Latent Left Ventricular Outflow Tract Research Articles

Unmasking Obstruction in Hypertrophic Cardiomyopathy With Postprandial Resting and Treadmill Stress Echocardiography

Latent left ventricular outflow tract obstruction (LVOTO) is an important cause of symptoms in patients with hypertrophic cardiomyopathy (HCM) but can be challenging to provoke. To examine the value of postprandial resting and stress echocardiography and utilization of invasive or enhanced drug therapies (surgical myectomy, alcohol septal ablation, disopyramide, and mavacamten) in patients with postprandial LVOTO. Consecutive HCM patients without LVOTO underwent routine and postprandial echocardiography at rest, with provocation (Valsalva and standing) and after symptom-limited treadmill stress. Among 252 patients (mean age, 58years, 39% women), postprandial LVOT gradients were higher compared with routine echocardiography at rest (median, 9.0 [0-38.0] vs 0 [0-14.0] mm Hg; P<.0001) and with provocation (18.5 [0-70.3] vs 1.5 [0-41.0] mm Hg; P<.0001). Postprandial exercise stress echocardiogram (PPXSE) gradients were higher in a subset of 44 patients who underwent both postprandial and fasting stress echocardiography (47.0 [5.3-81.0] vs 17.5 [0-46.0] mm Hg; P<.0001). In total, 49 (19.5%) patients achieved the ≥50mm Hg threshold under routine conditions (rest/provocation); 90 (35.7%) additional patients achieved postprandial gradients ≥50mm Hg (rest/provocation/exercise), 38 (15.1%) with PPXSE alone. A total of 71 patients were treated with 91 invasive or enhanced drug therapies, 32 (45.1%) of whom had gradients ≥50mm Hg only after eating (rest/provocation) and 8 (11.3%) only with PPXSE, with symptom relief in the majority. Postprandial echocardiography was useful at unmasking LVOTO in more than one-third of patients who did not have high gradients otherwise. Eating before echocardiography is a powerful provocative tool in the evaluation of patients with HCM.

Sitting maneuver to uncover latent left ventricular outflow tract obstruction in patients without hypertrophic cardiomyopathy

BackgroundLeft ventricular outflow tract obstruction [LVOTO; pressure gradient (PG) ≥30 mmHg] is observed in some patients without hypertrophic cardiomyopathy (HCM), and it may develop especially in older patients without HCM (non-HCM). The aim of this study is to investigate if the Valsalva or an upright sitting maneuver can unveil latent LVOTO in patients with non-HCM. MethodsA total of 33 non-HCM patients with a late peaking or dagger-shaped pulsed Doppler waveform of the LVOT and PG <30 mmHg were included. The Doppler flow velocity of the LVOT was measured at rest, after the Valsalva and a sitting maneuver. Peak PG of ≥30 mmHg after either maneuver was defined as latent LVOTO. The angle between the left ventricular septum and the aorta in the parasternal long-axis view and the apical three-chamber view was measured. ResultsTwenty (61 %) of the 33 patients (mean age 74 ± 9 years) were diagnosed with latent LVOTO. Of these, five (25 %) patients were diagnosed after both the Valsalva and sitting maneuver, and 15 (75 %) were diagnosed only after the sitting maneuver. The latent LVOTO group had a significantly smaller angle than the no-LVOTO group between the ventricular septum and the aorta in the parasternal long axis views (107 ± 8° vs. 117 ± 8°, p < 0.01). ConclusionThe sitting maneuver is better than the Valsalva maneuver in unveiling latent LVOTO in older, non-HCM patients.

Midterm results of latent outflow tract obstruction in hypertrophic cardiomyopathy after septal myectomy: A propensity score-matched study.

The midterm clinical outcomes of patients with latent left ventricular outflow tract (LVOT) obstruction who undergo septal myectomy are unclear. Therefore, this study aimed to evaluate the clinical outcomes of patients with latent LVOT obstruction who underwent septal myectomy. We studied 34 patients with hypertrophic cardiomyopathy (HCM) and latent LVOT obstruction who underwent septal myectomy in 2011-2019 at Anzhen Hospital. After 2:1 propensity score matching, the study cohort included 34 patients with latent LVOT obstruction and 68 patients with resting LVOT obstruction. Compared to patients with resting LVOT obstruction, patients with latent LVOT obstruction had a thinner interventricular septal thickness (18.2 ± 3.2 mm vs. 20.4 ± 5.6 mm; p = .01), while the proportion of moderate or severe mitral regurgitation was significantly higher (26.5% vs. 5.9%; p = .003). Moreover, the proportion of mitral valve procedures (26.5% vs. 5.9%; p = .004) was significantly higher in patients with latent LVOT obstruction. However, there was no intergroup difference in cardiovascular death (5.9% vs. 1.5%, p = .26). Furthermore, the 5-year survival rates after sudden cardiac death (100.0% vs. 91.7%; p = .26) and cardiovascular death (95.5% vs. 89.0%; p = .32) were similar between HCM patients with latent versus resting LVOT obstruction. Midterm clinical outcomes were similar and excellent in a matched cohort of HCM patients with latent versus resting LVOT obstruction after septal myectomy.

Repetitive Squat-to-Stand Provocation of Dynamic Left Ventricular Outflow Tract Obstruction in Hypertrophic Cardiomyopathy

Left ventricular outflow tract (LVOT) obstruction is a determinant in the management of patients with hypertrophic cardiomyopathy, including candidacy for septal reduction therapy and risk stratification for sudden cardiac death. 1 Elliott P.M. Gimeno J.R. Tomé M.T. Shah J. Ward D. Thaman R. et al. Left ventricular outflow tract obstruction and sudden death risk in patients with hypertrophic cardiomyopathy. Eur Heart J. 2006; 27: 1933-1941 Crossref PubMed Scopus (262) Google Scholar ,2 Ommen S.R. Mital S. Burke M.A. Day S.M. Deswal A. Elliott P. et al. 2020 AHA/ACC guideline for the diagnosis and treatment of patients with hypertrophic cardiomyopathy. J Am Coll Cardiol. 2020; 76: e159-e240 Crossref PubMed Scopus (136) Google Scholar Obstruction is defined as a maximal instantaneous gradient ≥ 30 mm Hg, and severe obstruction is defined as a maximal instantaneous gradient ≥ 50 mm Hg. 2 Ommen S.R. Mital S. Burke M.A. Day S.M. Deswal A. Elliott P. et al. 2020 AHA/ACC guideline for the diagnosis and treatment of patients with hypertrophic cardiomyopathy. J Am Coll Cardiol. 2020; 76: e159-e240 Crossref PubMed Scopus (136) Google Scholar Several provocative maneuvers have been used to elicit latent obstruction, including the Valsalva maneuver, amyl nitrite inhalation, and exercise on a treadmill or bike. 3 Marwick T.H. Nakatani S. Haluska B. Thomas J.D. Lever H.M. Provocation of latent left ventricular outflow tract gradients with amyl nitrite and exercise in hypertrophic cardiomyopathy. Am J Cardiol. 1995; 75: 805-809 Abstract Full Text PDF PubMed Scopus (74) Google Scholar , 4 Jensen M.K. Havndrup O. Pecini R. Dalsgaard M. Hassager C. Helqvist S. et al. Comparison of Valsalva manoeuvre and exercise in echocardiographic evaluation of left ventricular outflow tract obstruction in hypertrophic cardiomyopathy. Eur J Echocardiogr. 2010; 11: 763-769 Crossref PubMed Scopus (24) Google Scholar , 5 Shah J.S. Esteban M.T.T. Thaman R. Sharma R. Mist B. Pantazis A. et al. Prevalence of exercise-induced left ventricular outflow tract obstruction in symptomatic patients with non-obstructive hypertrophic cardiomyopathy. Heart. 2008; 94: 1288-1294 Crossref PubMed Scopus (165) Google Scholar During a recent shortage of amyl nitrite, our practice implemented a repetitive squat-to-stand maneuver as an adjunct to the Valsalva maneuver when assessing for LVOT obstruction. We sought to evaluate the efficacy of this repetitive squat-to-stand maneuver in eliciting LVOT obstruction compared with the Valsalva maneuver in a retrospective study.

Hypertrophic cardiomyopathy with latent obstruction: Clinical characteristics and surgical results

BackgroundThe role of mitral subvalvular anomalies in the etiology of latent left ventricular outflow tract (LVOT) obstruction has rarely been reported; and the results of surgical treatment for latent LVOT obstruction have been infrequently reported as a separate group by other medical centers other than Mayo clinic. MethodsAmong 292 eligible patients, 45 with resting gradients <30 mmHg had provoked obstruction. Their clinical characteristics and surgical results were compared with those of 247 patients with resting LVOT obstruction. The patients were followed up for a median of 13 months. ResultsComparatively, patients with latent obstruction were younger (51.6±12.1 years vs. 57.2±11.6 years, p=0.003) and had higher prevalence of mitral subvalvular abnormalities (73.3% vs. 16.2%, p<0.001) and basal variant of hypertrophic cardiomyopathy (84.5% vs. 62.0%, p=0.014), less marked septal thickness (16.9±2.8 mm vs. 18.6±3.8 mm, p=0.005), lower resting gradients (22.2±5.7 mmHg vs. 93.0±25.7 mmHg, p < 0.001), and lower mitral regurgitation severity (median, 2.0 vs. 3.0, p<0.001). After surgery, no surgical death occurred in patients with latent LVOT obstruction. Only one (2.2%) patient from the latent group developed complete atrioventricular block. No follow-up death or reoperation was recorded with a significant improvement in New York Heart Association functional status in either group. The provoked LVOT gradients of patients with latent obstruction decreased sharply from the preoperative value (11.8±3.7 mmHg vs. 89.8±16.4 mmHg, p < 0.001), with no occurrence of residual obstruction. ConclusionsSymptomatic patients with latent LVOT obstruction may have a higher prevalence of mitral subvalvular abnormalities and have less marked septal hypertrophy; and concomitant mitral management during myectomy for the treatment of this patient group achieved excellent results.

Myocardial Bridge or Something Else?

In this E-Challenge, the authors report on a patient with symptoms of exertional dyspnea and angina, scheduled to have surgical unroofing of an identified myocardial bridge (MB). An MB is very common in patients with hypertrophic cardiomyopathy (HCM). Intraoperative transesophageal echocardiography with provocative maneuvers revealed the patient had a systolic anterior motion of the mitral valve with septal contact and resulting outflow tract obstruction despite the notable absence of significant basal septal hypertrophy. HCM has many phenotypic variants that can make the identification of patients with latent left ventricular outflow tract obstruction difficult in the absence of a high index of suspicion. In this report, the authors discuss the association between MBs and HCM and the importance of recognizing phenotypic variants of HCM.

Latent outflow tract obstruction in hypertrophic cardiomyopathy: Clinical characteristics and outcomes of septal myectomy

ObjectiveThis investigation analyzed clinical characteristics of patients with hypertrophic cardiomyopathy (HCM) and latent left ventricular outflow tract (LVOT) and outcomes following septal myectomy. MethodsWe reviewed patients with HCM and LVOT obstruction undergoing septal myectomy from 2001 to 2016 at our center. Follow-up data on functional status were obtained through mailed survey questionnaires. ResultsThere were 629 (31.8%) patients with latent obstruction (resting LVOT gradient <30 mm Hg, provoked gradient >30 mm Hg) among 1981 patients undergoing septal myectomy. Patients with latent obstruction were more likely to be male (65.7% vs 51.8%, P < .001), but there were no important differences in other clinical characteristics. The New York Heart Association functional classes and measured/predicted maximal oxygen consumption (62 [51, 72] vs 60 [48, 72], P = .158) in cardiopulmonary exercise tests were comparable between the 2 groups. Patients with latent obstruction had both lower septal thickness and lower posterior wall thickness. Median intraoperative provoked pressure gradient decreased from 96 (68, 126) mm Hg to 0 (0, 6) mm Hg after myectomy (P < .001). There was no difference in early (<30 days) deaths (3/629 vs 5/1352, P = .726) and long-term survival between patients with latent obstruction and resting obstruction. In follow-up, both general health status and New York Heart Association functional class were significantly improved following septal myectomy. ConclusionsPatients with HCM and latent LVOT obstruction generally have milder left ventricular hypertrophy but similarly impaired functional capacity compared to those with resting obstruction. Septal myectomy improves functional capacity and symptoms.

An echocardiographic study of left ventricular torsion in patients with latent obstructive hypertrophic cardiomyopathy

Objective To explore the changes of left ventricular torsion function in patients with latent obstructive hypertrophic cardiomyopathy(HCM), and provide quantitative informations for clinical evaluation of cardiac function. Methods A total of 49 consecutive patients with HCM without left ventricular outflow tract obstruction at rest were enrolled.All subjects underwent exercise stress echocardiography. After exercise left ventricular outflow tract pressure gradient(LVOT-PG)≥30 mmHg was positive for exercise stress test (latent obstruction), while LVOT-PG<30 mmHg was negative for exercise stress test (non-obstruction). An ultrasound system obtained two-dimensional ultrasound images of resting and moving peaks. The global longitudinal strain (GLS), global circumferential strain (GCS), global radial strain (GRS) of the left ventricle 16 segments and left ventricular rotation, twist were analysis using off-line EchoPAC software. The differences of the above parameters were compared between the two groups. Results There were no significant differences in GLS, GRS, GCS and Rotation-B between the two groups in resting and peak period of exercise (all P>0.05), GRS in both groups were significantly increased compared with that before exercise (all P 0.05). Conclusions Left ventricular torsion function is significantly changed in rest and after exercise in latent obstructive HCM patients, providing valuable quantitative information for clinical comprehensive evaluation of cardiac function. Key words: Echocardiography, stress; Latent left ventricular outflow tract obstruction; Cardiomyopathy, hypertrophic; Two-dimensional strain; Left ventricular twist

Conventional cardiopulmonary resuscitation-induced refractory cardiac arrest due to latent left ventricular outflow tract obstruction due to a sigmoid septum: a case report

BackgroundPatients with left ventricular outflow tract obstruction who do not exhibit a dynamic pressure gradient at rest, experience pressure gradient increases of ≥ 30 mmHg only during specific situations; this is called latent left ventricular outflow tract obstruction. It is provoked by increased cardiac contraction and preload and afterload depletion. There are a few reports of patients with it developing cardiac arrest. We present a case of latent left ventricular outflow tract obstruction in which the patient with a sigmoid septum experienced refractory pulseless electrical activity due to conventional advanced cardiac life support.Case presentationA 73-year-old Asian woman on escitalopram and lorazepam was transported to our hospital for chest and back pain with altered consciousness. On arrival, she was in shock and developed pulseless electrical activity. After initiation of conventional cardiopulmonary resuscitation according to adult advanced cardiovascular life support guidelines, she could not regain spontaneous circulation. She was ultimately resuscitated via venoarterial extracorporeal membrane oxygenation initiation. The only abnormal laboratory result at admission was anemia. Her hemodynamic status stabilized after red blood cell transfusion, and venoarterial extracorporeal membrane oxygenation was subsequently terminated. Transthoracic echocardiography showed a sigmoid septum; dobutamine-infused Doppler echocardiography revealed a significant outflow gradient, and continuous monitoring showed Brockenbrough–Braunwald sign, which confirmed a diagnosis of latent left ventricular outflow tract obstruction due to a sigmoid septum. As a result, carvedilol and verapamil were initiated. A follow-up dobutamine-infused Doppler echocardiography showed a reduction of outflow gradient, and she was discharged without any sequelae. Latent left ventricular outflow tract obstruction worsened due to increasing cardiac contraction and the depletion of preload and afterload. Depleted preload occurred due to dehydration and anemia, whereas depleted afterload occurred due to the prescribed drugs, which subsequently caused pulseless electrical activity. Moreover, β-stimulation from the adrenaline probably enhanced the hypercontractile state and caused refractory pulseless electrical activity in our case.ConclusionsPatients with latent left ventricular outflow tract obstruction can progress to cardiogenic shock and pulseless electrical activity due to increased cardiac contraction and depletion of preload and afterload. We should consider the patient’s underlying conditions that induced pulseless electrical activity.

Manifestation of Latent Left Ventricular Outflow Tract Obstruction in the Acute Phase of Takotsubo Cardiomyopathy.

Objective Left ventricular outflow tract (LVOT) obstruction is a complication in 15-25% of patients with Takotsubo cardiomyopathy and sometimes leads to catastrophic outcomes, such as cardiogenic shock or cardiac rupture. However, the underlying mechanisms have not been clarified. Methods and Results We experienced 22 cases of Takotsubo cardiomyopathy during 3 years, and 4 of these 22 cases were complicated with LVOT obstruction in the acute phase (mean age 79±5 years, 1 man, 21 women). The LVOT pressure gradient in the acute phase was 100±17 mmHg. Transthoracic echocardiogram (TTE) revealed left ventricular hypertrophy (LVH) in one case and sigmoid-shaped septum without LVH in three cases. The complete resolution of the LVOT obstruction was achieved in a few days with normalization of the left ventricular wall motion following administration of beta-blockers. A dobutamine provocation test after normalization of the left ventricular wall motion reproduced the LVOT obstruction in all cases and revealed the presence of latent LVOT obstruction. Conclusion The manifestation of latent LVOT obstruction in the acute phase of Takotsubo cardiomyopathy is one potential reason for the complication of LVOT obstruction with Takotsubo cardiomyopathy.

Manifestation of latent left ventricular outflow tract obstruction caused by acute myocardial infarction: An important complication of acute myocardial infarction

BackgroundAlthough transient left ventricular outflow tract (LVOT) obstruction is reported as a complication with acute myocardial infarction (AMI), the mechanisms and features of LVOT obstruction in AMI are unclear. Methods and resultsHerein, we present two cases of transient LVOT obstruction with anteroseptal AMI. The features of these two cases were one-vessel disease (1-VD) of the left anterior descending artery (LAD) and maintenance of blood flow to the major septal branch (SB). Moreover, LVOT obstruction was revealed after dobutamine infusion in the chronic phase and the aorto-septal angle was low in these two cases, meaning that latent LVOT obstruction was due to sigmoid-shaped septum. ConclusionsLatent LVOT obstruction would be manifested in the acute phase of AMI. 1-VD of LAD and the maintenance of major SB blood flow are important factors with respect to the manifestation of latent LVOT obstruction.

Comparison of Valsalva manoeuvre and exercise in echocardiographic evaluation of left ventricular outflow tract obstruction in hypertrophic cardiomyopathy

Several methods are used to induce latent left ventricular outflow tract (LVOT) gradients in patients with hypertrophic cardiomyopathy (HCM). We compared LVOT gradients induced by Valsalva manoeuvre (VM) and exercise echocardiography (EE) in patients with HCM treated with percutaneous transluminal septal myocardial ablation (PTSMA). Left ventricular outflow tract gradients were measured at rest, during VM, and during EE in 57 patients 3.8 ± 2.8 years after PTSMA. Measurement succeeded in all patients during VM and in 96% during EE. There were no differences in LVOT gradients between VM [17 (9-33) mmHg] and EE [18 (10-30) mmHg, P = 0.31] [median (inter-quartile range)], but the differences ranged from -45 to 84 mmHg in individual patients. In 93% of patients, EE had no influence on the categorization into manifest-, latent- or non-obstructive phenotypes. The 7%, who revealed LVOT gradients ≥30 mmHg only during EE, did not reach LVOT gradients of 50 mmHg. Patients improving two New York Heart Association (NYHA) classes after PTSMA had higher baseline LVOT gradients during VM [115 (72-160) vs. 88 (54-114) mmHg, P = 0.04] and a larger reduction in VM-induced LVOT gradients [80 (48-139) vs. 61 (28-83) mmHg, P = 0.02] than patients improving one NYHA class. Valsalva manoeuvre and EE induce similar degrees of LVOT gradient, but categorization into obstructive phenotypes was not influenced by EE in more than 90% of patients. Valsalva manoeuvre should be the primary choice of stress modality in HCM patients treated with PTSMA, but EE is essential for the clinical management of the entire cohort.

A Patient with a Sigmoid-Shaped Septum who Complained of Chest Pain with Latent Left Ventricular Outflow Tract Obstruction and was Diagnosed by Dobutamine Stress Echocardiography

胸痛を主訴に来院し，虚血性心疾患が疑われ冠動脈造影が施行されるも有意冠動脈狭窄は認めず．経胸壁心エコーおよびドブタミン負荷心エコーにて潜在性左室流出路狭窄 (latent LVOTO) を有する S 字状中隔 (Sigmoid septum) と診断した一例を報告する．一般に Sigmoid septum は臨床的意義が少ないとされるが，胸痛等の症状を有する例の中には latent LVOTO を認めることがあり，注意を要する．

Dobutamine Stress Echocardiography Unmasks Acute Worsening of Mitral Regurgitation with Latent Left Ventricular Outflow Tract Obstruction Behind Diastolic Heart Failure in Hypertensive Heart Disease

In a 57-year-old woman who was referred as refractory diastolic heart failure, dobutamine stress echocardiography facilitated the diagnosis of acute worsening of mitral regurgitation accompanied with latent left ventricular outflow tract obstruction as a cause of recurrent flash pulmonary edema. Echocardiography revealed the presence of sigmoid septum and concentric left ventricular hypertrophy, being consistent with hypertensive heart disease. Dobutamine induced systolic anterior motion of the mitral valve (SAM) with massive mitral regurgitation, resulting in sudden hypotension with dyspnea. The class Ia antiarrhythmic drug, cibenzoline, reduced the SAM during a dobutamine stress test, followed by no recurrence of flash pulmonary edema.

Latent left ventricular outflow tract obstruction induced by abnormal hypertrophic papillary muscle caused myocardial ischemia

Left ventricular outflow tract (LVOT) obstruction is a typical recognized feature in hypertrophic cardiomyopathy. However, it has been shown in other clinical scenarios such as acute ischemia. In some patients, LVOT obstruction may only be detectable with provocation testing such as exercise stress. Accurate and timely diagnosis, therefore, relies on recognizing an echocardiographic substrate in which LVOT obstruction may occur, such as ventricular hypertrophy. This report describes the case of a patient presenting with effort ECG and signs of myocardial ischemia, with no significant narrowing of coronary arteries but with latent LVOT obstruction due to the presence of an abnormal hypertrophic papillary muscle instead of a typical ventricle hypertrophy.

Acute Myocardial Ischemia Associated with Latent Left Ventricular Outflow Tract Obstruction in the Absence of Left Ventricular Hypertrophy

Left ventricular outflow tract obstruction (LVOTO) is a recognized feature in hypertrophic cardiomyopathy, but can occur in other clinical scenarios such as acute myocardial ischemia. In some patients, LVOTO may only be detectable with provocation testing such as exercise stress. Accurate and timely diagnosis, therefore, relies on recognizing an echocardiographic substrate in which LVOTO may occur, such as ventricular hypertrophy. The investigators describe two cases of latent LVOTO, presenting with acute myocardial ischemia in the absence of obstructive coronary artery disease, in which the diagnosis was delayed because of the absence of hypertrophy, or other recognizable substrate, on the resting echocardiographic study, but became evident during exercise echocardiography.

Resting Echocardiographic Features of Latent Left Ventricular Outflow Obstruction in Hypertrophic Cardiomyopathy

We determined resting echocardiographic features predictive of latent left ventricular (LV) outflow obstruction in 50 consecutive patients with nonobstructive hypertrophic cardiomyopathy (26 provocable, 24 nonprovocable with amyl nitrite inhalation) to have a better understanding of the pathophysiology of this condition and to identify such patients without pharmacologic provocation. Measurements included wall thickness, type of hypertrophy, LV outflow tract diameter, degree of mitral systolic anterior motion, outflow pressure gradient, and ventricular volume. The direction of the ejection streamline was measured to assess the magnitude of the drag force acting on the mitral valve. Thirteen of 16 patients (81%) with proximal septal bulge were provocable, whereas only 3 of 8 patients (38%) with asymmetric septal hypertrophy and 10 of 26 (38%) with concentric hypertrophy were provocable (p <0.05). LV outflow tract was significantly narrower and the angle between the ejection flow and the mitral valve was larger in provocable patients. The sensitivity for predicting provocable patients by a combination of a narrow outflow tract (≤2 cm) and a large angle ( ≥35°) was 65%, with a specificity of 80% and a positive predictive value of 79%. When these criteria were combined with the presence of septal bulge, the sensitivity was 35%, but the specificity and the positive predictive value were both 100%. Patients with nonobstructive hypertrophic cardiomyopathy with proximal septal bulge, a narrow LV outflow tract, and an oblique angle between the ejection flow and the mitral valve appeared to be predisposed for latent outflow obstruction. These features are consistent with the presence of the large Venturi and drag forces. Thus, the left ventricle, which is capable of increasing both the Venturi and the drag forces on the basis of the morphologic change, contributes to the development of outflow obstruction with amyl nitrite inhalation.(Am J Cardiol 1996;78:622–667)

Provocation of latent left ventricular outflow tract gradients with amyl nitrite and exercise in hypertrophic cardiomyopathy

Amyl nitrite may be used to provoke latent gradients in patients with hypertrophic cardiomyopathy (HC) without significant resting outflow tract gradients, but afterload reduction may not be comparable to a more physiologic Stressor such as symptom-limited exercise testing. This study compared the ability of amyl nitrite and exercise testing to provoke outflow tract gradients in 57 patients (40 men and 17 women, mean age ± SD 49 ± 16 years) with HC (septal thickness 19 ± 5 mm, average resting gradient 13 ± 10 mm Hg) who underwent echocardiography at rest, after amyl nitrite inhalation, and after maximal exercise. No significant gradient (< 50 mm Hg) was induced after either provocation in 26 patients (46%); in 15 patients (26%), inducibility was achieved after both stressors, in 6 (11%) after exercise only, and in 10 (18%) after amyl only. Patients with amyl-induced gradients differed from those in whom gradients were noninducible on the basis of smaller outflow tract dimensions (p < 0.001), larger resting gradients (p < 0.001), and a greater prevalence of “septal bulge” morphology (p = 0.02). Those with exercise-induced gradients were able to attain a greater workload (p = 0.07), have larger resting gradients (p = 0.02), and also tended to have a septal bulge morphology (p ≤0.01). Although outflow tract obstruction increased to similar levels after amyl nitrite (49 ± 39 mm Hg) and symptom-limited exercise (47 ± 39 mm Hg), gradients induced by exercise and amyl correlated poorly (r = 0.54). Gradients were the same (within 10%) with both stressors in 14 patients (25%), greater with exercise in 25 (44%), and greater with amyl in 18 patients (32%). Measurement of outflow tract gradients after exercise should be included in the assessment of patients with HC with suspected latent outflow obstruction, particularly in younger patients without amyl-induced outflow tract gradients.

763-5 Provocation of Latent Left Ventricular Outflow Tract Gradients with Amyl Nitrite and Exercise in Patients with Hypertrophic Cardiomyopathy

In pts with hypertrophic cardiomyopathy (HCM) who have obstructive symptoms without significant resting outflow tract gradients, amyl nitrite may be used to provoke latent obstruction. However, the provocative effect of afterload reduction may not be comparable to a more physiologic method such as symptom-limited exercise stress testing. This study compared the ability of amyl nitrite and exercise testing to provoke outflow tract gradients in the same pts. Sixty-one pts (age 49 ± 17y, 43 male) with non-obstructive HCM (septal thickness 19 ± 5 mm, resting outflow tract gradient 15 ± 14 mmHg) underwent echocardiography at rest, following amyl nitrite inhalation, and after maximal exercise. Twenty-six pts (43%) remained without significant inducible gradients «50 mmHg) after either provocation, 17 (28%) became inducible after both stressors, 7 (11%) after exercise only, and 11 (18%) after amyl only. Although obstruction increased to similar levels after amyl nitrite (50 ± 38 mmHg) and after symptom-limited exercise (49 ± 39 mmHg), gradients induced by exercise and amyl correlated poorly (r = 0.54). Gradients were the same with both stressors in 15 patients (EO group), greater with exercise in 26 (EX group), and greater with amyl in 20 patients (AM group). Differences between amyl and exercise were unrelated to drug therapy. EQ(n = 15) EX(n = 26) AM (n = 20) p Age (ys) 37 ± 15 47 ± 17 61 ± 9 p &lt; 0.001 EQ vs AM Septum (mm) 21 ± 5 20 ± 6 17 ± 3 p &lt; 0.01 EQ vs AM Ex HR (% predicted) 73 ± 23 96 ± 9 82 ± 16 p &lt; 0.001 EQ vs EX Exercise RPP (× 10 3 ) 21.4±8.2 33.9 ± 7.7 24.3 ± 85 p &lt; 0.001 EQ vs EX Amyl gradient (mmHg) 40 ± 39 37 ± 33 76 ± 34 p &lt; 0.001 EQ vs AM Ex gradient (mmHg) 40 ± 39 67 ± 42 33 ± 25 p &lt; 0.03 EQ vs EX Over 50% of pts with non-obstructive HCM at rest have inducible gradients which may explain inlermittent symptoms. Measurement of gradients after AM and EX should be included in the assessment of pts with HCM with suspected latent outflow obstruction. Pts with a preponderant AM response are older and have less hypertrophy. EX is particularly indicated in younger patients without AM-induced gradients.