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European Heart Journal Advance Access originally published online on June 14, 2006
European Heart Journal 2006 27(14):1725-1731; doi:10.1093/eurheartj/ehl101
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© The European Society of Cardiology 2006. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

Interpretation of electrocardiographic abnormalities in hypertrophic cardiomyopathy with cardiac magnetic resonance

Carlos A. Dumont1, Lorenzo Monserrat1,*, Rafaela Soler2, Esther Rodríguez2, Xusto Fernandez1, Jesús Peteiro1, Alberto Bouzas1, Beatriz Bouzas1 and Alfonso Castro-Beiras1

1 Department of Cardiology, Juan Canalejo Hospital, Xubias de Arriba 84, 15006 La Coruña, Spain
2 Department of Radiology, Juan Canalejo Hospital, La Coruña, Spain

Received 23 December 2005; revised 17 May 2006; accepted 30 May 2006; online publish-ahead-of-print 14 June 2006.

* Corresponding author. Tel: +34 981 178184; fax: +34 981 178258. E-mail address: lorenzo_monserrat{at}canalejo.org


   Abstract
Top
 Abstract
Introduction
 Methods
 Results
 Discussion
 Conclusions
 Acknowledgements
 References
 
Aims To clarify the mechanisms of electrocardiographic abnormalities in hypertrophic cardiomyopathy, 102 patients were examined with cardiac magnetic resonance. Distribution and magnitude of hypertrophy and late-enhancement were correlated with electrocardiographic abnormalities.

Methods and results Abnormal Q waves were associated with greater upper anterior septal thickness (22±7 mm vs. 18±5 mm, P=0.001) and increased ratios of upper anterior septum to mean inferolateral (P=0.01), anterolateral (P=0.002), apical (P=0.001), and right ventricular (P=0.001) wall thickness. There was no relation between abnormal Q waves and late-enhancement, except for Q waves ≥40 ms (P=0.02). Conduction disturbances and absent septal Q waves were associated with late-enhancement (89 vs. 45%, P=0.01 and 75 vs. 39%, P=0.002, respectively). The depth of negative T waves was related to an increased ratio of the mean thickness between apical and basal level (P=0.01), and to the presence of apical late-enhancement (P=0.03).

Conclusion Abnormal Q waves reflect the interrelation between upper anterior septal thickness and other regions of the left and right ventricles, and wider Q waves are associated with late-enhancement. Conduction disturbances and absent septal Q waves are associated with late-enhancement. The depth of negative T waves is related to craniocaudal asymmetry and apical late-enhancement.

Key Words: Hypertrophy • Cardiomyopathy • Electrocardiography • Magnetic resonance imaging


   Introduction
Top
 Abstract
 Introduction
Methods
 Results
 Discussion
 Conclusions
 Acknowledgements
 References
 
Hypertrophic cardiomyopathy (HCM) is a genetic cardiac disease with a heterogeneous phenotypic expression.1,2 A variety of abnormalities may be present in the 12-lead electrocardiogram in patients with HCM.3–13 The mechanisms of the electrocardiographic changes have been previously studied using echocardiography or left ventriculography with controversial results.5–13 Contemporary cardiac magnetic resonance (CMR) provides high-resolution tomographic images of the entire left and right ventricle chambers, allowing a precise visualization of myocardial wall thickness and affords greater accuracy than echocardiography in assessing the magnitude of left ventricular (LV) hypertrophy, particularly in anterolateral and apical regions.14,15 Furthermore, CMR imaging is a diagnostic technique in which focally increased myocardial fibrosis (late contrast-enhanced MR imaging) may be detected.16–19 Hence, we examined the relation between the magnitude and distribution of LV hypertrophy and the presence of late gadolinium enhancement (LGE) and the occurrence of abnormal Q waves, negative T waves of different amplitude, tall positive T waves, bundle branch block (BBB), and the absence of normal Q waves in leads I-avL and V5-6 in a large group of patients with HCM, in an attempt to clarify the significance of electrocardiographic patterns in this disease.


   Methods
Top
 Abstract
 Introduction
 Methods
Results
 Discussion
 Conclusions
 Acknowledgements
 References
 
Study patients
CMR studies were performed for research indications over a 26-month period in 108 consecutive patients from our cohort of 360. One patient presented claustrophobia, two were excluded for poor image quality or technical limitations, and three for known or suspected coronary artery disease (CAD). Consequently, the remaining 102 patients comprised the final study group. Patients with implantable cardioverter-defibrillators (ICDs) (n=13), pacemakers (n=35), and atrial fibrillation (AF)(n=80) were not referred to CMR imaging. Patients who underwent myectomy (n=2), alcohol septal ablation (n=5), or valve replacement (n=5) prior to CMR were excluded. Based on previous electrocardiographic studies in HCM and taking into account the superior accuracy of CMR over echocardiography, and its limited availability, a sample size of around 100 patients was considered appropriate for this study.

HCM was diagnosed by the presence of a non-dilated and hypertrophied left ventricle (maximal wall thickness ≥15 mm in adult index patients or ≥13 mm in adult relatives of a HCM patient) in the absence of another cardiac or systemic disease (e.g. hypertension or aortic stenosis) capable of producing the magnitude of hypertrophy observed.20–22

Informed consent was obtained from all patients and the Institutional Committee on Human Research approved the study protocol.

Electrocardiographic procedure and criteria
Standard 12-lead ECG was obtained just before the time of CMR imaging with patients in the supine position during quiet respiration. Sensitivity of different ECG criteria for determining LV hypertrophy (Cornell voltage, Sokolow and Lyon index, and Romhilt-Estes point score) and right ventricular hypertrophy (R/S ratio >1 in lead V1 with R>0.5 mV and right axis deviation ≥90°)3 were analysed; as well as the presence of bundle branch blocks, negative T waves of different amplitude (≥5 mm and ≥10 mm), increased positive T waves (≥10 mm), abnormal Q waves (≥0.04 s in duration, ≥25% of the R wave in depth or ≥3 mm in depth in at least two contiguous leads except avR)10,11,13,23–25 and the absence of normal Q waves in leads I-avL and V5–V6.

Previous studies suggested that Q waves are present when increased electrical forces of hypertrophied ventricular septum are unopposed by forces from the right ventricle, the apex, or the posterior wall.11,13 We compared each LV segment measurement, and the maximal right ventricular wall thickness in patients with and without abnormal Q waves, and calculated the following ratios: the maximal upper or middle ventricular septum segment divided by (a) the mean wall thickness of anterolateral and (b) posterolateral segments, (c) the maximal right ventricular measurement, and (d) the mean apical wall thickness in order to assess the electrical forces that may alter the magnitude and direction of the initial QRS vector and influence on the presence of abnormal Q waves.

CMR protocol
Magnetic resonance images were obtained with a 1.5T system (Gyroscan NT; Philips Medical Systems, Best, The Netherlands) in conjunction with a phased-array body coil and electrocardiogram gating. Cine-MR images of the left ventricle were obtained using a turbo gradient recalled echo sequence (repetition time ms/echo time ms, 11/4; flip angle, 20°; field of view, 100x400 mm2; matrix, 147x256; section thickness, 10 mm, 1 mm gap between slices). The cine-MR sequences were obtained in the following planes: a short-axis view of the left ventricle from base to apex with eight to ten sections: one horizontal long axis view of the left ventricle and one vertical long axis view in two left atrium–left ventricle chambers. Endocardial and epicardial borders were outlined on the short-axis cine images in order to calculate the end-diastolic and end-systolic volumes, stroke volume, left myocardial mass, and the LV ejection fraction (EF), using standard ventricular analysis software (EasyVision, version 4.0; Philips Medical Systems). A 0.2 mmol/kg of body weight bolus of gadopentetate dimeglumine (Dotarem; Guerbet, France) was injected at 5 mL/s and flushed with 20 mL of normal saline solution using a power injector. LGE was considered present when the signal intensity of any area within the myocardium was highly hyperintense (excluded artifact images) in a sequence performed with a non-selective inversion pulse adjusted to null the myocardium and acquired up to 10 min after injection of contrast medium. The inversion time to null the signal of the normal myocardium was adjusted manually in each patient between 200 and 350 ms (mean value: 274.25±49.40 ms); flip angle, 15°; field of view, 100x400 mm2; matrix, 144x256; section thickness, 10 mm.26 Five images were obtained at optimal suppression of normal myocardium: three short axis views taken at the base, midpapillary muscles, and the apex, one horizontal long axis view, and one vertical long axis view. The American Heart Association 17-segment model for the left ventricle27 was used to analyse wall thickness, contractile function, and delayed enhancement per segment. Three representative short-axis slices obtained at the base, mid-ventricle, and apex were divided into six, six, and four segments, respectively. The true apex (segment 17) was analysed on the horizontal or vertical long axis of the left ventricle. Endocardial contours at end-diastole and end-systole on the short-axis cine data sets were manually traced for LV volume measurements and were computed with the modified Simpson rule.

All CMR images were analysed on a satellite workstation console with commercial image post-processing software (EasyVision, version 4.0; Philips Medical Systems) by two radiologists with experience in cardiac MR imaging (R.S. and E.R.), whose joint opinion was reached by consensus.

The patterns of LV hypertrophy by CMR were defined, as asymmetric when a ratio ≥1.3 of septum to free wall was present and apical when both an apical wall thickness ≥15 mm and a ratio ≥1.3 of maximum LV short-axis thickness at the apical level to the basal level were present.14

Statistical analysis
Data were analysed using the SPSS software (version 12.0). Continuous variables were expressed as mean±SD and were analysed with the Mann–Whitney and the Kruskal–Wallis tests or with the unpaired t-test and the one-way ANOVA test when normally distributed. Relationships between continuous variables were tested by linear regression. Categorical variables were expressed as a percentage and compared by {chi}2 test. {chi}2 for trend was used to test for an association between groups of electrocardiographic abnormalities and dichotomous variables. Logistic regression analysis was performed to assess which factors were independently associated with giant negative T waves. The following variables, which were considered potential determinants, were included in the model: craniocaudal asymmetry, apical hypertrophy, apical LGE, and midventricular obstruction. A two-tailed probability value of <0.05 was considered statistically significant. As P-values were not adjusted for multiple testing, they have to be considered as descriptive.


   Results
Top
 Abstract
 Introduction
 Methods
 Results
Discussion
 Conclusions
 Acknowledgements
 References
 
Clinical and cardiac magnetic imaging characteristics
The clinical and CMR features are summarized in Table 1. The age ranged from 16 to 78 years (mean: 51 years). There were 65 (64%) men and 37 (36%) women. Of the 102 patients, 100 (98%) were asymptomatic or had only mild symptoms (NYHA I or II) at the time of enrolment.


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  		Table 1 Clinical and CMR features

 
The mean LV thickness was 14±3 mm and the mean maximal wall thickness was 23±6 mm (13–42 mm). Asymmetrical hypertrophy was present in 65 patients (64%), symmetric in 25 (24%), and apical in 12 (12%). Hypertrophy was observed most frequently in anterior and posterior portions of the upper and middle septum. Mean right ventricular wall thickness was 5±2 (range: 3–10 mm). Right ventricular hypertrophy (>5 mm) was present in 30 patients (29%) with a positive correlation between mean LV and maximal right ventricular wall thickness (r=0.4; P<0.001). Right ventricular hypertrophy was associated with distal hypertrophy (apical 57%, basal and apical 44%, and only basal 18%, P=0.002).

Fifty patients (49%) had late-enhancement which occurred most frequently within hypertrophied regions of the interventricular septum (Figure 1). Septal late-enhancement showed a positive correlation with maximum septal thickness (r=0.6, P<0.001). In general, late-enhancement occurred in a patchy distribution with a diffuse or confluent transmural (>75% wall thickness involved) pattern.


Figure 1011
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  		Figure 1 Occurrence of late-enhancement in each LV segment. American Heart Association 17-segment model for the left ventricle (1, basal anterior; 2, basal anteroseptal; 3, basal inferoseptal; 4, basal inferior; 5, basal inferolateral; 6, basal anterolateral; 7, mid anterior; 8, mid anteroseptal; 9, mid inferoseptal; 10, mid inferior; 11, mid inferolateral; 12, mid anterolateral; 13, apical anterior; 14, apical septal; 15, apical inferior; 16, apical lateral; 17, true apical).

 
Electrocardiographic findings
Six patients (6%) with LV hypertrophy confined to the upper anterior septum presented ECG within normal limits. These patients presented the following baseline characteristics: mean age 48±8, 83% male, 17% presence of hypertension, 33% chest pain, 17% previous syncope and subaortic gradient ≥30 mmHg, 50% family history of HCM, and a mean maximum wall thickness of 17 mm (range: 13–20). None of these patients had NSVT, abnormal blood pressure response to exercise, episode of AF, family history of sudden death, or late-enhancement on CMR imaging.

Thirty-six patients (35%) did not fulfil any ECG criteria for LV hypertrophy, in which LV mass was significantly lower than in patients with criteria (161±65 vs. 220±81, P<0.001). The highest sensitivity among the criteria for LV hypertrophy was achieved by the Romhilt-Estes score (≥5) (57%). Of the 13 patients with LV wall thickness ≥30 mm, 9 (70%) had criteria for LV hypertrophy with the Romhilt-Estes score, 9 (70%) with the Cornell voltage, and 6 (46%) with the Sokolow-Lyon voltage. Statistically significant correlation was present between maximum LV wall thickness and the Romhilt-Estes score (r=0.36, P<0.001). Of the 30 patients with right ventricular hypertrophy only two had electrocardiographic criteria of right ventricular hypertrophy. Excluding nine patients with bundle branch block, there was no relation between patients with and without LGE in terms of PR segment and QRS duration, but those with LGE presented longer QTc intervals (437±30 ms vs. 415±28 ms, P=0.001).

Abnormal Q waves
Patients who had ECG abnormalities that could mask the presence of Q waves were excluded [three with left bundle branch block (LBBB)]. Thirty-five (35%) of the 99 remaining patients had abnormal Q waves. There was no consistent relation between the presence of abnormal Q waves and the presence of LGE, only 20 (57%) had LGE when compared with 27 (42%) patients without abnormal Q waves (P=0.1). However, patients with Q waves ≥40 ms had a higher proportion of LGE (15/20 patients, 75%) than patients with Q <40 ms (5/15 patients, 33%) and without Q waves (27/64 patients, 47%) (P=0.02) (Figure 2). Among patients with LGE there was no difference of transmural LGE in patients with Q ≥40 ms (10/15, 67%), Q <40 ms (3/5, 60%), and without Q waves (13/27, 48%) (P=0.5). Abnormal Q waves were associated with greater upper anterior septal thickness (22±7 mm vs. 18±5 mm, P=0.001) and an increase in the ratios of upper anterior septum to mean inferolateral (1.7±0.6 vs. 1.5±0.4; P=0.01), mean anterolateral (1.8±0.6 vs. 1.4±0.5; P=0.002), mean apical (1.8±0.6 vs. 1.4±0.5, P=0.001), and mean right ventricular (4.8±2 vs. 3.3±1, P=0.001) wall thickness segments.


Figure 1012
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  		Figure 2 (A) Electrocardiogram in a patient with extensive hypertrophy involving substantial portions of both ventricular septum and apex, showing abnormal Q waves ≥40 ms in leads I and avL. (B) End-diastolic horizontal long axis cine-MR image shows asymmetrical diffuse thickening of the septum and concentric hypertrophy of the apex. (C) Horizontal long axis late-enhancement MR image obtained at similar level demonstrates confluent mural high signal intensity at the thickened septum.

 
Among patients with Q waves <40 ms, they were located in lateral leads in nine (four septal LGE), inferior in three (one septal LGE), and inferolateral in three (no LGE). Among patients with Q waves ≥40 ms, they were located in lateral leads in 11 (eight septal LGE), inferior in five (two septal and two inferior LGE), inferolateral in three (two septal LGE) and V1–V3 in one (anterior LGE). None of the patients with abnormal Q waves had hypertrophy confined to apical region.

There was no significant difference in clinical and CMR features in patients with and without Q waves, except for a higher proportion of family history of HCM in patients with abnormal Q waves (43 vs. 23%, P=0.04). Seven (53%) of 13 patients with severe hypertrophy (≥30 mm) had abnormal Q waves.

Absence of the septal Q wave
The absence of normal Q waves in leads I-avL and V5–V6 was found in 24 (24%) patients (patients with LBBB excluded). It was statistically significant associated with the presence of LGE, 18 (75%) patients compared with 29 (39%) of 75 patients with Q waves (P=0.002). It occurs in septal (10 patients), anterior (seven patients), and inferior (one patient) segments. Abnormal Q waves were seen in four (17%) of 24 patients with absent septal Q waves, compared with 31 (41%) of 75 patients with normal Q waves (P=0.03). Maximum septal thickness was not different between patients with absent septal Q waves and patients with Q waves in leads I-avL and V5–V6 (21±6 mm vs. 21±7 mm, P=0.9).

Conduction disturbances
Nine (9%) of the 102 patients presented conduction disturbances, three left and six right bundle branch block. All but one of them (89%) had septal LGE (transmural), compared with 42 (45%) of 93 patients without conduction disturbances (P=0.01). The presence of conduction disturbances was associated with greater maximum septal thickness (26±8 mm vs. 21±6 mm, P=0.02), more segments with LGE (mean: 2.2±1.7 vs.1.2±1.9, P=0.01), and with the presence of chest pain (67 vs. 31%, P=0.03) and AF episodes (22 vs. 3%, P=0.01). It was also associated with an increased LV mass (254±100 vs. 195±77 g, P=0.03) and lower EF (66±9 vs. 75±7%, P=0.002). Two of the patients with LBBB had an abnormal Q wave in avL. Among patients with right bundle branch block, five had abnormal Q waves.

Negative T wave
The nine patients with conduction disturbance were excluded from T wave analysis. The depth of negative T waves was related to greater mean apical thickness, an increase in the ratio of the mean thickness between apical and basal level, and to the presence of midventricular obstruction and apical LGE (Table 2) (Figure 3). By logistic regression analysis, apical LGE and craniocaudal asymmetry were independently associated with giant negative T waves (P=0.03 and P=0.01, respectively).


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  		Table 2 Relation between the presence and depth of negative T waves and CMR findings

 

Figure 1013
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  		Figure 3 (A) Electrocardiogram in a patient with extensive hypertrophy involving substantial portions of the apex, showing giant negative T waves. (B) CMR image in horizontal long axis view of the left ventricle demonstrates apical late-enhancement.

 
None of the 18 patients with tall positive T waves (>10 mm) had apical hypertrophy and only 5 (28%) showed LGE compared with 45 (53%) of 84 patients without tall T waves (P=0.04). There was no difference in wall thickness measurements and clinical features between patients with and without tall T waves.


   Discussion
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
Conclusions
 Acknowledgements
 References
 
12-lead electrocardiography has traditionally been an integral part of the evaluation of patients with HCM. The ECG pattern has frequently been used to make inferences regarding the phenotypic expression of this disease, usually the magnitude and extent of LV hypertrophy. In this context, most of its knowledge is based on previous echocardiographic studies. CMR imaging is a technique that enables us to evaluate cardiac structure, function, and tissue characteristics (LGE) with high image resolution. In addition, it has been shown that the extent of LGE CMR correlates inversely with the EF and is associated with progressive ventricular dilatation and greater than or equal to two clinical markers of sudden death.17,18 To the best of our knowledge, this is the first study in which a combination of cine-MR and late-enhancement sequences was used to assess the significance of ECG abnormalities in HCM.

Even though electrocardiographic abnormalities are sometimes the initial or the only manifestation of HCM in genetically affected individuals,23–25,28–32 our study confirms that some patients with overt disease may have normal ECGs. This finding supports that the screening of family members in HCM should always include both ECG and echocardiography or CMR.

The magnitude of LV hypertrophy in HCM has been linked to prognosis, with a direct relation between wall thickness and the risk for sudden death.33 We identified a statistically significant relation between Romhilt-Estes score and maximum LV wall thickness.

The majority of patients with right ventricular hypertrophy on CMR did not have ECG criteria for RVH. This may be explained by the fact that for RVH to be manifested on the ECG, it must be severe enough to overcome the concealing effects of the larger LV forces.3

Abnormal Q wave
Abnormal Q waves are often the initial ECG abnormality in patients with HCM. They occur in the earliest stage of this disease, preceding echocardiographic abnormalities.28–32 Abnormal Q waves may disappear with age because the frequency of abnormal Q waves is lower in middle-age patients than in teens, and because the leads showing abnormal Q waves are different between teens (inferolateral) and older patients (I-avL).32 In general, Q waves in HCM are considered to be formed by two mechanisms: (i) loss of electrical forces because of transmural myocardial fibrosis and (ii) abnormal electrical activation of hypertrophied ventricular septum.9–11,13 From our findings, it is suggested that abnormal Q waves in older patients are present when electrical forces of the upper anterior septum are of such magnitude that they cancel out electrical forces from other regions of the left and right ventricles (moderate septal hypertrophy with mild or no hypertrophy of other segments or marked septal hypertrophy with moderate hypertrophy of other segments). We did not find an association between abnormal Q waves and LGE, except for patients with Q waves ≥40 ms.

The absence of normal Q waves
Net initial QRS forces are directed rightward and anteriorly, causing small Q waves in leads I, aVL, V5–V6. The absence of septal Q has been correlated with significant clinical, pathologic, and even pathophysiologic abnormalities such as fibrosis in the middle third of the ventricular septum, first degree LBBB, proximal left anterior descending CAD (except in diabetics), and with Q-waves infarction.34,35 Interestingly, we found a significant association between absent septal Q wave and LGE. This finding may be explained by an abnormal septum or slow conduction in septal fibres of the LBBB, which result in reversal of the septal activation (right-to-left and front-to-back).36

Conduction disturbances
Conduction system disease was not an uncommon feature in our study population. Our study has shown that conduction disturbances in patients with HCM are associated with septal fibrosis (late-enhancement), a substratum that must be taken into account when assessing unexplained syncope in these patients. We found that patients with conduction disturbances have a greater expression of this disease, increased maximum LV thickness, mass and number of segments with LGE, and decreased EF.

Negative T wave
Based on previous Japanese studies, the ECG pattern characterized by giant negative T waves is used as a marker for patients with a morphologic form of HCM in which hypertrophy is present primarily in the apical region of the LV.5,6 However, most patients with apical form of HCM studied outside of Asia have not shown this characteristic.37 Moreover, previous reports have found that giant negative T waves are present in a small number of patients with morphologic forms of HCM other than the apical variety.7,8,12

In the present study, giant T waves are related to distal hypertrophy with craniocaudal asymmetry and apical LGE. It has been recently demonstrated that patients with more severe distal LVH often display cavity obliteration, which imposes an increased pressure load on the hypertrophied apical myocardium, increasing its oxygen demand and impairing coronary flow through extravascular compression of the coronary artery, leading to ischaemia, and fibrosis replacement.38

Tall positive T waves have been seen exclusively in patients with only basal hypertrophy. It was speculated that conduction delay in the anterior division of the LBBB due to fibrosis replacement or disarray causes a posterior shift of the QRS vector along with a resulting anterior shift of the T wave and the consequent relatively tall T wave in the right- to mid-precordial leads.5 In our study, none of the patients with tall T waves had apical hypertrophy and they presented a lower proportion of LGE. There was no difference in wall thickness measurements between patients with and without tall T waves. Perhaps, the presence of subendocardial ischaemia may play a role in tall T waves development.


   Conclusions
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Conclusions
Acknowledgements
 References
 
Our findings demonstrate that (i) normal ECG or an ECG without criteria of LVH occurs not uncommonly in patients with HCM (6 and 35%, respectively), (ii) abnormal Q waves are primarily a function of the inter-relation of upper anterior septal thickness and other regions of the left and right ventricles, and in patients with wider Q waves myocardial fibrosis may also play a role, (iii) the absence of normal septal Q wave is strongly associated with the presence of myocardial fibrosis, (iv) conduction disturbances are associated with a greater expression of this disease, with most of them presenting septal fibrosis, (v) the depth of the negative T wave is related to distal hypertrophy with craniocaudal asymmetry and apical late-enhancement.

Study limitations
First, because many analyses were made, some chance associations may have been found. Second, most of our comparisons are based on small subgroup analyses, not being able to draw definite conclusions, however, the superior accuracy of CMR over two-dimensional echocardiography (used in previous studies) makes the sample size acceptable. Third, most patients included in this study were middle-aged, and the distribution of hypertrophy and the degree of fibrosis might be different in younger patients with HCM. Fourth, most of the patients were either asymptomatic or only mildly symptomatic and ECG abnormalities could have different implications in more severely symptomatic patients. Fifth, although all patients with documented CAD were excluded from this study, only patients with typical chest pain or symptoms indicative of coronary disease with coronary risk factors underwent coronary angiography, being possible that some patients with CAD were included.


   Acknowledgements
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Conclusions
 Acknowledgements
References
 
Dr Dumont is a Research Fellow of the BBVA-Carolina Foundation, Spain. Dr Monserrat is supported by the Sanofi-Aventis Foundation. Dr Fernandez, Dr Monserrat, and Dr Castro-Beiras are supported by the National Cardiovascular Research Network-Instituto de Salud Carlos III (RECAVA), Spain.

Conflict of interest: none declared.


   References
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Conclusions
 Acknowledgements
 References
 

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Redefining cardiomyopathies: the role of cardiovascular magnetic resonance imaging: reply
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