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Does the Post-Systolic Shortening of the Left Ventricle by Tissue Doppler Imaging Predict Coronary Artery Disease?


1 Department of Cardiovascular, Faculty of Medicine, Zagazig University, Zagazig, Egypt
*Corresponding author: Hanan Radwan, MD, Lecturer of Cardiology, Faculty of Medicine, Zagazig University, Zagazig City, Sharkia Governorate, Egypt. Tel: +20-1066381472, +20-1093310207, E-mail: hananradwan67@yahoo.com.
Archives of Cardiovascular Imaging. 4(2): e41788 , DOI: 10.5812/acvi.41788
Article Type: Research Article; Received: Mar 30, 2016; Revised: Apr 16, 2016; Accepted: Apr 30, 2016; epub: May 28, 2016; collection: May 2016

Abstract


Background: Abnormalities in the velocity and pattern of myocardial shortening on tissue Doppler imaging (TDI) have been proposed to aid in the noninvasive diagnosis of coronary artery disease (CAD).

Objectives: We investigated the diagnostic value of post-systolic shortening (PSS), a delayed ejection velocity of the myocardium after the closure of the aortic valve, on TDI in the diagnosis of CAD among patients with chest pain and normal resting wall motion on standard 2D echocardiography.

Methods: Eighty consecutive patients (49% female) with typical ischemic chest pain but without prior myocardial infarction, coronary revascularization, arrhythmia, or heart failure, who had no regional wall motion abnormalities on resting echocardiography and who were scheduled to undergo coronary angiography, were selected. TDI was performed in each patient before coronary angiography at 2 levels (basal and mid left ventricle [LV]) in each of the 4 LV walls (i.e., septal, anterior, inferior, and lateral). Coronary angiography was performed and interpreted per standard clinical protocols.

Results: Compared to the patients with normal coronaries, those with angiographic CAD showed significantly increased myocardial isovolumic relaxation time (IVRT) velocity (P < 0.001) and significantly prolonged IVRT (P < 0.001) at the septal, anterior, inferior, and lateral LV walls. With a cutoff value > 4.0 m/sec, a positive PSS velocity had about 65% sensitivity and 85% specificity with a positive predictive value > 90% in predicting angiographic CAD.

Conclusions: Among patients with chest pain and normal LV wall motion on 2D echocardiography, a prominent and prolonged IVRT on TDI may help predict the presence of significant CAD.

Keywords: Coronary Artery Disease; Echocardiography; Tissue Doppler Imaging; Post-Systolic Shortening

1. Background


Several noninvasive techniques such as exercise electrocardiography, myocardial scintigraphy, and echocardiography are routinely used for the detection of coronary artery disease (CAD). These modalities, however, have several inherent limitations in every day clinical practice. For example, exercise electrocardiography, although the most widely used method, has moderate sensitivity and specificity for the detection of CAD (1, 2). Myocardial scintigraphy may have higher sensitivity and specificity for the detection of CAD, but it is operationally a complex test and its use is generally limited to specialized institutions (3). Echocardiography is an easily available, reliable, and safe imaging modality proven to be highly useful in the identification and management of patients with CAD. Traditionally, the diagnosis of CAD on echocardiography has been based on the demonstration of segmental abnormalities in wall motion in the resting state or during exercise or pharmacological stress (4). Nonetheless, a substantial number of patients who eventually go on to develop different clinical syndromes of CAD do not display segmental wall motion abnormalities, either at rest or during stress testing. Furthermore, certain patient characteristics (e.g., some cases of left bundle branch block) may limit the interpretation of abnormalities in wall motion, thereby precluding a proper diagnosis of CAD (5-7). Identifying other more sensitive echocardiographic markers of CAD is, therefore, potentially interesting.

Spectral tissue Doppler imaging (TDI) is a simple echocardiographic technique that provides velocity measurements of the myocardial wall in standard cardiac ultrasound diagnostic equipment (8, 9). The velocity of shortening during systole is reduced in the ischemic myocardial tissue with abnormal deformation and deformation rates (10, 11). Additionally, post-systolic shortening (PSS) a delayed ejection motion of left ventricular (LV) myocardium after the aortic valve closure during the isovolumic relaxation (IVR) phase has been demonstrated in the ischemic myocardium in human (12, 13)as well as in experimental animal models (14). Several studies have suggested that a positive PSS velocity, at rest or during dobutamine stress, may be a marker of the severely ischemic myocardium (15, 16).

The present study was conducted to examine the diagnostic value of spectral TDI, especially PSS, in the noninvasive diagnosis of CAD among patients with chest pain and normal resting wall motion on standard 2D echocardiography.

2. Methods


The study was done in the cardiology department of Zagazig University hospital, Egypt. Eighty consecutive patients (39 females) scheduled to undergo coronary angiography for further evaluation of typical ischemic chest pain were selected. Patients with prior myocardial infarction (n = 12), coronary revascularization (n = 7), arrhythmia or pacing rhythm (n = 3), and cardiomyopathy with heart failure (n = 6) were excluded as were patients who showed regional wall motion abnormalities on resting echocardiography (n = 14) or who had inadequate ultrasound images (n = 2). TDI, performed in each patient before coronary angiography, was used to measure myocardial tissue velocity at 2 levels (basal LV and mid LV) in each of the 4 LV walls (i.e., anterior, inferior, lateral, and septal).

After written informed consent, complete history including history of CAD risk factors was obtained from each participant. Hypertension was defined as a systolic blood pressure ≥ 140 mmHg; a diastolic blood pressure ≥ 90 mmHg; or by the self-report of physician diagnosis with the concomitant use of antihypertensive medications (17). Diabetes mellitus was diagnosed as per the 2004 criteria of the American diabetic association as fasting blood sugar ≥ 126 mg% or 2-hour post-prandial blood sugar ≥ 200 mg% (18). Dyslipidemia was diagnosed according to the criteria of the national cholesterol education program adult treatment panel III or when the patients were taking lipid-lowering agents (19). Family history of premature CAD was considered positive on the basis of diagnosed CAD in a male first-degree relative before age 55 years or in a female first-degree relative before age 65 years (20). Smoking was defined as a current or former smoker having quit < 2 years previously. Standard physical examination was performed in each patient, and 12-lead surface ECG was obtained. All patients were in sinus rhythm.

2.1. Echocardiography

Echocardiographic evaluation was done using commercially available equipment (HP- 5500, Sonos Ultrasound) with a 2- to 3-MHz transducer. The examinations were done with the patient in the left lateral position utilizing the left parasternal long-axis and short-axis views and the apical 4-, 5-, and 2-chamber views. 2D, M-mode, and Doppler echocardiographic assessment was performed for all patients. Left atrial (LA) and LV internal dimensions were measured, and LV ejection fraction and fractional shortening were calculated. Regional wall motion analysis was performed in accordance with the American society of echocardiography’s guidelines, and patients with regional wall motion abnormalities were excluded (21). The assessment of LV diastolic function was performed using Doppler examination of the mitral valve flow pattern. The transducer was positioned in the apical 4-chamber view. The sample volume marker was positioned at the level of the tips of the mitral valve leaflets.

2.2. Tissue Doppler Imaging

Spectral TDI measurements were done at annular and mid-LV levels for LV walls in SAIL format (i.e., septal, anterior, inferior, and lateral) in the apical 4- and 2-chamber views (8 points in each patient). A fixed sampling gate of 8 mm was placed equidistant between the endocardial and epicardial borders. The spectral Doppler signal parameters were adjusted to obtain adequate Nyquist limits using the lowest filter settings. Gain was adjusted to minimize noise and to eliminate the signals produced by the blood flow, with continuous ECG monitoring so as to time the cardiac cycle events. From spectral TDI tracings at each point of interrogation, peak myocardial tissue velocity was measured at 5 time points of 1 cardiac cycle: during the isovolumic contraction (IVC) phase (IVC velocity, which begins with the appearance of the QRS complex), during the systolic ejection phase (S velocity, which begins after the R wave and extends to the end of the T wave), during the IVR phase (PSS velocity), during early diastolic filling (E’ velocity, which follows the T wave of ECG), and during the atrial contraction phase (A’ velocity, which follows the P wave of ECG). The velocities were recorded for 5 cardiac cycles at a sweep speed = 50 mm/s. Peak PSS velocity and the duration of isovolumic relaxation time (IVRT) were recorded. PSS velocity was defined as an upward spike found between the end of the systolic ejection phase and the onset of the early diastolic relaxation phase and PSS duration (IVRT from the end of the wave S’ to the beginning of the wave E’) (Figure 1).

Figure 1.
Example of a Normal PW-TDI Spectral Curve
2.3. Coronary Angiography

Coronary angiography was performed by experienced cardiologists for clinical indications as deemed necessary by the treating physician and was interpreted by the consensus opinion of 2 physicians, who were unaware of the TDI findings. A separate written informed consent was obtained from each patient, and the procedure was performed in standard manner using the retrograde percutaneous transfemoral approach. Briefly, under septic precautions, femoral arterial access was obtained using the Judkins technique; the femoral sheath was placed; standard left and right coronary catheters preloaded with 0.035-inch tapered, movable core J-wires were advanced through the sheath; and coronary angiography was performed in multiple projections. The coronary angiograms were interpreted off-line by the cardiologist in standard clinical format. For the present study, a coronary artery stenosis was considered significant if it caused > 70% luminal stenosis. The presence of CAD, the number of affected arteries, and the arteries involved were noted.

2.4. Ethics

An informed written consent was obtained from each patient according to the declaration of Helsinki and the rules of the local ethics committee of the faculty of medicine, Zagazig University, Egypt.

2.5. Reproducibility of Measurements

Ten patients were randomly selected to determine the reproducibility of the measurements of the duration of a positive IVR. Spectral TDI tracings were analyzed by a single observer on 2 occasions (intraobserver variability) and by 2 independent observers (interobserver variability). The mean values of the absolute difference in the measurements were 12 ± 24 ms (intraobserver variability) and 14 ± 33 ms (interobserver variability) for the duration of a positive IVR.

2.6. Statistical Analysis

Statistical package for social sciences, version 19.0 (Chicago, IL) was used for data analysis. The data are presented as means± SDs for the continuously distributed variables or as numbers (%) for the categorical variables. The Student t-test and the χ2 test, as appropriate, were used to compare the variables between the different groups. The receiver operating characteristics (ROC) curve was drawn upon to identify the cutoff values for PSS velocity in different LV segments to identify patients with angiographic CAD. The highest values of basal and apical PSS velocities at each LV wall were employed to determine whether PSS velocity at the corresponding wall exceeded the empirically identified cutoff value. The diagnostic performance of PSS in detecting CAD was assessed by comparison against the angiographic findings as the gold standard using sensitivity data and the Cohen kappa statistic. The values are presented as means ± SDs or as numbers (%) unless otherwise specified. Statistical significance was determined as a P value < 0.05.

3. Results


Among the 80 patients selected for this study, 60 were found to have significant CAD on angiography. Among these, 46 (77%) had disease in the left anterior descending artery or its main diagonal branch, 13 (22%) in the left circumflex or its main obtuse marginal branch, and 11 (18%) in the right coronary artery. Seventy-two percent, 18%, and 10% patients respectively had 1-, 2-, and 3-vessel disease; the left main was not involved in any patient. Compared to the patients without CAD, the patients with CAD were older, were more often men, and had a significantly higher prevalence of major risk factors including smoking, dyslipidemia, and family history of premature CAD, though not hypertension or diabetes (Table 1).

Table 1.
Demographic and Other Characteristics of the Study Subjectsa

On echocardiography, LA size and LV internal dimensions were similar between the patients with CAD and those without CAD. Global LV systolic function was also similar between the 2 groups. The patients with CAD more often had diastolic LV dysfunction than those without CAD (Table 1).

On spectral TDI, the patients with CAD displayed generally lower average systolic tissue velocities and higher average tissue velocities during IVC than the patients in the non-CAD group (Tables 2 - 6). The patients with CAD had significantly higher PSS velocities than those without CAD at all the myocardial segments interrogated (i.e., septal (Table 2), anterior (Table 3), inferior (Table 4), and lateral (Table 5)). Further, the duration of PSS was significantly greater among the patients with CAD than those without CAD at all studied myocardial segments (Figure 2A and 2B). The patients with CAD also had a lower mitral annulus E’ velocity and a greater A’ velocity than those without CAD, suggestive of diastolic dysfunction in the former group.

Table 2.
Tissue Doppler Findings at Left Ventricular Septal Wall
Table 3.
Tissue Doppler Findings at Left Ventricular Anterior Wall
Table 4.
Tissue Doppler Findings at Left Ventricular Inferior Wall
Table 5.
Tissue Doppler Findings at Left Ventricular Lateral Wall
Table 6.
Diagnostic Performance of PSS Velocity in the Detection of Significant CADa
Figure 2.
A, Myocardial Velocity (V) by Spectral Tissue DOPPLER Imaging; B, Tissue Doppler Imaging Parameters in the Patients With Coronary Artery Disease

In the sensitivity analyses, using cutoff values of 4.4 m/s, 4.8 m/s, 4.1 m/s, and 4.2 m/s to define significantly positive PSS velocity for the septal, lateral, anterior, and inferior LV walls respectively we found that the sensitivity in predicting CAD ranged from 63% to 73% while specificity was between 80% and 85%. PSS velocity had a positive predictive value of about 92% but the negative predictive value was only between 40% and 50%. The coefficient of agreement (kappa statistic) between positive PSS velocity and angiography in identifying the patients with CAD ranged from 0.57 at the anterior wall to 0.67 at the septal wall (Figure 3, Table 6).

Figure 3.
Receiver Operating Characteristics (ROC) Curve for Predicting Significant Coronary Artery Disease Using Positive Post-Systolic Shortening Velocity

4. Discussion


Traditionally, TDI has been used to evaluate diastolic function and LV filling pressures (23). Clinical studies have shown that TDI confers diagnostic and prognostic information incremental to conventional echocardiography in some cardiac diseases (24). In the present study, we demonstrated that abnormalities on TDI especially a prominent PSS velocity strongly correlated with the presence of angiographically significant CAD. Our data suggest that TDI could be a useful adjunct in the noninvasive diagnosis of CAD in patients presenting with chest pain.

While the detection of regional wall motion abnormalities on standard 2D echocardiography provides an easy and confident biomarker of CAD, the detection of significant CAD in the face of normal segmental wall motion continues to be a challenge. Stress echocardiography improves the sensitivity and specificity of testing (25), but it is technically more cumbersome and the subjective evaluation of regional wall motion abnormalities necessitates highly trained personnel. On the other hand, TDI is a simple and easily available modality that can be performed by the bedside without the need for stress testing or contrast injections. The results of the present study showed that the patients with angiographically significant CAD had a significantly increased myocardial tissue velocity during the IVR phase (PSS) compared to those without angiographic CAD; the duration of IVR was also significantly more prolonged in the patients with CAD than in those with normal epicardial coronary arteries.

In the non-ischemic ventricle, the IVC period is dominated by a positive velocity spike of a short duration, which represents a slight longitudinal shortening before LV ejection. During IVRT, there is a pattern opposite to that during the IVC period with a negative velocity spike of a short duration representing a slight elongation before the onset of filling. Possibly, the twisting and untwisting effects may have contributed to the IVC and IVR velocities. During severe ischemia, early-ejection Doppler velocities remain positive and, therefore, do not reflect the marked impairment of myocardial function. The mechanism of the positive early-ejection velocity in the dyskinetic myocardium is not clear, but it might represent cardiac translational motion or tethering effects resulting from contractions in the other myocardial segments. The dominant systolic velocity component during severe ischemia is a large negative velocity spike during the IVC period. During severe ischemia, IVR velocities reverse and a large positive velocity component (PSS of the ischemic myocardium) persists throughout the entire IVR period, and in some cases continues after the early-diastolic LA/LV pressure crossover. Accordingly, in the severely ischemic and dyskinetic myocardium, IVC and IVR velocities are the strongest markers of myocardial dysfunction. Myocardial ejection velocities have very low amplitudes and appear to be influenced by tethering effects and/or translational motion (15).

Abnormalities in myocardial tissue velocities in the ischemic myocardium have been reported by several investigators (10, 11, 15, 26-31). In a canine model, Edvardsen et al. (15) studied the effect of ischemia on cardiac pressure and myocardial tissue velocities and found that moderate ischemia caused a reduction in regional systolic shortening and in peak systolic velocities, whereas severe ischemia induced systolic lengthening with preserved positive peak myocardial velocity during ejection in anesthetized dogs. Lee et al. (28) found significantly lower myocardial S and mitral annular E’ velocities on TDI in patients with stable CAD than in controls subjects without CAD. In a recent study involving 84 patients with angina pectoris with a normal LV ejection fraction, Hoffman et al. (31) found reduced average S and average E’ velocities on color TDI in patients with reversible ischemia on myocardial single-photon emission computed tomography (SPECT) imaging and angiographic CAD but not in patients with false-positive SPECT imaging. Our observation of reduced myocardial S velocity and mitral annulus E’ velocity among patients with CAD is consistent with these earlier reports.

A particularly interesting finding in the present study was the significantly increased velocity and duration of IVRT in the patients with CAD. PSS is a delayed LV myocardial ejection motion post aortic valve closure. About 2 decades ago, Kondo et al. (27) using digital subtraction high-frame-rate echocardiography, demonstrated that a delayed outward LV wall motion in the IVR phase was indicative of CAD. Later, Derumeaux et al. (10) found that a prominent PSS velocity on spectral TDI indicated severely ischemic myocardium. Subsequently, several other investigators reported the prominence of PSS in the ischemic myocardium (12-16, 29, 32, 33). Edvardsen et al. (15) noted that severe myocardial ischemia induced by the clamping of the left anterior descending coronary artery induced a prominent PSS. Voigt et al. (16) found that on dobutamine stress echocardiography, PSS was as a marker of the presence of significant CAD. In a study of 138 patients by Onishi et al. (33) a positive PSS velocity on spectral TDI at annular and mid LV levels in the apical 4- and 2-chamber views at rest predicted the presence of significant CAD on subsequent thallium-201 myocardial perfusion SPECT and coronary angiography. In a more recent study, Onishi et al. (34) studied 59 patients with suspected CAD with normal LV wall motion at rest using TDI; PSS velocity was an independent predictor of the presence of significant CAD.

In the present study, TDI was found to have a reasonably good diagnostic performance for detecting CAD. Overall, with a velocity cutoff > 4 m/s for PSS, the sensitivity in predicting CAD was between 63% and 73% and specificity was between 80% and 85%. In the sample population that consisted of patients with chest pain, PSS had a positive predictive value of about 92% but the negative predictive value was only between 40% and 50%. Interestingly, there was a reasonably good agreement between PSS and angiography in identifying patients with CAD with the kappa statistic ranging from 0.57 to 0.67.

Our finding of a more prominent IVRT in the patients with CAD than in those without CAD is also consistent with several earlier observations (33-35). Maciel et al. (35) analyzed 168 segments of the LV using TDI and found that patients with CAD diagnosed with coronary angiography, SPECT, or dobutamine stress echocardiography had a positive PSS velocity with an IVRT duration between 80 and 120 ms. Onishi et al. (34) also found that a prolonged duration of IVRT was positively correlated with the presence of significant lesions on coronary angiography.

Thus, the results of the present study indicated that among the patients presenting with chest pain, those who ultimately were found to have angiographically significant CAD displayed a characteristic pattern on TDI: reduced systolic tissue velocity, prominent and prolonged IVRT of the LV, and reduced E’ velocity at the mitral annulus. Taken together, our findings suggest that TDI could be a useful adjunct in the noninvasive diagnosis of CAD among patients with chest pain who have normal wall motion on standard 2D echocardiography. The demonstration of the characteristic pattern of abnormalities on TDI and, in particular, a prominent and prolonged IVRT of the LV myocardium could help positively identify patients likely to have significant CAD and thereby improve cardiac risk stratification and patient selection for invasive diagnostic procedures. Accordingly, TDI could be incorporated into the diagnostic armamentarium in chest pain pathways to more accurately triage patients in the emergency and outpatient clinics.

4.1. Limitations

A limitation of the present study is its relatively small sample size. Patients with low ejection fractions or earlier myocardial infarction, who constitute a substantial number of those referred for coronary angiography in every day practice, were not included. These factors could limit the generalizability of our findings. Further, due to the high prevalence of CAD in the study sample, the negative predictive value of TDI was small. Larger studies including subjects from the general community would be needed to more accurately explore the performance of TDI in the diagnosis of CAD. We only considered angiographically significant luminal narrowing in epicardial coronary arteries to define CAD. However, research has shown that myocardial infarction often develops at the site of non-flow-limiting coronary lesions. Finally, our study may not be considered immune to some inherent limitations of TDI as an imaging modality. For instance, the rotation of the heart in addition to its apical-basal movement and tethering of circumscribed dysfunctional myocardial segments by normal adjacent segments may affect the assessment of regional myocardial function. Corrected PSS duration (PSS c) was not calculated because the heart rate data were not available. As there is myocardial velocity heterogeneity and the data on the Doppler signals in IVC, IVR phases (in the normal human population) are lacking. Consequently, more investigations are needed on the utility of TDI focusing on the IVR and IVC phases and describing their Doppler signal (positivity or negativity) or their clinical implications.

Acknowledgments

The authors thank the staff of the cardiovascular department of Zagazig University Hospital for their expert input and detailed evaluations. Many thanks are also due to our patients, who participated in the study.

Footnotes

Conflict of Interests: The authors declare that there is no conflict of interest.
Funding/Support: This research did not receive any specific grant from any funding agency in the public, commercial, or not-for-profit sector.

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Table 1.

Demographic and Other Characteristics of the Study Subjectsa

CharacteristicStudy GroupP Value
CAD (n = 60)Non-CAD (n = 20)
Age, y62.1 ± 5.555.6 ± 8.6< 0.001
Sex0.053
Female33 (55)6 (30)
Male27(45)12(70)
Diabetes27 (45)12 (60)0.24
Hypertension40 (66.7)10 (50)0.18
Smoking29 (48.3)4 (20)0.026
Dyslipidemia35 (58.3)4 (20)0.003
Family history33 (55)6 (30)0.053
SBP, mm Hg130 ± 16129 ± 150.84
DBP, mm Hg80 ± 879 ± 70.77
LA size, mm34.7 ± 3.735.3 ± 3.30.49
LVED, mm45.7 ± 3.345.0 ± 3.40.37
LVES, mm27.3 ± 2.727.2 ± 2.50.92
LVEF, %70.4 ± 5.568.9 ± 5.40.29
FS, %39.2 ± 3.138.2 ± 3.10.24
Mitral E/A ratio0.71 ± 0.10.72 ± 0.10.87
Abbreviations: CAD, coronary artery disease; DBP, diastolic blood pressure; FS, fractional shortening; LA, left atrium; LVED, left ventricular end-diastolic diameter; LVEF, left ventricular ejection fraction; LVES, left ventricular end-systolic diameter; SBP, systolic blood pressure.
a Values are presented as means ± SD for the continuously distributed variables and as No. (%) for the categorical variables.

Table 2.

Tissue Doppler Findings at Left Ventricular Septal Wall

VariableStudy GroupP Value
CAD (n = 60)Non-CAD (n = 20)
Mid-Level
S velocity, m/s8 ± 2.413.2 ± 2.3< 0.001
IVC velocity, m/s10 ± 39.1 ± 2> 0.05
PSS velocity, m/s4.3 ± 3.44 ± 1.6< 0.05
PSS duration, ms82.5 ± 6716 ± 39< 0.001
E’ velocity, m/s9.7 ± 2.410.6 ± 3.1NS
A’ velocity, m/s12.7 ± 4.313.7 ± 3NS
Basal Level
S velocity, m/s10.5 ± 2.911.7 ± 2.1> 0.05
IVC velocity, m/s11.4 ± 48.5 ± 2< 0.05
PSS velocity, m/s7.2 ± 4.22.4 ± 0.95< 0.001
PSS duration, ms107.7 ± 5416.5 ± 40< 0.001
E’ velocity, m/s11 ± 2.513.6 ± 2.4< 0.001
A’ velocity, m/s16.1 ± 4.69.6 ± 2.5< 0.001
Abbreviations: CAD, coronary artery disease; IVC, velocity of isovolumic contraction; NS, not significant; PSS, post-systolic shortening.

Table 6.

Diagnostic Performance of PSS Velocity in the Detection of Significant CADa

Left Ventricular Territory Examined
Septal WallLateral WallAnterior WallInferior Wall
PSS velocity cutoff, m/s4.44.84.14.2
Sensitivity63.369.563.373.3
Specificity85.08580.080.0
PPV92.892.290.491.6
NPV44.7051.242.150.0
Patients with positive PSS
CAD group37 (61.6)34 (56.6)52 (86.7)40 (73.3)
Non-CAD group3 (15.5)3 (15.0)2 (10.0)3 (15.0)
P< 0.001< 0.001< 0.001< 0.001
ƙ0.670.690.570.61
Abbreviations: CAD, coronary artery disease; NPV, negative predictive value; PPV, positive predictive value; PSS, post-systolic shortening; TDI, tissue Doppler imaging.
a Values are expressed as No. (%) or %.

Table 3.

Tissue Doppler Findings at Left Ventricular Anterior Wall

VariableStudy GroupP Value
CAD (n = 60)Non-CAD (n = 20)
Mid-Level
S velocity, m/s6.9 ± 1.912.2 ± 2.5< 0.001
IVC velocity, m/s9.1 ± 3.29.5 ± 2.4> 0.05
PSS velocity, m/s4.1 ± 3.51.1 ± 2.8< 0.05
PSS duration, ms82.4 ± 66.617.3 ± 4.1< 0.001
E’ velocity, m/s8.7 ± 2.410.8 ± 2.9< 0.05
A’ velocity, m/s10.2 ± 3.812.2 ± 4.4> 0.05
Basal Level
S velocity, m/s9.5 ± 3.59.8 ± 2.9> 0.05
IVC velocity, m/s11.7 ± 3.38.7 ± 2< 0.001
PSS velocity, m/s6.3 ± 5.51.2 ± 2.7< 0.001
PSS duration, ms102.5 ± 43.320.6 ± 42.4< 0.001
E’ velocity, m/s12.2 ± 3.113.4 ± 3.1> 0.05
A’ velocity, m/s16.2 ± 5.39.9 ± 3.4< 0.001
Abbreviations: CAD, coronary artery disease; IVC, velocity of isovolumic contraction; PSS, post-systolic shortening.

Table 4.

Tissue Doppler Findings at Left Ventricular Inferior Wall

VariableStudy GroupP Value
CAD (n = 60)Non-CAD (n = 20)
Mid-Level
S velocity, m/s9 ± 3.49.9 ±2.7> 0.05
IVC velocity, m/s9 ± 36.8 ± 2.2< 0.05
PSS velocity, m/s5.3 ± 3.51 ± 4.9< 0.001
PSS duration, ms102.8 ± 69.516 ± 39.2< 0.001
E’ velocity, m/s9 ± 2.29.5 ± 3> 0.05
A’ velocity, m/s11.9 ± 3.413.1 ± 2.9> 0.05
Basal Level
S velocity, m/s9.6 ± 3.59.8 ± 2.9> 0.05
IVC velocity, m/s11.7 ± 3.48.8 ± 2< 0.001
PSS velocity, m/s6.3 ± 5.61.3 ± 2.8< 0.001
PSS duration, ms82.9 ± 55.921.8 ± 44.9< 0.001
E’ velocity, m/s11.2 ± 2.312.7 ± 2.4< 0.05
A’ velocity, m/s15.7 ± 4.310.5 ± 3< 0.001
Abbreviations: CAD, coronary artery disease; IVC, velocity of isovolumic contraction; PSS, post-systolic shortening.

Table 5.

Tissue Doppler Findings at Left Ventricular Lateral Wall

VariableStudy GroupP Value
CAD (n = 60)Non-CAD (n = 20)
Mid-Level
S velocity, m/s7.9 ± 312.9 ± 2.9< 0.001
IVC velocity, m/s10.2 ± 38.8 ± 2.4< 0.05
PSS velocity, m/s4.6 ± 3.72.6 ± 0.85< 0.001
PSS duration, ms84.5 ± 6434 ± 11< 0.001
E’ velocity, m/s10.6 ± 3.411 ± 2.6< 0.05
A’ velocity, m/s10.3 ± 3.39 ± 3.2> 0.05
Basal Level
S velocity, m/s11.3 ± 4.413.1 ± 2.9> 0.05
IVC velocity, m/s11.6 ± 3.910.5 ± 3.3> 0.05
PSS velocity, m/s6.9 ± 4.91.5 ± 3.2< 0.001
PSS duration, ms96.5 ± 50.221 ± 43< 0.001
E’ velocity, m/s12.4 ± 4.113.6 ± 2.9> 0.05
A’ velocity, m/s16.1 ± 4.610.3 ± 2.6< 0.001
Abbreviations: CAD, coronary artery disease; IVC, velocity of isovolumic contraction; PSS, post-systolic shortening.

Figure 1.

Example of a Normal PW-TDI Spectral Curve
Note the immediate representation of the mechanical events in the various phases of the cardiac cycle. It is possible to measure time intervals using the traces of the ECG and/or the phonocardiogram as reference. (See the panel below). Sm, positive wave of systolic contraction; Em, negative early diastolic wave; Am, negative end-diastolic wave; IVCT, isovolumetric contraction time or pre-contraction; IVRT, isovolumetric relaxation time (Citro et al. (22)).

Figure 2.

A, Myocardial Velocity (V) by Spectral Tissue DOPPLER Imaging; B, Tissue Doppler Imaging Parameters in the Patients With Coronary Artery Disease
Prominent positive myocardial V during the isovolumic relaxation phase (IVR). Show revered E/A ratio, IVR velocities reverse and a large positive velocity component (PSS) persists throughout the entire IVR period and increased duration of IVRT. 1, E velocity; 2, PSS, post-systolic shortening; 3, IVRT, isovolumic relaxation time.

Figure 3.

Receiver Operating Characteristics (ROC) Curve for Predicting Significant Coronary Artery Disease Using Positive Post-Systolic Shortening Velocity