), and/or contrast enhancement values (7) that were >2 standard deviations (SDs) from control group mean values. Ten subjects in this group had evidence of focal plaques in the carotids (5) and/or aorta (6). Compared with the remaining 30 subjects, these 22 had significantly higher levels of interleukin‐6 (3.53 ± 2.46 vs. 1.97 ± 1.37 pg/mL, P= 0.004), C‐reactive protein (0.56 ± 0.98 vs. 0.30 ± 0.52 mg/dL, P= 0.019), vascular cell adhesion molecule‐1 (572 ± 153 vs. 471 ± 130 ng/mL, P= 0.012), and intercellular adhesion molecule‐1 (244 ± 80 vs. 202 ± 45 ng/mL, P= 0.015), and nonsignificant differences in levels of E‐selectin (46.1 ± 18.9 vs. 42.3 ± 11.3 ng/mL, P= 0.369). Thus, MRI characteristics of the aorta and carotid arteries were associated with elevated serum markers of inflammation, frequently in the absence of definite atheroma. MRI of large arteries may provide a new approach to investigate the contribution of inflammation to atherogenesis. J. Magn. Reson. Imaging 2001;14:698–704. © 2001 Wiley‐Liss, Inc.

The purposes of our study were to investigate the benefits of using a single dose of an extracellular contrast agent for coronary magnetic resonance angiography (CMRA) and to determine the relative benefits of arterial‐phase vs. delayed‐phase image acquisition. The right coronary artery was imaged in 10 healthy adults using a breath‐hold, two‐dimensional fast gradient echo pulse sequence designed for vessel tracking (multiphase, multislice image acquisition). Pre‐ and postcontrast CMRA was performed. Postcontrast imaging consisted of arterial‐ and delayed‐phase CMRA following a 15 mL bolus (single dose) of contrast media and of delayed‐phase imaging following a cumulative 45 mL contrast dose (triple dose). Contrast‐enhanced CMRA provided a significantly higher (P< 0.001) signal‐to‐noise ratio (SNR) and contrast‐to‐noise ratio (CNR) than noncontrast CMRA. CNR was highest for single‐dose arterial‐phase CMRA (13.1 ± 4.5) and triple‐dose delayed‐phase CMRA (13.0 ± 4.8), followed by single‐dose delayed‐phase CMRA (8.4 ± 3.5) and noncontrast CMRA (4.2 ± 1.8). Single‐dose arterial‐phase CMRA provided the best visualization of the distal right coronary artery and was preferred for blinded physician assessments. We concluded that utilization of a single dose of extracellular contrast media improves CMRA, especially if timed for arterial‐phase imaging. J. Magn. Reson. Imaging 2001;13:682–689. © 2001 Wiley‐Liss, Inc.

Fast gradient-echo sequences that use an echo-train readout are becoming more widely used, particularly for imaging the heart. An important issue for these sequences involves determining the optimal duration for the echo-train readout. In normal volunteer scans and theoretically the echo-train readout duration was varied from 2.4 to 32.8 msec. Myocardial signal-to-noise ratio (SNR), myocardium-tag signal difference-to-noise ratio (SDNR), flow artifact-to-noise ratio (FNR), and geometric distortion were measured and/or calculated. Our results showed that to obtain high SNR, SDNR, and data acquisition efficiency while minimizing FNR and geometric distortion, the readout duration should be 10–15 msec at 1.5 T. J. Magn. Reson. Imaging 2000;11:75–80. Published 2000 Wiley-Liss, Inc.

Although magnetic resonance imaging (MRI) is capable of imaging various physiological parameters associated with the heart valves, it has generally been difficult to visualize the valve leaflets directly. The aortic valve was imaged in 120 patients referred for cardiac MRI to assess myocardial volumes or mass. The average patient age was 37 and ranged from 9 to 75 years. Heart rate ranged from 43 to 100 bpm. Imaging was performed on a 1.5 T scanner equipped with enhanced gradients and a cardiac phased-array coil. A double inversion recovery fast spin-echo sequence was used to acquire short-axis images of the aortic valve in a breathhold (15 ± 3 seconds). All three leaflets of the aortic valve were seen in 102 of 120 studies (85%). Two leaflets were detected in another 15 subjects. No leaflets were seen in three individuals. Seven cases of a bicuspid or thickened aortic valves were clearly distinguished from normal valves. The signal-to-noise ratio of aortic leaflets (14 ± 5) was significantly higher than that of the residual blood signal in the aortic root (7 ± 4, P &lt; 0.001). MR images showed the aortic valve leaflets in a high fraction of people with suspected normal aortic valves and detected seven cases of abnormal aortic valves. The potential of MRI to study both the anatomic and functional consequences of valvular heart disease warrants further study. J. Magn. Reson. Imaging 1999;10:771–777. © 1999 Wiley-Liss, Inc.

Velocity‐encoded phase contrast magnetic resonance imaging (MRI) has the potential to quantify regional myocardial contractile function with a sensitivity to motion comparable to implanted ultrasonic crystals. An MRI sequence and post‐processing algorithm were developed to measure myocardial velocity gradients on a 1.5 T MRI scanner. These methods were validated on a rotating phantom and applied to dogs before (n= 11) and during prolonged coronary occlusion (n= 5). In phantom validation studies, the average absolute error corresponded to motion equivalent to 0.03 ± 0.04 mm (mean ± SD) during the repetition time of the experiment. Rigid body corrections during post‐processing significantly simplified the interpretation of myocardial velocity vectors. In vivo, rigid body motion contributes substantially to the recorded myocardial velocities in systole and diastole and can give the false impression of regional wall motion abnormalities. After rigid body correction, normal systolic and diastolic velocity vectors in short‐axis views of the left ventricle were primarily directed toward the center of the left ventricle. Transmural radial strain rate was 2.0 ± 0.6 sec−1during systole and −3.6 ± 1.1 sec−1during early diastole in normal canine hearts. Ischemic myocardium was easily discriminated from normal left ventricle by velocity‐encoded phase contrast MRI both qualitatively and quantitatively (P< 0.01 in systole and P< 0.05 in early diastole). Although the myocardial velocity images have a spatial resolution on the order of a millimeter, the velocity encoding describes the mechanical consequences of focal myocardial ischemia with sensitivity to submillimeter displacement of the pixels. The three‐dimensional nature of velocity‐encoded MRI is particularly well suited to the study of the complex motion of the heart in vivo. Magn Reson Med 42:98–109, 1999. © 1999 Wiley‐Liss, Inc.

A segmented k‐space fast gradient‐echo pulse sequence with an echo‐train readout (FGRE‐ET) was developed for high‐quality cine imaging of the heart in reduced scan times. Using segmented FGRE‐ET, cine images of the heart can be acquired in as few as 1–5 heart beats and do not display the geometric distortion and flow‐related artifacts typically associated with cardiac echoplanar imaging (EPI). Segmented FGRE‐ET was compared with conventional segmented FGRE and with conventional multi‐phase EPI in normal volunteers. Segmented FGRE‐ET was found to have reduced temporal blurring compared with segmented FGRE for cine imaging in 4 heart beats (P< 0.05). Also, segmented FGRE‐ET did not display geometric distortion characteristic of conventional EPI (P< 0.05). Segmented FGRE‐ET may be particularly applicable to functional cardiac stress testing because it allows versatile cine imaging in very short breath‐holds. Magn Reson Med 41:609–613, 1999. Published 1999 Wiley‐Liss, Inc.

A segmented k-space fast gradient-echo pulse sequence with an echo-train readout (FGRE-ET) was developed for high-quality cine imaging of the heart in reduced scan times. Using segmented FGRE-ET, cine images of the heart can be acquired in as few as 1–5 heart beats and do not display the geometric distortion and flow-related artifacts typically associated with cardiac echoplanar imaging (EPI). Segmented FGRE-ET was compared with conventional segmented FGRE and with conventional multi-phase EPI in normal volunteers. Segmented FGRE-ET was found to have reduced temporal blurring compared with segmented FGRE for cine imaging in 4 heart beats (P &lt; 0.05). Also, segmented FGRE-ET did not display geometric distortion characteristic of conventional EPI (P &lt; 0.05). Segmented FGRE-ET may be particularly applicable to functional cardiac stress testing because it allows versatile cine imaging in very short breath-holds. Magn Reson Med 41:609–613, 1999. Published 1999 Wiley-Liss, Inc.

A method is proposed to reconstruct multiphase images that accurately depicts the entire cardiac cycle. A segmented, gradient‐recalled‐echo sequence (FASTCARD) was modified to acquire data continuously. Images were reconstructed retrospectively by selecting views from each heartbeat based on cardiac phase rather than the time elapsed from the QRS complex. Cardiac phase was calculated using a model that compensates for beat‐to‐beat heart rate changes. Images collected using cardiac phase to order reconstruction (CAPTOR) depict the entire cardiac cycle and lack the temporal gap that is characteristic of prospectively reconstructed sequences. Time‐volume curves of the left ventricle capture the contribution of atrial contraction to end‐diastolic volume (EDV). Transmitral phase‐contrast flow measurements show a second peak inflow (awave) that is absent in the standard sequence. Because atrial contraction contributes to ventricular EDV, images using CAPTOR potentially may provide a more reliable measure of EDV, stroke volume, and ejection fraction than standard techniques.

Introduction:Stress perfusion cardiovascular magnetic resonance (CMR) and PET data suggest the presence of microvascular dysfunction in non-ischaemic dilated cardiomyopathy (DCM) but its impact on clinical outcomes is unknown.Hypothesis:Impaired global stress myocardial blood flow (MBF) and myocardial perfusion reserve (MPR) are associated with increased risk of adverse cardiovascular (CV) events.Methods:Adenosine stress perfusion CMR was undertaken on consecutive DCM patients.Stress and rest global MBF and MPR were derived using a modified Fermi-constrained deconvolution algorithm and follow-up data was collected. The primary outcome was a composite of CV death, CV hospitalization and major arrhythmic events. Cumulative incidence curves were constructed for the primary endpoint, stratified by the median value for stress MBF and a threshold of 1.5 for MPR, selected due to prognostic significance in other cardiac conditions. Cox proportional hazards modelling was performed, adjusting for age, sex, LVEF and midwall fibrosis.Results:Of 97 patients (63 men, median age 51 years, median LVEF 43%) followed up for median 1661 days, 17 met the primary endpoint. Stress MBF and MPR increased in line with a rise in LVEF (both p=0.01); there was no trend between rest MBF and LVEF (p=0.77). MBF below median and MPR<1.5 were significantly associated with increased cumulative incidence of the primary endpoint (log-rank p=0.02 and p=0.01, Fig 1). On multivariable modelling, a decreased rate of the primary outcome was associated with increased MPR (HR 0.44; 95%CI 0.2-0.96; p=0.04), with a non-significant increase in stress MBF (HR 0.69; 95%CI 0.46-1.06; p=0.09) and had no association with rest MBF (HR 1.08; 95%CI 0.47-2.46; p=0.86).Conclusion:Impaired MPR, driven by reduced stress MBF is associated with an increased risk of CV events, even after adjusting for LVEF. MPR may be a useful adjunct for DCM risk stratification and as a putative therapeutic target.

Aim:To determine whether stress cardiac magnetic resonance imaging (CMR) provides effective risk reclassification in patients with suspected stable coronary artery disease (CAD) in a multicentre setting across the United States.Methods:Using data from 13 sites, a cohort of 2349 consecutive patients (63?11 years, 53% male) presenting with chest pain and referred for stress CMR was followed for a median of 5.4 years. The primary outcome was major adverse cardiac events (MACE) defined as cardiovascular death, myocardial infarction (MI), hospitalization for congestive heart failure or late unplanned coronary artery bypass graft. The prognostic association of presence of ischemia and/or late gadolinium enhancement (LGE) with MACE was evaluated and the extent of net reclassification improvement (NRI) by CMR beyond a clinical risk model was determined.Results:There were 374 MACE during follow-up. Both ischemia and presence of LGE demonstrated a strong association with MACE (hazard ratio (HR)=3.27; 95% confidence intervals (95%CI) 2.64-4.05; P<0.001 and HR=3.29 (95%CI 2.68-4.04); p<0.001 respectively). Added in a model adjusted for age, sex, hypertension, smoking, diabetes, history of MI and left ventricular ejection fraction (LVEF), ischemia was the strongest predictor for MACE (HR=2.04, 95%CI 1.60-2.59, p<0.001). Adding presence of ischemia or LGE significantly improved model discrimination (C-statistic improvement=0.027 (p=0.001) for ischemia; 0.020 (p=0.008) for LGE; 0.037 (p<0.001) for both), beyond the best overall risk model. NRI by CMR across predefined risk categories (low <10%, intermediate 10%-20%, and high >20%) was 14% (95%CI 13.4-20.6, p=0.001), while continuous NRI was 3.3 (95%CI 2.2-4.4, p<0.001). CMR reclassified 49% of patients at intermediate pre-test risk (32.5% to low risk; 16.5% to high risk) with corresponding changes in the observed MACE rates (1.01%/y and 6.16%/y for low and high post-test risk respectively).Conclusion:In a multicentre cohort of patients with suspected stable CAD, stress CMR effectively reclassified patient risk beyond standard clinical variables and LVEF, especially for those considered at intermediate risk. A CMR negative for ischemia and LGE was associated with a low annual rate of MACE.

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Aim Previous animal studies have demonstrated differences in perfusion and perfusion reserve between the subendocardium and subepicardium. 320-row computed tomography (CT) with sub-millimetre spatial resolution allows for the assessment of transmural differences in myocardial perfusion reserve (MPR) in humans. We aimed to test the hypothesis that MPR in all myocardial layers is determined by age, gender, and cardiovascular risk profile in patients with ischaemic symptoms or equivalent but without obstructive coronary artery disease (CAD). Methods and results A total of 149 patients enrolled in the CORE320 study with symptoms or signs of myocardial ischaemia and absence of significant CAD by invasive coronary angiography were scanned with static rest and stress CT perfusion. Myocardial attenuation densities were assessed at rest and during adenosine stress, segmented into 3 myocardial layers and 13 segments. MPR was higher in the subepicardium compared with the subendocardium (124% interquartile range [45, 235] vs. 68% [22,102], P < 0.001). Moreover, MPR in the septum was lower than in the inferolateral and anterolateral segments of the myocardium (55% [19, 104] vs. 89% [37, 168] and 124% [54, 270], P < 0.001). By multivariate analysis, high body mass index was significantly associated with reduced MPR in all myocardial layers when adjusted for cardiovascular risk factors (P = 0.02). Conclusion In symptomatic patients without significant coronary artery stenosis, distinct differences in endocardial–epicardial distribution of perfusion reserve may be demonstrated with static CT perfusion. Low MPR in all myocardial layers was observed specifically in obese patients.

Aims It remains controversial whether cardiovascular magnetic resonance imaging with gadolinium only enhances acutely infarcted or also salvaged myocardium. We hypothesized that enhancement of salvaged myocardium may be due to altered extracellular volume (ECV) and contrast kinetics compared with normal and infarcted myocardium. If so, these mechanisms could contribute to overestimation of acute myocardial infarction (AMI) size. Methods and results Imaging was performed at 1.5T ≤ 7 days after AMI with serial T1 mapping and volumetric early (5 min post-contrast) and late (20 min post-contrast) gadolinium enhancement imaging. Infarcts were classified as transmural (>75% transmural extent) or non-transmural. Patients with non-transmural infarctions (n = 15) had shorter duration of symptoms before reperfusion (P = 0.02), lower peak troponin (P = 0.008), and less microvascular obstruction (P < 0.001) than patients with transmural infarcts (n = 22). The size of enhancement at 5 min was greater than at 20 min (18.7 ± 12.7 vs. 12.1 ± 7.0%, P = 0.003) in non-transmural infarctions, but similar in transmural infarctions (23.0 ± 10.0 vs. 21.9 ± 9.9%, P = 0.21). ECV of salvaged myocardium was greater than normal (39.5 ± 5.8 vs. 24.1 ± 3.1%) but less than infarcted myocardium (50.5 ± 6.0%, both P < 0.001). In kinetic studies of non-transmural infarctions, salvaged and infarcted myocardium had similar T1 at 4 min but different T1 at 8–20 min post-contrast. Conclusion The extent of gadolinium enhancement in AMI is modulated by ECV and contrast kinetics. Image acquisition too early after contrast administration resulted in overestimation of infarct size in non-transmural infarctions due to enhancement of salvaged myocardium.