The International Journal of Cardiovascular Imaging

, Volume 26, Issue 5, pp 527–535

Echocardiography in stress cardiomyopathy and acute LVOT obstruction


    • Division of Cardiovascular Medicine, Department of Internal MedicineUniversity of Missouri
    • Cardiology SectionHarry S Truman VA Medical Center
  • Gong-Yuan Xie
    • Division of Cardiovascular Medicine, Department of Internal MedicineUniversity of Missouri
  • Kevin C. Dellsperger
    • Division of Cardiovascular Medicine, Department of Internal MedicineUniversity of Missouri
    • Center for Health Care QualityUniversity of Missouri

DOI: 10.1007/s10554-010-9590-7

Cite this article as:
Chockalingam, A., Xie, G. & Dellsperger, K.C. Int J Cardiovasc Imaging (2010) 26: 527. doi:10.1007/s10554-010-9590-7


Widespread use of echocardiography has contributed to more frequent recognition of takotsubo stress cardiomyopathy. Initial presentation is similar to acute coronary syndrome and the acute course can be complicated by heart failure, arrhythmias, dynamic left ventricular outflow tract obstruction, hypotension and death. We briefly review the clinical presentation and propose a unified diagnostic algorithm for cardiologists acutely managing this cardiac emergency. We highlight the central role of echocardiography and emphasize the nuances of this peculiar acute cardiomyopathy from an echocardiographers’ perspective.


Stress cardiomyopathyLV outflow obstructionEchocardiography


Stress cardiomyopathy, also called apical ballooning syndrome or Takotsubo cardiomyopathy, manifests as sudden onset reversible dysfunction predominantly affecting the apical and mid left ventricular (LV) segments [1, 2]. Typically seen in post menopausal women, this is thought to be due to catecholaminergic excess from severe emotional or physical stress [3]. Echocardiography plays a central role in the diagnosis and management of stress cardiomyopathy (SC) and left ventricular outflow tract obstruction (LVOTO). The ability to rapidly perform bedside echocardiography with Doppler imaging places this modality in the center of schema to understand cardiac function and quantify various associated abnormalities in this situation. Reliance on non-invasive hemodynamics, frequent cardiac biomarker testing and widespread performance of echocardiography in critical care settings likely accounts for the recent increased frequency of SC recognition.

Prevalence of stress cardiomyopathy

One serial echocardiographic study suggests up to a quarter of all critically ill hospitalized patients may develop SC [4]. The true incidence is probably lower but prevalence would vary significantly based on severity of illness and the population screened for SC [5]. Initial presentation can range from an incidental finding during routine echocardiography to a presentation suggesting acute coronary syndrome (ACS) or cardiogenic shock. Symptoms may include angina, dyspnea, heart failure and/or new onset arrhythmia. ECG may manifest ischemia-like ST-T wave changes and cardiac enzymes are generally modestly elevated. Dynamic LV outflow tract obstruction (LVOTO) may occur in up to a fourth of SC subjects [6, 7].

In our institution, we have diagnosed SC in 21 patients in the past 3–4 years with evidence of LVOTO in 6 of them. The majority were older women who presented with symptoms similar to acute coronary syndrome such as acute onset angina, dyspnea, tachyarrhythmia, ischemic ECG changes, cardiac enzyme elevation or hypotension. Coronary angiography excluded culprit lesions in all except 2 patients when comorbidities precluded invasive studies. Serial echocardiography conclusively diagnosed SC in all patients by documentation of normalization of cardiac function over days to weeks. One 74 year old male without evident stress manifested apex sparing severe basal hypokinesia which normalized over 2 weeks. Another woman developed classical features of SC on 2 occasions 1 year apart—first without any ‘stressful’ precipitant and the second episode following a prolonged back surgery. Mitral regurgitation can be moderate to severe at the time of SC diagnosis but typically reduces to insignificant levels after LVOTO is relieved [7]. There was no acute mortality in our series.

Diagnosis of stress cardiomyopathy

Early in our evaluation of SC echocardiograms, we reported moderate to severe LV dysfunction with ejection fraction (EF) in the 25–40% range. Although the wall thickness is reduced in the akinetic apical LV segments, SC does not manifest the thinned hyperechogenic fibrosis signal characteristic of evolved transmural myocardial infarction. Initial echocardiography performed at the time of presentation may not distinguish the regional wall motion abnormalities (RWMA) of SC from acute myocardial infarction (MI) [8]. Importantly, the pattern of RWMA is segmental rather than global and predominantly is seen in an apical distribution which does not necessarily correlate with defined coronary territories.

As echocardiographers, we are trained to evaluate for RWMA and attribute these abnormalities to various coronary territories. On first inspection, SC appears like an evolving left anterior descending (LAD) infarction with akinesia of the apex, apical anterior wall and septum. On closer inspection of 2D images from the apical 4 and 2 chamber views, typical SC manifests as symmetrical RWMA extending equally into the apical inferior and lateral walls (Fig. 1) [9]. Table 1 outlines the various aspects of SC evaluated by echocardiography.
Fig. 1

2D echocardiographic imaging in apical 4 chamber view in diastole (a) and systole (b), and lower row shows apical 2 chamber view in diastole (c) and systole (d). The typical, symmetrical mid and apical left ventricular akinesia is evident in systolic images b and d

Table 1

The role of echocardiography in diagnosis of stress cardiomyopathy and LV dynamic obstruction

SC, LVOTO component

Best evaluated in

Additional comments

1. LV global function

Standard views

Reproducible estimate of global cardiac function


Apical views

Echo contrast may optimize endocardial definition

3. Mitral SAM

PLX, A5C, mitral M mode

 Detection of SAM is initial step

 Next, level and severity of LVOTO, hemodynamic and LV stress and MR are determined.

4. LVOT resting and peak gradients

A5C, A3C

Determine contribution of medications, Inotropes, loading state

LV wall stress = LVOT gradient + Systolic BP

5. Mid-cavity obstruction

A4C, A5C

Hyperdynamic states with volume depletion typically manifest in this manner

6. Mitral regurgitation


Recovery near total when MR is eccentric without structural abnormalities of valves

7. Pulmonary hypertension

TR Doppler in A4C view

Likely reflects baseline cardiopulmonary status and not SC

8. RA filling pressures

Subcostal IVC M-mode

When low helps guide volume replacement

Relative or actual compensatory hypercontractility of basal segments is evident in a majority of SC patients. Variants of SC can manifest as ‘reverse Takotsubo cardiomyopathy’ (with mid-cavity hypokinesia and apical sparing), focal RWMA, global LV hypokinesia as well as RV dysfunction [1012]. These variants of SC may be harder to diagnose by echocardiography alone, especially if the RWMA overlaps with a particular coronary territory. Coronary angiographic documentation of patent vessels with certain clinical settings (older women, mental stress, physiological strain) and laboratory findings (disproportionately low levels of troponin and CK-MB for size of MI by ECG, RWMA) raises the probability of SC in these instances. The time course for normalization of cardiac function is variable with some recovering systolic function in days while others may take weeks to improve. Echocardiography is the most readily available tool to determine improvements in RWMA serially over short time intervals noninvasively and reproducibly.

The modified Mayo criteria for SC diagnosis require ECG changes and angiographic proof of patent coronaries [5]. Due to the clinical and electrocardiographic similarity between ACS and SC, cardiac catheterization should not be delayed in patients with angina or ST elevations. Many patients with suspected ACS are however not candidates for invasive therapy due to age or comorbidity. In high risk patients with ongoing acute medical- surgical issues, catheterization may be delayed or reserved for hemodynamic instability. Also, coexistence of coronary artery disease does not exclude the diagnosis of SC [13]. The diagnosis of SC is probable when angiography reveals no culprit lesions and LV apical ballooning is typically seen. The definitive diagnosis of SC is however confirmed when echocardiography repeated after few days to weeks documents complete normalization of LV RWMA and EF (Fig. 2).
Fig. 2

Role of echocardiography in the diagnosis of stress cardiomyopathy. STEMI denotes ST segment elevation myocardial infarction

Prevalence of acute LVOT obstruction

In our experience, LVOTO is a highly variable finding that is dependent on loading conditions, medications, heart rate and circulating catecholamine levels [7, 14]. Anterior mitral leaflet (AML) systolic anterior motion (SAM) is classically demonstrated in 70% of hypertrophic cardiomyopathy (HCM) patients at rest or with exercise [15]. Another well recognized setting for transient LVOTO is in about 10% of patients undergoing dobutamine stress echocardiography [16]. Similarly, use of inotropes in critical care settings also predisposes to LVOTO [14]. About 25% of SC subjects likely manifest LVOTO [6]. Loading conditions may alter LVOTO severity significantly and it may thus be a transient phenomenon.

LVOTO can be precipitated when a small left ventricle (due to volume loss, diuretics) develops hyper contractility, especially in the basal segments (due to excess endogenous or infused catecholamines) that results in crowding of the outflow area especially in patients with underlying left ventricular hypertrophy. The sum of systolic BP (e.g. 120 mmHg) and peak LVOT pressure gradient (e.g. 100 mmHg) is used to estimate the acute systolic subendocardial wall stress. This sudden LV strain can lead to subendocardial ischemia and possibly acute myocardial stunning and as well as SC [7]. Since LVOTO can be transient it is crucial to perform the echocardiogram when the murmur is audible. Simultaneous documentation of BP is essential to calculate the total LV wall stress.

When the LVOTO is significant, a late peaking systolic ejection murmur can be appreciated maximally in the left third intercostal space. Hypotension may ‘paradoxically’ worsen with standard intravenous inotropes mimicking ACS with cardiogenic shock. 2D imaging in the parasternal long and apical 5 chamber views are best suited to study the severity and duration of SAM [7]. Mitral valve level M-mode from the parasternal long axis view, when obtainable, may provide adequate temporal resolution to study the severity and duration of AML-septal proximity [14].

Color Doppler guided pulse interrogation in apical long axis and 5 chamber views can help localize the level of obstruction. Next, to quantify the severity of SAM, continuous wave (CW) Doppler is applied using 2D and color Doppler guidance. This results in the late peaking ‘dagger’ shaped CW Doppler envelope peculiar to dynamic LVOTO (Fig. 3). When milder peak CW Doppler gradients are recorded, valsalva maneuver can accentuate classical LVOTO by reducing LV chamber size [14].
Fig. 3

Continuous wave (CW) Doppler imaging in apical long axis view demonstrating late peaking dynamic LVOTO gradient of over 150 mmHg (peak velocity 6.5 m/s)

Mitral regurgitation

Papillary muscle geometry is altered by the dysfunctional LV in SC causing mild central mitral regurgitation (MR). As LV function normalizes, this MR would resolve [7, 14]. On the other hand, when there is LVOTO, SAM results in the anterior leaflet not approximating with PML during systole. Posteriorly directed, late systolic MR that improves with resolution of SAM is typically seen in SC with LVOTO. Transesophageal echocardiography (TEE) may provide anatomic details and functional understanding that may direct repair of the mitral apparatus. Very rarely, when structurally abnormal, mitral valve replacement may be needed to relieve the MR and LVOTO [17].

Hemodynamics evaluation

Various mechanisms can lead to hypotension in SC [5, 17]. First, the acute reduction in LV function may directly reduce cardiac output due to reduction in stroke volume. Second, the basal hypercontractility related venturi effect could draw the anterior mitral leaflet towards the interventricular septum in systole. The SAM and resultant acute LVOTO could limit forward flow and lower systemic pressures. Third, SAM related AML displacement results in acute mitral regurgitation and a new low pressure alternative for the LV stroke volume. Fourth, tachyarrhythmias like atrial fibrillation with rapid ventricular rates may be the dominant reason for hypotension in some SC subjects. Finally, SC is easily mistaken for ACS with ‘cardiogenic shock’ due to the anginal symptoms, ischemia-like ECG changes and cardiac enzyme elevations both in the ER and critical care settings. This initiates management with maneuvers to increase cardiac output such as inotropic agents like dobutamine and dopamine or intra aortic balloon counterpulsation—all these actions can worsen LVOTO and cause further hemodynamic deterioration. This sets up a vicious cycle where more interventions become indicated for worsening hypotension.

We believe there is a wide spectrum of the SC- LVOTO presentations and at least in some situations LVOTO precipitates SC due to the sudden increase in wall stress or reduction in cardiac output [7]. A comprehensive transthoracic echocardiogram would diagnose SC and in the majority of instances quantify the relative contribution of the various factors leading to hypotension in each individual situation. To determine response to therapy, auscultation could provide most of the needed information if close attention is paid to the severity, duration and late peaking nature of the LVOTO systolic ejection murmur. However, since many of these patients are in critical care units which are inherently noisy, softer murmurs may go undetected by auscultation.

Management issues in SC and LVOTO

The available literature is anecdotal and a clear consensus as to the management of SC has not emerged thus far. The scope of this review does not allow for a detailed review of management. Being a transient and completely reversible condition by definition, the mainstay of SC management is supportive. Chest discomfort may not respond to nitrates but typically does not persist. Pulmonary edema could require diuretics and respiratory support. LVOTO can be managed similar to hypertrophic cardiomyopathy with outflow obstruction. Figure 4 outlines the management of LVOTO based on hemodynamics and response to initial therapy with fluids and beta blockers. We have recently reported the interventions that could potentially help in these critically ill patients (Table 2) [14].
Fig. 4

Management of LV outflow obstruction with hypotension based on hemodynamics and response to therapy

Table 2

Various acute interventions and long term measures to counter dynamic LVOTO

Acute SC/LVOTO management

Long term options for SC/LVOTO

IV ß blockers—Metoprolol bolus or Esmolol drip

Maintenance oral ß blockers

Target heart rate ≤ 60 bpm

IV Verapamil or Diltiazem drip

Oral long acting Verapamil or Diltiazem

Target heart rate ≤ 60 bpm

IV Fluids

Ensure adequate hydration—especially in hot weather and during exercise

Discontinue inotropic agents

Avoid Digoxin and minimize cardiac stimulants like caffeine

Phenylephrine infusion for hypotension/sepsis (vasopressor without inotropy)

Hypertension- aggressive control < 130/80 mmHg

Discontinue β agonist if possible-Levalbuterol’s selectivity may limit cardiac stimulation making it β agonist of choice

Minimize long-term β agonist use for bronchospasm/COPD

Disopyramide or amiodarone

Stress reduction, meditation and relaxation techniques

Minimize diuretics and nitrates

Regular exercise

3D, Tissue Doppler, strain and contrast echo in SC/LVOTO

Emerging literature suggests tissue Doppler imaging, regional strain imaging and time-volume curves from 3D echo image modeling may offer visually better demonstration of the RWMA of SC with higher diagnostic sensitivity [18, 19]. Microbubble echocardiographic contrast can improve image quality in intubated critically ill patients, obesity and with issues like chronic lung disease. Contrast ventriculography improves endocardial definition, excludes apical thrombus and can also demonstrate myocardial perfusion abnormalities. These techniques, along with magnetic resonance and cardiac CT imaging, may improve the diagnostic accuracy in variant and subtle forms of SC.


Transesophageal echo (TEE) may help clarify the diagnosis when TTE windows are suboptimal. LV hypertrophy and septal morphology can be better characterized. SAM and LVOTO level can be demonstrated with better spatial and temporal resolution. Mitral valve leaflet and chordal anatomy can be correlated with mitral regurgitation severity to guide therapy. In atypical situations, with borderline or focal basal septal hypertrophy, TEE done electively after resolution of LVOTO may be valuable in planning further management. TEE may provide anatomic details that may direct repair or replacement of the mitral apparatus when significant MR persists after SC and LVOTO resolve.

Recurrent SC/LVOTO

Over a 4 year follow-up period, 2–10% of SC patients can have a recurrence [5]. We have seen recurrence of SC following prolonged surgery. Consideration and exclusion of conditions known to produce excessive sympathetic stimulation such as pheochromocytoma is important especially in recurrent cases [20]. Minor troponin increases disproportional to the extensive LV dysfunction would favor SC. In instances where similar precipitants and symptoms are associated with recurrence of the LV apical RWMA, echocardiography guided medical management with close hemodynamic monitoring is sufficient. In our experience, repeat 2D echo may confirm significant improvement or even normalization of LV function in as short an interval as 2–5 days. When the clinical presentation varies significantly from the initial SC episode repeat catheterization may be needed to exclude ‘new’ CAD. In one situation we diagnosed chordal SAM with acute LVOTO and hypotension with focal SC manifest as anterior apical hypokinesia. The same patient developed classical SC a year later following a prolonged spine surgery- this time with severe LV dysfunction and classical apical ballooning. We feel recurrent SC can be reasonably diagnosed without cardiac catheterization in most instances. ECG ST-T changes and classical stressors may not be evident always. However, LV function recovery by repeat echocardiography is needed to confirm the diagnosis of recurrent SC.

Longitudinal follow of SC/LVOTO

The long term prognosis of SC appears relatively benign from the available literature [21, 22]. Acutely there is excess morbidity from hypotension, heart failure and associated medical conditions. Arrhythmia and free wall rupture may complicate when LVOTO is severe and LV is unable to cope with the sudden increase in afterload [2325]. However, after the acute episode resolves, the outcomes are not different from age matched healthy controls. Inotropes and dehydration should be avoided [5]. Although studies have not shown a reduction in recurrence with any medication, we routinely use beta blockers to blunt future potential catecholaminergic insults. Optimal risk factor control may help and there may not be any additional merit in repeating echocardiograms periodically unless new symptoms develop.


Stress cardiomyopathy is increasingly recognized in the emergency room, critical care units and cardiology practices due to widespread use of echocardiography. 2D and Doppler studies provide real time detailed evaluation of various aspects of this problem including LV dysfunction, mitral regurgitation and LVOT obstruction. Disproportionally large RWMA and demonstration of cardiac functional recovery without revascularization are central to the diagnosis. Serial monitoring of response to therapy, identification of recurrence and long term follow-up are also best done with echocardiography.

Funding sources

VISN 15 Veterans Administration Research award to A Chockalingam.

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© Springer Science+Business Media, B.V. 2010