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Year : 2020  |  Volume : 4  |  Issue : 2  |  Page : 154-160

Significance of Tissue Doppler Echocardiography-Based Dispersion Index of Myocardial Velocities in the Differentiation of Ischemic and Nonischemic Cardiomyopathy: A Novel Echocardiographic Parameter

Department of Cardiology, Osmania Medical College/General Hospital, Afzalgunj, Hyderabad, Telangana, India

Date of Submission19-Sep-2019
Date of Decision05-Jan-2020
Date of Acceptance27-Jan-2020
Date of Web Publication19-Aug-2020

Correspondence Address:
Dr. Nagula Praveen
Department of Cardiology, Quli Qutub Shah Building, First Floor, Osmania Medical College/General Hospital, Afzalgunj, Hyderabad - 500 012, Telangana
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jiae.jiae_47_19

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Background: Tissue Doppler imaging (TDI) echocardiography, an objective method for the quantification of left ventricular (LV) function, can detect subtle alterations in contractility both in rest and stress echocardiography. Aim: The study aims were to (1) compare TDI parameters in patients with heart failure (HF) of ischemic and nonischemic etiology, (2) to differentiate both subsets based on velocity dispersion index (VDI) at mitral valve, and (3) to identify parameters that help in identifying the ischemic etiology of HF. Materials and Methods: Patients with symptomatic HF (NYHA class ≥II; LV ejection fraction <40%) were included in the study. Patients with aortic and mitral valve diseases, prosthetic valves, and cor pulmonale were excluded from the study. All patients underwent coronary angiography after stabilization. A total of 100 patients admitted between May 2017 and October 2018 were enrolled. Results: The mean age of presentation was earlier in nonischemic group compared to that of ischemic group of HF (43.4 ± 10.91 vs. 54.06 ± 10.40; P= 0.001). No significant differences in the mitral inflow velocities by conventional Doppler were found. The mean mitral TDI velocities were lower in the nonischemic group compared to those of the ischemic group. Systolic VDI, V s' >25.40 (sensitivity 91.7% and specificity 100%), and diastolic VDI, V e' >17.35 (sensitivity 86.7% and specificity 87.5%), were associated with the probability of diagnosing the ischemic cause of HF. Conclusions: VDIs help in the differentiation of ischemic and nonischemic etiologies of HF compared to the conventional echocardiography.

Keywords: Cardiomyopathy, heart failure, tissue Doppler imaging, velocity dispersion index

How to cite this article:
Sandeep N, Adikesava Naidu O, Srinivas R, Praveen N, Krishna Malakonda Reddy P. Significance of Tissue Doppler Echocardiography-Based Dispersion Index of Myocardial Velocities in the Differentiation of Ischemic and Nonischemic Cardiomyopathy: A Novel Echocardiographic Parameter. J Indian Acad Echocardiogr Cardiovasc Imaging 2020;4:154-60

How to cite this URL:
Sandeep N, Adikesava Naidu O, Srinivas R, Praveen N, Krishna Malakonda Reddy P. Significance of Tissue Doppler Echocardiography-Based Dispersion Index of Myocardial Velocities in the Differentiation of Ischemic and Nonischemic Cardiomyopathy: A Novel Echocardiographic Parameter. J Indian Acad Echocardiogr Cardiovasc Imaging [serial online] 2020 [cited 2021 Oct 24];4:154-60. Available from: https://www.jiaecho.org/text.asp?2020/4/2/154/292628

  Introduction Top

Differentiating ischemic from nonischemic causes of left ventricular (LV) systolic dysfunction has profound clinical and therapeutic implications in patients with chronic heart failure (HF). Ischemic etiology is probable in patients with a history of myocardial infarction, whereas cardiomyopathies are most probably nonischemic. However, it is not definite; an overlap of symptoms can be present in both subsets. Imaging techniques help in establishing the etiology of LV dysfunction, but there is a need of an optimal strategy. Tissue Doppler imaging (TDI) echocardiography is an objective method for the quantification of LV function, as opposed to the subjective visual assessment of the wall motion in rest and stress echocardiography.[1]

The risk of HF, a major health burden, increases with age, and the burden is more with the growing life expectancy of the Indian population. There is a dearth of data regarding the incidence or prevalence of HF not only from India but also worldwide.[1] The current estimates show the incidence of HF in India to be varying from 1.3 to 23 million.[2]

The definition of cardiomyopathies was given by 2013 World Heart Federation classification.[3] The ischemic etiology of cardiomyopathy (ICMP) was defined by Felker et al.[4] and that of non-ICMP (NICMP) was given by Packer et al.[5] The differentiation between ICMP and NICMP is of paramount importance because revascularization has a mortality benefit in ICMP, whereas for a patient with NICMP, there is no need for either high-dose antiplatelet therapy or expeditious revascularization.[6] The differentiation is often not straightforward and may need a lot of imaging modalities.

Stress 201 Tl myocardial scintigraphy,[7] positron emission tomography, electron-beam computed tomography, magnetic resonance imaging, and transthoracic high-frequency coronary echocardiography are effective in differentiating ICMP from NICMP but are more complex and less portable approaches.[6] Because of the limitations of the noninvasive tests, coronary angiography, with increased risk in these patients, is frequently undertaken.[8]

The regional function is dependent on the number of normally functioning myocytes and is reduced with myocyte necrosis and replacement fibrosis. Shan et al. showed for the first time that Em and Sm are strongly dependent on the percent of interstitial fibrosis in patients with coronary artery disease (CAD) and LV regional dysfunction.[9] With an increase in interstitial fibrosis, there is a decrease in Sm and Em.

Em velocity, a parameter of myocardial relaxation, is dependent on receptors influencing the LV lusitropic state.[10] The Am velocity, secondary to passive ventricular motion, had no significant relation with the beta-adrenergic receptor density. These observations support the active ventricular myocardium contribution to Sm and Em and suggest that Am is perhaps reflective of passive ventricular motion or maybe more dependent on atrial myocardium function.

Regional diastolic wall motion will be impaired at baseline in ischemic myocardial segments, even with preserved systolic contraction.[11] Ischemia impairs the diastolic myocardial wall motion earlier than the systolic contraction of the left ventricle. Evaluation of regional LV diastolic function could be a good strategy in identifying myocardial regions with impaired coronary artery flow and reduced myocardial perfusion.[11],[12]

Plewka et al.[13] analyzed the performance of the left ventricle in HF patients with severe systolic dysfunction using PWTDI and found no significant differences between the two groups either in LV ejection fraction (LVEF) or in wall motion score index. Among the TDI parameters, Em was significantly lower in patients after myocardial infarction than in dilated cardiomyopathy group (DCMP), whereas there were no differences in Sm and Am velocities.

A new TDI index was proposed by Plewka et al.,[13] reflecting the heterogeneous distribution of longitudinal systolic and diastolic myocardial velocities in different LV walls. This index allowed for an optimal discrimination between ischemic and nonischemic causes. Systolic velocity dispersion index (SVDI) >20% was associated with the probability of ischemic cause of CHF with a high sensitivity of 97%, a specificity of 100%, a positive predictive value of 100%, a negative predictive value of 97%, and an accuracy of 98%.

Because of the anatomic arrangement of myocardial fibers, a degree of heterogeneous contractility is present even in a healthy heart.[14] The level of heterogeneity is expressed by velocity dispersion index (VDI). The mean dispersion index of systolic and diastolic velocities in patients after myocardial infarction is approximately twice higher than that in DCMP patients.[13] This could be due to the different level of longitudinal fiber destruction in these groups of patients.

In many patients with DCMP, contractility is commonly impaired along both the short and long axes. Schwarz et al.[15] observed an increase in fiber diameter in patients with DCMP. An increase in fibrosis and reduction in myofibrils and myofibrillar mass were observed when the ejection fraction declined. Alternatively, the dilatation of the left ventricle might change the fiber orientation, resulting in a more circumferential fiber arrangement, with relatively uniform transmural fiber shortening. These changes result in a certain degree of functional heterogeneity in patients with DCMP that are consistent with previous reports of regional wall motion abnormalities.[16]

Aims and objectives

The aims and objectives were to compare TDI parameters among the patients with ischemic and nonischemic causes of LV dysfunction, to use a high degree of heterogeneity on TDI at different sites around the mitral annulus in differentiating them, and to identify the parameters that may indicate an ICMP.

Patient population

This was a prospective observational study with a study population of 100 patients.

Inclusion criteria

Patients with symptomatic HF (NYHA functional class ≥II), globally reduced wall motion contractility with moderate LV dysfunction (LVEF <40%) by echocardiography using the modified Simpson's method in sinus rhythm, were enrolled in the study.

Exclusion criteria

Patients with moderate aortic and/or mitral stenosis, prosthetic valves, significant mitral annular calcification, and cor pulmonale were excluded from the study.

  Materials and Methods Top

Written informed consent has been taken from all the eligible patients admitted between May 2017 and October 2018. The ethical committee of the institution approved the study. Written proformas were filled up during the inclusion of patients, which contained epidemiological information (age, sex, occupation, and place), questionnaires for risk factor evaluation (alcohol, hypertension, diabetes mellitus, and smoking), information of clinical presentation (dyspnea, chest pain, etc.), and clinical signs.

The patients enrolled were on HF medications, and on comparison between groups regarding the use of the medications (diuretics, angiotensin-converting enzyme inhibitors/angiotensin receptor blocker antagonists, mineralocorticoid receptor antagonists, beta-blockers, etc.), it was found to be statistically not significant.

Patients were scheduled to undergo diagnostic coronary angiography after evaluation with TDI on six mitral annular sites for three consecutive beats and then averaged for each site. Systolic (Vs'), early (Ve'), and late (Va') diastolic mitral annular VDIs among the six mitral annular sites were calculated, and data were collected, compiled, and analyzed.

Coronary angiography

CAD is a pathological process characterized by atherosclerotic plaque accumulation in the epicardial arteries, whether obstructive or nonobstructive. Obstructive CAD was defined as at least 50% stenosis of luminal diameter of the left main coronary artery (LMCA) or at least 70% stenosis of luminal diameter of at least one of the major epicardial coronary arteries. Nonsignificant lesion was defined as <30% stenosis of luminal diameter of any epicardial artery. Intermediate lesion was defined as 30%–50% stenosis of luminal diameter of LMCA, or 30%–70% stenosis of luminal diameter of one of the major epicardial arteries.[17] The ICMP was diagnosed for patients with ≥50% luminal diameter stenosis of the left main or ≥70% proximal left descending anterior coronary artery, or ≥2 major epicardial coronary arteries; otherwise, patients were diagnosed as having NICMP.[17]

Conventional M-mode, two-dimensional, and Doppler echocardiography

Each patient underwent echocardiography independently by an experienced cardiologist with transthoracic M-mode, two-dimensional (2D), and Doppler imaging using the Philips iE33 echo machine (Philips Medical Systems, Andover, MA, USA) before coronary angiography was performed. The person doing the echocardiography was blinded to the study protocol (only one cardiologist had done the echocardiography of the patients enrolled in the study). The echocardiography was done as per the American College of Cardiology/American Heart Association 2015 guidelines of chamber quantification, at the time of admission.[18] The LV end-diastolic volume, LV end-systolic volume, and LVEF were assessed on apical two-chamber and four-chamber views using the modified Simpson's rule.

Transmitral early (E) and late (A) diastolic flow velocities and deceleration time of early diastolic flow velocities were measured using the conventional Doppler echocardiography.

Pulsed-wave tissue Doppler imaging

In each patient, the sample volume used was positioned parallel to the transducer without angle correction on each mitral annular site. The values of mitral annular velocities were determined at six sites for three consecutive beats using three apical views (four-chamber, two-chamber, and apical long-axis views). The six mitral annular sites were anterior, inferior, septal, lateral, inferolateral, and anteroseptal areas at the central part of the junction of the left atrium and the left ventricle on each mitral annular site.

The two TDI parameters calculated for each patient included the average values of s', e', and a' of the six mitral annular sites and the VDIs of s', e', and a' (Vs', Ve', and Va'), defined as the ratio of the standard deviation (SD) to the average value of TDI velocity of s', a', and e'[13],[19] [Figure 1].
Figure 1: Various sites around the mitral annulus where tissue Doppler imaging (TDI) parameters are calculated[13]

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Statistical analysis

Quantitative data were expressed as mean value ± SD. Qualitative data were expressed as number (percentage). Comparison of qualitative data was assessed by the Chi-square test and comparison of quantitative data by Student's t-test. A receiver operating characteristic curve (ROC) was constructed to establish the sensitivity and specificity of cutoff values for TDI parameters. P < 0.05 was considered statistically significant. SPSS version 17.0 for Windows (SPSS, Inc., Chicago, IL, USA) was used for data analysis.

  Results Top

The present study included 100 patients with moderate LV dysfunction. All the participants underwent TDI, and the parameters were noted. They were categorized into ischemic cardiomyopathy (n = 60) and nonischemic cardiomyopathy (n = 40) groups after the conventional angiography. [Table 1] shows the baseline characteristics of the study participants.
Table 1: Comparison of all the baseline clinical characteristics between two groups

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The mean age of presentation was earlier in NICMP compared to ischemic cardiomyopathy, with a decade earlier presentation (43.4 ± 10.91 vs. 54.06 ± 10.40, P = 0.001). Patients were more symptomatic in ICMP group compared to NICMP group (24 vs. 19, P = 0.002). The CKD patients and those with PVD were more common in ICMP compared to NICMP [Table 1].

On comparison of the conventional 2D volumes, the left ventricle volumes were high in NICMP group compared to ICMP group (103.42 ± 7.82 vs. 101.08 ± 13.47, P = 0.002) and there was more depressed LVEF (29.90 ± 5.66 vs. 31.13 ± 5.61, P = 0.05). There was no significant difference in the mitral inflow velocities by conventional Doppler [Table 2].
Table 2: Comparison of conventional two-dimensional and Doppler echo findings

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The mean mitral tissue Doppler velocities were statistically significantly lower compared to those of the ischemic group. The VDIs, Ve', Va', and Vs', were low in NICMP group compared to the ICMP group (Ve'– 13.47 ± 3.36 vs. 22.50 ± 4.95, P = 0.001; Va'– 17.26 ± 4.11 vs. 19.78 ± 4.40, P = 0.005; Vs'– 15.50 ± 3.67 vs. 30.42 ± 3.32, P = 0.007, respectively [Table 2], [Figure 2].
Figure 2: Bar diagram showing the dispersion indices and ejection fraction among both groups. ICMP:Ischemic cardiomyopathy, SD: Standard deviation, NICMP: Non ischemic cardiomyopathy

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The values of VDI for the effective diagnosis of ICMP compared to the NICMP were plotted in the ROC characteristic analysis, and the area under the curve (AUC) and statistical significance for each value were calculated. A Ve' value of 17.35 cm/s for diagnosing ischemic cardiomyopathy had a sensitivity of 86.7% and a specificity of 87.5% with an AUC of 0.931. The cutoff values of Va' and Vs' above which diagnosing the ICMP was appropriate were 20.40 cm/s (sensitivity of 91.7% and specificity of 100%) and 25.40 cm/s (sensitivity of 50% and specificity of 75%), with AUC being 0.998 and 0.665, respectively [Figure 3].
Figure 3: Receiver operating curve (ROC) analysis for Ve', Vs', Va'. AUC: Area under the curve

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  Discussion Top

The results of this study demonstrated that patients with ICMP were older (54 ± 10) and had a history of typical angina more than those in the NICMP group.

The transmitral flow pattern remains the most effective means of routinely measuring diastolic function and predicting poor prognoses in patients with LV dysfunction.[20] However, these measurements cannot reveal any difference between patients with ICMP and NICMP.[21]

In our observation, among the TDI parameters, Em velocity is significantly lower in patients with ICMP than in NICMP group (P = 0.002), whereas there were no differences in Sm and Am velocities. In addition, progressive dilatation of the LV cavity and decrease of LVEF are common in patients diagnosed with NICM and in the latter stages of ICMP due to the re-modeling process, possibly explaining the findings in this study of the higher degree of LV volumes as well as lower ejection fractions.[22],[23]

In patients diagnosed with ICMP, a different level of abnormalities in longitudinal axis velocities can be expected because of the different level of ischemia with regions of stunned, hibernated myocardium and regions of postinfarction necrosis.[24] While depending on the number and extent of normally functioning myocytes, the regional function is reduced with myocyte necrosis and replacement fibrosis.[25]

Shan et al.[9] found that in patients diagnosed with ischemic LV dysfunction, Sm and Em velocities heavily depend on both the percentage of interstitial fibrosis and the myocardial beta-adrenergic receptor density, which is abnormal during HF.

The present study suggests that the VDI parameter could be useful as an additional noninvasive test for the differential diagnosis in patients with LV systolic dysfunction. SVDI, Vs'>25.40, and diastolic VDI, Ve'>17.35, were associated with the probability of ischemic cause of HF with good sensitivity and specificity.

In the study by Lee et al.,[19], systolic and late diastolic mitral annular velocities did not differ in the level of VDI. However, in the study by Plewka et al.,[13] all the three TDI parameters, systolic, early, and late diastolic, differed in the level of VDI. The results of the present study are on par with those seen in the study by Plewka et al.[13] [Table 3].
Table 3: Tissue Doppler imaging dispersion values compared to previous studies

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Previous studies have suggested that in patients with systolic dysfunction, abnormal coronary microcirculatory function may impair myocardial perfusion and cause metabolic changes. These studies also have demonstrated that the severity of reduction in myocardial blood flow predicts adverse outcomes, such as death and progressive HF, in patients with LV dysfunction, and is associated with the deterioration of LV systolic function over time.[26],[27] These studies may correspond to our results that a high Ve' value provides incremental and valuable information for prognostication in patients diagnosed with advanced LV dysfunction.

Study limitations

This is a single-center study with a limited number of patients. Baseline differences in confounding factors such as age, sex, and ejection fraction will affect the results in the present study. Continuing the study for a further period would have overcome this limitation. The differentiation of ICMP from NICMP solely based on the conventional angiographic criteria is not entirely precise as it is just a luminogram.

Cardiomyopathy of unknown cause may coexist with CAD so that the CAD may not be the cause of ventricular dysfunction.[26] Myocardial infarctions can occur at a site with nonobstructive CAD (at locations with 50% stenosis by angiography),[27] or secondary to spasm, cocaine, emboli, etc. Nonischemic cardiomyopathy etiology was not evaluated. Extrapolating the findings of the study to heterogeneous NICMP groups is limited. NICMP may originate from small-vessel disease and is not devoid of CAD.

Accurately recording the mitral annular diastolic velocity requires a parallel alignment between the ultrasound beam and the mitral annular sites on PWDTI. The angle of incidence may not be exactly parallel because of changes in mitral annular geometry due to a markedly dilated left ventricle, which was observed in some patients in this study. In this study, PWTDI was recorded at different mitral annular sites, not during the same beat. Recording different annular sites (septal and lateral) during the same beat is one advantage of color TDI, but this technique may be limited by underestimated velocities.[28] It is also possible that pharmacological treatment could influence TDI velocities and dispersion. Quintana et al.[29] showed significantly lower TDI systolic velocities in patients treated with beta-blockers. A limitation of velocity measurements by TDI is that these data may be affected by cardiac rotation or whole heart motion.

Evaluation in large number of patients and follow-up with change in the initial values to the medical therapy have to be carried out for the prognostic significance of the VDI.

  Conclusions Top

TDI echocardiography allows the quantitative, reproducible, and noninvasive analysis of LV function in patients with HF. TDI Em and the VDI of Vs', Ve', and Va differentiate ischemic and nonischemic cardiomyopathy. These parameters are complementary to clinical and standard echocardiographic findings and facilitate the qualification for invasive procedures in patients with difficult-to-diagnose cardiomyopathy.


We acknowledge the support of cardiology staff for effective conduction of the study.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

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  [Figure 1], [Figure 2], [Figure 3]

  [Table 1], [Table 2], [Table 3]


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