Dynamic Left Ventricular Outflow Tract Obstruction Research Articles

Usefulness of Cibenzoline Stress Echocardiography to Determine Severity of Aortic Stenosis in a Patient with Combined Left Ventricular Outflow Tract Obstruction and Aortic Stenosis

Left ventricular outflow tract obstruction (LVOTO) is sometimes accompanied by aortic stenosis (AS). Reliable estimation of the true severity of AS is often difficult because it cannot be discriminated from dual stenosis. A 75-year-old woman was referred to our hospital due to traumatic hemopneumothorax with exertional dyspnea. Echocardiography revealed AS and LVOTO by chance. A continuous Doppler echocardiography revealed a late-systolic peaking dagger-shaped profile with a 6.0 m/s of peak jet velocity across the LVOT and aortic valve, but it was difficult to discriminate between the coexisting peak flows. For an accurate evaluation of AS, we performed landiolol (short acting beta-blocker) and cibenzoline (Na+ channel-blocking agent) stress echocardiography with simultaneous recordings of both left ventricular and aortic pressure by catheter examination. Cibenzoline successfully eliminated the LVOTO, but landiolol did not. Cibenzoline stress echocardiography enabled us to evaluate the AS severity as less than moderate, resulting in proper decision-making. The findings in this case clearly showed that cibenzoline stress echocardiography has a potential utility for determining AS severity in a patient with coexistent dynamic LVOTO.

A Tale of Two Pressures- Medical Management Dilemmas in Post-TAVR LVOT Obstruction

Background Systolic anterior motion (SAM) of the anterior mitral valve leaflet after transcatheter aortic valve replacement (TAVR) is an extremely rare pathophysiologic phenomenon leading to left ventricular outflow tract (LVOT) obstruction. We report a case of post-TAVR LVOT obstruction leading to pulmonary edema and respiratory failure successfully treated medically with fluid challenges. Case Presentation A 91-year-old woman with severe symptomatic aortic stenosis and New York Heart Association (NYHA) functional class III was referred to our institution for TAVR evaluation. Patient was deemed to be intermediate risk based on Society of Thoracic Surgeon (STS) score of 4.7%. The baseline transthoracic echocardiogram confirmed the presence of severe aortic stenosis with peak aortic jet velocity of 5.5 m/s, aortic valve area of 0.8 cm2and mean gradient > 40 mmHg with preserved left ventricular function and mild mitral regurgitation. No intra-ventricular gradient, septal wall hypertrophy or SAM of the anterior mitral valve leaflet was noted. Patient underwent successful transfemoral TAVR with a 29 mm Medtronic Evolut PRO valve. Angiography confirmed proper valve position and no paravalvular leak. Post-procedural echocardiogram demonstrated adequate prosthesis performance with new-onset of SAM dynamic LVOT obstruction and concomitant severe mitral regurgitation leading to systolic flow reversal in both left and right pulmonary veins and apical tethering of the anterior mitral leaflet. Postoperative course was further complicated by Enterococcus sepsis leading to atrial fibrillation with rapid ventricular response resulting in systemic hypotension, pulmonary edema and impending respiratory failure. Despite the congestion in the pulmonary vasculature, the decision was made to optimize diastolic filling and preload by titrated beta-blockade and serial fluid challenges with 250 mL boluses. Patient was able to increase forward stroke volume leading to improvements in mean arterial pressure and resolution of pulmonary congestion. Conclusions The mechanism leading to SAM and LVOT obstruction after TAVR implant is poorly elucidated and rarely reported in the literature. Chronic aortic stenosis results in increased afterload to the LV that is compensated by elevated intra-ventricular pressure to allow adequate systemic perfusion. The increased intra-ventricular pressure also prevents septal inward motion and thus keeps LVOT unobstructed. With TAVR and the relief of the fixed obstruction, intra-ventricular pressure drops simultaneously with a reduction in LVOT cross-sectional area due to an increased flow velocity. A pressure gradient is created between the left atrium and LVOT that pulls the anterior mitral leaflet toward the LVOT creating a dynamic LVOT obstruction. Every effort should be made to optimize diastolic filling and contractility through titrated beta-blockade and fluid challenge.

A case report: haemodynamic instability due to true dynamic left ventricular outflow tract obstruction and systolic anterior motion following resuscitation: reversal of haemodynamics on supportive veno-arterial extracorporeal membrane oxygenation.

BackgroundObstruction of the left ventricular outflow tract (LVOT) as seen in hypertrophic cardiomyopathy is a dynamic condition with a wide range of clinical presentations and symptoms.Case summaryWe report the use of veno-arterial extracorporeal membrane oxygenation in a female patient who was resuscitated after out-of-hospital cardiac arrest. Soon after admission the patient developed critical haemodynamic compromise due to severe obstruction of the left ventricle outflow tract and systolic anterior motion (SAM) of the mitral valve. Veno-arterial extracorporeal membrane oxygenation restored haemodynamics and was weaned after 4 days without any haemodynamic compromise due to SAM. The patient was discharged from the intensive care unit at Day 13, and after 3 days at the coronary care unit, she was discharged to ambulatory follow-up with no sequelae.DiscussionVeno-arterial extracorporeal membrane oxygenation restored haemodynamic stability in this patient with dynamic severe LVOT obstruction following cardiac arrest.

Takotsubo Cardiomyopathy With Left Ventricular Outflow Tract Obstruction and Shock

SESSION TITLE: Heart Failure and Cardiogenic Shock SESSION TYPE: Affiliate Case Report Poster PRESENTED ON: Tuesday, October 31, 2017 at 01:30 PM - 02:30 PM INTRODUCTION: Takotsubo cardiomyopathy (TCM), also known as apical ballooning syndrome, mimics acute coronary syndrome. We report a unique case of a female who presented as STEMI with hypotension, and was found to have TCM causing significant Left ventricular outflow tract (LVOT) obstruction. CASE PRESENTATION: A 70-year-old female with history of hypertension, hyperlipidemia presented to our ER with exertional shortness of breath and chest pain. She denied any recent stress. She was hypotensive with BP of 80/43 mmHg and had bibasilar pulmonary rales. Lab showed BNP of 1673 pg/ml and positive cardiac troponins which increased from 3.76 to 4.25 ng/ml. Chest X-ray revealed pulmonary vascular congestion. EKG showed ST-elevation in anterior leads. ECHO showed EF of 35% with akinetic LV apex and dynamic LV outflow tract obstruction with peak velocity of approximately 4 m/s. Patient underwent cardiac catheterization that showed clean coronaries. Left ventriculogram showed basal hypokinesis with apical ballooning during systole (Figure 1). The above findings along with ST-elevation on EKG were consistent with TCM. Thus, the diagnosis of TCM with LVOT obstruction was established. She was medically managed with beta-blockers. Repeat ECHO performed 5-days later showed complete recovery of LV systolic function with resolution of apical ballooning. She was later discharged home in a stable condition and she continued to do well at 3-month follow up. DISCUSSION: TCM is known to cause transient systolic LV dysfunction and ST-T changes on ECG following various triggering factors. Our case is an example of a rare presentation of TCM causing LVOT obstruction and hypotension initially mimicking STEMI. A review of literature suggests that only 10-20% of patients with TCM develop cardiogenic shock. Hypotension may develop in patients with TCM due to multiple mechanisms such as left ventricular systolic dysfunction, significant mitral regurgitation secondary to systolic anterior motion of the mitral valve, dynamic LVOT obstruction, or a combination of these factors (1). As the management of cardiogenic shock due to LVOT obstruction is very different from other causes of cardiogenic shock, all patients with suspected TCM causing shock should first undergo ECHO to rule out LVOT obstruction. Inotropic agents and intraaortic balloon pump (IABP) used for the treatment of cardiogenic shock due to STEMI can paradoxically increase LVOT pressure gradients and worsen the dynamic gradient in patients with TCM and LVOT obstruction (1). This can lead to worsening of shock and catastrophic sequelae. CONCLUSIONS: In patients with hypotension and ECHO suggestive of TCM, LVOT obstruction must be ruled out. Inotropic agents and IABP are relatively contraindicated in cardiogenic shock due to LVOT obstruction. Thus, timely diagnosis and appropriate management of TCM with LVOT obstruction is imperative. Reference #1: Shah BN, et al. JACC Sep 2011;58(11);1195-1196. DOI:10.1016/j.jacc.2011.03.062 DISCLOSURE: The following authors have nothing to disclose: Parita Soni, Sameer Chadha, Nidhi Aggarwal, Anand Kumar Rai, Yizhak Kupfer, Bilal Mailk No Product/Research Disclosure Information

Late-onset dynamic outflow tract gradient in the setting of tako-tsubo cardiomyopathy: An interesting phenomenon with potential implications?

In clinical practice, dynamic left ventricular outflow tract obstruction (LVOTO) in the setting of tako-tsubo cardiomyopathy (TTC) has been regarded as an early-onset complication typically emerging in accordance with wall motion abnormalities. However, dynamic LVOTO has, very rarely, been reported as a late-onset phenomenon in the setting of TTC as well (arising in the late stage or after recovery). Accordingly, the present paper aims to highlight clinical relevance and potential implications of late-onset LVOTO in the setting of TTC.

Left Ventricular Outflow Tract Obstruction—be Prepared!

The current trend to treat hypotension in critically ill patients is to place a greater emphasis on inotropic support and less on fluid resuscitation in order to limit the potential harm from fluid overload. This combination may trigger left ventricular outflow tract obstruction (LVOTO) in susceptible patients. Although LVOTO is classically described in patients with hypertrophic cardiomyopathy it has been reported in other conditions including septic shock, apical ballooning syndrome, myocardial infarction, respiratory failure, and post valvular surgery. It is more common in the elderly, females, and in patients with hypertension, diabetes, and chronic vascular disease because of predisposing anatomical conditions such as left ventricular hypertrophy, small left ventricle size, sigmoid septum and alterations in the positions of the aortic and mitral valve annular planes. The onset of LVOTO is largely unpredictable due to a complex interplay between preload, afterload, heart rhythm and rate in susceptible patients. The consequences of missing this treatable condition may lead to life-threatening hypotension refractory to, or exacerbated by, a further increase in inotropic support. Dynamic LVOTO should be considered in any hypotensive intensive care patient. Echocardiography is perhaps the best tool to assess LVOTO and its underlying pathophysiology in the critically ill. Detection of LVOTO is a relatively simple task using a combination of two-dimensional, M-mode and spectral Doppler imaging by an operator alert to the possible diagnosis.

Graves Induced Reversible LVOT Obstruction.

<p>Left ventricular outflow tract (LVOT) obstruction is most commonly associated with hypertrophic cardiomyopathy (HCM). Dynamic LVOT obstruction has been described in various clinical settings including Takotsubo cardiomyopathy, sepsis, treatment with adrenergic agonists and in the setting of acute anterior wall myocardial infarction. Reversible LVOT obstruction has been reported after treatment of pheochromocytoma. A common denominatorin these cases is increased inotropy of the basal LV segments, secondary to catecholamine excess, resulting in obliteration of the LVOT. We report the case of a 59 year old male with a structurally normal heart who developed symptomatic LVOT obstruction in the setting of Graves disease. His symptoms and LVOT gradient completely resolved once his thyroid function normalized with appropriate treatment. To our knowledge this is the first case report of hyperthyroidism induced reversible LVOT obstruction. </p>

Valsalva maneuver in echocardiography.

The Valsalva maneuver is an easily performed maneuver with an interesting hemodynamic effect which can be used to aid accurate echocardiographic diagnosis. However, correct adequate performance is often missed. Here, we aim to describe the performance of an adequate Valsalva maneuver and the correct interpretation of its effect. The Valsalva hemodynamic effect consists of four basic phases which can be used in echocardiography to yield an accurate diagnosis. Valsalva is used to decrease preload and provoke left ventricular outflow tract (LVOT) gradient in dynamic LVOT obstruction. In addition, a decrease in E/A ratio in mitral inflow >50% with Valsalva correlates with increased LV filling pressure and diastolic dysfunction. Valsalva also momentarily increases RA pressure and helps to unmask a patent foramen ovale with the use of saline contrast.

Dynamic obstruction in hypertrophic cardiomyopathy.

The present article reviews the recent advances in the echocardiographic assessment of left ventricular outflow tract (LVOT) obstruction in hypertrophic cardiomyopathy (HCM). In particular, it highlights the role of novel imaging techniques in promoting our understanding of the pathophysiology of obstruction and discusses the prognostic value of information obtained from exercise echocardiography and the emerging role of image-guidance technologies for interventional relief of obstruction. The advent of novel echocardiography technologies, such as vector flow mapping, continues to expand our understanding of the exact mechanism of systolic anterior motion leading to dynamic LVOT obstruction by providing new insights into the interaction between pathologic mitral geometry and the left ventricular flow field. New studies provide evidence for the prognostic value of exercise echocardiography in the assessment of patients with HCM. Myocardial contrast perfusion imaging can delineate the anatomy of septal perforator arteries and identify the downstream septal perfusion bed, which is critical for safely guiding the procedure of alcohol septal ablation. Echocardiography represents a versatile, continuously evolving, and easily repeatable technique, allowing truly dynamic imaging studies, and is therefore most appropriate to evaluate a dynamic disease condition such as LVOT obstruction in HCM. It provides profound insights into the pathophysiology of LVOT obstruction, information on its clinical impact, and guidance for its relief by interventional strategies.

Systolic Anterior Motion of the Mitral Valve and Three-Dimensional Echocardiography

DYNAMIC LEFT VENTRICULAR outflow tract (LVOT) obstruction due to systolic anterior motion (SAM) of the mitral valve (MV) after MV repair is a well-known phenomenon.1 Clinically significant SAM can cause LVOT obstruction and hemodynamic instability regardless of the presence of mitral regurgitation (MR). Two-dimensional (2D) transesophageal echocardiographic (TEE) appearance of dynamic LVOT obstruction consists of SAM, turbulence on color-flow Doppler in the LVOT, and eccentric mitral regurgitation.

Acute Effects of Ivabradine on Dynamic Obstruction of the Left Ventricular Outflow Tract in Cats with Preclinical Hypertrophic Cardiomyopathy

BackgroundIvabradine is a negative chronotropic drug with minimal effects on central hemodynamics. Its effect on dynamic obstruction of the left ventricular outflow tract (LVOT) in cats with hypertrophic cardiomyopathy (HCM) remains unknown.Hypothesis/ObjectivesIvabradine reduces dynamic obstruction of the LVOT in cats with HCM.AnimalsTwenty‐eight client‐owned cats with preclinical HCM and dynamic LVOT obstruction.MethodsRandomized, double‐blind, active‐control single dose study. Cats received a single dose of either ivabradine (0.3 mg/kg PO) or atenolol (2 mg/kg PO). Heart rate, echocardiographic variables, and systolic blood pressure (SBP) were recorded before and 3 hours after drug administration. Statistical comparisons were made using ANCOVA.ResultsPeak velocity in the LVOT was significantly decreased compared to baseline for both drugs; however, the effect was more prominent with atenolol (mean reduction 2.53 m/s; 95% CI 2.07–3.13 m/s) compared to ivabradine (mean reduction 0.32 m/s; 95% CI −0.04 to 0.71 m/s; P < .0001). Echocardiographic indices of systolic function were largely unchanged by ivabradine, but significantly reduced by atenolol.Conclusions and Clinical ImportanceA single dose of ivabradine decreases dynamic LVOT obstruction in cats with HCM, but the clinical effect is negligible and inferior compared to that achieved by atenolol.

Hypertrophic cardiomyopathy: part 1 - introduction, pathology and pathophysiology.

Hypertrophic cardiomyopathy (HCM) is the most common genetic cardiovascular disease with many genotype and phenotype variations. Earlier terminologies, hypertrophic obstructive cardiomyopathy and idiopathic hypertrophic sub-aortic stenosis are no longer used to describe this entity. Patients present with or without left ventricular outflow tract (LVOT) obstruction. Resting or provocative LVOT obstruction occurs in 70% of patients and is the most common cause of heart failure. The pathology and pathophysiology of HCM includes hypertrophy of the left ventricle with or without right ventricular hypertrophy, systolic anterior motion of mitral valve, dynamic and mechanical LVOT obstruction, mitral regurgitation, diastolic dysfunction, myocardial ischemia, and fibrosis. Thorough understanding of pathology and pathophysiology is important for anesthetic and surgical management.

Surgical treatment for obstructive hypertrophic cardiomyopathy

Keywords Hypertrophic cardiomyopathy Mitral valvereplacement Septal myectomyHypertrophic cardiomyopathy (HCM) is one of the mostcommon genetic diseases affecting myocardium with widevariety of clinical manifestation, hemodynamic character-istics, anatomic morphology, and natural history. Patientswith HCM may develop limiting symptoms due to dynamicleft ventricular outflow tract obstruction (LVOTO) andassociated mitral regurgitation (MR) due to systolic ante-rior motion (SAM) of the anterior mitral leaflet [1]. Forthose who have severe symptoms unresponsive to maxi-mum medical therapy including beta-blockers and antiar-rhythmic drugs such as disopyramide or cibenzoline,surgical left ventricular septal myectomy has been thestandard option. It has been shown that septal myectomysignificantly decreases LVOT gradient and associated MRand provides excellent long-term outcomes.Although the basic transaortic approach for performinga septal myectomy has been known for over 40 years, theoperation remains technically challenging and results areoperator dependent to a high degree [2]. This procedurecarries many tips and pitfalls. Incisions or excisions madetoo deep may create ventricular septal defects or ventric-ular perforations, both of which increase surgical mortalitysignificantly. Poor visualization of the anatomy below theaortic valve can result in injury to mitral leaflets or chor-dae. Incorrect placement of incisions or excessive tractioncan produce complete heart block, requiring permanentpacemakers. Inadequate myocardial protection of thehypertrophied heart can cause difficulty in defibrillationand low cardiac output, which may require mechanicalcirculatory support. The aortic valve is always at risk forinjury from instruments passed through the valve andmanipulated within the ventricle. Therefore, it is under-standable that overly conservative surgical attitudes maysometimes prevail, resulting in limited myocardial resec-tion and consequent incomplete relief or early return ofLVOTO and symptoms. Even if adequate resection issurgically obtained at the level of the basal septum, mid-ventricular obstruction and/or MR associated with abnor-mal papillary muscles and/or chordae, and other musclebundles may persist, and additional procedures maybecome necessary [3].As Furukawa et al. [4] reported their surgical case in thisissue of the GTCS, in which mitral valve replacement(MVR) was required because of residual LVOTO and MRafter standard septal myectomy, surgeons performing thisprocedure should always think about options for residualLVOTO and MR. Because SAM plays an essential role forLVOTO and MR, additional procedures such as mitralvalve plasty including Alfieri’s stitch or MVR with low-profile prosthesis can be effective alternatives. It was firstreported by Cooley et al. that MVR using mechanicalvalves eliminate MR and can relief LVOTO and symptomsin patients with obstructive HCM [5]. Because MVR is asimple and highly reproducible procedure, it can be anattractive option for those who have residual LVOTO andMR even after standard septal myectomy although thoseundergoing MVR with mechanical valve require life-longanticoagulation therapy.

Symptomatic Exercise-Induced Left Ventricular Outflow Tract Obstruction without Left Ventricular Hypertrophy

Left ventricular (LV) outflow tract obstruction (LVOTO) is most commonly seen in patients with hypertrophic cardiomyopathy. Postexercise dynamic LVOTO (DLVOTO) has been infrequently identified in symptomatic patients without LV hypertrophy, and its pathophysiology is not well established. The aim of this study was to identify echocardiographic abnormalities that might explain the dynamic development of systolic anterior motion, mitral-septal contact, and LVOTO in these patients. Patients with DLVOTO and normal wall thickness were compared with 20 age-matched and gender-matched controls with normal stress echocardiographic findings. Two other groups were also compared: patients with DLVOTO and mild segmental hypertrophy (segmental wall thickness ≤15 mm) and patients with normal left ventricles but DLVOTO after dobutamine stress. Six symptomatic patients were identified (mean age, 48 ± 9 years; range, 37-60 years; five men) with normal wall thickness who developed DLVOTO after exercise during a 6-year period. Five had been hospitalized for cardiac symptoms. The mean postexercise LV outflow tract gradient caused by systolic anterior motion mitral-septal contact was 107 ± 55 mm Hg (range, 64-200 mm Hg). All patients had echocardiographic LV wall thicknesses in the normal range (≤12 mm). Structural abnormalities of the mitral valve were identified in all six patients. These were elongated posterior leaflets (2.0 vs 1.5 cm, P < .0005), elongated anterior leaflets (3.2 vs 2.6 cm, P= .015), increased protrusion height of the mitral valve beyond the mitral annular plane (2.6 vs 0.6 cm, P < .00001), and residual protruding portions of the mitral valve leaflets (0.85 vs 0.24 cm, P < .005). There was anterior positioning of the papillary muscles in the LV cavity, with a greater distance from the plane of the papillary muscles to the posterior wall (1.8 vs 1.3 cm, P= .03). In two patients, potentially provoking medications were stopped; two patients received β-blockers, with reductions of angina. Medium-term prognosis was good; no patient had died after 3.5 years. The mitral valve abnormalities in the 10 patients with DLVOTO and mild segmental hypertrophy were qualitatively and quantitatively very similar to those in patients with DLVOTO without hypertrophy. In contrast, the valves of patients with dobutamine stress DLVOTO were not elongated, but 50% had residual mitral leaflets that protruded past the coaptation point by ≥5 mm. DLVOTO after exercise can occur in the absence of LV hypertrophy and may be associated with high gradients and cardiac symptoms. Elongated, redundant mitral valve leaflets with anterior position of the papillary muscles appear to cause the postexercise obstruction.

Anesthetic management of a patient with hypertrophic cardiomyopathy and patent ductus arteriosus

Anesthetic management of a patient with hypertrophic cardiomyopathy and patent ductus arteriosus

Paradoxical Heart Failure Precipitated by Profound Dehydration: Intraventricular Dynamic Obstruction and Significant Mitral Regurgitation in a Volume-Depleted Heart

Occurrence of dynamic left ventricular outflow tract (LVOT) obstruction is not infrequent in critically ill patients, and it is associated with potential danger. Here, we report a case of transient heart failure with hemodynamic deterioration paradoxically induced by extreme dehydration. This article describes clinical features of the patient and echocardiographic findings of dynamic LVOT obstruction and significant mitral regurgitation caused by systolic anterior motion of the mitral valve in a volume-depleted heart.

Dynamische Obstruktion des linksventrikulären Ausflusstrakts bei Lungenembolie

Left ventricular hypertrophy, dehydration, sepsis, vasodilatation, excessive sympathetic stimulation, pericardial tamponade and surgical treatment of the atrioventricular valve are known causes of left ventricular outflow tract (LVOT) obstruction. We report the rare case of a patient who developed dynamic LVOT obstruction as a complication of acute pulmonary embolism.

Alcohol septal ablation after transaortic valve implantation: The dynamic nature of left outflow tract obstruction

Transcatheter aortic valve implantation (TAVI) has emerged as a less invasive and potentially high efficacious procedure for the treatment of high-risk patients with symptomatic aortic stenosis. Appropriate patient selection for TAVI is a key component to ultimate clinical success. Herein, we describe a patient with left ventricular outflow tract (LVOT) obstruction that became apparent only following relief of aortic stenosis with TAVI. This report highlights the dynamic nature of LVOT obstruction, which was successfully treated in our patient with catheter-based alcohol septal ablation. The potential to unmask dynamic LVOT obstruction with TAVI should be an important consideration in patient selection for the procedure, and the postoperative assessment of these patients.

2011 ACCF/AHA Guideline for the Diagnosis and Treatment of Hypertrophic Cardiomyopathy: Executive Summary

2011;58;2703-2738; originally published online Nov 8, 2011; J. Am. Coll. Cardiol. W. Yancy Rakowski, Christine E. Seidman, Jeffrey A. Towbin, James E. Udelson, and Clyde Fifer, Mark S. Link, Srihari S. Naidu, Rick A. Nishimura, Steve R. Ommen, Harry Bernard J. Gersh, Barry J. Maron, Robert O. Bonow, Joseph A. Dearani, Michael A. Thoracic Surgeons Society for Cardiovascular Angiography and Interventions, and Society of Nuclear Cardiology, Heart Failure Society of America, Heart Rhythm Society, of Thoracic Surgery, American Society of Echocardiography, American Society Developed in Collaboration With the American Association for Guidelines Cardiology Foundation/American Heart Association Task Force on Practice Cardiomyopathy: Executive Summary: A Report of the American College of 2011 ACCF/AHA Guideline for the Diagnosis and Treatment of Hypertrophic This information is current as of May 14, 2012 http://content.onlinejacc.org/cgi/content/full/58/25/2703 located on the World Wide Web at: The online version of this article, along with updated information and services, is

Left ventricular cavity obliteration during dobutamine stress echocardiography in diabetic patients

Prevalence of dynamic left ventricular outflow tract obstruction (DLVO) during dobutamine stress-echo (DSE) seems disproportionally high among diabetic patients. We retrospectively identified 212 diabetic (D+) and 212 non diabetic (D-) subjects, who underwent DSE for suspected coronary artery disease (CAD); we evaluated DSE-induced DLVO prevalence and correlates. During DSE, 105 patients in D+ (50%) and 83 in D- group (39%, P = 0.032) developed a DLVO, with similar maximum gradient (94 ± 49 mmHg in D+ vs. 86 ± 49 mmHg in D-, P = NS). D+ and D- patients with DLVO showed reduced LV end-diastolic and end-systolic dimension. Compared with diabetic subjects without DLVO, diabetic patients with DLVO had higher left ventricular (LV) ejection fraction (EF), lower LV mass index; diastolic function was normal in a higher proportion of cases. Non diabetic patients with moderate or severe DLVO had higher LV EF compared with patients without DLVO. At multivariate analysis, in D+ patients, the only independent predictor was a smaller LV end-diastolic diameter (HR 0.779, CI 0.655-0.926, P = 0.005); in D- patients lower age (HR 0.878, CI 0.806-0.957, P = 0.003), higher LV EF (HR 1.087, CI 1.003-1.177, P = 0.042) and lower peak WMSI (HR 0.017, CI 0.001-0.325, P = 0.007) were associated to presence of DLVO. In D+ patients, during a median follow-up of 924 ± 134 days, we observed 11 new cardiac events, only 1 in patients with DLVO (P = 0.0041). DSE-provoked DLVO had a very high prevalence in patients evaluated for suspected CAD, especially among diabetic patients; echocardiographic predictors were a reduced LV dimension in D+ and a preserved systolic function, both at rest and at peak stress, in D- patients.