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European Journal of Echocardiography 2005 6(5):351-357; doi:10.1016/j.euje.2004.12.006
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Copyright © 2005, The European Society of Cardiology

Myocardial contractility is early affected in systemic sclerosis: A Tissue Doppler echocardiography study

Christophe Meunea,*, Yannick Allanoreb, Olivier Pascalc, Jean-Yves Devauxd, Odile Dessaultd, Denis Duboca, Simon Webera and André Kahanb

aDepartment of Cardiology, Cochin Hospital, AP-HP, René Descartes University, 27 rue du Fg St-Jacques, 75014 Paris, France
bDepartment of Rheumatology A, Cochin Hospital, AP-HP, René Descartes University, 27 rue du Fg St-Jacques, 75014 Paris, France
cDepartment of Cardiology, Kremlin-Biçêtre Hospital, AP-HP, Kremlin-Biçêtre, France
dDepartment of Nuclear Medicine, Cochin Hospital, AP-HP, René Descartes University, 27 rue du Fg St-Jacques, 75014 Paris, France

Received 7 September 2004; received in revised form 12 December 2004; accepted after revision 29 December 2004.

* Corresponding author. Tel.: +33 1 58 41 16 21; fax: +33 1 58 41 16 05. christophe.meune{at}cch.ap-hop-paris.fr


    Abstract
 Top
 Abstract
 Introduction
 Material and methods
 Results
 Discussion
 Study limitations
 References
 
Aims

Systemic sclerosis (SSc) is a connective tissue disorder characterized by frequent myocardial involvement. Alteration in left ventricular (LV) function is reported to be rare; however, it may be underestimated by conventional measurements. Our aim was to prospectively investigate LV function in SSc patients, using Tissue Doppler echocardiography (TDE), a modern and accurate method of assessing myocardial function.

Methods and results

Seventeen consecutive SSc patients with normal cardiac examination, pulmonary artery pressure (PAP) and radionuclide LV ejection fraction (EF) were prospectively investigated. Myocardial perfusion was investigated using single-photon-emission computerized tomography (SPECT). Echocardiography (ECHO), systolic and diastolic strain-rate (SR) measured in the posterior wall by TDE were used to investigate myocardial function, and compared with results of 15 matched controls.

All patients (53±8 years; 14 women; systolic PAP 33±6mmHg; LVEF 67±8%) had myocardial SPECT perfusion abnormalities. Despite normal ECHO, they had lower systolic SR than controls (1.7±0.5 versus 3.8±1.7cm–1, p<0.0001), and lower diastolic SR (3.7±1.5 versus 5.6±1.2cm–1, p=0.0004). Ten SSc patients had reduced systolic SR<1.7cm–1 and 11 reduced diastolic SR<3.5cm–1.

Conclusion

Frequent abnormal myocardial perfusion is confirmed in SSc patients. Reduced contractility is also frequent as detected by TDE, despite normal radionuclide LVEF.

Keywords: Echocardiography; Tissue Doppler; Systemic sclerosis; Left ventricular function


    Introduction
 Top
 Abstract
 Introduction
 Material and methods
 Results
 Discussion
 Study limitations
 References
 
Systemic sclerosis (SSc) is a connective tissue disease characterized by widespread vascular lesions leading to systemic fibrosis. A growing body of evidence suggests that vascular system impairment may be the primary target of the disease1–3 and that myocardial lesions are manifestations of focal ischemic injury resulting from abnormal vasoreactivity, with or without accompanying structural vascular disease.4–7 Single-photon-emission computerized tomography (SPECT), echocardiography or radionuclide ventriculography are performed in order to detect perfusion abnormalities and left ventricular (LV) dysfunction, respectively.8 Myocardial perfusion abnormalities are very common,2,3 but reduced contractility seems to be far less frequent as estimated by conventional measurements. It can be speculated that using a more sensitive method, myocardial dysfunction will be more frequently detected, offering the opportunity of more accurate follow-up and earlier treatment.9,10

The recent development of Tissue Doppler echocardiography (TDE) allows direct measurement of myocardial velocities and strain-rate (SR).11 Previous studies have demonstrated that SR was a powerful indicator of myocardial contraction, independent of myocardial translational motion, and far more sensitive than conventional echocardiography.12,13 The aim of our study was to investigate LV function in SSc patients with apparent normal LV ejection fraction (EF) using TDE.


    Material and methods
 Top
 Abstract
 Introduction
 Material and methods
 Results
 Discussion
 Study limitations
 References
 
Consecutive SSc patients referred to our institution for cardiac screening during a 6 months-period were considered for inclusion after informed consent. Additional inclusion criteria were (a) normal pulmonary artery pressure, (b) normal cardiac examination and (c) normal radionuclide LVEF.

SSc was defined according to the American College of Rheumatology criteria for systemic sclerosis; 9 had the limited and 8 the diffuse cutaneous form of the disease.14

No patient had known atherosclerotic heart disease; vasoactive drugs were stopped at least 5 half-lives before evaluation. All patients underwent physical examination, laboratory testing (blood cell count, serum creatinine, creatine phospho-kinase [CPK], lactico-deshydrogenase [LDH], anti-nuclear, anti-centromere, anti-topoisomerase 1 antibodies), CT-scan, pulmonary function testing, myocardial SPECT, radionuclide ventriculography, echocardiography and TDE imaging. Strain-rate (SR) determined by TDE was then compared to 15 gender age matched controls. The healthy cardiac status of the control subjects was confirmed by the absence of relevant cardiac medical history, normal cardiac examination, ECG and echocardiography.

Single-photon-emission computed tomography
Myocardial perfusion was investigated by Thallium-201 SPECT as previously described,2 in a 17-segment model using a semi-quantitative score; 4 for normal, 3 for mild reduction (not definitely abnormal), 2 for moderate reduction (definitely abnormal), 1 for severe reduction and 0 for absent uptake.15 Patients were considered to have myocardial involvement if they had: 1/reduced global perfusion score<50 and 2/at least 2 segments with abnormal perfusion score. Two practitioners performed all scoring independently.

Radionuclide ventriculography
All patients underwent radionuclide ventriculography as previously described7. LV ejection fraction (EF) was measured, after in vitro red cell labeling with 555MBq technetium-99m, by a two-region-of-interest with an automatic thresholding technique for background subtraction. A LVEF≥55% was defined as normal. All measurements were performed by 2 practitioners independently.

Echocardiographic measurements
All standard echocardiography and TDE were performed with an ATL HDI5000 system (ATL ultrasound, Bothell, Washington, DC) equipped with Tissue Doppler, second harmonic imaging technologies and a 2–3.5MHz phased array transducer. Conventional measurements including LV cavity dimensions, wall thickness, fractional shortening (FR) and transmitral flow velocities were made according to the guidelines of the American and European Societies of Echocardiography.

Myocardial velocities were measured in the posterior wall from a parasternal short axis view at the level of the papillary muscle on M-mode TDE recordings. Special attention was made on correct alignment of the beam to be perpendicular to the LV wall. Off-line TDE measurements were made by 2 cardiologists according to a blind protocol with the HDI Lab software package installed in a standard PC workstation as follows:

- Lines that were drawn manually in the sub-endocardium and in the sub-epicardium to determine velocity patterns over time.
- Peak systolic velocity, defined as maximal velocity during LV ejection time, was determined from endocardial (Endo VSYS) and epicardial (Epi VSYS) velocity patterns. Early diastolic velocity was determined from endocardial (Endo VDIA) and epicardial (Epi VDIA) patterns.
- Peak systolic and early diastolic strain-rate (SR) was defined as the maximal transmural velocity gradient during systolic (SRSYS) and early diastolic (SRDIA) times and was calculated as: SR (s–1)=(Endo V–Epi V)/d (where d is the distance between endocardium and epicardium).
- Lastly, patients were investigated for the presence of post-systolic shortening. SR determination is provided in one patient and control at baseline on Fig. 1.


Figure 1
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Figure 1 Example of myocardial sub-endocardial (black) and sub-epicardial (grey) velocity patterns extracted from TDE acquisitions, and corresponding strain-rate in a representative patient with SSc and a control.

 
Statistical analysis
Statistical analysis was performed using Statview software (Abacus concept, Berkeley, USA, 1998). Data were expressed as means±standard deviation (SD). Patients with SSc were compared with controls using Student's t-test for comparison of normally distributed continuous variables and chi-square analysis for differences in frequency. Subgroups analysis in SSc patients were examined using Mann–Whitney test. Linear regression and Spearman correlation tests were used to determine the existence of correlations between variables. A p value<0.05 was necessary for statistical significance in all comparisons.


    Results
 Top
 Abstract
 Introduction
 Material and methods
 Results
 Discussion
 Study limitations
 References
 
Of 20 consecutive SSc patients screened, 3 had reduced LVEF (39%, 48% and 49%) and were not included in the present study.

The mean characteristics of the 17 patients enrolled are summarized in Table 1. No difference was demonstrated between SSc patients and control subjects regarding demographic characteristics, heart rate, blood pressure, and all patients had normal cardiac examination. No patient had any coronary artery disease risk factors (including glycemic and lipid status) except for hereditary which was not investigated. None exhibits atrioventricular conduction defect, one had incomplete right bundle branch block and one had complete right bundle branch block. All SSc patients had myocardial perfusion abnormalities (mean global perfusion score 32.5±6.8; mean±SD number of segments with defects 12.9±2.9). Results of radionuclide LVEF and ECHO in SSc patients and controls are shown in Table 2. SSc patients had increased systolic pulmonary artery pressure when compared to controls (33±6 versus 28±4mmHg, p=0.006) although all values remained within normal ranges (<40mmHg). There was a trend for increased LV mass, no significant difference for FR. Transmitral flow velocities analysis showed a trend for more patients having relaxation abnormalities as demonstrated with an E/A ratio<1 (7/17 patients with SSc versus 4/15 controls, p=0.38), although the global E/A ratio did not differ between both groups (Table 2).


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Table 1 Clinical and biological characteristics of SSc patients

 


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Table 2 Results of radionuclide ventriculography at rest and ECHO in SSc patients and control subjects

 
The inter-observer variability for SRSYS and SRDIA were 0.19 and 0.22, respectively. All SSc patients had normal radionuclide LVEF; however, when compared to controls, they had lower SRSYS (1.7±0.5 versus 3.8±1.7s–1, p<0.0001) and lower SRDIA (3.7±1.5 versus 5.6±1.2s–1, p=0.0004) (Table 2, Fig. 2). No patients had post-systolic shortening. The lowest values of systolic and diastolic SR in controls were 1.7s–1 and 3.5s–1 in this study; 10 SSc patients had reduced SRSYS<1.7 and 11 had reduced SRDIA<3.5s–1.


Figure 2
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Figure 2 Systolic and diastolic strain-rate (TDE) in SSc patients and controls. Statistical analysis with Student's paired-t test (p<0.05 for statistical significance).

 
Systolic and diastolic SR correlated with LVEF (r=0.576, p=0.02 and r=0.816, p=0.001), whereas no correlation was found with demographic criteria, cutaneous form of the disease and other SSc characteristics including pulmonary artery pressure and pulmonary function tests.

SSc patients with diffuse cutaneous sub-type had reduced mean forced vital capacity when compared with limited cutaneous sub-type (75±18% versus 99±12%, p=0.006) and mean DLCO/hemoglobin (67±19% versus 84±10%, p=0.029), whereas no difference was demonstrated regarding thallium perfusion score, LVEF, echocardiographic parameters and DTE values.


    Discussion
 Top
 Abstract
 Introduction
 Material and methods
 Results
 Discussion
 Study limitations
 References
 
The main findings of our study indicate that (1) TDE is an accurate and sensitive method to examine contractility in SSc and should be considered in this setting, (2) abnormal myocardial function may be present in patients with SSc despite normal echocardiographic and radionuclide LVEF.

Assessment of LV function in patients with suspected cardiomyopathy is commonly performed by echocardiography or radionuclide ventriculography. Some measurements such as end-diastolic diameter, fractional shortening, or LVEF are used in routine clinical practice. These indexes are, however, load-dependent, and do not systematically reflect the contractile state of the myocardium. TDE is a new method that allows the direct and reliable measurement of myocardial regional contractility.11–13 Myocardial SR is calculated from the local difference in wall motion velocity, and is known as an index of contractility independent of myocardial translational motion, more sensitive than conventional echocardiography, and less dependent of loading conditions than conventional methods.12,13,16–18 Besides their concordance with these studies, our TDE observations also demonstrated frequent LV systolic and diastolic alterations in patients with SSc.

SSc is a widespread tissue disorder and several studies have demonstrated a high prevalence of myocardial involvement using SPECT2,3; our results are in accordance with these studies. Previous studies, using conventional measurements, have reported low prevalence of systolic dysfunction and variable alteration in diastolic function in SSc.2,3,7,8,19,20 However, it should be suspected that LV systolic dysfunction might be underevaluated by conventional measurements. Indeed, 2 studies have demonstrated the existence of reduced resting LVEF in 2/19 and 3/26 SSc patients with limited and diffuse SSc, respectively, and also the existence of an abnormal systolic function in 7/19 and 12/26, respectively, by either abnormal resting LVEF or inadequate raise in LVEF during exercise.3,21 Our results are in accordance with these previous results as we observed a low prevalence of abnormal resting LVEF (3/20 consecutive SSc patients screened), but demonstrated that SSc patients with normal resting LVEF have lower systolic and diastolic SR than controls. When regarding individual data, 10/17 and 11/17 SSc patients had reduced systolic SR<1.7 and diastolic SR<3.5s–1. As systolic and diastolic SR are respective markers of myocardial systolic and diastolic regional function, our results suggest that our patients have both types of dysfunction.13,16,22 In our study, we only investigated radial SR from the inferior wall; therefore, our results must be interpreted as a reduction in regional function and not in global function. Moreover, analyzing longitudinal strain-rate might be even more relevant as longitudinal contraction is mainly caused by sub-endocardial fibers, which are sensitive to ischemia.23 In a recent study using TDE, their authors demonstrated the coexistence of reduced E/A transmitral flow, with altered longitudinal diastolic velocities and no systolic alteration in 19 SSc women.24 Their control population, however, tended to be younger than SSc patients (43.6 years versus 51.7 years in SSc), which may account for part of the differences. Moreover, we observed a trend for more patients having relaxation abnormalities (7/17 versus 4/15), with no difference in the mean E/A ration, but with a lower E/A ratio in our control population as compared to their controls. Other discrepancy between both studies include the observation of isolated abnormal longitudinal diastolic velocities in their study, while we documented altered systolic and diastolic SR. Interpretation could be that our population have more serious heart involvement, and we documented myocardial perfusion abnormalities in all patients, whereas neither myocardial perfusion nor pulmonary function is provided in their study. Lastly, they only investigated myocardial velocities, which are known to be less sensitive indexes of contractility as compared to SR.12,16

In our study, systolic and diastolic SR correlated with LVEF, whereas they did not correlate with pulmonary involvement nor with pulmonary arterial pressure confirming previous reports stating that both myocardial and pulmonary involvement are independent.2–6

Our results show a high prevalence of myocardial dysfunction in SSc patients, both in the diffuse and limited cutaneous forms of the disease, which illustrates the striking cardiac involvement in this disease. Our observations may have important clinical implications, since we demonstrated the presence of both systolic and diastolic dysfunction in few SSc patients whose clinical condition was normal and whose radionuclide LVEF was normal. Moreover, vasoactive drugs including ACE inhibitors and calcium channel blockers have been demonstrated to mitigate myocardial perfusion and function abnormalities2,7,9 using conventional techniques; they may be effective to prevent early myocardial dysfunction and warrant further studies.


    Study limitations
 Top
 Abstract
 Introduction
 Material and methods
 Results
 Discussion
 Study limitations
 References
 
TDE was limited to a section of the posterior wall of the LV, due to the angle-dependency of the method. Strict interpretation of our result is that regional contractility is affected in SSc. However, as perfusion abnormalities on SPECT were diffused and not confined to the posterior wall, we assume that the abnormalities observed in this confined may be representative of the entire LV.

In this study, controls tended to have lower systolic and diastolic blood pressure and myocardial mass than SSc, although not significant. However, we cannot exclude that it accounts, at least in part, in the variations in diastolic strain-rate. Moreover, although our population had no other conventional atherosclerosis risk factor, it may favor coronary artery disease, and therefore reduces systolic and diastolic performances.

These results demonstrate striking rate of function abnormalities; although TDE provide meaningful data in other population of patients with cardiac involvement, only longitudinal studies will evaluate the impact of reduced SR on clinical events and prognosis.

In conclusion, there is a high prevalence of abnormal myocardial systolic and diastolic function assessed by TDE in SSc patients, despite normal global LVEF. TDE allows early detection of myocardial dysfunction. TDE, which is far more sensitive than conventional techniques, could be proposed for the early detection of myocardial dysfunction and for the follow-up of SSc patients.


    References
 Top
 Abstract
 Introduction
 Material and methods
 Results
 Discussion
 Study limitations
 References
 

  1. D'Angelo W.A., Fries J.F., Masi A.T., Schulman L.E. Pathologic observations in systemic sclerosis (scleroderma): a study of fifty-eight autopsy cases and fifty-eight matched controls. Am J Med (1969) 46:428–440.[CrossRef][Web of Science][Medline]
  2. Kahan A., Devaux J.Y., Amor B., Menkes C.J., Weber S., Nittenberg A., et al. Nifedipine and thallium-201 myocardial perfusion in progressive systemic sclerosis. N Engl J Med (1986) 314:1397–1402.[Abstract]
  3. Follansbee W.P., Curtiss E.I., Medsger T.A. Jr., Steen V., Uretsky B.F., Owens G.R., et al. Physiologic abnormalities of cardiac function in progressive systemic sclerosis with diffuse scleroderma. N Engl J Med (1984) 310:142–148.[Abstract]
  4. Steen V.D., Follansbee W.P., Conte C.G., Medsger T.A. Jr. Thallium perfusion defects predict subsequent cardiac dysfunction in patients with systemic sclerosis. Arthritis Rheum (1996) 39:677–681.[Web of Science][Medline]
  5. Kahan A., Nitenberg A., Foult J.M., Amor B., Menkes C.J., Devaux J.Y., et al. Decreased coronary reserve in primary scleroderma myocardial disease. Arthritis Rheum (1985) 28:637–646.[Web of Science][Medline]
  6. Ellis W.W., Baer A.N., Robertson R.M., Pincus T., Kronenberg M.W. Left ventricular dysfunction induced by cold exposure in patients with systemic sclerosis. Am J Med (1986) 80:385–392.[CrossRef][Web of Science][Medline]
  7. Kahan A., Devaux J.Y., Amor B., Menkes C.J., Weber S., Guérin F., et al. Pharmacodynamic effect of nicardipine on left ventricular function in systemic sclerosis. J Cardiovasc Pharmacol (1990) 15:249–253.[Web of Science][Medline]
  8. Candell-Riera J., Armanda-Gil L., Simeón C.P., Castel-Conesa J., Fonollosa-Pla V., Garcia-Del-Castillo H., et al. Comprehensive noninvasive assessment of cardiac involvement in limited systemic sclerosis. Arthritis Rheum (1996) 39:1138–1145.[Medline]
  9. Kahan A., Devaux J.Y., Amor B., Menkes C.J., Weber S., Venot A., et al. The effect of captopril on thallium 201 myocardial perfusion in systemic sclerosis. Clin Pharmacol Ther (1990) 47:483–489.[Web of Science][Medline]
  10. The SOLVD investigators. Effect of enalapril on mortality and the development of heart failure in asymptomatic patients with reduced left ventricular ejection fractions. N Engl J Med (1992) 327:685–691.[Abstract]
  11. Sutherland G.R., Stewart M.J., Groundstroem K.W., Moran C.M., Fleming A., Guell-Peris F.J., et al. Color Doppler myocardial imaging: a new technique for the assessment of myocardial function. J Am Soc Echocardiogr (1994) 7:441–458.[Medline]
  12. Uematsu M., Nakatani S., Yamagishi M., Matsuda H., Miyatake K. Usefulness of myocardial velocity gradient derived from two-dimensional tissue Doppler imaging as an indicator of regional myocardial contraction independent of translational motion assessed in atrial septal defect. Am J Cardiol (1997) 79:237–241.[CrossRef][Web of Science][Medline]
  13. Meune C., Pascal O., Bécane H.M., héloire F., Christoforou D., Laforet P., et al. Reliable detection of early myocardial dysfunction by Tissue Doppler echocardiography in Becker's muscular dystrophy. Heart (2004) 90:947–948.[Free Full Text]
  14. LeRoy E.C., Black C., Fleischmajer R., Jablonska S., Krieg T., Medsger T.A. Jr., et al. Scleroderma (systemic sclerosis). Classification, subset and pathogenesis. J Rheumatol (1988) 15:202–205.[Web of Science][Medline]
  15. Cerqueira MD, Weissman NJ, Dilsizian V, Jacobs AK, Kaul S, Laskey WJ, et al. for the American Heart Association Writing Group on Myocardial Segmentation and Registration for cardiac Imaging. Circulation 2002;105:539–542.
  16. Greenberg N.L., Firstenberg M.S., Castro P.L., Main M., Travaglini A., Odabashian J.A., et al. Doppler-derived myocardial systolic strain-rate is a strong indicator of left ventricular contractility. Circulation (2002) 105:99–105.[Abstract/Free Full Text]
  17. Shimizu Y., Uematsu M., Nagaya N., Yamagishi M., Yamamoto H., Miyatake K., et al. Myocardial velocity gradient reflects the severity of myocardial damage regardless of the presence or absence of mitral regurgitation. J Am Soc Echograph (2003) 16:246–253.
  18. Derumeaux G., Mulder P., Richard V., Chagraoui A., Nafeh C., Bauer F., et al. Tissue Doppler imaging differentiates physiological from pathological pressure-overload left ventricular hypertrophy in rats. Circulation (2002) 105:1602–1608.[Abstract/Free Full Text]
  19. Giunta A., Tirri E., Maione S., Cangianiello S., Mele A., De Luca A., et al. Right ventricular diastolic abnormalities in systemic sclerosis. Relation to left ventricular involvement and pulmonary hypertension. Ann Rheum Dis (2000) 59:94–98.[Abstract/Free Full Text]
  20. Meune C., Allanore Y., Devaux J.Y., Dessault O., Duboc D., Weber S., et al. High prevalence of right ventricular systolic dysfunction in early systemic sclerosis. J Rheumatol (2004) 31:1941–1945.[Abstract/Free Full Text]
  21. Handa R., Gupta K., Malhotra A., Jain P., Kamath P.K., Aggarwal P., et al. Cardiac involvement in limited systemic sclerosis: non-invasive assessment in asymptomatic patients. Clin Rheumatol (1999) 18:136–139.[CrossRef][Web of Science][Medline]
  22. Shimizu Y., Uematsu M., Shimizu H., Nakamura K., Yamagishi M., Miyatake K. Peak negative myocardial velocity gradient in early diastole as a noninvasive indicator of left ventricular diastolic function: comparison with transmitral flow indices. J Am Coll Cardiol (1998) 32:1418–1425.[Abstract/Free Full Text]
  23. Pellerin D., Sharma R., Elliott P., Veyrat C. Tissue Doppler, strain, and strain rate echocardiography for the assessment of left and right systolic ventricular function. Heart (2003) 89:iii9–iii17.[Abstract/Free Full Text]
  24. Plazak W., Zabinska-Plazak E., Wojas-Pelc A., Podolec P., Olszowska M., Tracz W., et al. Heart structure and function in systemic sclerosis. Eur J Dermatol (2002) 12:257–262.[Web of Science][Medline]

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