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Published online before print December 21, 2005, 10.1148/radiol.2382041822

(Radiology 2005;238:640.)

A more recent version of this article appeared on December 1, 2005
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© RSNA, 2005

Musculoskeletal Imaging

Pathologic Skeletal Muscle Perfusion in Patients with Myositis: Detection with Quantitative Contrast-enhanced US—Initial Results1

Marc-André Weber, MD, MSc, Martin Krix, MD, MSc, Uta Jappe, MD, MSc, Hagen B. Huttner, MD, Marius Hartmann, MD, Uta Meyding-Lamadé, MD, Marco Essig, MD, Christoph Fiehn, MD, Hans-Ulrich Kauczor, MD and Stefan Delorme, MD

1 From the Department of Radiology, German Cancer Research Center, Im Neuenheimer Feld 280, D-69120 Heidelberg, Germany (M.A.W., M.K., M.E., H.U.K., S.D.); Departments of Dermatology (U.J.), Neurology (H.B.H., U.M.), and Neuroradiology (M.H.), University of Heidelberg, Heidelberg, Germany; and Department of Hematology, Oncology, and Rheumatology, Clinic for Internal Medicine V, University of Heidelberg and Center of Rheumatic Diseases, Baden-Baden, Germany (C.F.). From the 2004 RSNA Annual Meeting. Received October 20, 2004; revision requested December 27; revision received January 20, 2005; accepted February 21; final version accepted February 21. Address correspondence to M.A.W. (e-mail: m.a.weber{at}dkfz.de).


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 References
 
Purpose: To prospectively determine whether contrast material–enhanced ultrasonography (US) can depict inflammation-induced changes in muscle perfusion for patients suspected of having dermatomyositis or polymyositis and to compare these findings with those of magnetic resonance (MR) imaging and muscle biopsy.

Materials and Methods: Institutional review board approval and informed consent were obtained. Perfusion in skeletal muscles was quantified with contrast-enhanced intermittent power Doppler US by applying a modified model that analyzed the replenishment kinetics of microbubbles. In 22 patients (16 women, six men; mean age, 52 years ± 17) who were suspected of having myositis and in 10 healthy volunteers (two women, eight men; mean age, 28 years ± 4), contrast-enhanced US of the clinically affected right biceps muscle was performed to measure blood flow, blood volume, and blood flow velocity. Additionally, the right upper arm was examined with a 1.5-T unit by using three different MR imaging techniques. Findings were compared with the results of clinical examinations and muscle biopsy. Data for perfusion-related parameters obtained at contrast-enhanced US were analyzed by using a nonparametric Mann-Whitney U test.

Results: Eight patients had histologically confirmed myositis and showed significantly higher blood flow velocity (P = .01), blood flow (P = .001), and blood volume (P = .002) at contrast-enhanced US than did patients who did not have myositis. Blood flow velocity (P = .001) and blood flow (P = .002) were significantly higher in patients with myositis than in volunteers. An increase in signal intensity on T2-weighted MR images was found in all patients with myositis, while contrast material enhancement on fat-suppressed T1-weighted MR images was found in only four of seven patients with myositis.

Conclusion: Initial results show that contrast-enhanced US is a feasible method for noninvasively demonstrating increased perfusion in the involved muscle groups in patients with myositis.

© RSNA, 2005


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 References
 
Idiopathic inflammatory myopathies have in common the presence of moderate to severe muscle weakness and autoimmune inflammation in the muscle, the precise cause of which is still unknown (1). These disorders are clinically important because they are potentially treatable with corticosteroids, immunosuppressive agents, and intravenous immunoglobulins (1,2). Idiopathic inflammatory myopathies can be differentiated into three major and distinct subsets: dermatomyositis, polymyositis, and sporadic inclusion body myositis (1,2). Differential diagnoses include endocrine disease, neurogenic disease, dystrophies, and metabolic myopathies. The classic clinical diagnosis of both polymyositis and dermatomyositis is determined on the basis of clinical presentation, medical history, and elevated creatine kinase activity and can be determined by using invasive procedures, such as electromyography and muscle biopsy (1). Serum creatine kinase levels, however, may be normal or only mildly elevated in patients with dermatomyositis, inclusion body myositis, or focal forms of myositis (2), and needle electromyographic signs are not disease specific. Hence, although these procedures are useful in confirming active myopathy, such procedures are not useful in correctly classifying it. Until now, only muscle biopsy allowed for the correct establishment of a definite diagnosis (1,2).

Noninvasive diagnostic modalities, such as computed tomography (CT), magnetic resonance (MR) imaging, and ultrasonography (US), are able to demonstrate muscular edema, fluid collections, fatty infiltration, atrophy, fibrosis, and calcifications. Because MR imaging is sensitive to the presence of edema and offers better tissue differentiation, current MR imaging with fat-suppressed T2-weighted techniques appears to be more efficient than US or CT in the diagnosis and management of inflammatory myopathies (3). MR imaging has also been proposed as a means to guide biopsy in an area of active disease, thereby reducing the problem of sampling error (2–4). A good correlation between signal intensity on T2-weighted MR images, disease activity, and muscle function has been observed, and MR imaging has been used to monitor the progression of disease. These changes in signal intensity, however, are not specific for myositis (2,3). Although MR imaging is now the imaging modality of choice in this issue, reduced availability, patient discomfort, and exclusion of certain patients with indwelling metal objects, such as pacemakers, are disadvantages (5).

Among the soft tissues, muscle is best suited to US examination (6). The availability and ease of use of US makes it preferable to MR imaging (6). The detection of possible alterations in muscle vascularity in patients with myositis by using power Doppler US has been the focus of earlier studies (7,8). Muscle vascularity was hypothesized to correlate with the disease duration of myositis (8). Quantification of muscular capillary perfusion, however, was not possible by using power Doppler US. Contrast material–enhanced US is highly sensitive to blood flow, even within the capillaries, which is a prerequisite for correctly measuring tissue perfusion (9). By using replenishment kinetics after the destruction of intravenously injected microbubbles at US, determination of perfusion-related parameters, such as blood flow velocity, blood flow, and blood volume, has become possible (9,10). These techniques have been well evaluated for measuring perfusion in the myocardium (9) and in experimentally induced tumors of small animals (10,11). In principle, contrast-enhanced US allows for the quantification of perfusion in all tissues that are accessible with US (9). Data on physiologic and pathologic skeletal muscle perfusion, however, which is especially low at rest and therefore requires highly sensitive imaging, is lacking. Thus, the aim of our study was to prospectively determine whether contrast-enhanced US can depict inflammation-induced changes in muscle perfusion in patients who are suspected of having dermatomyositis or polymyositis and to compare these findings with those of MR imaging and muscle biopsy.


   MATERIALS AND METHODS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
 References
 
Patients and Volunteers
Twenty-two consecutive patients (16 women, six men; mean age, 52 years ± 17 [standard deviation]) who were clinically suspected of having dermatomyositis or polymyositis with apparent involvement of the upper extremities were included in the study from January 2003 to August 2004. Clinical suspicion of dermatomyositis or polymyositis was established after neurologic, dermatologic, and/or rheumatologic examination by the referring clinician (U.J., H.B.H., U.M., C.F.) and was based on the following findings: symmetric, proximally accentuated limb weakness; elevated levels of serum skeletal muscle enzymes, such as creatine kinase, aldolase, lactate dehydrogenase, and the transaminases; and myopathic findings at electromyography, such as an increased spontaneous activity with fibrillations, complex repetitive discharges, and positive sharp waves (1). Because creatine kinase is the most sensitive muscle enzyme, a creatine kinase level of greater than 145 IU/L was classified as elevated. A characteristic skin affection, such as an erythematous rash on the face, neck, and anterior chest or a Gottron rash, indicated dermatomyositis (1). The patients were then referred for contrast-enhanced US and MR imaging of the muscle. Patients with absolute or relative contraindications for the US contrast agent galactose-palmitic acid (Levovist; Schering, Berlin, Germany) were excluded; contraindications included galactosaemia, severe heart failure, severe pulmonary disease, pregnancy, and myocardial infarction within the preceding 2 weeks. Patients who required monitoring, such as those in intensive care, were also excluded.

Patients had a mean creatine kinase level of 1138 IU/L ± 1131 at the time of assessment. Mean muscle strength, as scored according to the grading system proposed by the Medical Research Council of Great Britain, was 4.0 ± 1.0 on a six-point scale. A score of 0 indicated complete paralysis; a score of 1, minimal contraction; a score of 2, active movement with gravity eliminated; a score of 3, weak contraction against gravity; a score of 4, active movement against gravity and resistance; and a score of 5, normal strength (12).

Clinically, polymyositis was suspected by the referring clinician in 14 patients, and dermatomyositis was suspected by the referring clinician in eight patients. All patients who were suspected of having dermatomyositis exhibited a suspicious skin rash. One patient had a history of underlying connective tissue disease, and a diagnosis of polymyositis with associated scleroderma (overlap syndrome) was made.

At the time of assessment, three patients received antihypertensive medication, and mean systolic and mean diastolic blood pressure, as measured in millimeters of mercury, were 123 mm Hg ± 10 and 82 mm Hg ± 7, respectively. At follow up, five patients with confirmed myositis underwent serial contrast-enhanced US, which was performed while patients received immunosuppressive therapy.

Prior to patient enrollment (ie, from November 2002 to December 2002), 10 healthy volunteers (two women, eight men; mean age, 28 years ± 4) with no evidence or history of muscular or cardiovascular disease (ie, all with a muscle strength score of 5, normal creatine kinase levels, and normal gray-scale muscular US findings) were examined by using contrast-enhanced US and MR imaging for comparison as a healthy subgroup. At the time of assessment, no volunteer received any medication. Mean systolic blood pressure was 117 mm Hg ± 9, and mean diastolic blood pressure was 78 mm Hg ± 5. The study was approved by the institutional review board and was conducted according to the declaration of Helsinki. Informed consent was obtained from all volunteers and patients after the nature of the examination had been fully explained.

Contrast-enhanced US Examination
Quantification of perfusion by using contrast-enhanced US.—In this study, blood flow, blood volume, and blood flow velocity were calculated in the muscles by analyzing the replenishment kinetics of microbubbles after their destruction with a high-energy US pulse. US contrast agent (ie, microbubbles) can be destroyed in a chosen region of interest (ROI) by using high-energy US (high-mechanical-index US). Replenishment kinetics describes the refilling of microbubbles from outside the ROI where contrast agent is still present. Because US signals can be measured even from stationary microbubbles, capillary blood flow can be visualized by using this approach whenever microbubbles are given enough time to fill the small vessels. The maximum US signal intensity measured after complete refilling is proportional to the blood volume in the ROI, and the initial increase in replenishment indicates the mean blood flow velocity of all vessels in the ROI (9). Thus, blood flow can be defined as f ~ B · v, where B is blood volume and v is blood flow velocity (9). Perfusion, p, is the blood flow normalized on the tissue volume V (p ~ f/V).

Limitations of this model, which was introduced by Wei et al (9), include the assumption of a constant velocity of refilling and the neglect of the different directions of the vessels inside the examined ROI and, thus, a neglect of blood flow, which depends on the alignment of the vessels (13). Because of these limitations, we used a previously developed multivessel model to describe replenishment curves. This model takes into account the different directions and different amounts of blood flow that are found in vessels inside the ROI and is therefore able to more comprehensively and consistently calculate tissue perfusion (13). According to this model, after the destruction of microbubbles by using high-mechanical-index US techniques such as power Doppler US, replenishment is initially linear with time. Once the vessels in the ROI that are perpendicular to the US section and that demonstrate the maximum blood flow velocity of all vessels are completely refilled, a nonlinear increase in US signal intensity (which is approximately equal to microbubble concentration) occurs and is followed by saturation behavior to maximum (13). Therefore, it is not necessary to measure the entire detailed replenishment curve to derive perfusion-related parameters. To perform US examinations that are easily applicable in a clinical setting, it is sufficient to obtain the first measurement at an early time point (ie, at the initial increase of the replenishment curve) and the second measurement at a late phase of replenishment (ie, at the maximum plateau). The blood volume is then proportional to the parameter maximum—that is, to the maximum plateau of the replenishment curve—and the blood flow velocity can be obtained as v = d · m/(2/3max), where d is the US beam width; m is the slope of the initial linear increase of the replenishment curve starting at zero (after baseline correction), which can be calculated from the early time point measurement (13); and max is the maximum of the replenishment curve.

To further simplify the examination protocol for use in the clinical setting, we used a contrast agent bolus technique for the quantification of muscle perfusion (10,13) rather than the continuous contrast agent infusion technique that was proposed by Wei et al (9). The early phases of replenishment were then measured by using the maximum US signal intensity after bolus injection in a representatively chosen ROI with a high frame rate of 1.67 sec–1 and a pulsing interval time of 0.6 second; it was assumed that this measurement would be part of the initial linear phase of replenishment (Fig 1). To reduce measurement errors, the two values obtained directly before and after the maximum were included, and the mean of these five values above baseline was calculated (Fig 1). To obtain the late phase of replenishment, the transducer was slowly but continuously moved over the muscle starting at 75 seconds after contrast material injection. We therefore assumed that these contrast-enhanced US signals were measured in regions where ultrasound had not previously destroyed microbubbles and that changes in the systemic concentration of microbubbles were small during the late phase. The mean of all values that were obtained during the movement of the transducer was used as a measurement of the maximum plateau of the replenishment curve (Fig 1).



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  		Figure 1: Graph demonstrates measured US signal intensity in right biceps muscle of healthy volunteer after contrast material injection. Signal intensity is superimposed on an idealized sketch (line) of the data by using our examination protocol for perfusion quantification, which is based on replenishment kinetics. Initially, the maximum of the signal intensity-time curve obtained by using a high US frame rate allows for the calculation of the early replenishment values, whereas movement of the US transducer at later phases provides measurement after complete replenishment.

 
Examination protocol.—Muscle perfusion was measured by using contrast-enhanced US after the patient or volunteer had rested for 20 minutes on a stretcher in a cool (68°F [20°C]), quiet, and darkened room. The US device (Sequoia 512; Siemens-Acuson, Mountain View, Calif) used a linear-array transducer (15L8w; Siemens-Acuson) with power Doppler US (transmission frequency, 7 MHz). Most of the US device settings were standard. Importantly, the acoustic power of the power Doppler US device was maximal (mechanical index, 1.9) and sensitivity was minimal to reduce motion artifacts and to ensure that the detected signals were mainly from the destroyed microbubbles (maximum pulse repetition rate, 0.69). Further settings included a beam width of 0.8 mm (10), a triggered frame rate of 1.67 sec–1 (10), an ROI size of 2.00 x 2.75 cm, an ROI depth of more than 0.5 cm, and a focus depth of 1.5 cm.

All US examinations were performed by the same operator (M.A.W.), and a second radiologist (M.K.) was present for ROI placement in consensus. Both radiologists had 5 years of experience in the field of musculoskeletal US. After choosing a representative US section in the clinically involved biceps muscle of the right arm, a single bolus of 10 mL galactose-palmitic acid (300 mg/mL) was infused into a left cubital vein for 5 seconds and was followed by an injection of 15 mL 0.9% sodium chloride. Next, a continuous US video clip was acquired. The color pixels in the ROI were measured to quantify the power Doppler video intensity by using an external computer-based quantification tool (Data Pro; Noesis, Courtaboeuf, France) (13). Initially, the probe rested at the same position in the representative cross section of the biceps muscle, thereby reflecting the measurement of the initial phase of replenishment. Seventy-five seconds after contrast material injection, the linear-array transducer was slowly moved to the proximal end of the biceps muscle perpendicular to the representative cross section. The baseline revised signal intensity reflects the late phase of refilling (Fig 1) (13). The whole measurement lasted about 2 minutes. For acute muscle inflammation, US criteria on gray-scale images included hyperechoic muscle fibers, hypoechoic fibroadipose septa (reverse image of normal), and increased muscle diameter (6,14,15). Criteria for muscle atrophy were a hyperechoic muscle with diminution of the hypoechoic muscle bundles (6).

MR Examination and Interpretation
MR imaging was performed with a clinical 1.5-T unit (Magnetom Symphony; Siemens, Erlangen, Germany) by using a surface coil for signal reception. MR imaging was performed in all but one patient with dermatomyositis. Before contrast material injection, MR images were obtained with a T1-weighted spin-echo MR imaging sequence (450/8.7 [repetition time msec/echo time msec]; matrix, 448 x 448; section thickness, 8 mm), a transverse fat-suppressed T2-weighted turbo spin-echo MR imaging sequence (3970/98; matrix, 448 x 448; section thickness, 8 mm), and a coronal short tau inversion-recovery MR imaging sequence (5080/66/140 [repetition time msec/echo time msec/inversion time msec]; matrix, 381 x 448; section thickness, 7 mm). After administration of a single dose of gadopentetate dimeglumine (Magnevist; Schering), transverse images were acquired with a fat-suppressed T1-weighted spin-echo MR imaging sequence (678/8.7; matrix, 448 x 448; section thickness, 8 mm). Contrast material was not given to volunteers to avoid unnecessarily exposing them to the risk of adverse events.

Image interpretation was performed by two readers in consensus (M.A.W. and M.H., with 5 and 12 years of experience in the field of musculoskeletal MR imaging, respectively). The presence of edema and/or contrast material enhancement was used as a criterion for inflammatory autoimmune myopathies (16). Muscle edema was defined as an area of localized hyperintensity on T2-weighted MR images and was considered to be the most important criterion for myositis, particularly when lesions were symmetric, the most prominent in proximal muscles, and diffuse rather than localized (4,5,17). Fatty infiltration, which was defined as areas that demonstrated a signal intensity equivalent to that of subcutaneous fat on T1-weighted MR images, was interpreted as a sign of chronic inflammation (4,5,16,17). A reticular pattern (ie, edematous changes) in the subcutaneous fat tissue was interpreted as an indication of dermatomyositis (4,5,17). The MR imaging criterion for muscle atrophy was a reduction in the cross-sectional area of a muscle that was qualitatively assessed by two readers in consensus by using the opposite side or other muscle groups for comparison. The readers were asked to assess in a dichotomous fashion whether these criteria were identified.

Histologic Characteristics
Muscle biopsy was performed by a neurologist (H.B.H.) who had 2 years of experience in muscle biopsy. The biopsy procedure was guided by using clinical, electromyographic, and MR imaging findings to reduce the problem of sampling error before beginning immunosuppressive therapy. In 18 patients, biopsy material was obtained from the clinically affected right biceps brachii muscle. In one patient, biopsy was performed on the right triceps brachii muscle because MR imaging showed edema and contrast material enhancement in this muscle;the biceps muscle, however, was not affected to a major extent on MR images. In this same patient, both the biceps and triceps muscles showed clinical muscle weakness. In three patients with a proximal accentuated tetraparesis, biopsy was performed on the right quadriceps femoris muscle. In these three patients, myositis was not confirmed histologically, and MR imaging showed no edema or contrast material uptake in the biceps and quadriceps muscles; electromyography, however, showed a myopathic pattern in the quadriceps muscle.

Histologic criteria for dermatomyositis included perifascicular atrophy and the presence of an inflammatory infiltrate that was either predominantly perivascular or located within the interfascicular septae and around rather than within the fascicles (1). Criteria for polymyositis included the presence of multifocal lymphocytic infiltrates that surrounded and invaded healthy muscle fibers. The additional presence of rimmed vacuoles and congophilic amyloid deposits within or next to the vacuoles, however, were indicative of inclusion body myositis (1).

Statistical Analysis
Data entry procedures and statistical analyses were performed with a computer software program (SPSS for Windows, version 11.5.1; SPSS, Chicago, Ill). For statistical test comparisons, nonparametric rather than parametric methods were applied because of the relatively low number of patients and volunteers that were available for analysis. The normality of distribution of the measured values could not be guaranteed. Data for perfusion-related parameters that were obtained at contrast-enhanced US (ie, blood volume, blood flow, and blood flow velocity) were analyzed separately by using a nonparametric Mann-Whitney U test (level of significance, P = .05). For each significant difference that was found, the corresponding statistical power was calculated by using the effect size approach (nQuery Advisor, version 5.0; Statistical Solutions, Saugus, Mass). Results were expressed as the mean ± standard deviation.


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
DISCUSSION
 References
 
Histologic Results and US Parameters
In our study group, polymyositis was ultimately confirmed in three patients, and dermatomyositis was ultimately confirmed in five patients. Both conditions were diagnosed at histologic analysis and were substantiated by means of subsequent clinical course. At the time of assessment, one of the eight patients received antihypertensive medication (mean systolic blood pressure, 124 mm Hg ± 12; mean diastolic blood pressure, 83 mm Hg ± 8). In 14 patients, inflammatory myopathy was excluded at histologic analysis, and the absence of myositis was confirmed by means of subsequent clinical course. For these 14 patients, the final diagnosis was alcoholic myopathy in one patient, dystrophic myopathy in one patient, end-stage myopathy in one patient, fibromyalgia in four patients, mixed connective tissue disease in one patient, neurogenic myopathy in one patient, polymyalgia rheumatica in two patients, psychosomatic disturbance in one patient, scleroderma in one patient, and Sjögren syndrome in one patient. At the time of assessment, two of these 14 patients received antihypertensive medication (mean systolic blood pressure, 123 mm Hg ± 8; mean diastolic blood pressure, 81 mm Hg ± 7).

US parameters for muscle perfusion—that is, blood volume, blood flow, and blood flow velocity—are summarized in Table 1 for patients and volunteers and are presented as box plots in Figure 2 . In detail, patients with histologically proved myositis had significantly higher blood flow velocity (P = .01, power = 87%), blood flow (P = .001, power = 96%), and blood volume (P = .002, power = 95%) than did patients with histologic exclusion of myositis (Fig 3). Blood flow velocity (P = .001, power = 92%) and blood flow (P = .002, power = 88%) were significantly higher in patients with myositis than in the volunteers. Blood volumes in patients with myositis were substantially higher than those in the volunteers (P = .06). Blood flow in volunteers and in patients without myositis was not significantly different (P = .64). Blood volume, however, was significantly higher in volunteers than in patients without myositis (P = .004, power = 80%). The patients without confirmation of myositis were older than the volunteers (mean age of all patients without myositis, 53 years). No muscle atrophy was found in volunteers; muscle atrophy was, however, found in four patients without myositis. Blood flow velocity was significantly lower in volunteers than in patients without myositis (P = .018, power = 80%).


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  		Table 1. Parameters of Muscle Perfusion as Measured at Contrast-enhanced US

 


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  		Figure 2a: Box plots of (a) blood volume, (b) blood flow velocity, and (c) blood flow for patients and volunteers, as measured by using contrast-enhanced US. Error bars indicate 10th and 90th percentile. Patients with histologically confirmed myositis had the highest values compared with volunteers and patients without histologic confirmation of myositis.

 


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  		Figure 2b: Box plots of (a) blood volume, (b) blood flow velocity, and (c) blood flow for patients and volunteers, as measured by using contrast-enhanced US. Error bars indicate 10th and 90th percentile. Patients with histologically confirmed myositis had the highest values compared with volunteers and patients without histologic confirmation of myositis.

 


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  		Figure 2c: Box plots of (a) blood volume, (b) blood flow velocity, and (c) blood flow for patients and volunteers, as measured by using contrast-enhanced US. Error bars indicate 10th and 90th percentile. Patients with histologically confirmed myositis had the highest values compared with volunteers and patients without histologic confirmation of myositis.

 


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  		Figure 3a: Power Doppler US (7-MHz) images of right biceps muscle after bolus injection of 10 mL galactose-palmitic acid at a depth of 1.5 cm (focus area). Transverse images demonstrate initial increase and maximum plateau of microbubble replenishment. Contrast-enhanced power Doppler US signals clearly demonstrate higher microbubble concentration in muscle tissue of patient with polymyositis owing to higher muscle perfusion. (a, b) Histologically confirmed polymyositis in a 45-year-old woman. (a) Distinct early replenishment is observed 30 seconds after injection (blood flow, 22.7 arbitrary units [au]). (b) Increased contrast material enhancement can be seen within the capillaries in an area without previous destruction of microbubbles 75 seconds after injection (blood volume, 11.8 au). (c, d) Polymyalgia rheumatica in a 77-year-old woman. (c) Nearly no initial increase in microbubble replenishment is seen 30 seconds after injection (blood flow, 0.3 au). (d) Distinctly reduced maximum plateau of US contrast material enhancement is observed in an area without previous destruction of microbubbles 75 seconds after injection (blood volume, 1.7 arbitrary units [au]). (e, f) Images in a 30-year-old male volunteer. (e) Initial increase in microbubble replenishment is observed 30 seconds after injection (blood flow, 2.2 au). (f) Maximum plateau of US contrast material enhancement can be seen 75 seconds after injection (blood volume, 8.5 au).

 


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  		Figure 3b: Power Doppler US (7-MHz) images of right biceps muscle after bolus injection of 10 mL galactose-palmitic acid at a depth of 1.5 cm (focus area). Transverse images demonstrate initial increase and maximum plateau of microbubble replenishment. Contrast-enhanced power Doppler US signals clearly demonstrate higher microbubble concentration in muscle tissue of patient with polymyositis owing to higher muscle perfusion. (a, b) Histologically confirmed polymyositis in a 45-year-old woman. (a) Distinct early replenishment is observed 30 seconds after injection (blood flow, 22.7 arbitrary units [au]). (b) Increased contrast material enhancement can be seen within the capillaries in an area without previous destruction of microbubbles 75 seconds after injection (blood volume, 11.8 au). (c, d) Polymyalgia rheumatica in a 77-year-old woman. (c) Nearly no initial increase in microbubble replenishment is seen 30 seconds after injection (blood flow, 0.3 au). (d) Distinctly reduced maximum plateau of US contrast material enhancement is observed in an area without previous destruction of microbubbles 75 seconds after injection (blood volume, 1.7 arbitrary units [au]). (e, f) Images in a 30-year-old male volunteer. (e) Initial increase in microbubble replenishment is observed 30 seconds after injection (blood flow, 2.2 au). (f) Maximum plateau of US contrast material enhancement can be seen 75 seconds after injection (blood volume, 8.5 au).

 


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  		Figure 3c: Power Doppler US (7-MHz) images of right biceps muscle after bolus injection of 10 mL galactose-palmitic acid at a depth of 1.5 cm (focus area). Transverse images demonstrate initial increase and maximum plateau of microbubble replenishment. Contrast-enhanced power Doppler US signals clearly demonstrate higher microbubble concentration in muscle tissue of patient with polymyositis owing to higher muscle perfusion. (a, b) Histologically confirmed polymyositis in a 45-year-old woman. (a) Distinct early replenishment is observed 30 seconds after injection (blood flow, 22.7 arbitrary units [au]). (b) Increased contrast material enhancement can be seen within the capillaries in an area without previous destruction of microbubbles 75 seconds after injection (blood volume, 11.8 au). (c, d) Polymyalgia rheumatica in a 77-year-old woman. (c) Nearly no initial increase in microbubble replenishment is seen 30 seconds after injection (blood flow, 0.3 au). (d) Distinctly reduced maximum plateau of US contrast material enhancement is observed in an area without previous destruction of microbubbles 75 seconds after injection (blood volume, 1.7 arbitrary units [au]). (e, f) Images in a 30-year-old male volunteer. (e) Initial increase in microbubble replenishment is observed 30 seconds after injection (blood flow, 2.2 au). (f) Maximum plateau of US contrast material enhancement can be seen 75 seconds after injection (blood volume, 8.5 au).

 


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  		Figure 3d: Power Doppler US (7-MHz) images of right biceps muscle after bolus injection of 10 mL galactose-palmitic acid at a depth of 1.5 cm (focus area). Transverse images demonstrate initial increase and maximum plateau of microbubble replenishment. Contrast-enhanced power Doppler US signals clearly demonstrate higher microbubble concentration in muscle tissue of patient with polymyositis owing to higher muscle perfusion. (a, b) Histologically confirmed polymyositis in a 45-year-old woman. (a) Distinct early replenishment is observed 30 seconds after injection (blood flow, 22.7 arbitrary units [au]). (b) Increased contrast material enhancement can be seen within the capillaries in an area without previous destruction of microbubbles 75 seconds after injection (blood volume, 11.8 au). (c, d) Polymyalgia rheumatica in a 77-year-old woman. (c) Nearly no initial increase in microbubble replenishment is seen 30 seconds after injection (blood flow, 0.3 au). (d) Distinctly reduced maximum plateau of US contrast material enhancement is observed in an area without previous destruction of microbubbles 75 seconds after injection (blood volume, 1.7 arbitrary units [au]). (e, f) Images in a 30-year-old male volunteer. (e) Initial increase in microbubble replenishment is observed 30 seconds after injection (blood flow, 2.2 au). (f) Maximum plateau of US contrast material enhancement can be seen 75 seconds after injection (blood volume, 8.5 au).

 


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  		Figure 3e: Power Doppler US (7-MHz) images of right biceps muscle after bolus injection of 10 mL galactose-palmitic acid at a depth of 1.5 cm (focus area). Transverse images demonstrate initial increase and maximum plateau of microbubble replenishment. Contrast-enhanced power Doppler US signals clearly demonstrate higher microbubble concentration in muscle tissue of patient with polymyositis owing to higher muscle perfusion. (a, b) Histologically confirmed polymyositis in a 45-year-old woman. (a) Distinct early replenishment is observed 30 seconds after injection (blood flow, 22.7 arbitrary units [au]). (b) Increased contrast material enhancement can be seen within the capillaries in an area without previous destruction of microbubbles 75 seconds after injection (blood volume, 11.8 au). (c, d) Polymyalgia rheumatica in a 77-year-old woman. (c) Nearly no initial increase in microbubble replenishment is seen 30 seconds after injection (blood flow, 0.3 au). (d) Distinctly reduced maximum plateau of US contrast material enhancement is observed in an area without previous destruction of microbubbles 75 seconds after injection (blood volume, 1.7 arbitrary units [au]). (e, f) Images in a 30-year-old male volunteer. (e) Initial increase in microbubble replenishment is observed 30 seconds after injection (blood flow, 2.2 au). (f) Maximum plateau of US contrast material enhancement can be seen 75 seconds after injection (blood volume, 8.5 au).

 


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  		Figure 3f: Power Doppler US (7-MHz) images of right biceps muscle after bolus injection of 10 mL galactose-palmitic acid at a depth of 1.5 cm (focus area). Transverse images demonstrate initial increase and maximum plateau of microbubble replenishment. Contrast-enhanced power Doppler US signals clearly demonstrate higher microbubble concentration in muscle tissue of patient with polymyositis owing to higher muscle perfusion. (a, b) Histologically confirmed polymyositis in a 45-year-old woman. (a) Distinct early replenishment is observed 30 seconds after injection (blood flow, 22.7 arbitrary units [au]). (b) Increased contrast material enhancement can be seen within the capillaries in an area without previous destruction of microbubbles 75 seconds after injection (blood volume, 11.8 au). (c, d) Polymyalgia rheumatica in a 77-year-old woman. (c) Nearly no initial increase in microbubble replenishment is seen 30 seconds after injection (blood flow, 0.3 au). (d) Distinctly reduced maximum plateau of US contrast material enhancement is observed in an area without previous destruction of microbubbles 75 seconds after injection (blood volume, 1.7 arbitrary units [au]). (e, f) Images in a 30-year-old male volunteer. (e) Initial increase in microbubble replenishment is observed 30 seconds after injection (blood flow, 2.2 au). (f) Maximum plateau of US contrast material enhancement can be seen 75 seconds after injection (blood volume, 8.5 au).

 
Muscle inflammation was detected at gray-scale US in four patients, two of whom were ultimately confirmed as having dermatomyositis. The other two patients were ultimately confirmed as having polymyositis. All four patients showed increased muscle perfusion (mean blood volume, 12.5 au [arbitrary units] ± 7.7; mean blood flow, 21.8 au ± 20.7; mean blood flow velocity, 1.5 mm/sec ± 0.7). For mean blood volume, arbitrary units ~ milliliters, and for mean blood flow, arbitrary units ~ (mL · min–1)/100 g tissue.

Muscular atrophy was detected in four patients at gray-scale US. Two of these patients were ultimately confirmed as having polymyalgia rheumatica, one as having end-stage myopathy, and one as having a psychosomatic disturbance. Each of these patients showed low muscle perfusion (mean blood volume, 1.5 au ± 0.9; mean blood flow, 0.5 au ± 0.6; mean blood flow velocity, 0.2 mm/sec ± 0.2). In all volunteers, the results of gray-scale US were normal.

MR Imaging
At T2-weighted MR imaging, all patients with confirmed dermatomyositis or polymyositis had areas of increased muscular signal intensity; none had areas of atrophy or fatty infiltration (Fig 4). Increased signal intensity on T2-weighted MR images was found in one of 14 patients with histologic exclusion of myositis. Contrast material enhancement on fat-suppressed T1-weighted MR images was found in four of seven patients with myositis. No contrast material enhancement was observed in the absence of increased signal intensity on T2-weighted MR images. A reticular pattern in the subcutaneous tissue, which was used as a criterion for dermatomyositis, was found on fat-suppressed T2-weighted MR images in three of four patients with dermatomyositis (Fig 5). Muscular atrophy was detected in the same four patients at US and MR imaging. Fatty infiltration was observed in two patients at MR imaging. One of these patients had end-stage myopathy, and the other patient had polymyalgia rheumatica; both showed muscle atrophy. In all volunteers, unenhanced MR images were normal.



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  		Figure 4a: Confirmed polymyositis and associated scleroderma in 60-year-old man. (a) Transverse fat-suppressed T2-weighted turbo spin-echo (3970/98) MR image demonstrates absence of atrophy. Area of increased signal intensity indicates inflammation (arrow). (b) Transverse power Doppler US image of respective area 75 seconds after injection of 10 mL galactose-palmitic acid shows distinct increased maximum plateau.

 


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  		Figure 4b: Confirmed polymyositis and associated scleroderma in 60-year-old man. (a) Transverse fat-suppressed T2-weighted turbo spin-echo (3970/98) MR image demonstrates absence of atrophy. Area of increased signal intensity indicates inflammation (arrow). (b) Transverse power Doppler US image of respective area 75 seconds after injection of 10 mL galactose-palmitic acid shows distinct increased maximum plateau.

 


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  		Figure 5a: Confirmed dermatomyositis in a 54-year-old woman. (a) Transverse T1-weighted spin-echo (450/8.7), (b) transverse contrast-enhanced fat-suppressed T1-weighted turbo spin-echo (678/8.7), (c) transverse T2-weighted turbo spin-echo (6785/120), and (d) sagittal short tau inversion-recovery (4890/60) MR images demonstrate triceps brachii muscle, which served as a biopsy site. Images show peripheral edema and contrast material enhancement that were not profound (arrow in b and c). Biceps muscle was not affected to a major extent. Muscle volume is preserved, and no fatty infiltration is visible. A reticular pattern in the subcutaneous tissue could be observed on d (arrow). Increased signal intensity may represent edema and/or inflammatory infiltration. On the left side of a–c, a field inhomogeneity is visible within the subcutaneous fat tissue. (e) Transverse power Doppler US (7-MHz) image of right biceps muscle obtained at a depth of 1.5 cm shows no distinct increase in maximum plateau 75 seconds after bolus injection of 10 mL galactose-palmitic acid. This finding demonstrates that myositis may be spotty and that, for screening purposes, it may be useful to examine more than one muscle group with contrast-enhanced US.

 


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  		Figure 5b: Confirmed dermatomyositis in a 54-year-old woman. (a) Transverse T1-weighted spin-echo (450/8.7), (b) transverse contrast-enhanced fat-suppressed T1-weighted turbo spin-echo (678/8.7), (c) transverse T2-weighted turbo spin-echo (6785/120), and (d) sagittal short tau inversion-recovery (4890/60) MR images demonstrate triceps brachii muscle, which served as a biopsy site. Images show peripheral edema and contrast material enhancement that were not profound (arrow in b and c). Biceps muscle was not affected to a major extent. Muscle volume is preserved, and no fatty infiltration is visible. A reticular pattern in the subcutaneous tissue could be observed on d (arrow). Increased signal intensity may represent edema and/or inflammatory infiltration. On the left side of a–c, a field inhomogeneity is visible within the subcutaneous fat tissue. (e) Transverse power Doppler US (7-MHz) image of right biceps muscle obtained at a depth of 1.5 cm shows no distinct increase in maximum plateau 75 seconds after bolus injection of 10 mL galactose-palmitic acid. This finding demonstrates that myositis may be spotty and that, for screening purposes, it may be useful to examine more than one muscle group with contrast-enhanced US.

 


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  		Figure 5c: Confirmed dermatomyositis in a 54-year-old woman. (a) Transverse T1-weighted spin-echo (450/8.7), (b) transverse contrast-enhanced fat-suppressed T1-weighted turbo spin-echo (678/8.7), (c) transverse T2-weighted turbo spin-echo (6785/120), and (d) sagittal short tau inversion-recovery (4890/60) MR images demonstrate triceps brachii muscle, which served as a biopsy site. Images show peripheral edema and contrast material enhancement that were not profound (arrow in b and c). Biceps muscle was not affected to a major extent. Muscle volume is preserved, and no fatty infiltration is visible. A reticular pattern in the subcutaneous tissue could be observed on d (arrow). Increased signal intensity may represent edema and/or inflammatory infiltration. On the left side of a–c, a field inhomogeneity is visible within the subcutaneous fat tissue. (e) Transverse power Doppler US (7-MHz) image of right biceps muscle obtained at a depth of 1.5 cm shows no distinct increase in maximum plateau 75 seconds after bolus injection of 10 mL galactose-palmitic acid. This finding demonstrates that myositis may be spotty and that, for screening purposes, it may be useful to examine more than one muscle group with contrast-enhanced US.

 


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  		Figure 5d: Confirmed dermatomyositis in a 54-year-old woman. (a) Transverse T1-weighted spin-echo (450/8.7), (b) transverse contrast-enhanced fat-suppressed T1-weighted turbo spin-echo (678/8.7), (c) transverse T2-weighted turbo spin-echo (6785/120), and (d) sagittal short tau inversion-recovery (4890/60) MR images demonstrate triceps brachii muscle, which served as a biopsy site. Images show peripheral edema and contrast material enhancement that were not profound (arrow in b and c). Biceps muscle was not affected to a major extent. Muscle volume is preserved, and no fatty infiltration is visible. A reticular pattern in the subcutaneous tissue could be observed on d (arrow). Increased signal intensity may represent edema and/or inflammatory infiltration. On the left side of a–c, a field inhomogeneity is visible within the subcutaneous fat tissue. (e) Transverse power Doppler US (7-MHz) image of right biceps muscle obtained at a depth of 1.5 cm shows no distinct increase in maximum plateau 75 seconds after bolus injection of 10 mL galactose-palmitic acid. This finding demonstrates that myositis may be spotty and that, for screening purposes, it may be useful to examine more than one muscle group with contrast-enhanced US.

 


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  		Figure 5e: Confirmed dermatomyositis in a 54-year-old woman. (a) Transverse T1-weighted spin-echo (450/8.7), (b) transverse contrast-enhanced fat-suppressed T1-weighted turbo spin-echo (678/8.7), (c) transverse T2-weighted turbo spin-echo (6785/120), and (d) sagittal short tau inversion-recovery (4890/60) MR images demonstrate triceps brachii muscle, which served as a biopsy site. Images show peripheral edema and contrast material enhancement that were not profound (arrow in b and c). Biceps muscle was not affected to a major extent. Muscle volume is preserved, and no fatty infiltration is visible. A reticular pattern in the subcutaneous tissue could be observed on d (arrow). Increased signal intensity may represent edema and/or inflammatory infiltration. On the left side of a–c, a field inhomogeneity is visible within the subcutaneous fat tissue. (e) Transverse power Doppler US (7-MHz) image of right biceps muscle obtained at a depth of 1.5 cm shows no distinct increase in maximum plateau 75 seconds after bolus injection of 10 mL galactose-palmitic acid. This finding demonstrates that myositis may be spotty and that, for screening purposes, it may be useful to examine more than one muscle group with contrast-enhanced US.

 
Follow-up
Five patients (four women, one man; mean age, 57 years ± 8) who had confirmed myositis (two with polymyositis and dermatomyositis and one with overlap syndrome) and, compared with healthy volunteers, elevated perfusion-related parameters underwent serial assessments after immunosuppressive therapy, which was performed after an average interval of 2 months. An additional third contrast-enhanced US examination performed 4 months after the initial examination was available in two patients. Table 2 lists the changes in perfusion-related parameters, creatine kinase values, and muscle strength scores, which were determined according to the Medical Research Council grading system. Muscle strength improved, while creatine kinase decreased at follow-up. In all patients, contrast-enhanced US demonstrated a reduction of blood flow (Fig 6).


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  		Table 2. Follow-up in Five Patients with Confirmed Myositis Who Underwent Immunosuppressive Therapy

 


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  		Figure 6: Graph demonstrates follow-up results in five patients with confirmed myositis who underwent immunosuppressive therapy. Blood flow values were calculated by using contrast-enhanced US findings. Concomitant with an improvement in clinical symptoms, a reduction in muscle blood flow was noted with immunosuppressive therapy. The second and third examination took place after 2 and 4 months, respectively.

 

   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
References
 
In this study we demonstrate that, by using contrast-enhanced US, patients with typical histologic features of polymyositis and dermatomyositis have significantly increased muscle perfusion. The perfusion-related parameter of blood flow achieved the best statistical significance and therefore may serve as an additional diagnostic tool. Conventional myosonography can show muscle edema only in cases of acute dermatomyositis and polymyositis because of increased echogenicity. In less active myositis, however, echogenicity can also be slightly reduced (18). To date, only a few studies have examined the detection of vascular patterns in patients with myositis by using US. Meng and coworkers (8) found significantly higher vascularity scores in patients with dermatomyositis and polymyositis than in control subjects by using power Doppler US. A limitation of their study was that all patients were receiving immunosuppressive therapy at the time of the examination, and the control subjects received no medication. Because Meng et al used a four-point score to assess US findings, muscular perfusion was not calculated and could only be assessed subjectively as a surrogate parameter by the observers during power Doppler US image analysis (8).

In accordance with previous observations (5,19,20), we found that patients with acute dermatomyositis and polymyositis had areas of increased muscular signal intensity on T2-weighted MR images; this is considered the most important finding in the different types of autoimmune inflammatory myopathies (4,17). This finding is also thought to be a good sign of disease activity and may be caused by an abnormal cellular infiltrate or edema (4). Although muscle edema may be an early sign of inflammatory myopathy, this finding is nonspecific and has been described in other conditions, including metabolic or traumatic changes, neuropathies, muscular dystrophies, myotonic dystrophy, and necrotic changes, such as rhabdomyolysis or diabetic muscle infarction, or even after physical exercise (4,17,18). In our study, edema was detected in all patients with confirmed myositis, while contrast material enhancement on T1-weighted MR images was detected in only four of seven patients with confirmed myositis. No contrast material enhancement was observed in the absence of increased signal intensity on T2-weighted MR images. As described previously (4,16,18), the sensitivity of contrast-enhanced images for this disease does not seem to be higher than that of images obtained with T2-weighted MR imaging. Contrast material enhancement seems to be more of a feature of an acute muscle inflammation, such as in pyomyositis. In pyomyositis, contrast material enhancement is found in most patients with ill-defined borders (15).

Increased perfusion that is detected at contrast-enhanced US and increased signal intensity on T2-weighted MR images were correlated in our study. Both findings could be interpreted as parameters that indicated myositis. Idiopathic inflammatory myopathies are histologically characterized by perivascular and intrafascicular inflammatory infiltrates—mainly T cells and macrophages—and often by the degeneration and regeneration of fibers (4,21). It has been proposed that, as indicated at MR imaging, possible mechanisms of muscle edema (inflammatory infiltrates are regularly associated with muscle edema) include an absolute increase of interstitial fluid content, a relative decrease of intracellular space content, and an increase of microcirculation (18). Our contrast-enhanced US findings suggest that the latter finding may indeed play a role. Moreover, an increase in signal intensity on gadolinium-enhanced MR images in patients with acute myositis has been interpreted as inflammatory hypervascularization (18).

Muscle biopsy is mandatory to confirm the diagnosis of inflammatory myopathy because biopsy demonstrates inflammatory infiltrates and is therefore the most crucial test for establishing the diagnosis. The inflammation, however, may be spotty, and multiple muscle biopsies may have to be performed in different muscles whenever a patient meets the clinical criteria but the sample is not of diagnostic quality (1,18). Electromyography can be painful, is time-consuming, and can also cause a local necrosis-induced myositis that interferes with subsequent analysis of biopsy material. Noninvasive contrast-enhanced US, by demonstrating an elevated muscular perfusion in inflammatory myopathy, is an additional imaging modality that can be used to detect a suitable biopsy site in patients with typical clinical signs of myositis and previous negative or nonspecific biopsy results. Furthermore, results of contrast-enhanced US may guide therapeutic decisions in patients who meet the clinical criteria for myositis whenever a biopsy is not possible or multiple biopsy findings are inconclusive. Therefore, MR imaging or contrast-enhanced US could be proposed instead of electromyography for choosing the biopsy site and thus could reduce the 10%–25% false-negative rate for biopsy when performed without imaging guidance (5,20,22).

Evaluating the response to treatment and the activity of myositis requires reliable clinical and laboratory criteria. Treatment monitoring in patients with dermatomyositis and polymyositis is primarily made on the basis of neurologic examination, which assesses muscle strength by manual testing and evaluation of serum creatine kinase concentration. A decrease in serum creatine kinase concentration, normalization of edema at MR imaging, and improved muscle strength, however, do not always coincide. Sometimes "treating" the creatine kinase instead of improving the clinically important muscle weakness was done (1,3,23). The preliminary results of our study suggest that, in patients who are undergoing specific treatment, contrast-enhanced US might be beneficial in demonstrating alterations in muscular perfusion. The quantitative measures of perfusion that are provided at contrast-enhanced US may be especially valuable for the serial assessment of responses to treatment in clinical trials. We propose that a reduction in perfusion values to the levels found in volunteers should be considered to be a sign of response to therapy.

Although our preliminary contrast-enhanced US results are promising, the number of patients in our study is limited, and therefore our results need to be confirmed by larger studies. Another limitation of contrast-enhanced US to quantify the perfusion-related parameters of blood flow and blood flow velocity is that only one extremity can be assessed after a single contrast material injection. Blood volume, however, can be quantified in all muscles that are accessible with US after a single administration of contrast material. Newer US techniques that are specific to contrast agents allow for a faster and more sensitive measurement of replenishment kinetics (24). Therefore, such techniques may improve the quantification of perfusion in large muscle volumes after a single contrast material injection. Thus, multiple contrast material injections for the examination of possible widespread muscular involvement of myositis could be avoided. This might be interesting for screening purposes because idiopathic inflammatory myopathies include a diverse group of conditions ranging from focal disorders that are confined to a single muscle to diffuse disorders (2). If all perfusion-related parameters are of interest, contrast-enhanced US should be used after a thorough neurologic examination. By doing this, muscles that are possibly affected by myositis can be identified owing to the manifestation of paresis, and both the number of examined muscle groups and the number of contrast material injections can be reduced.

In conclusion, the results of our preliminary study show that contrast-enhanced US is a clinically feasible method to quantify skeletal muscle perfusion. Moreover, contrast-enhanced US is able to noninvasively demonstrate increased perfusion in the involved muscle groups for patients with myositis.


   ACKNOWLEDGMENTS
 
The authors thank Ivan Zuna, PhD, for statistical advice.


   FOOTNOTES
 

Abbreviations: ROI = region of interest

Author contributions: Guarantors of integrity of entire study, M.A.W., M.K., H.U.K., S.D.; study concepts/study design or data acquisition or data analysis/interpretation, all authors; manuscript drafting or manuscript revision for important intellectual content, all authors; approval of final version of submitted manuscript, all authors; literature research, M.A.W., M.K., M.H.; clinical studies, M.A.W., M.K., U.J., H.B.H., M.H., U.M., C.F.; statistical analysis, M.A.W., M.K.; and manuscript editing, M.A.W., M.K., U.J., U.M., H.U.K., S.D.


   References
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 References
 

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