| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Cardiac Imaging |
-Tropomyosin Gene1
1 From the Depts of Clin Radiology (P.S., H.M., H.J.A.), Medicine (K.P., P.J., M.L., J.K.), and Clin Physiology and Nuclear Medicine (M.H.S., J.T.K., E.V., T.L.), Kuopio Univ Hosp, Puijonlaaksontie 2, 70210 Kuopio, Finland; Niuvanniemi Hosp, Kuopio, Finland (J.T.K.); Dept of Radiology, Turku Univ, Turku, Finland (P.N.); and Dept of Radiology, Helsinki Univ Central Hosp, Helsinki, Finland (K.L., H.J.A.). From the 2000 RSNA scientific assembly. Received Nov 25, 2001; revision requested Feb 5, 2002; revision received Apr 8; accepted Jun 24. Supported by Kuopio Univ Hosp Research Grants 5063502 and 410K29, Helsinki Univ Central Hospital Research Fund Grant TYH0220, the Radiological Society of Finland, Orion Research Funds, the Ida Montin Foundation, and the Instrumentarium Science Foundation. Address correspondence to P.S. (e-mail: petri.sipola@kuh.fi).
 |
ABSTRACT |
|---|
 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODSRESULTS DISCUSSIONREFERENCES |
|---|
-tropomyosin gene and to evaluate the association between hypertrophy and perfusion.
MATERIALS AND METHODS: Rest-stress first-pass MR imaging with gadopentetate dimeglumine was performed in 17 patients with HCM and the Asp175Asn substitution in the -tropomyosin gene and in five control subjects. Global and segmental first-pass reserve index (FPR) measurements were derived from signal intensity versus time curves. Left ventricular (LV) wall thickness and LV mass index were measured on cine MR images. The Mann-Whitney test was used to evaluate the difference in FPR between the patient group and the control group. The Spearman correlation was used to evaluate the association between LV hypertrophy and FPR.
RESULTS: Global FPR was significantly lower in the patients with HCM than in the control subjects (1.12 ± 0.35 vs 1.80 ± 0.58, P = .015). In patients with HCM, maximal LV wall thickness and LV mass index correlated negatively with global FPR (r = -0.723, P = .001 and r = -0.598, P = .011, respectively). At the regional level, segmental FPR correlated inversely with LV wall thickness (r = -0.389; P < .001) in patients with HCM.
CONCLUSION: First-pass MR imaging facilitates global and regional evaluation of perfusion impairment in patients with HCM. The severity of perfusion impairment is associated with the degree of LV hypertrophy.
© RSNA, 2002
Index terms: Genes and genetics • Heart, cardiomyopathy, 511.1935 • Heart, hypertrophy, 511.871 • Heart, perfusion, 511.12144 • Heart, MR, 511.12143 • Magnetic resonance (MR), perfusion study, 511.12144
|
INTRODUCTION |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTS DISCUSSIONREFERENCES |
|---|
Breath-hold cine MR imaging provides information on left ventricular (LV) mass and segmental wall thickness with good spatial resolution (15-19). Cine MR imaging in combination with first-pass MR imaging enables assessment of the relationships between regions of myocardial hypertrophy and perfusion in the same imaging session.
The purposes of our study were (a) to assess first-pass MR imaging in the evaluation of perfusion impairment in a genetically homogeneous population of patients with HCM and the Asp175Asn substitution of the -tropomyosin (TPM1) gene, and (b) to evaluate the association between hypertrophy and perfusion.
|
MATERIALS AND METHODS |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTS DISCUSSIONREFERENCES |
|---|
Patients with HCM and Genetic Analysis
The region in eastern Finland in which Kuopio University Hospital is located is home to a population of about 250,000 individuals. All patients who are suspected or confirmed to have HCM in this area are referred to the Division of Cardiology of the Department of Medicine of Kuopio University Hospital for diagnosis and treatment. According to hospital records, all unrelated patients from this area who were suspected or confirmed to have HCM were previously evaluated at Kuopio University Hospital by the same cardiologist (J.K.). Altogether, 36 unrelated patients over 16 years of age who fulfilled the criteria for definite HCM were identified between January 1990 and December 1996 (20).
In the index patients, the clinical diagnosis of HCM was established on the basis of the finding of maximal LV wall thickness of at least 15 mm at two-dimensional echocardiography in the absence of other causes of ventricular hypertrophy such as arterial hypertension (20). Clinical diagnosis of HCM in adult relatives of the probands was established on the basis of the diagnostic criteria of McKenna et al (21). Briefly, relatives with maximal LV wall thickness of at least 13 mm at two-dimensional echocardiography in the absence of other causes of ventricular hypertrophy, as well as those who were observed to have abnormal Q waves at electrocardiography (ECG), were classified as having HCM (21).
Genetic screening for variants in genes encoding sarcomeric proteins was performed by means of polymerase chain reaction analysis with the single-strand conformation polymorphism method and direct sequencing; details of these methods have been previously described (20).
Of the 36 consecutive unrelated patients with HCM in the Kuopio area, four had the Asp175Asn substitution of the TPM1 gene, accounting for 11% of all HCM cases in this area (20). Of the 37 relatives of these four index patients, 22 were found to have the same Asp175Asn substitution of the TPM1 gene. In addition, four members of one family from western Finland with the identical TPM1 gene mutation were included in the study. Thus, a total of 30 patients with HCM and the Asp175Asn substitution of the TPM1 gene were identified.
Six of these patients were unwilling to participate. Two patients with bronchial asthma were excluded because adenosine stress was contraindicated in these patients in an MR imaging environment. Two patients could not be imaged with the body array coil owing to obesity. ECG triggering failed during the first pass of contrast medium in two patients. Contrast medium injection was mistimed in one patient. The population of the present study ultimately consisted of 17 adult subjects from five families with the Asp175Asn substitution of the TPM1 gene, which has been shown to be a rare cause of HCM (22) with benign or intermediary phenotype (23).
Control Subjects
Twelve control subjects (six men, six women; age range, 23–60 years) who did not have documented cardiac or other chronic diseases and were not taking any kind of medication were recruited. All control subjects underwent clinical evaluation by a cardiologist (J.K.) and blood pressure measurement, ECG, and cardiac echocardiography. If no findings of disease were observed, the subject was accepted as a control subject. In addition, all five control subjects (two men, three women; age range, 50–60 years) in whom rest-stress MR perfusion imaging was performed had undergone diagnostic coronary angiography to exclude coronary artery disease within the previous year. All these control subjects had normal coronary arteries at coronary angiography.
Clinical Evaluation
All patients with HCM in the present study participated in a clinical interview and underwent physical examination, 12-lead ECG, and echocardiography. The physical examination included measurement of height, weight, and arterial blood pressure at rest. Echocardiographic evaluation of patients with HCM was performed with a Sonos 1000 or 5500 scanner (Hewlett-Packard, Palo Alto, Calif) and a 2.5-MHz transducer. All tracings were analyzed according to the standards of the American Society of Echocardiography (24). Coronary angiography was performed in 15 of 17 patients with HCM to exclude coronary artery disease. Coronary artery stenoses exceeding 50% were particularly documented, but stenoses less than 50% were also noted. The two patients who did not undergo angiography were 43- and 35-year-old women without cardiovascular risk factors. All coronary angiograms were obtained by the same cardiologist (J.K.) and were evaluated by two cardiologists (J.K. and K.P.).
An identical study protocol was followed with the 12 control subjects. Adenosine stress MR imaging was performed in the five control subjects who had undergone diagnostic coronary angiography. The remaining seven control subjects did not undergo coronary angiography and underwent MR imaging without adenosine stress being induced.
MR Imaging
MR imaging was performed with a 1.5-T clinical MR imaging unit (Magnetom Vision; Siemens Medical Systems, Erlangen, Germany). A phased-array body coil was used as a receiver. ECG readings, blood pressure, pulse wave, and peripheral oxygen saturation were monitored during the study with an MR-compatible control monitor (Datex-Ohmeda AS/3 MRI patient monitor; Instrumentarium, Datex-Ohmeda Division, Helsinki, Finland). In addition, precordial electrodes were applied for ECG gating of the image acquisition. All study subjects were imaged by the same radiologist (P.S.).
After scout views were obtained, the first pass of the contrast medium was assessed with acquisition of images at three LV short-axis planes: at the levels of the mitral valve chordae, the papillary muscle, and the apex. The first pass in the myocardium was observed with an inversion-recovery snapshot fast low-angle shot sequence (25). The parameters for first-pass MR imaging were as follows: repetition time msec/echo time msec/inversion time msec, 4.5/2.2/300; 8° flip angle; 128 x 128 data matrix; 10-mm section thickness; and a 250–280-mm field of view with a 256 x 256 interpolated matrix. Before imaging with contrast medium was performed, the baseline signal intensity (SI) level was assessed.
Myocardial first pass was assessed after injection of a 0.05-mmol bolus of gadopentetate dimeglumine (Magnevist; Schering, Berlin, Germany) per kilogram of body weight into the right antecubital vein through an 18-gauge cannula. The volume of the bolus was 5–13 mL (0.1 mL/kg). The injection was performed at a speed of 5 mL/sec with an MR-compatible power injector (Spectris, Medrad, Pittsburgh, Pa). The bolus of contrast medium was followed by a 10-mL bolus of saline. Immediately after injection of the contrast agent, the patient was asked to hold his or her breath. An image at each anatomic position listed above was acquired every 3–4 seconds, for a total of 15 images at each level.
After first-pass MR imaging with the patient at rest, short-axis MR cine images of the entire LV were obtained during the patient’s breath hold. The parameters for MR cine imaging were as follows: repetition time msec/echo time msec, 60/4.8 with fivefold k-space segmentation; 20° flip angle; 110 x 256 data matrix; and a 280–320-mm field of view with a 256 x 256 interpolated matrix.
Half an hour after the injection of gadopentetate dimeglumine while the patient was at rest, maximal vasodilatation was induced with a continuous infusion of 140 µg/kg/min of adenosine (Adenoscan; Sanofi Winthrop Pharmaceuticals, Morrisville, Pa) for 6 minutes. Each patient had refrained from ingesting caffeine for 24 hours before the examination. The first-pass MR imaging sequence was performed 3 minutes after the initiation of continuous adenosine infusion. Gadopentetate dimeglumine was injected through a separate line to prevent an adverse bolus effect of adenosine.
All patients with HCM underwent MR imaging at rest and during adenosine infusion (rest-stress injections). Five of 12 control subjects (the rest-stress injection control group) underwent MR imaging at rest and during adenosine infusion. Seven of 12 control subjects (the two-injections-at-rest control group) underwent MR imaging without stress. The second injection of gadopentetate dimeglumine was administered half an hour after the first in both control groups. To observe the effect of adenosine on first-pass reserve index (FPR) parameters, results in the rest-stress injection control group were compared with results in the two-injections-at-rest control group. To observe the differences in FPR between patients with HCM and control subjects, FPR parameters in patients with HCM were compared with those in subjects in the rest-stress injection control group.
Image Analysis
Assessment of segmental LV wall thickness.—All anatomic measurements on MR images were performed by the same radiologist (P.S.). Anatomic evaluation was performed with Numaris software (Siemens Medical Systems). LV wall thickness was evaluated in a short-axis orientation at the levels of the mitral valve chordae, the papillary muscle, and the apex (Fig 1). On each end-diastolic short-axis MR image of the LV at the levels of the mitral valve chordae and the papillary muscle, the LV was divided into five segments: anterior, lateral, and posterior free walls, and anterior and posterior septa. On MR images obtained at the apical level, the LV was divided into free wall and septum. The wall thickness of each segment was measured, and the maximal wall thickness in the LV at any location was noted. Papillary muscles, ventricular trabeculations, and the right ventricular moderator band were not included in the measurements of wall thicknesses.
|
Analysis of first-pass MR images.—Regions of interest for the same 12 tissue segments evaluated in the segmental wall thickness analysis were drawn by the same radiologist (P.S.) on the first-pass MR images. All of the SI versus time curves were fitted by the same physicist (M.H.S.), who was blinded to all the clinical data of the subjects. Data points were fitted with the extended Freundlich model of the right-skewed curve with Origin 5.0 software (Microcal Software, Northampton, Mass) according to the following equation:
|
Only first-pass data points (7.2 points ± 1.2 [SD]) were included in the fitting procedure to avoid the effect of recirculation. Maximal SI increase was determined from the fitted curves. The SI change rate was calculated as SI increase versus time. The FPR was calculated as the ratio of the SI change rate at stress to that at rest according to the following equation:
|
If an SI curve was continuously ascending or if it ended in a plateau, the curve was excluded from the analysis. Methodologic errors involved in SI change rate calculations were evaluated (M.H.S., J.T.K.) by generating SI noise against the observed SI versus time curves. The observed variation in SI before the arrival of the contrast agent in the myocardial area was used as a seed for this purpose. SI versus time curves generated in this manner were fitted, and the SI change rate was calculated. This rate was compared with the observed SI change rate. The mean 95% probability of signal noise and fitting errors being involved in the observed SI change rates was ± 16% (2 SDs).
Assessment of Reproducibility of Measurements
For the evaluation of intraobserver variation in the assessment of perfusion parameters, one radiologist (P.S.) drew new regions of interest for 30 myocardial segments 1 month after the original analysis. A physicist (M.H.S.) fitted SI versus time curves to these new data. For the evaluation of interobserver variation, 30 myocardial segments were drawn (M.H.S.) and fitted (P.S.).
Statistical Analysis
The Mann-Whitney test was used to evaluate the differences in maximal LV wall thickness, LV mass index, hemodynamic response, and FPR parameters between the groups. The Spearman correlation was used to assess the correlations within each group between LV mass index and global FPR, LV maximal end-diastolic wall thickness and global FPR, and segmental wall thickness and segmental FPR. The paired-samples t test and the Pearson correlation were used to evaluate intra- and interobserver variation in the assessment of FPR parameters. Statistical analysis was performed with a statistical software package (SPSS Windows 9.0; SPSS, Chicago, Ill). Data are presented as means ± SDs.
|
RESULTS |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTS DISCUSSIONREFERENCES |
|---|
|
Clinical and echocardiographic findings in the control subjects are also shown in Table 1. All control subjects had normal blood pressure and ECG findings, as well as normal echocardiograms.
Findings at Coronary Angiography
Coronary angiography was performed in 15 of 17 patients with HCM. Thirteen (87%) of these patients had no signs of coronary artery disease. One patient with HCM had stenoses greater than 50% in all three main branches at coronary angiography, and another patient with HCM had stenosis greater than 50% in the left anterior descending coronary artery. The other patients with HCM had anatomically normal coronary arteries.
Coronary angiography was performed in the five subjects in the rest-stress injection control group; no coronary artery stenoses were found.
LV Anatomy at MR Imaging
In three of the patients with HCM, the maximal LV wall thickness was less than 13 mm (range, 10–31 mm), whereas it was less than 13 mm (range, 7–12 mm) in all the control subjects. The mean maximal wall thickness in the patients with HCM was 20.1 mm ± 5.6, whereas it was 9.9 mm ± 1.6 in the control subjects (P < .001). LV mass index was somewhat higher in patients with HCM than in control subjects (79 g/m2 ± 26 vs 65 g/m2 ± 9, P = .080).
Hemodynamics at Rest and during Adenosine Stress
There was no statistically significant difference in hemodynamic response between the patients with HCM and the subjects in the rest-stress injection control group (data not shown). In all individuals who underwent adenosine stress MR imaging (17 patients with HCM and five control subjects), the mean heart rate increased during adenosine infusion from 67 beats per minute ± 9 to 87 beats per minute ± 10 (P < .001). Mean systolic blood pressure was 153 mm Hg ± 18 at rest; it remained at the same level (156 mm Hg ± 25) during adenosine infusion (P = .087). The corresponding values for diastolic blood pressure were 79 mm Hg ± 18 and 74 mm Hg ± 11 (P = .360). Thus, because heart rate changed, the mean rate-pressure product increased from 10,279 ± 2,057 to 13,586 ± 2,927 (P < .001).
Effect of Adenosine on First-Pass Parameters
The effect of adenosine on first-pass parameters was studied by comparing results in the rest-stress injection control group with those in the two-injections-at-rest control group. The results are summarized in Table 2. At rest, no significant difference was observed in time-to-peak values, SI increase, or SI change rate between the rest-stress injection control group and the two-injections-at-rest control group. For the second injection, the time to peak was shorter and the SI change rate was higher in the rest-stress injection control group than in the two-injections-at-rest control group. As a result, the mean SI change rate ratio was, on average, 2.6 times higher in the rest-stress injection control group than in the two-injections-at-rest control group (1.80 ± 0.58 vs 0.71 ± 0.16, P = .003).
|
This difference did not result from a difference in baseline values between the patients with HCM and the subjects in the rest-stress injection control group because baseline levels before the at-rest injection (15 AU ± 6 vs 15 AU ± 5, P = .866) and before the stress injection were nearly equal (35 AU ± 16 vs 37 AU ± 10, P = .933) in both groups. Due to the longer time to peak and the smaller SI increase, global FPR was smaller in the patients with HCM than in the subjects in the rest-stress injection control group (1.12 ± 0.35 vs 1.80 ± 0.58, P = .015) (Fig 2).
|
Correlation of First-Pass Parameters with LV Hypertrophy
In patients with HCM, maximal LV wall thickness and LV mass index correlated negatively with global FPR (r = -0.723, P = .001 and r = -0.598, P = .011, respectively) (Figs 3, 4). In the rest-stress injection control group, no correlation was observed (data not shown).
|
|
|
Intra- and Interobserver Reproducibility of MR Imaging Measurements
The results of reproducibility measurements are summarized in Table 3. The individual components of first-pass perfusion parameters were highly reproducible. Reproducibility was best in the assessment of the SI increase of the first-pass curves. Because of the nature of the FPR parameter (which is a combination of four parameters), the reproducibility of assessments of FPR was somewhat weaker than the reproducibility of time-to-peak or SI increase values but was still reasonably good (intraobserver r = 0.791, P < .001, mean difference = 0.0 ± 0.4; interobserver r = 0.710, P < .001, mean difference = 0.1 ± 0.4).
|
|
DISCUSSION |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTS DISCUSSIONREFERENCES |
|---|
In this study, a relatively low-dose (0.05 mmol/kg) bolus of gadopentetate dimeglumine was injected into a peripheral vein, and the first pass of the bolus was observed with an inversion-recovery gradient-echo sequence. SI versus time curves were fitted, and the SI increase, time to peak, and maximal SI increase were calculated for 12 LV segments. The segmental FPR was derived as a ratio of SI change rate values observed at adenosine stress MR imaging to those observed at at-rest MR imaging.
The fitting of SI versus time curves provides two advantages compared with the use of raw data points only. First, it smooths image-to-image variability. Second, it uses data points from the descending part of the SI versus time curve.
Limitations of Perfusion Analysis with First-Pass MR Perfusion Imaging
We assessed first-pass parameters in a semiquantitative estimate of myocardial perfusion. With optimal conditions, as when contrast medium is injected into the left atrium, this approach has been proved to yield measurements that have a close correlation with microsphere myocardial blood flow measurements (29). This method has also been shown to be sensitive in the detection of perfusion abnormalities in patients with coronary artery disease (2,30). However, to the best of our knowledge, this was the first study in which the first-pass MR technique was used to depict perfusion abnormalities in patients with HCM.
The changes in these parameters do not necessarily reflect alterations in perfusion only; rather, they also reflect alterations in systemic circulation. Also, dispersion and delay in the bolus of contrast material entering the myocardium can affect the SI change rate. It seems unlikely, however, that the observed findings of impaired first-pass indices in patients with HCM can be explained by these factors. Global LV systolic function measured as an ejection fraction was normal in all the study participants, there was no difference in hemodynamic parameters during adenosine stress between the patients with HCM and the control subjects, and, finally, the body weight-adjusted volume of contrast agent, the injection rate, and the cannula site were the same for all individuals.
First-pass enhancement was evaluated with gadopentetate dimeglumine as a contrast agent. During the first pass of this agent through the capillary network, about half of the agent leaks out of the vessel into the interstitial space (31,32). Thus, the alteration in the SI increase may be due not only to altered flow but also to changes in the interstitial space or extraction efficiency.
If one were to perform a perfusion study with both an intravascular contrast agent and a small molecular compound such as gadopentetate dimeglumine, one could possibly differentiate the specific components of perfusion abnormalities in patients with HCM. This approach may be especially informative in patients with HCM, since the basic cause of perfusion abnormalities is unknown. Ischemia in HCM may be caused by small-vessel disease, myocardial bridging, impaired diastolic relaxation, or a decreased capillaries-to-myocardial fiber ratio (4).
The calculated SI change rate ratio in the two-injections-at-rest control group was only 0.71 instead of the anticipated 1.00. This result implies that these methods have a tendency to result in underestimation of the true perfusion reserve. This finding is probably related to the influence of residual myocardial gadolinium in the second first-pass curve. Further studies are needed to clarify the influence of residual myocardial gadolinium in the second first-pass curve.
Comparison with Previous Studies
Our findings of impaired perfusion in patients with HCM compared with control subjects are in concordance with those of studies in which single photon emission computed tomography with thallium 201 (7), PET with nitrogen 13 (9,10), transesophageal echo Doppler ultrasonography (12), and velocity-encoded cine MR imaging (13) were used to evaluate patients with HCM. The inverse association between LV mass and global perfusion reserve in these patients has also been previously demonstrated (13).
In previous studies, results have been inconsistent for assessment of perfusion impairment in hypertrophied areas of LV compared with nonhypertrophied areas of LV in patients with HCM. Camici et al (9) and Tadamura et al (10) compared data from echocardiographic measurements of LV hypertrophy with PET perfusion data. In the study of Camici et al (9), no association between hypertrophy and perfusion was found, whereas in the study of Tadamura et al (10), perfusion in pediatric patients was clearly more impaired in the hypertrophied septum than in the normal lateral wall.
We found that the segmental FPR in patients with HCM was lower in hypertrophied LV segments than in other segments. Our approach, which combines first-pass MR and cine MR imaging in the same imaging session and segment-by-segment comparison of the results (as demonstrated in Fig 1), facilitates better comparison between anatomic features and perfusion within individual hearts than previously used methods in which data from different imaging modalities were combined. In addition, in previous studies, hypertrophy has been evaluated with echocardiography, which does not allow the myocardium to be visualized as comprehensively as MR imaging does (18,19,33).
Clinical Implications
It has been suggested that ischemia is a potential risk factor for sudden cardiac death in patients with HCM, especially young patients (8,34). Furthermore, the extent of LV hypertrophy seems to be related to the risk of sudden death (35). The present study suggests that one factor explaining the increased risk of sudden death in patients with HCM and severe LV hypertrophy might be myocardial ischemia. First-pass MR perfusion imaging is a promising method that can be used to assess the role of myocardial ischemia in the stratification of risk in patients with HCM.
|
FOOTNOTES |
|---|
Author contributions: Guarantors of integrity of entire study, P.S., K.L., J.T.K., M.L., J.K., H.J.A.; study concepts, P.S., J.T.K., H.M., K.P., M.L., J.K., H.J.A.; study design, P.S., K.L., E.V., T.L., J.K., H.J.A.; literature research, P.S., M.H.S., J.T.K.; clinical studies, P.S., T.L., J.K.; data acquisition, P.S., P.J., J.K.; data analysis/interpretation, P.S., K.L., M.H.S., P.N., J.T.K., J.K., H.J.A.; statistical analysis, P.S., J.T.K., E.V., H.M., H.J.A.; manuscript preparation, P.S., K.L., M.H.S., J.T.K., P.N., J.K., H.J.A.; manuscript definition of intellectual content, P.S., K.L., J.T.K., E.V., H.M., M.L., J.K., H.J.A.; manuscript editing, P.S., K.L., K.P., H.M., P.J., J.K., M.L., H.J.A.; manuscript revision/review, P.S., K.L., J.T.K., T.L., K.P., J.K., H.J.A.; manuscript final version approval, all authors.
Abbreviations: AU = arbitrary units,
ECG = electrocardiography,
FPR = first-pass reserve index,
HCM = hypertrophic cardiomyopathy,
LV = left ventricle,
SI = signal intensity,
TPM1 = -tropomyosin
|
REFERENCES |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTS DISCUSSIONREFERENCES |
|---|
This article has been cited by other articles:
|
|
 |
|
  R. Gebker, C. Jahnke, I. Paetsch, B. Schnackenburg, S. Kozerke, A. Bornstedt, E. Fleck, and E. Nagel MR Myocardial Perfusion Imaging with k-Space and Time Broad-Use Linear Acquisition Speed-up Technique: Feasibility Study Radiology, December 1, 2007; 245(3): 863 - 871. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 O. I I Soliman, P. Knaapen, M. L Geleijnse, P. A Dijkmans, A. M Anwar, A. Nemes, M. Michels, W. B Vletter, A. A Lammertsma, and F. J ten Cate Assessment of intravascular and extravascular mechanisms of myocardial perfusion abnormalities in obstructive hypertrophic cardiomyopathy by myocardial contrast echocardiography Heart, October 1, 2007; 93(10): 1204 - 1212. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. E. Petersen, M. Jerosch-Herold, L. E. Hudsmith, M. D. Robson, J. M. Francis, H. A. Doll, J. B. Selvanayagam, S. Neubauer, and H. Watkins Evidence for Microvascular Dysfunction in Hypertrophic Cardiomyopathy: New Insights From Multiparametric Magnetic Resonance Imaging Circulation, May 8, 2007; 115(18): 2418 - 2425. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Sipola, K. Lauerma, P. Jaaskelainen, M. Laakso, K. Peuhkurinen, H. Manninen, H. J. Aronen, and J. Kuusisto Cine MR Imaging of Myocardial Contractile Impairment in Patients with Hypertrophic Cardiomyopathy Attributable to Asp175Asn Mutation in the {alpha}-Tropomyosin Gene Radiology, September 1, 2005; 236(3): 815 - 824. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y. Amano, S. Kumita, M. Takayama, and T. Kumazaki Comparison of Contrast-Enhanced MRI with Iodine-123 BMIPP for Detection of Myocardial Damage in Hypertrophic Cardiomyopathy Am. J. Roentgenol., August 1, 2005; 185(2): 312 - 318. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. J. Pennell, U. P. Sechtem, C. B. Higgins, W. J. Manning, G. M. Pohost, F. E. Rademakers, A. C. van Rossum, L. J. Shaw, and E. K. Yucel Clinical indications for cardiovascular magnetic resonance (CMR): Consensus Panel report Eur. Heart J., November 1, 2004; 25(21): 1940 - 1965. [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| RADIOLOGY | RADIOGRAPHICS | RSNA JOURNALS ONLINE |
