Automated Deep Learning Based Cardiac Quantification in Hypertrophic Cardiomyopathy: A Comparative Study with Manual Segmentation

A 48-year-old man, with only a history of mild systemic hypertension, was initially evaluated after presenting with symptoms of exertional dyspnea occurring predominantly with inclines. At that time, an abnormal 12-lead ECG was obtained demonstrating left ventricular hypertrophy by conventional voltage criteria, prompting additional testing with a 2-dimensional echocardiogram that showed normal systolic function (ejection fraction=65%), with 14-mm ventricular septal thickness and 12 mm in the posterolateral wall, and mild systolic anterior motion (SAM) of the mitral valve (bend of anterior leaflet into outflow tract without septal contact). A stress nuclear stress test showed no myocardial ischemia at rest or at peak exercise with a normal blood pressure response and no arrhythmias or ST-T changes during exercise or in recovery. The patient was prescribed a β-blocker for treatment of systemic hypertension. During the next 2 years, the patient developed more limiting exertional symptoms with routine activities. β-Blocker dosage was increased, and a repeat echocardiogram demonstrated similar findings to the initial study, borderline left ventricular (LV) wall thickness despite well-controlled blood pressure. The abnormal ECG, and mild SAM at rest, raised consideration for a diagnosis of hypertrophic cardiomyopathy (HCM) and management for limiting heart failure symptoms. HCM is often suspected in a patient based on the presence of cardiovascular symptoms, detection of abnormal ECG, systolic ejection murmur on routine examination, or as part of pedigree screening.1,2 Abnormalities on ECG are present in >90% of patients with HCM, although no specific ECG pattern is pathognomonic.1 Clinical diagnosis of HCM can reliably be made in the majority of patients with 2-dimensional transthoracic echocardiography by imaging increased LV wall thickness (≥15 mm) with a nondilated cavity in the absence of any disease known to cause LV hypertrophy of that magnitude (ie, systemic hypertension or aortic stenosis).1–5 In …

An asymptomatic athletic 42-year-old man has an abnormal 12-lead ECG obtained during his initial employment examination at a new job (Figure 1). He had no family history of hypertrophic cardiomyopathy (HCM) or unexplained sudden deaths. Echocardiogram demonstrated a 13-mm ventricular septal thickness without systolic anterior motion of the mitral valve. The patient exercised on a standard Bruce protocol stress (exercise) echocardiogram for 12 minutes, without symptoms or arrhythmias, and with appropriate blood pressure augmentation. In the immediate recovery period, systolic anterior motion was absent and outflow tract velocities were normal. A 24-hour ambulatory (Holter) ECG demonstrated normal sinus rhythm without ventricular ectopy. This clinical evaluation left a number of unanswered questions for the patient regarding the diagnosis of HCM, prognosis, and whether a genetic heart disease was present in his family. Figure 1. Abnormal 12-lead ECG in a 42-year-old man demonstrating normal sinus rhythm with left anterior fascicular block, RSR′ in leads V1 and V2, and left ventricular hypertrophy. Since the early 1970s, cardiovascular imaging has played a critical role in describing the structure and function of the heart in HCM.1–5 Indeed, HCM is a disorder uniquely suited to noninvasive imaging, given HCM’s characteristic heterogeneous morphology and hemodynamics, including dynamic left ventricular (LV) outflow obstruction.2,3 For much of 40 years, echocardiography has been the dominant imaging technique, first with rudimentary M-mode and then ultimately 2-dimentional imaging and Doppler,2 now widely available and accessible. The past decade has witnessed the introduction of cardiac magnetic resonance (CMR) into clinical HCM practice.1,3–10 This contemporary technique provides images with high spatial and temporal resolution and sharp contrast between the myocardial border and blood pool, allowing precise measurements of LV wall thickness and complete tomographic reconstruction of the entire cardiac chamber (without …

Hypertrophic Cardiomyopathy

Because of its wide availability, low cost, versatility, and clinical use, stress echocardiography has become increasingly recognized as a valuable tool in the assessment of patients with regurgitant valvular heart disease. Exercise testing is favored compared with pharmacological stress testing for risk stratification in asymptomatic patients and can identify what might otherwise be considered as a moderate valve disease. It has been shown to provide insights into exertional symptoms disproportionate to resting hemodynamics in these patients and to facilitate individual risk stratification. Aggravation of valvular regurgitation severity, exercise-induced pulmonary hypertension (PHT), impaired left ventricular (LV) contractile reserve, inducible ischemia, dynamic LV dyssynchrony, and altered exercise capacity, together with the development of symptoms during exercise echocardiography, provide the clinician with straightforward prognostic information, therefore enabling a more accurate definition of the optimal timing of intervention in patients with valvular regurgitation.1,2 In contrast, dobutamine stress echocardiography has little value in cases of valvular regurgitation. Dobutamine infusion is almost systematically associated with a decrease in the severity of regurgitation; however, it might be of interest in the detection of LV contractile reserve and inducible ischemia. The most common form of exercise used in conjunction with echocardiography is immediate postexercise imaging on a treadmill or upright bicycle ergometer. However, semisupine exercise testing on an appropriate tilted table allows continuous echocardiographic monitoring, which represents an advantageous tool for quantifying changes in valvular regurgitation severity, LV function, and pulmonary pressure (Table). This exercise stress echocardiography modality (ie, per-exercise echocardiography) is the most used in Europe, and we strongly suggest this approach in the setting of valvular heart disease to detect evanescent changes. A symptom-limited graded exercise test is recommended, and ≥80% of the age-predicted upper heart rate should be reached in the absence of symptoms. The test is adapted to the clinical conditions …

BackgroundCardiovascular magnetic resonance (CMR) imaging in patients with hypertrophic cardiomyopathy (HCM) enables the assessment of not only left ventricular (LV) hypertrophy and scarring but also the severity of mitral regurgitation. CMR assessment of mitral regurgitation is primarily based on the difference between LV stroke volume (LVSV) and aortic forward flow (Ao) measured using the phase-contrast (PC) technique. However, LV outflow tract (LVOT) obstruction causing turbulent, non-laminar flow in the ascending aorta may impact the accuracy of aortic flow quantification, leading to false conclusions regarding mitral regurgitation severity. Thus, we decided to quantify mitral regurgitation in patients with HCM using Ao or, alternatively, main pulmonary artery forward flow (MPA) for mitral regurgitation volume (MRvol) calculations.MethodsThe analysis included 143 prospectively recruited subjects with HCM and 15 controls. MRvol was calculated as the difference between LVSV computed with either the inclusion (LVSVincl) or exclusion (LVSVexcl) of papillary muscles and trabeculations from the blood pool and either Ao (MRvolAoi or MRvolAoe) or MPA (MRvolMPAi or MRvolMPAe). The presence or absence of LVOT obstruction was determined based on Doppler echocardiography findings.ResultsMRvolAoi was higher than MRvolMPAi in HCM patients with LVOT obstruction [47.0 ml, interquartile range (IQR) = 31.5–60.0 vs. 35.5 ml, IQR = 26.0–51.0; p < 0.0001] but not in non-obstructive HCM patients (23.0 ml, IQR = 16.0–32.0 vs. 24.0 ml, IQR = 15.3–32.0; p = 0.26) or controls (18.0 ml, IQR = 14.3–21.8 vs. 20.0 ml, IQR = 14.3–22.0; p = 0.89). In contrast to controls and HCM patients without LVOT obstruction, in HCM patients with LVOT obstruction, aortic flow-based MRvol (MRvolAoi) was higher than pulmonary-based findings (MRvolMPAi) (bias = 9.5 ml; limits of agreement: −11.7–30.7 with a difference of 47 ml in the extreme case). The differences between aortic-based and pulmonary-based MRvol values calculated using LVSVexcl mirrored those derived using LVSVincl. However, MRvol values calculated using LVSVexcl were lower in all the groups analyzed (HCM with LVOT obstruction, HCM without LVOT obstruction, and controls) and with all methods of MRvol quantification used (p ≤ 0.0001 for all comparisons).ConclusionsIn HCM patients, LVOT obstruction significantly affects the estimation of aortic flow, leading to its underestimation and, consequently, to higher MRvol values than those obtained with MPA-based MRvol calculations.

Differentiation between hypertrophic cardiomyopathy (HCM) patients and healthy athletes (HA) is a common clinical conundrum. We aimed to analyze cardiac magnetic resonance (CMR) characteristics of HA, sedentary HCM and athletic HCM patients and to determine CMR parameters which can help to diagnose HCM in athletes. Male sedentary HCM patients with slightly elevated maximal end-diastolic wall thickness (EDWT 13–18 mm, n=40, 47.6±14.7y) and HA (n=30, 27.5±5.6y) were consecutively enrolled. Additionally, athletes with HCM were enrolled (n=16, 29.6±13.4 y), where a comprehensive investigation confirmed the diagnosis of HCM. We determined conventional CMR parameters (left ventricular (LV) ejection fraction (EF), end-diastolic (EDVi) and end-systolic volume index, mass index (Mi)), derived parameters such as EDWT/LVEDVi, LVM/LVEDV ratio and strain parameters such as global longitudinal (GLS), radial (GRS) and circumferential strain (GCS), SD of peak LS and CS using feature tracking. Presence of late gadolinium enhancement (LGE) was also determined. CMR parameters representing LV hypertrophy pattern or LV function were analyzed using a logistic regression to detect the best CMR parameters to predict HCM in athletes. To differentiate between HA and athletes with HCM optimal cut-off values for CMR parameters were calculated using receiver operating curve analysis. Comparing the three groups significant differences were found regarding conventional and derived CMR parameters and strain values. None of the HA showed LGE, 75% of athletic HCM and 82% of sedentary HCM patients showed LGE. The univariate regression model showed that LVEF, EDWT, EDWT/LVMi, LVM/LVEDV, GCS, GRS, SD of peak LS and CS are determinants of the diagnosis of HCM among athletes. Multivariate regression revealed that EDWT/LVMi and GCS are independent disease predictors in athletes (p&amp;lt;0.05). Cut-off value for GCS ≤−32.5 and for EDWT/LVEDVi &amp;gt;0.126 discriminate athletic HCM from HA with a sensitivity of 81.3 and 87.5% (AUC 0.93), and a specificity of 96.7 and 83.3% (AUC 0.95), respectively (Figure 1). CMR characteristics of sedentary and athletic HCM may differ, therefore establishing diagnostic parameters based on comparison between athletic HCM and HA is essential. CMR based strain and derived parameters may help to differentiate between physiological and pathological left ventricular hypertrophy in athletes. Figure 1 Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): National Research, Development and Innovation Office of Hungary (NKFIA) and National Research, Development and Innovation Office (NFKIH) of Hungary.

Chronic secondary mitral regurgitation (SMR) is a complex entity that is often clinically underappreciated.1 It complicates either ischemic heart disease or dilated cardiomyopathy; its prevalence varies among series but may reach ≤50% in patients with heart failure.2 When present, SMR may exhibit a broad range of severity and confers an adverse prognosis, which is worse with increasing severity of mitral regurgitation (MR).3,4 The management of SMR poses a unique set of challenges, based partly on the complexity of the valve disorder and the still-evolving adoption of the optimal therapeutic approach.5 Noninvasive imaging and, in particular, echocardiography, plays a critical role for the initial and longitudinal assessment, for individual risk stratification and outcome prediction, and for guiding intervention in patients with chronic SMR.6 SMR develops because of a combination of mitral leaflet tethering secondary to left ventricular (LV) dilatation/deformation with papillary displacement/discoordination, annular dilatation/dysfunction, insufficient LV-generated closing forces attributable to reduction of LV contractility, and global LV/papillary muscle dyssynchrony.1,5 Tethering of the mitral leaflets is the principal lesion of SMR and results in restriction of systolic leaflet motion, namely type IIIb of Carpentier’s classification. SMR does not typically occur in global LV dysfunction without tethering. However, once tethering occurs, leaflet closure is further impaired by LV dysfunction because there is decreased force opposing tethering.6–9 The key event in the pathogenesis of SMR is the distortion of normal LV geometry—regional and global LV remodeling—with subsequent apical and lateral displacement of papillary muscles, which, in turn, draws the chordae tendineae away from the line of coaptation.7,8 The extent of LV systolic dysfunction and dilatation is weakly correlated to the degree of SMR unless accompanied by geometric distortion in the region of the papillary muscles.1,9 …

Spectrum and Clinical Significance of Systolic Function and Myocardial Fibrosis Assessed by Cardiovascular Magnetic Resonance in Hypertrophic Cardiomyopathy

Background In hypertrophic cardiomyopathy (HCM) patients, quantification of left ventricular (LV) mass carries important prognostic implications. Two-dimensional echocardiography (2DE) has limited accuracy for LV mass calculation, due to plane position errors, geometric assumptions and asymmetric distribution of LV hypertrophy in HCM. Purpose We aimed to explore: (1) the accuracy of three-dimensional echocardiography (3DE) vs 2DE to quantify LV mass in HCM compared to cardiac magnetic resonance (CMR); (2) the relationship of 3DE LV mass with non-sustained ventricular tachycardia (NSVT) and late gadolinium enhancement (LGE)≥15% by CMR. Methods In consecutive HCM patients referred to our Cardiomyopathy Clinic between 2020 and 2023, 2DE and 3DE were used to assess LV mass. LV systolic function was assessed by 3DE ejection fraction (LVEF) and peak global 2D longitudinal strain (2DGLS). Clinical, 24h ECG Holter and CMR data were collected. Results A total of 180 HCM patients (pts, age 58±18 years, 55% men) were enrolled. Apical HCM was present in 56 pts (31%) and obstructive HCM in 69 pts (38%). Maximal LV wall thickness (MWT) by 2DE was 19.5±4.6 mm. LV mass was 150±51 g/m2 by 2DE, 80±25 g/m2 by 3DE, and 79±26 g/m2 by CMR. Fifty-seven pts (32%) had evidence of NSVT at ECG Holter monitoring. LGE≥15% was present in 32% pts. Aim #1: In a subset of 63 pts who underwent CMR, 3DE LV mass was strongly correlated with CMR LV mass (r=0.85, p&amp;lt;0.001), while 2DE LV mass was not (p=0.38). LV mass by 3DE showed a better agreement with LV mass (bias 3.8 g/m2, LOA -25 to 32 g/m2) by CMR than 2DE (bias 68 g/m2, LOA -35 to 172 g/m2). Aim #2: In the entire cohort, 3DE LV mass had a stronger association compared to 2DE LV mass with the presence of LGE≥15% (AUC 0.68 for 3DE versus 0.56 for 2DE, p=0.08) and NSVT (AUC 0.65 for 3DE versus 0.54 for 2DE, p=0.06). By multivariable analysis, LV mass by 3DE was an independent predictor of LGE≥15% (HR 1.03) and of NSVT (HR 1.03), outperforming 2DGLS and MWT in the latter regression. Using the Youden Index from ROC curve, the optimal cutoff for predicting LGE≥15% using 3DE mass was 87 g/m² (sensitivity 47%, specificity 91%). The addition of 3DE LV mass to a model including 2DE MWT, 2DE LV mass and 2DGLS had a significant incremental value for the prediction of LGE≥15% (Figure 1). Conclusions In HCM patients, LV mass by 3DE was strongly correlated to LV mass by CMR and was an independent predictor of significant LV myocardial fibrosis and ventricular arrhythmias. In centers with low access to CMR, implementation of 3DE to measure LV mass in HCM patients may improve arrhythmic risk stratification compared to 2DE.

Major advances in the field of pediatric cardiology and cardiac surgery over the last several decades have led to a dramatic improvement in survival rates for most forms of congenital heart disease (CHD). For example, hypoplastic left heart syndrome, a previously lethal defect, now has early survival rates up to 90% at major centers.1 These improved outcomes have produced a growing population of survivors with complex CHD who are now reaching adulthood (Figure 1). During this period, improvements in surgical and medical treatments have been accompanied by developments in diagnostic modalities. Echocardiography has replaced catheterization as the primary diagnostic modality, and it is now uncommon for newborn infants to undergo catheterization for purely diagnostic purposes. Although echocardiography remains the bedrock of noninvasive cardiac imaging, the array of diagnostic modalities and techniques available continue to grow and this has spawned the specialty of “noninvasive cardiac imaging” and the need for the “cardiac imager” to be adept in all the different modalities. Figure 1. Percentage of patients under the age of 1 year (grey bars) and over the age of 18 years (black bars) undergoing echocardiography at Children’s Hospital Boston from 1983 through 2006. Note the reverse trends of these age groups reflecting the steady increase in the proportion of adult patients with congenital heart disease. Although the absolute number of infants undergoing echocardiography during this time period has increased, their proportion has steadily declined. Echocardiography, cardiac magnetic resonance (CMR), and cardiac computed tomography (CCT) are the primary modalities used for noninvasive cardiac imaging in patients with CHD. Nuclear scintigraphy is used in selected circumstances. The Table summarizes the strengths and weaknesses of each modality. Figure 2 shows temporal trends in utilization for the various noninvasive cardiac imaging techniques at our center. It is clear that echocardiography is the most frequently …

Characterization of atrial histology in a patient with hypertrophic cardiomyopathy: Possible evidence of a primary atrial myopathy

MitraClipTM-implantation has been shown to significantly reduce mitral regurgitation (MR) in patients with high surgical risk. Whereas hemodynamic and echocardiographic studies suggest a reduction in left ventricular (LV) volumes and an increase in cardiac output following the intervention, there is very limited data on assessment of volumetric and functional changes after MitraClipTM-implantation using cardiac magnetic resonance (CMR) imaging, the considered method of choice in such a scenario. Methods Patients with moderate to severe MR, high surgical risk and absence of contraindications to CMR imaging underwent MitraClipTM-implantation and CMR imaging on a 1.5 Tesla scanner (Intera, CV, Philips Medical Systems) before and within seven days after the procedure. In addition to volumetric and flow studies, myocardial feature tracking (FT) technology for quantification of myocardial wall mechanics was applied. From steady-state free precession images of short axis views LV maximal circumferential (ECCSAX) and radial (ERRSAX) and of the 4-chamber view LV longitudinal (ELL4CH) and radial (ERR4CH) strain was calculated using dedicated prototype software (TomTec, Germany). Results Twenty patients (age: 76 ± 8 years) with functional MR (n = 15) or degenerative MR (n = 5) with a median Euroscore of 33 (range 17-62) underwent the MitraClipprocedure and CMR imaging. Detailed results of volumetric assessment of the LV and right ventricle (RV) as well as calculated mitral and tricuspid regurgitation fraction are summarized within the table. There was a 44% relative reduction in MR fraction after MitraClipTMimplantation. In this severely compromised patient population (mean pre-implant cardiac index of 1.7 L/min/m2), there were smaller LV enddiastolic volumes after the intervention, but reduced total stroke volume at unchanged effective LV stroke volume (=net aortic forward flow) and

The impairment of atrial function and atrial-ventricular coupling in diseases with left ventricular (LV) hypertrophy has been increasingly recognized. This study compares left atrium (LA) and right atrium (RA) function, as well as LA-LV coupling, in patients with hypertrophic cardiomyopathy (HCM) and hypertension (HTN) with preserved LV ejection fraction (EF), using cardiovascular magnetic resonance feature tracking (CMR-FT). Fifty-eight HCM patients, 44 HTN patients, and 25 healthy controls were retrospectively enrolled. LA and RA functions were compared among the three groups. LA-LV correlations were evaluated in the HCM and HTN groups. LA reservoir (LA total EF, ɛs, and SRs), conduit (LA passive EF, ɛe, SRe), and booster pump (LA booster EF, ɛa, SRa) functions were significantly impaired in HCM and HTN patients compared to healthy controls (HCM vs. HTN vs. healthy controls: ɛs, 24.8 ± 9.8% vs. 31.3 ± 9.3% vs. 25.2 ± 7.2%; ɛe, 11.7 ± 6.7% vs. 16.8 ± 6.9% vs. 25.5 ± 7.5%; ɛa, 13.1 ± 5.8% vs. 14.6 ± 5.5% vs. 16.5 ± 4.5%, p < 0.05). Reservoir and conduit functions were more impaired in HCM patients compared to HTN patients (p < 0.05). LA strains demonstrated significant correlations with LV EF, LV mass index, LV MWT, global longitudinal strain parameters, and native T1 in HCM patients (p < 0.05). The only correlations in HTN were observed between LA reservoir strain (ɛs) and booster pump strain (ɛa) with LV GLS (p < 0.05). RA reservoir function (RA ɛs, SRs) and conduit function (RA ɛe, SRe) were significantly impaired in HCM and HTN patients (p < 0.05), while RA booster pump function (RA ɛa, SRa) was preserved. LA functions were impaired in HCM and HTN patients with preserved LV EF, with reservoir and conduit functions more affected in HCM patients. Moreover, different LA-LV couplings were apparent in two different diseases, and abnormal LA-LV coupling was emphasized in HTN. Decreased RA reservoir and conduit strains were evident in both HCM and HTN, while booster pump strain was preserved.

Background Myocardial fibrosis is a hallmark of hypertrophic cardiomyopathy (HCM). Cardiac magnetic resonance (CMR) detects replacement fibrosis (RF) through late gadolinium enhancement (LGE) and interstitial fibrosis (IF) in apparently unscarred myocardium by T1 mapping-derived increased extracellular volume (ECV). Differently from LGE, to date only few small studies have explored the clinical significance of IF in HCM and a correlation between IF and diastolic dysfunction (DD) has been proposed. However, DD detection is challenging in this population since the accuracy of standard echocardiographic parameters is controversial, especially in presence of left ventricular outflow tract obstruction (LVOTO). Left atrial (LA) dysfunction is associated with high left ventricular (LV) filling pressures and may represent an early marker of DD in HCM. Purpose To explore the correlation between IF and LA dysfunction in HCM patients with preserved systolic function. Methods 93 consecutive HCM patients with preserved EF underwent a standard CMR scan. Semi-automatic threshold-based quantification of ventricular volumes, function and mass was performed. LA volumes (LAV) and function were evaluated by CMR feature-tracking (FT) analysis. The three atrial phasic functions were analyzed: (i) passive strain (εe), (ii) active strain (εa) and (iii) total strain (εs). LGE was quantified using the standard deviations (SDs) method (≥4 SDs). IF was assessed by T1 mapping-derived ECV quantification in remote myocardium (r-ECV). A matched group of 15 healthy subjects (HS) served as controls. Results Compared to HS, HCM patients showed increased LAV (LAV max: HS 39±9ml, HCM 59±20 ml; LAV min: HS 16±4 ml, HCM 34±17 ml; p&amp;lt;0.001), reduced LA EF (HS 61±3%, HCM 45±12%, p&amp;lt;0.001), impaired εs (HS 40±7%, HCM 29±11%, p&amp;lt;0.001) and εe (HS 26±7%, HCM 15±7%, p&amp;lt;0.001). No differences in εa were observed (HS 13±4%, HCM 14±7%, p 0.56). HCM patients were divided into 2 groups according to the presence of IF, defined as r-ECV values ≥29%. The two ECV groups did not differ in terms of LV EF, LA EF, LAV, LA area, E/E', LGE, LV mass, maximal wall thickness and LVOTO (all p&amp;gt;0.05). HCM patients with increased r-ECV showed significantly impaired LA function in terms of all three strain parameters vs. normal r-ECV group (HCM r-ECV &amp;lt;29%: εs 31±12%, εe15±7%, εa 15±5%; HCM r-ECV≥29%: εs 24±7%, εe 12±4%, εa 12±5%; all p&amp;lt;0.05). Conclusions In HCM patients increased r-ECV correlates with LA dysfunction, hinting towards a possible role for IF in determining altered LV relaxation and DD. LA strain in controls and HCM ECV groups Funding Acknowledgement Type of funding source: None

Evaluation of patients with primary mitral valve insufficiency (MI) is best supported by quantitative measures. Cardiovascular magnetic resonance imaging (CMR) offers flow and cardiac chamber volume quantification. We studied cardiac remodelling with CMR to determine MI regurgitation volumes (MIVol) related to severe MI. In total, 24, 20, and 28 patients determined to have mild, moderate, and severe primary MI, respectively, were studied. Combining cine stacks with phase-contrast velocity mapping across the ascending aorta, CMR-determined MIVol was reproducibly obtained as the difference between left ventricular (LV) stroke volume and aortic forward flow (Aoflow). With increasing MI severity, MIVol, left heart volumes, and pulmonary venous diameters increased (P < 0.01). Severe MI with LV end-systolic diameter of 40 mm was signified by MIVol >40 mL, MI regurgitant fraction >0.30, LV end-diastolic volume (LVEDV(i)) >108 mL m(-2), and a total left heart volume >188 mL m(-2) with dilated pulmonary veins and a LVEDV/right ventricular EDV ratio >1.2. In severe MI, LV ejection fraction was unaffected, but the Aoflow and the peak ejection rate indexed to LVEDV were lowered (P < 0.05). In surgical patients, the MIVol correlated to the decrease in LV dimension after valve surgery (P < 0.02). CMR provides a reproducible quantitative technique for evaluation of MI, as MIVol and cardiac chamber volumes can be held against diagnostic cut-off values. The Aoflow and peak ejection rate indexed to LVEDV may reveal early LV systolic dysfunction in patients with severe MI. Severe MI is related to lower MI regurgitation volume and fraction than previously believed.