Graphical abstract
Keywords: Stress echocardiography, Ultrasound contrast agent, Myocardial contrast echocardiography, Dilated cardiomyopathy
Highlights
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UEAs in stress echocardiography improve endocardial definition and RWMA detection.
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MCE provides diagnostic information incremental to wall motion assessment.
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MCE helps differentiate ischemic vs nonischemic cardiomyopathy.
Introduction
In current guidelines, the use of ultrasound-enhancing agents (UEAs) is recommended to enhance endocardial definition and to accurately determine global and regional left ventricular (LV) function.1 Their use in stress echocardiography has improved the feasibility and reliability of detecting regional wall motion abnormality (RWMA).2 With dedicated machine settings, myocardial contrast echocardiography (MCE) can also be performed to assess resting and stress myocardial perfusion. We present a case that illustrates the benefits of UEAs in the evaluation of LV volumes and ejection fraction, RWMA, and myocardial perfusion in a patient undergoing treadmill exercise stress echocardiography for suspected coronary artery disease (CAD).
Case Presentation
A 52-year-old woman was referred to the cardiology clinic with a 1-year history of exertional breathlessness and atypical chest pain. They had a medical history of type 2 diabetes mellitus, hypercholesterolemia, and hypertension. They were an ex-smoker (30 pack-years). There was no family history of cardiovascular disease. Medications included perindopril, metformin, simvastatin, allopurinol, and esomeprazole. On clinical examination, they had an elevated body mass index of 31.9 kg/m2, a regular heart rate of 94 beats/min, and blood pressure of 132/70 mm Hg. Heart sounds were normal, with no murmurs and no peripheral edema. The chest was clear to auscultation, without any wheeze or crackles. Electrocardiography demonstrated sinus rhythm at 94 beats/min with left-axis deviation and left bundle branch block (LBBB), with a QRS duration of 144 ms. Laboratory analysis revealed normal full blood count, renal profile, liver function, and thyroid function test results. Brain natriuretic peptide was 75 ng/L (0-111 ng/L), total cholesterol was 5.5 mmol/L, and low-density lipoprotein was mildly elevated at 3.5 mmol/L.
Because of the cardiovascular risk factors and clinical presentation, resting and stress echocardiography was performed to evaluate LV function and determine whether there was any evidence of inducible ischemia. At rest, the LV cavity was mildly dilated, with mild increased LV wall thickness (11 mm). Precontrast images showed suboptimal endocardial definition, particularly of the anterior wall. Images were improved following intravenous UEA (sulfur hexafluoride) administration (Figure 1, Video 1). LV volumes were higher with contrast (LV end-diastolic volume index 71 mL/m2, LV end-systolic volume index 40 mL/m2) than noncontrast imaging (56 and 32 mL/m2, respectively). There was mild impairment of LV systolic function, with an LV ejection fraction (LVEF) of 44%. Global longitudinal strain was markedly reduced at −6%. There was resting hypokinesis of the midapical septum and midapical anterolateral walls. Right ventricular size and systolic function were normal, and there was no significant valvular disease. The patient performed only 3.5 minutes of Bruce-protocol treadmill exercise, reaching 103% of the age-predicted target heart rate. The test was terminated by dyspnea rather than chest pain. Postexercise echocardiographic images were acquired using an initial small intravenous bolus of ultrasound contrast followed by a continuous infusion. Images were rapidly acquired for LV regional wall motion analysis using a very low mechanical index (MI) and quad-screen display. This was immediately followed by myocardial perfusion assessment using triggered replenishment of end-systolic images at a 1:1 trigger. All imaging was completed within 90 to 120 seconds of the termination of exercise. The findings revealed marked end-systolic LV cavity dilatation (LV end-diastolic volume index 72 mL/m2, LV end-systolic volume index 64 mL/m2) and global deterioration in systolic function, with an LVEF of 22% (Figure 2, Video 2). The RWMA involving the midapical septum and midapical anterolateral walls observed at rest persisted following exercise. MCE revealed normal perfusion within all myocardial territories (Figure 3, Video 3). The impression was therefore that of a nonischemic cardiomyopathic process. Cardiac computed tomography demonstrated nonobstructed coronary arteries and an Agatston coronary artery calcium score of zero (Figure 4). Subsequent cardiovascular magnetic resonance (CMR) imaging confirmed mild LV dilatation (LV end-diastolic volume index 97 mL/m2, LV end-systolic volume index 53 mL/m2) and an LVEF of 46%. Adenosine stress perfusion CMR imaging showed no demonstrable evidence of microvascular dysfunction. There was no myocardial fibrosis or scarring seen with late gadolinium enhancement. The working diagnosis was that of a nonischemic dilated cardiomyopathy (DCM), and the patient was referred to the inherited cardiac conditions clinic for genetic counseling and heart failure optimization. Echocardiography at 18 months initially showed ongoing mild LV global systolic dysfunction with an LVEF of 46%. Following the optimization of oral heart failure therapy, repeat CMR at 3 years revealed a normalized LVEF of 60%.
Figure 1.
Two-dimensional transthoracic echocardiography without (A-C) and with (D-F) administration of a UEA, apical four-chamber (A4ch), apical three-chamber (A3ch), and apical two-chamber (A2ch) end-diastolic (ED) and end-systolic (ES) views acquired at baseline (rest stage), demonstrates suboptimal unenhanced endocardial definition (arrows) that improved after contrast, mild LV dilation, and mildly reduced global LV systolic function with regional hypokinesis in the midapical septum and anterolateral wall segments that is better appreciated after UEA administration.
Figure 2.
Two-dimensional transthoracic echocardiography with administration of a UEA, apical four-chamber (A4ch) and apical two-chamber (A2ch) end-diastolic (ED) and end-systolic (ES) views acquired at baseline (left) and after 3.5 minutes of treadmill exercise (right), demonstrate marked LV cavity dilatation and severely reduced global LV systolic function without new RWMAs.
Figure 3.
MCE (continuous infusion) using triggered replenishment interval at a 1:1 trigger and low MI (0.09-0.11) on postexercise end-systolic displays, apical four-chamber (A4ch), apical three-chamber (A3ch), and apical two-chamber (A2ch) views, demonstrates the bright white frame that masks the LV myocardium during a high-MI (1.0) flash sequence (A), homogenous black myocardium immediately after flash imaging, which confirms microbubble destruction (B); and frame-by-frame systolic imaging with progressive replenishment of contrast within all segments of the myocardium (C, D); 2 seconds after flash imaging, there is homogenous opacification of the myocardium without a visualized subendocardial perfusion defect.
Figure 4.
Cardiac computed tomography, multiplanar curvilinear coronary reconstructions of the left anterior descending coronary artery (LAD), first diagonal branch (D1), left circumflex coronary artery (LCX), and right coronary artery (RCA), demonstrates nonobstructed epicardial coronary arteries.
Discussion
This case highlights the versatility and added value of UEAs to (1) enhance LV endocardial definition for the accurate measurement of LV volumes and LVEF; (2) evaluate stress-induced RWMAs; (3) assess myocardial perfusion during stress echocardiography; (4) improve the feasibility of performing stress echocardiography in obese patients; and (5) allow comprehensive ischemia testing in LBBB, evaluating both wall motion and perfusion.
As expected, LV volumes were higher with contrast-enhanced echocardiography compared with standard two-dimensional imaging, enabling accurate tracing of the compacted LV myocardium.3 This was of particular importance in the setting of DCM, as contrast use reclassified the LV cavity size from the nondilated to dilated category. Currently, there are no universally accepted reference ranges for contrast-enhanced LV volumes. Similarly, both echocardiographic techniques underestimated LV volumes compared with CMR imaging.4,5
Despite a strong evidence base, UEAs for LV opacification remain underused in clinical practice.6 In addition, although UEAs may be used for wall motion analysis in stress echocardiography, combined myocardial perfusion assessment is rarely performed. This is considered particularly challenging in conjunction with treadmill exercise echocardiography because of the need for rapid postexercise imaging at adequately high heart rates. Although MCE is performed after wall motion assessment, it has been shown that lower heart rates after stress may be adequate for perfusion assessment compared with wall motion analysis in the diagnosis of CAD.7 Consequently, combining immediate RWMA assessment followed by MCE, as in our case, may provide incremental diagnostic and prognostic information.8 In addition, our case reaffirms the benefit of UEAs in not only improving the feasibility of stress echocardiography in obese patients but also allowing the combined assessment of wall motion and perfusion in this challenging group of patients.9 Furthermore, our patient had LBBB, and under these circumstances, myocardial contrast echocardiographic perfusion assessment with UEAs may have an advantage over regional wall motion analysis alone in the diagnostic evaluation of CAD.10,11 Indeed, perfusion assessment by MCE may have better diagnostic accuracy than single-photon emission computed tomographic perfusion imaging because of the lower specificity of the latter technique related to the partial volume effect.10,11
In accordance with the ischemic cascade, myocardial perfusion abnormalities precede the onset of RWMA. In our case, the pattern of global LV dilatation and reduction in LVEF after exercise could have been indicative of widespread multivessel CAD. However, myocardial perfusion assessment using dedicated MCE settings provided insight into the etiology of LV dysfunction. The absence of perfusion defects on MCE meant the likely cause was nonischemic, and this was subsequently confirmed with cardiac computed tomography, showing nonobstructed coronary arteries. It has previously been shown that MCE can distinguish between nonischemic and ischemic causes of heart failure.12 The absence of an inducible subendocardial perfusion defect in the setting of LV impairment renders the presence of flow-limiting CAD highly unlikely, with a negative predictive value of 88%. A recent consensus statement and European Society of Cardiology guidelines on chronic coronary syndromes both recognize MCE as an adjunct to conventional stress echocardiography in the detection of chronic CAD.13,14 In addition, the 2023 American Heart Association/American College of Cardiology guidelines recommend the integration of stress echocardiography–derived coronary flow reserve into individualized risk stratification for chronic CAD.15 Therefore, in cases such as ours with negative results on MCE and no chest pain or ischemic electrocardiographic changes, invasive coronary angiography may be unnecessary. Conversely, some patients with idiopathic DCM manifest abnormal blood flow in the presence of nonobstructed epicardial coronary arteries. In these patients, coronary microcirculatory abnormalities have been implicated as the cause of abnormal blood flow and corresponding perfusion defects.16,17 During vasodilator stress MCE, an increase in myocardial blood volume has been linked to a positive response to optimal medical therapy in patients with DCM.18 Positron emission tomography–based studies reveal that myocardial blood flow is a powerful predictor of heart failure progression and cardiac death among patients with DCM.19 Our case supports this literature in that the absence of a perfusion defect was accompanied by favorable LV remodeling and medium-term improvement in global LV systolic function.
It is important to be aware of the pitfalls and limitations in performing and interpreting MCE in stress-induced global LV systolic dysfunction. False-negative interpretations may occur in the presence of too much contrast, leading to a generalized blooming artifact within the myocardium, creating the impression of normal perfusion. The correct rate of contrast delivery should be combined with judicious use of the gain settings at the lowest acceptable level to provide good endocardial definition. Equally, the confident exclusion of perfusion abnormalities may be confounded by attenuation artifact, rib shadowing, or insufficient myocardial contrast.20 In one study involving 560 segments, 19% could not be adequately visualized at baseline, and 74% of these were in the basal region.21 The failure to reach the target heart rate during dobutamine or exercise stress echocardiography may result in the false-negative exclusion of CAD. In a study comparing the accuracy of RWMA and MCE during dobutamine stress echocardiography for the diagnosis of CAD in 170 patients, the majority of reversible perfusion defects were observed without concomitant RWMA at an early or intermediate stage.7 Therefore, MCE can also enhance the sensitivity and accuracy of stress echocardiography in patients who fail to achieve the target heart rate, compared with RWMA assessment alone. MCE may underdetect CAD related to isolated right coronary artery stenosis. The sensitivity of MCE for detection of a ≥70% right coronary artery stenosis ranges from 52% to 60%, compared with 87% and 80% for the left anterior descending and left circumflex arteries, respectively.7,22 In a minority of cases with multivessel CAD, MCE may fail to demonstrate a perfusion abnormality. The sensitivity of MCE when combined with wall motion assessment for detection of multivessel CAD ranges from 91% to 95%.22,23 Therefore, a high index of suspicion must still be maintained in the small number of patients with high pretest probability of CAD and negative stress echocardiographic results.
There are a number of quality measures to ensure that acquisition and interpretation are optimal during stress MCE.20 Very low MI MCE settings should be used for both wall motion and perfusion analysis. A continuous intravenous infusion of contrast is preferred for myocardial perfusion assessment. The optimal MCE settings should be obtained at rest, and the same used postexercise. Optimal images require a steady state of contrast infusion needing adjustments to the rate of contrast infusion and gain settings to ensure good endocardial definition and homogeneous visualization of microbubbles within the myocardium. This is followed by flash-replenishment imaging, ensuring that a high enough mechanical ultrasound impulse (MI of 1.0) is applied to destroy the microbubbles within the myocardium while leaving enough contrast within the cavity to maintain good LV opacification. Perfusion assessment can be performed in real time or using triggered images in end-systole when the myocardium is thickest. In our experience, triggered images are more easily interpreted than real-time images. If there is inadequate uptake of microbubbles within the myocardium following flash imaging, the contrast infusion should be increased or the number of flash frames reduced. Inadequate destruction of microbubbles within the myocardium requires the opposite adjustments. Image acquisition should be continued until the complete replenishment of microbubbles within the myocardium.
During exercise testing, an intravenous bolus of contrast should be administered just before the termination of exercise to allow immediate postexercise imaging for regional wall motion. A small volume of only 0.2 to 0.3 mL should be used to avoid blooming artifacts and ensure adequate endocardial definition. While acquiring the LV quad-screen images, the nonscanning assistant should attach and start the intravenous infusion of contrast. The gain settings should be regularly optimized. Following the rapid acquisition of the LV wall motion images, perfusion assessment should be performed using the same principles as the resting perfusion methodology. A perfusion defect is usually observed first in the endocardium. An instantaneous full-thickness defect involving both endocardium and epicardium is more likely attributable to rib shadowing or attenuation artifact. Overall, the combined assessment of wall motion and perfusion should increase diagnostic confidence.
Conclusion
The use of UEAs during stress echocardiography improves the feasibility and reliability of the technique and may provide added diagnostic value with the inclusion of myocardial perfusion assessment. This could potentially avoid further unnecessary investigation. Operators performing regular stress echocardiography should be proficient in the use of UEAs for the assessment of both wall motion and myocardial perfusion.
Ethics Statement
The authors declare that the work described has been carried out in accordance with The Code of Ethics of the World Medical Association (Declaration of Helsinki) for experiments involving humans.
Consent Statement
Complete written informed consent was obtained from the patient (or appropriate parent, guardian, or power of attorney) for the publication of this study and accompanying images.
Funding Statement
The authors declare that this report did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.
Disclosure Statement
The authors report no conflict of interest.
Footnotes
Supplementary data related to this article can be found at https://doi.org/10.1016/j.case.2025.01.007.
Supplementary Data
Two-dimensional transthoracic echocardiography, initially without and subsequently with the administration of an UEA, displayed serially in the apical four-chamber, apical three-chamber, and apical two-chamber views acquired at baseline (rest stage), demonstrates suboptimal unenhanced endocardial delineation that improved after contrast, mild LV dilation, and mildly reduced global LV systolic function with regional hypokinesis in the midapical septum and anterolateral wall segments that is better appreciated after the UEA.
Two-dimensional transthoracic echocardiography with MCE (continuous infusion) using triggered replenishment interval at a 1:1 trigger and low MI (0.09-0.11) on postexercise serial displays in the apical four-chamber, apical three-chamber, and apical two-chamber views, demonstrate the bright white frame that masks the LV myocardium during a high-MI (1.0) flash sequence, then homogenous black myocardium immediately after flash imaging, which confirms microbubble destruction and rapid, progressive homogenous replenishment of myocardial contrast within all segments of the myocardium without a visualized subendocardial perfusion defect.
Two-dimensional transthoracic echocardiography with administration of a UEA, displayed serially in the apical four-chamber, apical three-chamber, apical two-chamber, parasternal long-axis, and parasternal short-axis views acquired after 3.5 minutes of treadmill exercise, demonstrates marked LV cavity dilatation and severely reduced global LV systolic function without new RWMAs.
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Associated Data
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Supplementary Materials
Two-dimensional transthoracic echocardiography, initially without and subsequently with the administration of an UEA, displayed serially in the apical four-chamber, apical three-chamber, and apical two-chamber views acquired at baseline (rest stage), demonstrates suboptimal unenhanced endocardial delineation that improved after contrast, mild LV dilation, and mildly reduced global LV systolic function with regional hypokinesis in the midapical septum and anterolateral wall segments that is better appreciated after the UEA.
Two-dimensional transthoracic echocardiography with MCE (continuous infusion) using triggered replenishment interval at a 1:1 trigger and low MI (0.09-0.11) on postexercise serial displays in the apical four-chamber, apical three-chamber, and apical two-chamber views, demonstrate the bright white frame that masks the LV myocardium during a high-MI (1.0) flash sequence, then homogenous black myocardium immediately after flash imaging, which confirms microbubble destruction and rapid, progressive homogenous replenishment of myocardial contrast within all segments of the myocardium without a visualized subendocardial perfusion defect.
Two-dimensional transthoracic echocardiography with administration of a UEA, displayed serially in the apical four-chamber, apical three-chamber, apical two-chamber, parasternal long-axis, and parasternal short-axis views acquired after 3.5 minutes of treadmill exercise, demonstrates marked LV cavity dilatation and severely reduced global LV systolic function without new RWMAs.