A human MYBPC3 mutation appearing about 10 centuries ago results in a hypertrophic cardiomyopathy with delayed onset, moderate evolution but with a risk of sudden death.

BACKGROUND: Hypertrophic Cardiomyopathy (HCM) is a genetically heterogeneous disease. One specific mutation in the MYBPC3 gene is highly prevalent in center east of France giving an opportunity to define the clinical profile of this specific mutation. METHODS: HCM probands were screened for mutation in the MYH7, MYBPC3, TNNT2 and TNNI3 genes. Carriers of the MYBPC3 IVS20-2A>G mutation were genotyped with 8 microsatellites flanking this gene. The age of this MYBPC3 mutation was inferred with the software ESTIAGE. The age at first symptom, diagnosis, first complication, first severe complication and the rate of sudden death were compared between carriers of the IVS20-2 mutation (group A) and carriers of all other mutations (group B) using time to event curves and log rank test. RESULTS: Out of 107 HCM probands, 45 had a single heterozygous mutation in one of the 4 tested sarcomeric genes including 9 patients with the MYBPC3 IVS20-2A>G mutation. The IVS20-2 mutation in these 9 patients and their 25 mutation carrier relatives was embedded in a common haplotype defined after genotyping 4 polymorphic markers on each side of the MYBPC3 gene. This result supports the hypothesis of a common ancestor. Furthermore, we evaluated that the mutation occurred about 47 generations ago, approximately at the 10th century.We then compared the clinical profile of the IVS20-2 mutation carriers (group A) and the carriers of all other mutations (group B). Age at onset of symptoms was similar in the 34 group A cases and the 73 group B cases but group A cases were diagnosed on average 15 years later (log rank test p = 0.022). Age of first complication and first severe complication was delayed in group A vs group B cases but the prevalence of sudden death and age at death was similar in both groups. CONCLUSION: A founder mutation arising at about the 10th century in the MYBPC3 gene accounts for 8.4% of all HCM in center east France and results in a cardiomyopathy starting late and evolving slowly but with an apparent risk of sudden death similar to other sarcomeric mutations.

Myocardial microvascular disease and major adverse cardiovascular events in patients with end-stage renal disease: rationale and design of the MICROCARD study.

BACKGROUND: Myocardial ischaemia, a consequence of coronary artery disease, is a major cause of death in patients with end-stage renal disease (ESRD). The pathophysiology and clinical presentation of coronary artery disease in ESRD patients seem to differ from non-ESRD patients with higher implication of myocardial microvascular disease (MMD), higher mortality, fewer myocardial infarctions, less significant coronary stenosis and low efficacy of well-established drugs such as statin and angiotensin-converting enzyme inhibitors. No study has investigated the presence of MMD and its clinical impact in ESRD patients. METHODS: We designed an observational prospective cohort study to investigate the prevalence of MMD and its association with major adverse cardiovascular events (MACE) in ESRD patients with a positive non-invasive test for myocardial ischaemia. Patients eligible for inclusion are those>18 years old receiving dialysis and/or undergoing investigation for kidney transplantation, who are referred to our renal clinic and meet all the inclusion criteria but none of the exclusion criteria. Patients with a positive test for myocardial ischaemia will be enrolled in the 'invasive group'. They will be further examined to detect simultaneously epicardial coronary stenosis by coronary angiography and MMD using pressure wire measurement of fractional flow reserve and coronary flow reserve followed by calculation of the index of microcirculatory resistance. Patients with a negative test for myocardial ischaemia will be enrolled in a 'control group' designed to verify whether the invasive group is indeed at high risk for MACE. Both groups will be followed up for 2 years to compare the incidence of MACE. CONCLUSION: The MICROCARD study will phenotype MMD and will investigate its relation with the incidence of MACE in ESRD patients with myocardial ischaemia. Clinicaltrial.gov NCT01291771.

Effect of cyclosporine on left ventricular remodeling after reperfused myocardial infarction.

OBJECTIVES: This study examined the effect of a single dose of cyclosporine administered at the time of reperfusion on left ventricular (LV) remodeling and function by cardiac magnetic resonance 5 days and 6 months after myocardial infarction. BACKGROUND: In a human study, administration of cyclosporine at the time of acute reperfusion was associated with a smaller infarct size. METHODS: Twenty-eight patients of the original cyclosporine study had an acute (at 5 days) and a follow-up (at 6 months) cardiac magnetic resonance study to determine LV volumes, mass, ejection fraction, myocardial wall thickness in infarcted and remote noninfarcted myocardium, and infarct size. RESULTS: There was a persistent reduction in infarct size at 6 months in the cyclosporine group compared with the control group of patients (29 +/- 15 g vs. 38 +/- 14 g; p = 0.04). There was a significant reduction of LV end-systolic volume (and a trend for LV end-diastolic volume; p = 0.07) in the cyclosporine group compared with the control group, both at 5 days and 6 months after infarction. There was no significant difference between the 2 groups in either global LV mass or regional wall thickness of the remote noninfarcted myocardium at 5 days or 6 months. Attenuation of LV dilation and improvement of LV ejection fraction by cyclosporine at 6 months were correlated with infarct size reduction. CONCLUSIONS: Cyclosporine used at the moment of acute myocardial infarction reperfusion persistently reduces infarct size and does not have a detrimental effect on LV remodeling. These results are preliminary and must be supported by further studies. (Ciclosporin A and Acute Myocardial Infarction; NCT00403728).

Preventing acute decrease in renal function induced by coronary angiography (PRECORD): a prospective randomized trial.

BACKGROUND: Infusion of saline attenuates the decrease in renal function induced by radiographic contrast agents among patients with chronic renal insufficiency. AIM: The Preventing Renal alteration in Coronary Disease (PRECORD) trial was a randomized trial to assess the effect on renal function of saline infusion during and after coronary angiography in 201 patients without severe chronic renal insufficiency (serum creatinine<140micromol/L). METHODS: All patients received standard oral hydration: 2000mL of tap water within the 24 hours after coronary angiography. Patients were randomized before the procedure to intravenous hydration (1000mL of 0.9% saline infusion) or no additional hydration. The infusion was started in the catheterization laboratory and continued for 24 hours. The primary endpoint was the change in calculated creatinine clearance between baseline and 24 hours after coronary angiography. The same ionic low osmolar radiographic contrast agent (ioxaglate) was used in all patients. RESULTS: Both groups had similar baseline characteristics, including age, serum creatinine, volume of contrast and proportion of patients undergoing ad hoc coronary angioplasty. The overall decrease in serum creatinine clearance 24 hours after the procedure was -3.44 (0.68)mL/min. The change in serum creatinine clearance 24 hours after the procedure was -2.81 (1.07)mL/min in the infusion group vs -4.09 (0.91)mL/min in the control group (p=0.38). CONCLUSION: Renal function is altered only slightly 24 hours after coronary angiography with standard oral hydration alone and is not affected by saline infusion started at the beginning of coronary angiography, even in patients with mild-to-moderate renal dysfunction.

Effect of cyclosporine on reperfusion injury in acute myocardial infarction.

BACKGROUND: Experimental evidence suggests that cyclosporine, which inhibits the opening of mitochondrial permeability-transition pores, attenuates lethal myocardial injury that occurs at the time of reperfusion. In this pilot trial, we sought to determine whether the administration of cyclosporine at the time of percutaneous coronary intervention (PCI) would limit the size of the infarct during acute myocardial infarction. METHODS: We randomly assigned 58 patients who presented with acute ST-elevation myocardial infarction to receive either an intravenous bolus of 2.5 mg of cyclosporine per kilogram of body weight (cyclosporine group) or normal saline (control group) immediately before undergoing PCI. Infarct size was assessed in all patients by measuring the release of creatine kinase and troponin I and in a subgroup of 27 patients by performing magnetic resonance imaging (MRI) on day 5 after infarction. RESULTS: The cyclosporine and control groups were similar with respect to ischemia time, the size of the area at risk, and the ejection fraction before PCI. The release of creatine kinase was significantly reduced in the cyclosporine group as compared with the control group (P=0.04). The release of troponin I was not significantly reduced (P=0.15). On day 5, the absolute mass of the area of hyperenhancement (i.e., infarcted tissue) on MRI was significantly reduced in the cyclosporine group as compared with the control group, with a median of 37 g (interquartile range, 21 to 51) versus 46 g (interquartile range, 20 to 65; P=0.04). No adverse effects of cyclosporine administration were detected. CONCLUSIONS: In our small, pilot trial, administration of cyclosporine at the time of reperfusion was associated with a smaller infarct by some measures than that seen with placebo. These data are preliminary and require confirmation in a larger clinical trial.

Long-term benefit of postconditioning.

BACKGROUND: We previously demonstrated that ischemic postconditioning decreases creatine kinase release, a surrogate marker for infarct size, in patients with acute myocardial infarction. Our objective was to determine whether ischemic postconditioning could afford (1) a persistent infarct size limitation and (2) an improved recovery of myocardial contractile function several months after infarction. METHODS AND RESULTS: Patients presenting within 6 hours of the onset of chest pain, with suspicion for a first ST-segment-elevation myocardial infarction, and for whom the clinical decision was made to treat with percutaneous coronary intervention, were eligible for enrollment. After reperfusion by direct stenting, 38 patients were randomly assigned to a control (no intervention; n=21) or postconditioned group (repeated inflation and deflation of the angioplasty balloon; n=17). Infarct size was assessed both by cardiac enzyme release during early reperfusion and by 201thallium single photon emission computed tomography at 6 months after acute myocardial infarction. At 1 year, global and regional contractile function was evaluated by echocardiography. At 6 months after acute myocardial infarction, single photon emission computed tomography rest-redistribution index (a surrogate for infarct size) averaged 11.8+/-10.3% versus 19.5+/-13.3% in the postconditioned versus control group (P=0.04), in agreement with the significant reduction in creatine kinase and troponin I release observed in the postconditioned versus control group (-40% and -47%, respectively). At 1 year, the postconditioned group exhibited a 7% increase in left ventricular ejection fraction compared with control (P=0.04). CONCLUSIONS: Postconditioning affords persistent infarct size reduction and improves long-term functional recovery in patients with acute myocardial infarction.

Mechanisms leading to reversible mechanical dysfunction in severe CAD: alternatives to myocardial stunning.

Patients with severe chronic coronary artery disease (CAD) exhibit a highly altered myocardial pattern of perfusion, metabolism, and mechanical performance. In this context, the diagnosis of stunning remains elusive not only because of methodological and logistic considerations, but also because of the pathophysiological characteristics of the myocardium of these patients. In addition, a number of alternative pathophysiological mechanisms may act by mimicking the functional manifestations usually attributed to stunning. The present review describes three mechanisms that could theoretically lead to reversible mechanical dysfunction in these patients: myocardial wall stress, the tethering effect, and myocardial expression and release of auto- and paracrine agents. Attention is focused on the role of these mechanisms in scintigraphically "normal" regions (i.e., regions usually showing normal perfusion, glucose metabolism, and cellular integrity as assessed by nuclear imaging techniques), in which stunning is usually considered, but these mechanisms could also operate throughout the viable myocardium. We hypothesize that reversion of these three mechanisms could partially explain the unexpected functional benefit after reperfusion recently highlighted by high-spatial-resolution imaging techniques.

Postconditioning the human heart.

BACKGROUND: In animal models, brief periods of ischemia performed just at the time of reperfusion can reduce infarct size, a phenomenon called postconditioning. In this prospective, randomized, controlled, multicenter study, we investigated whether postconditioning may protect the human heart during coronary angioplasty for acute myocardial infarction. METHODS AND RESULTS: Thirty patients, submitted to coronary angioplasty for ongoing acute myocardial infarction, contributed to the study. Patients were randomly assigned to either a control or a postconditioning group. After reperfusion by direct stenting, control subjects underwent no further intervention, whereas postconditioning was performed within 1 minute of reflow by 4 episodes of 1-minute inflation and 1-minute deflation of the angioplasty balloon. Infarct size was assessed by measuring total creatine kinase release over 72 hours. Area at risk and collateral blood flow were estimated on left ventricular and coronary angiograms. No adverse events occurred in the postconditioning group. Determinants of infarct size, including ischemia time, size of the area at risk, and collateral flow, were comparable between the 2 groups. Area under the curve of creatine kinase release was significantly reduced in the postconditioning compared with the control group, averaging 208 984+/-26 576 compared with 326,095+/-48,779 (arbitrary units) in control subjects, ie, a 36% reduction in infarct size. Blush grade, a marker of myocardial reperfusion, was significantly increased in postconditioned compared with control subjects: 2.44+/-0.17 versus 1.95+/-0.27, respectively (P<0.05). CONCLUSIONS: This study suggests that postconditioning by coronary angioplasty protects the human heart during acute myocardial infarction.

150 microgram intracoronary adenosine bolus for accurate fractional flow reserve assessment of angiographically intermediate coronary stenosis.

AIMS: Fractional flow reserve measurement is based upon achieving maximum hyperemia. A 40 microg intracoronary (IC) adenosine bolus sometimes seems insufficient, and we therefore sought to assess the possible role of 100-150 microg boli in routine. METHODS AND RESULTS: 108 intermediate (49+/-16%) stenoses were consecutively studied with 6F catheters. A history of myocardial infarction in the territory of the explored artery or myocardial hypertrophy were the exclusion criteria. Mean FFR was 0.82+/-0.12 with a 40 microg adenosine bolus and decreased to 0.80+/-0.12 and 0.80+/-13 respectively with 100microg and 150 microg boli (P<0.001 vs 40microg in both cases; 100 vs 150 microg, NS). The 40 microg bolus failed to diagnose 8 out of 30 (27%) significant stenoses (i.e., final FFR <0.75). The large boli led to 12 (11%) transient asymptomatic and spontaneously resolving AV blocks without other side-effects. CONCLUSION: FFR underestimated a quarter of intermediate stenoses with the currently used 40microg IC adenosine bolus. A large bolus up to 150 microg appears to be accurate and safe for routine FFR measurement.

Evolution of spontaneous atherosclerotic plaque rupture with medical therapy: long-term follow-up with intravascular ultrasound.

BACKGROUND: Ruptured coronary atheromatous plaque is generally considered to involve a high risk of subsequent clinical events. Few data are available on the natural evolution of non-culprit-lesion ruptured plaque. We therefore used serial intravascular ultrasound (IVUS) to study how such lesions, detected in the context of a first acute coronary syndrome with elevated troponin I levels, develop. METHODS AND RESULTS: Fourteen patients with 28 distinct plaque ruptures (2+/-1 per patient) without significant associated stenosis (minimal lumen cross-sectional area >4 mm2) were included and systematically treated with 40 mg statin and antiplatelet agent (clopidogrel and aspirin for > or =9 months). Mean clinical and IVUS follow-up was 22+/-13 months (median, 22 months). No clinical event related to the lesion under study occurred. On final IVUS examination, half (14 of 28) of the ruptured plaques had healed, and the degree of stenosis tended to diminish (stenosis, 22+/-17% versus 29+/-17% at baseline; P=0.056). No healing-prediction criterion could be identified. CONCLUSIONS: Nearly 2 years of follow-up found that spontaneous coronary atheromatous plaque rupture without significant stenosis detected on first acute coronary syndrome healed without significant plaque modification in 50% of cases with medical therapy.

Tagged MRI and PET in severe CAD: discrepancy between preoperative inotropic reserve and intramyocardial functional outcome after revascularization.

In severe coronary artery disease (CAD), it has been shown that intramyocardial inotropic reserve as assessed with tagged magnetic resonance imaging (MRI) is uniformly distributed among positron emission tomography (PET) patterns reflecting normal or concomitant reductions in perfusion and glucose metabolism. This preliminary study aimed to delineate the relationship between preoperative values of intramyocardial inotropic reserve (in different PET patterns of perfusion and glucose uptake) and intramyocardial functional outcome after surgical revascularization in severe CAD. Twelve patients underwent preoperative tagged MRI (baseline, 10 microg.kg(-1).min(-1) of dobutamine), H2 15O/[18F]fluorodeoxyglucose PET imaging, and postoperative resting tagged MRI. Regional midmyocardial circumferential shortening (Ecc, in %) and PET patterns (normal, match viable, mismatch viable, and infarcted) were assessed in three tagged MRI/PET short-axis slices. Ecc at baseline ranged from 12 +/- 6 to 8 +/- 5 and 4 +/- 4% in normal, match-viable, and infarcted regions, respectively (P <0.05) and was 8 +/- 5% in mismatch-viable regions. Of the 429 regions studied, 187 showed preoperative inotropic reserve with dobutamine, but 238 showed postoperative functional improvement. Postoperative functional improvement was less common in infarcted regions (41 vs. approximately 60% in the other PET patterns), but the extent of improvement was similar among PET patterns (approximately 6%). Postoperative functional improvement occurred in 53% of all (normal, match viable, and mismatch viable) regions without inotropic reserve. In severe CAD, revascularization affords greater intramyocardial functional benefit than expected from the evaluation of intramyocardial inotropic reserve with low-dose dobutamine. Postoperative functional improvement in PET-viable regions without inotropic reserve suggests that factors other than regionally enhanced perfusion contribute to such functional improvement.

Dobutamine-tagged MRI for inotropic reserve assessment in severe CAD: relationship with PET findings.

The impact of blood flow reductions on the intramyocardial inotropic reserve has not yet been established in coronary artery disease (CAD). We therefore evaluated in severe CAD the relationship between positron emission tomography (PET) patterns of perfusion and glucose uptake and the corresponding tagged magnetic resonance imaging (tagged MRI) values of midmyocardial strains under low-dose dobutamine. Eighteen patients underwent tagged MRI (at rest, with dobutamine) and H2(15)O/18F-fluorodeoxyglucose PET. Regional midmyocardial circumferential shortening (Ecc) and PET patterns (normal, match viable, mismatch viable, and infarcted) were assessed in three tagged MRI/PET short-axis slices. Regional Ecc at rest correlated with both perfusion (r = 0.49) and glucose uptake (r = 0.58). The presence of the inotropic reserve was similar in normal, match viable, and infarcted (approximately 40% of regions vs. 52% in mismatch viable, P < 0.05), but the extent of the increase after dobutamine was lower in infarcted regions (P = 0.06). Within each PET pattern, regions were grouped according to their Ecc values at rest into three categories (high, intermediate, and low contractile performance). In mismatch viable (hibernation), the inotropic reserve was similar among the three categories, but in the other PET patterns the presence and extent of the inotropic reserve was higher in those regions with lowest Ecc (without significant differences in perfusion). In severe CAD, the presence of the inotropic reserve assessed by midmyocardial changes under dobutamine does not relate to resting perfusion. At a similar level of perfusion, the presence of the inotropic reserve is inversely related to contractile performance at rest, but our results suggest that it may not be true for hibernating myocardium.

Myocardial perfusion and glucose uptake coupling in CAD patients.

PURPOSE: To evaluate coronary artery disease (CAD) patients regarding to their perfusion-glucose uptake relationship at rest for all myocardial regions and to determine whether this evaluation could typify patients with different positron emission tomography (PET)-pattern proportions and pathophysiological characteristics. METHODS: Rest/dipyridamole H(15)2O and 18FDG PET studies were performed in 23 patients with left ventricular dysfunction. Regional index (relative perfusion, %H(15)2O; relative glucose uptake, %18FDG) allowed to detect PERFUSION-metabolism mismatch (i.e. hibernation) and dipyridamole-induced reversible stress defects (RSD). RESULTS: The correlation (r) between %H(15)2O and % 18FDG at rest allowed definition of three groups: correlated (CORR; r > 0.7; n = 10), semicorrelated (SEMI; 0.5 < r < or = 0.7; n = 6) and uncorrelated (UNCO; r < or = 0.5; n = 7). In UNCO, 96% of regions had a %H(15)2O > or = 55% (p < 0.01 vs. 89 and 82% in SEMI and CORR) and 95% of regions had a %18FDG > or = 55% (p < 0.01 vs. 78 and 71% in SEMI and CORR). Mismatch proportions increased from CORR to SEMI and UNCO (11, 19 and 27%; p < 0.02) and proportion of regions with RSD was higher in UNCO and SEMI (25 and 24 vs. 6% in CORR; p < 0.01). Proportion of mismatch with RSD was at least three fold higher in UNCO (17/58) (p < 0.01 vs. 3/33 and 1/16 in SEMI and CORR). CONCLUSIONS: Analysis of perfusion and glucose uptake at rest allowed to typify three categories of CAD patients with different PET-patterns proportions, distinctive ranges of perfusion and glucose uptake and distinctive hyperemic response. Our results suggest that myocardial hibernation associated with defective hyperemic response is specific of patients with preserved perfusion and glucose uptake.

Cardiac retention of [11C]HED in genotyped long QT patients: a potential amplifier role for severity of the disease.

Although mutations in cardiac sodium and potassium channel genes are associated with congenital long QT syndrome (LQTS), a "modifier" role of the sympathetic nervous system was proposed to explain the distinct severity of the disease. We evaluated cardiac sympathetic innervation using [11C]hydroxyephedrine ([11C]HED) and positron emission tomography (PET) in genotyped LQTS patients. H215O and [11C]HED PET studies were performed in 11 patients (5 symptomatic) and 8 controls. Perfusion and [11C]HED images were depicted as 36-sector polar maps. Sectorial values of perfusion (H2O%), absolute (HEDRet) and relative retention (HED%Ret) of [11C]HED, and the ratio of HED%Ret to H2O% (HED%Ret/H2O%) were calculated. Normal databases were obtained from controls. Sectorial values below 2SD database values were defined as "outside sectors." Controls and patients showed similar sectorial perfusion. Sectorial HEDRet did not differ between groups, but means of HED%Ret were lower in three sectors for patients (P < 0.05). Three sectors from 3 controls had HED%Ret below 2SD, whereas 36 sectors in 9 patients were outside sectors (P < 0.01). In patients, average HED%Ret/H2O% was lower in 9 sectors (P < 0.05 vs. controls); 2 outside sectors were found in controls, but 43 outside sectors were found in patients (P < 0.01), 77% of them in the 5 symptomatic patients. Heterogeneous [11C]HED retention was localized in the septal, anterior, and lateral walls. Most LQTS patients showed a localized and decreased pattern of [11C]HED retention. The larger number of heterogeneous sectors in symptomatic patients suggests that sympathetic function could play an amplifier role for severity of the disease.

QT dynamicity and sudden death after myocardial infarction: results of a long-term follow-up study.

INTRODUCTION: The aim of this study was to determine whether impaired adaptation of the QT interval to changes in heart rate predicts sudden death after an acute myocardial infarction. METHODS AND RESULTS: The Groupe d'Etude du Pronostic de l'Infarctus du Myocarde (GREPI) trial was a prospective multicenter study designed to evaluate the long-term outcome of myocardial infarction. QT dynamicity was evaluated in 265 patients by analyzing 24-hour Holter recordings obtained 9 to 14 days after myocardial infarction. The linear regression slope of QT intervals measured to the apex and to the end of the T wave (QTe) plotted against RR intervals was calculated using a dedicated Holter algorithm. The value of QT/RR in predicting sudden death and total mortality was compared with those of ejection fraction, heart rate variability, and late potentials. Mean follow-up was 81 +/- 27 months. There were 73 deaths, of which 23 were sudden. Of all the parameters, an increased diurnal QTe/RR slope (>0.18) was the strongest independent predictor of sudden death (relative risk 6.07, confidence interval 1.48-24.95, P = 0.01). CONCLUSION: Increased diurnal QTe dynamicity is independently predictive of sudden death among patients with myocardial infarction. This simple parameter may help to stratify risk and select patients who may benefit from antiarrhythmic prophylaxis.

[Diagnosis of systolic heart failure]. / Diagnostic de l'insuffisance cardiaque systolique.

Most of patients with heart failure present a left ventricular systolic dysfunction usually, if not always, associated with a diastolic dysfunction. Clinical manifestations and physical examination allows a presumed diagnosis. Some signs guide toward a systolic heart failure: deviation of cardiac impulse, protodiastolic gallop, functional mitral insufficiency, radiological cardiomegaly associated with signs of postcapillary hypertension, anterior Q wave or complete left bundle branch block. Bed-side dosage of B-type natriuretic peptide is useful to make or exclude the diagnosis of heart failure in patients with acute dyspnea from various causes. Doppler echocardiography is essential to confirm the left ventricular systolic dysfunction and its mechanism: ischemic, valvular or myocardial. The value of shortening fraction is better than eye evaluation. Coronary angiography is indicated when the mechanism of heart failure is unclear and if the patient is relevant to revascularization.

Factor analysis of medical image sequences improves evaluation of first-pass MR imaging acquisitions for myocardial perfusion.

RATIONALE AND OBJECTIVES: Factor analysis of medical image sequences (FAMIS) applied to gadolinium chelate-enhanced subsecond magnetic resonance (MR) imaging was evaluated as a postprocessing method for assessing myocardial perfusion in coronary artery disease (CAD). MATERIALS AND METHODS: To assess the accuracy of motion correction, five normal volunteers underwent MR imaging at rest. Thirteen patients with well-documented CAD and no myocardial infarction underwent MR imaging at rest and after dipyridamole administration. After motion correction, a single myocardial tissue factor (FAMISt) image was obtained with FAMIS for each raw MR imaging series acquisition. To evaluate how FAMIS could improve the analysis of these acquisitions, five readers visually assessed myocardial perfusion with FAMISt and raw MR images, and a multicase, multireader receiver operating characteristic analysis was performed. RESULTS: FAMISt images significantly improved detection of the perfusion defects when compared with raw MR images (P = .002). Areas under the receiver operating characteristic curves ranged from 0.84 to 0.93 with FAMISt images and from 0.48 to 0.85 with raw MR images. CONCLUSION: FAMIS applied to first-pass MR imaging series provided myocardial perfusion images that improve the objective assessment of myocardial perfusion in patients with CAD.