Frequent occurrence of postbreakfast syncope due to carotid sinus syndrome after surgery for hypopharyngeal cancer: A case report.

RATIONALE: Syncope often occurs in patients with advanced head and neck cancers due to the stimulation of the autonomic nervous system by the tumor. Here, we describe a case of frequent syncopal episodes after laryngopharyngectomy for hypopharyngeal cancer. As all syncopal episodes were observed during the forenoon, we also evaluated the heart rate variability using ambulatory electrocardiography to determine why the syncopal episodes occurred during a specified period of the day. PATIENT CONCERNS: A 73-year-old Japanese man who underwent laryngopharyngectomy for recurrent hypopharyngeal cancer started experiencing frequent episodes of loss of consciousness that occurred during the same time period (10:00-12:00). He had never experienced syncopal episodes before the operation. From 23 to 41 days postoperatively, he experienced 9 syncopal episodes that occurred regardless of his posture. DIAGNOSES: Pharyngo-esophagoscopy revealed an anastomotic stricture between the free jejunum graft and the upper esophagus. Swallowing videofluoroscopy confirmed the dilatation of the jejunal autograft and a foreign body stuck on the oral side of the anastomosis. Contrast-enhanced computed tomography revealed that the carotid artery was slightly compressed by the edematous free jejunum. The patient was diagnosed with carotid sinus syndrome (CSS) as the free jejunum was dilated when consuming breakfast, which may have caused carotid sinus hypersensitivity and induced a medullary reflex. INTERVENTIONS: Administration of disopyramide was effective in preventing syncope. Heart rate variability analysis using ambulatory electrocardiography showed that parasympathetic dominancy shifted to sympathetic dominancy during 10:00 to 12:00. The significant time regularity of the syncopal episodes may have been affected by modified diurnal variation in autonomic tone activity. OUTCOMES: After the surgical release and re-anastomosis of the pharyngoesophageal stenosis via an open-neck approach, no recurrent episodes of syncope were reported. LESSONS: We reported a case of frequent syncopal episodes limited to the forenoon due to CSS after surgery for hypopharyngeal carcinoma. The patient was treated with anticholinergics followed by the release and re-anastomosis of the pharyngoesophageal stenosis. When syncope occurs after surgery for head and neck lesions, CSS due to postoperative structural changes should be considered as a differential diagnosis of syncope.

Structure-activity relationship and cardiac safety of 2-aryl-2-(pyridin-2-yl)acetamides as a new class of broad-spectrum anticonvulsants derived from Disopyramide.

A series of 2-aryl-2-(pyridin-2-yl)acetamides were synthesized and screened for their anticonvulsant activity in animal models of epilepsy. The compounds were broadly active in the 'classical' maximal electroshock seizure (MES) and subcutaneous Metrazol (scMET) tests as well as in the 6 Hz and kindling models of pharmacoresistant seizures. Furthermore, the compounds showed good therapeutic indices between anticonvulsant activity and motor impairment. Structure-activity relationship (SAR) trends clearly showed the highest activity resides in unsubstituted phenyl derivatives or compounds having ortho- and meta- substituents on the phenyl ring. The 2-aryl-2-(pyridin-2-yl)acetamides were derived by redesign of the cardiotoxic sodium channel blocker Disopyramide (DISO). Our results show that the compounds preserve the capability of the parent compound to inhibit voltage gated sodium currents in patch-clamp experiments; however, in contrast to DISO, a representative compound from the series 1 displays high levels of cardiac safety in a panel of in vitro and in vivo experiments.

Disopyramide use in infants and children with hypertrophic cardiomyopathy.

Hypertrophic cardiomyopathy has a range of clinical severity in children. Treatment options are limited, mainly on account of small patient size. Disopyramide is a sodium channel blocker with negative inotropic properties that effectively reduces left ventricular outflow tract gradients in adults with hypertrophic cardiomyopathy, but its efficacy in children is uncertain. A retrospective chart review of patients ⩽21 years of age with hypertrophic cardiomyopathy at our institution and treated with disopyramide was performed. Left ventricular outflow tract Doppler gradients before and after disopyramide initiation were compared as the primary outcome measure. Nine patients received disopyramide, with a median age of 5.6 years (range 6 days-12.9 years). The median left ventricular outflow tract Doppler gradient before initiation of disopyramide was 81 mmHg (range 30-132 mmHg); eight patients had post-initiation echocardiograms, in which the median lowest recorded Doppler gradient was 43 mmHg (range 15-100 mmHg), for a median % reduction of 58.2% (p=0.002). With median follow-up of 2.5 years, eight of nine patients were still alive, although disopyramide had been discontinued in six of the nine patients. Reasons for discontinuation included septal myomectomy (four patients), heart transplantation (one patient), and side effects (one patient). Disopyramide was effective for the relief of left ventricular outflow tract obstruction in children with hypertrophic cardiomyopathy, although longer-term data suggest that its efficacy is not sustained. In general, it was well tolerated. Further study in larger patient populations is warranted.

Safety of Outpatient Initiation of Disopyramide for Obstructive Hypertrophic Cardiomyopathy Patients.

BACKGROUND: Disopyramide is effective in ameliorating symptoms in patients with hypertrophic cardiomyopathy; however, its potential for proarrhythmic effect has raised concerns about its use in the ambulatory setting. The risk of initiating disopyramide in this manner has never been evaluated. METHODS AND RESULTS: All charts of patients seen in the outpatient hypertrophic cardiomyopathy clinic between 2010 and 2014 were screened for initiation of disopyramide and data were extracted. Disopyramide in our clinic is usually initiated at a dose of 300 mg daily and titrated during follow-up. A total of 2015 patients were seen in the clinic, including 168 who were started on disopyramide. There were no cardiac events within 3 months of disopyramide initiation. During long-term follow-up (255 patient-years; mean, 447 days; interquartile range, 201-779), only 2 patients developed cardiac events (syncope of unknown cause in both). Thirty-eight patients (23%) developed side effects of disopyramide and 18 (11%) stopped the drug because of these side effects. Of the patients continuing disopyramide long term, 63% remained free of septal reduction interventions at end of follow-up. Disopyramide at a dose of 300 mg prolonged the mean QTc interval by 19±23 ms; however, increasing the dose to 600 mg had no further significant effect. CONCLUSIONS: Initiation of disopyramide in the outpatient setting is safe and the risk of subsequent sudden cardiac death is low. Because of its QT-prolonging effect, precautions may be necessary in patients at higher risk of torsades de pointes.

Disopyramide for Hypertrophic Cardiomyopathy: A Pragmatic Reappraisal of an Old Drug.

Hypertrophic cardiomyopathy (HCM) is a genetic cardiac disorder characterized by unexplained left ventricular hypertrophy in the absence of other cardiac or systemic etiologies. Approximately two-thirds of patients with HCM develop left ventricular outflow tract (LVOT) obstruction with or without provocation, whereas nearly half develop heart failure with preserved ejection fraction. Medical management of heart failure with preserved ejection fraction is based on the presence of symptoms and LVOT obstruction and frequently includes ß-blockers or verapamil. Disopyramide is a class Ia antiarrhythmic that historically was used for the treatment of arrhythmias; however, its contemporary use is often reserved for patients with HCM who are persistently symptomatic despite ß-blockers or verapamil and have evidence of LVOT obstruction. The pharmacologic rationale for use of disopyramide is largely based on its strong negative inotropic property. Three clinical studies have showed significant improvements in heart failure symptoms and a reduction in the need for invasive therapy in patients treated with disopyramide. Appropriate dosing and monitoring of disopyramide are important to mitigate the potential for anticholinergic adverse events and proarrhythmias. Disopyramide is a safe and effective medication that reduces heart failure symptoms and LVOT gradient and delays the need for invasive therapy in patients with obstructive HCM.

Early-Morning Type Ventricular Fibrillation With J Wave.

A 67-year-old man who had cardiopulmonary arrest (CPA) at home was admitted to our institution. His spontaneous circulation was restored by bystander cardiopulmonary resuscitation (CPR) performed by his wife and an automated external defibrillator (AED). J waves were observed in the inferior leads of an electrocardiogram. We performed an implantable cardioverter defibrillator (ICD) implantation. After the ICD implantation, appropriate shocks due to ventricular fibrillation (VF) were observed on interrogation of the ICD at a frequency of twice a month. Most VF events occurred in the early morning between 1:00 to 6:00, and ventricular premature contractions (VPCs) were detected just before the occurrence of VF. Since the VF events always occurred in the early morning, we started long-acting disopyramide (150 mg/day, before bedtime), which has a muscarinic receptor blocking action. As a result, he has not received any appropriate ICD shocks for more than two years.

Effects of flecainide on left ventricular pressure gradient and symptoms in obstructive hypertrophic cardiomyopathy: a comparison of flecainide and disopyramide.

It remains unclear whether flecainide, a Class I antiarrhythmic drug, improves left ventricular pressure gradient (LVPG) or symptoms in patients with obstructive hypertrophic cardiomyopathy (HCM). Our study evaluated the long-term efficacy of flecainide, compared to disopyramide, when administered orally, on LVPG and symptoms in obstructive HCM patients. Among 164 obstructive HCM patients, 15 were administered oral flecainide therapy and 33 administered oral disopyramide therapy. LVPG declined from 79.8 ± 36.6 to 39.2 ± 36.7 mmHg (p = 0.003) after flecainide therapy and from 74.5 ± 26.4 to 31.4 ± 24.8 mmHg (p < 0.001) after disopyramide therapy. The percent reduction in LVPG was -47.9 ± 43.2 % in patients treated with flecainide, comparable to the results for those treated with disopyramide (-57.1 ± 33.0 %; p = 0.425). We found no significant differences in improvement in NYHA functional class between patients treated with flecainide and those treated with disopyramide (p = 0.331). Patients treated with flecainide exhibited no significant adverse side effects, and there was no need for myectomy or alcohol septal ablation to reduce LVPG and symptoms. Improvements in LVPG and symptoms were similar in patients treated with flecainide and patients treated with disopyramide, suggesting that flecainide is a potentially useful alternative for symptomatic obstructive HCM patients, particularly those with disopyramide-induced vagolytic side effects, narrow angle glaucoma, or prostatic hyperplasia and pre-existing urination difficulties. Our data must be viewed with caution, however, in view of the small number of study patients. Flecainide therapy will require further proof of safety before it can be routinely recommended in patients with symptomatic obstructive HCM.

Combined effect of disopyramide and erythromycin on ventricular repolarization in dogs with complete atrioventricular block.

The combined effects of disopyramide (DP) and erythromycin (EM) on ventricular repolarization and the inciden-ces of ventricular premature contractions (VPCs) and torsades de pointes (TdP) were investigated in 12 anesthetized dogs with complete atrioventricular block. Monophasic action potentials (MAPs) were measured from the left and right ventricular (LV and RV) endocardium. The right or left ventricle was paced at a cycle length of 750-1000 msec. Dogs were divided into 2 groups and given either intravenous DP at 3 mg/kg and then intravenous EM at 50 mg/kg (group 1, n = 8), or intravenous EM at 50 mg/kg and then intravenous DP at 3 mg/kg (group 2, n = 4). MAP duration at 90% repolarization (MAPD(90)) was measured before drug administration (baseline) and again after administration of each drug. RV MAPD(90) and LV MAPD(90) increased significantly (P < 0.02) after administration of each drug in group 1 (RV MAPD(90): from 247.0 ± 36.3 [baseline] to 283.5 ± 38.3 to 321.8 ± 56.7; LV MAPD(90): from 262.6 ± 49.1 (baseline) to 296.1 ± 58.8 to 351.0 ± 80.6). Early afterdepolarizations developed in 2 group 1 dogs after administration of DP and in 4 additional dogs after administration of EM. Frequent VPCs occurred in 1 dog after administration of DP and in 2 additional dogs after administration of EM, and TdP and ventricular tachycardias developed in 2 of the 3 dogs after administration of EM. Similar trends occurred in group 2. These results indicate a potentially fatal interaction between DP and EM administered in clinically relevant doses.

Negative ionotropic agents for the treatment of left ventricular outflow tract obstruction due to sigmoid septum and concentric left ventricular hypertrophy.

BACKGROUND: Negative ionotropic agents are established treatments for left ventricular outflow tract obstruction (LVOTO) in hypertrophic cardiomyopathy (HCM). However, their benefit in those with LVOTO without typical HCM is unclear. We evaluated if negative ionotropic agents are beneficial in treatment of LVOTO in patients without typical HCM. METHOD: In this retrospective cohort study, we evaluated echocardiograms and reviewed records of 15 patients with resting LVOT obstruction due to sigmoid septum (SS, n=9) and mild concentric left ventricular hypertrophy (LVH, n=6). Patients received treatment with sequential negative ionotropic agents (ß-blockers and disopyramide). Initial symptoms, presentation characteristics and echocardiographic characteristics pre and post treatment were evaluated. RESULTS: Fifteen patients (mean age 66.2 years, 46.7% male) were included. Dyspnoea (NYHA Class II/III) was reported as the initial symptom in all patients with four patients reporting chest pain. All patients had hypercontractile LV function at baseline (fractional shortening 46.29±8.77%) but had normal LVS/PW ratio (1.03±0.10). The mean resting LVOT gradient was 74.4±55.2 mmHg. Fourteen patients received initial ß-blocker therapy with a mean reduction in peak LVOT gradient of 40.9 mmHg seen in 11 patients that responded to therapy (p=0.02). Nine patients received disopyramide with a further 24.2±25.8 mmHg reduction in peak LVOT gradient observed in eight patients who tolerated treatment (p=0.04). Symptomatic improvement occurred in 80% of treated patients. CONCLUSIONS: In patients with LVOTO without typical HCM, sequential treatment with negative ionotropes is associated with a significant reduction in the degree of LVOTO and leads to symptomatic improvement.

Prospective comparative study of intravenous cibenzoline and disopyramide therapy in the treatment of paroxysmal atrial fibrillation after cardiovascular surgery.

BACKGROUND: It has been reported that approximately one-third of patients undergoing cardiovascular surgery experience paroxysmal atrial fibrillation (AF) during the postoperative period. There is, however, little information on the selection of anti-arrhythmic drugs for terminating postoperative paroxysmal AF. METHODS AND RESULTS: Between April 2007 and March 2009, 118 patients (76 men, 42 women, mean age 68+/-10 years) who had postoperative paroxysmal AF lasting > or =30 min were randomly assigned to receive either iv cibenzoline (70 mg, n=60) or disopyramide (50 mg, n=58) for terminating postoperative paroxysmal AF. The success rate of iv cibenzoline therapy (47%) was significantly greater than that of iv disopyramide therapy (24%; P<0.05). To identify clinical factors to increase the termination efficacy of iv cibenzoline, multivariate logistic regression was used to adjust for several covariates and to generate adjusted odds ratios (OR). The significant variables for the termination of paroxysmal AF after iv cibenzoline therapy were pretreatment with oral beta-adrenergic blockers (OR =8.224, P=0.030) and smaller left atrial dimensions (OR =0.879, P=0.039). CONCLUSIONS: The efficacy of iv cibenzoline for the termination of postoperative paroxysmal AF was significantly better than that of disopyramide, especially in patients with pre-administration of oral beta-adrenergic blockers and those with smaller left atrium.

Provokable left ventricular outflow tract obstruction in a patient without hypertrophy.

BACKGROUND: A 61-year-old man presented with shortness of breath and chest pain on exertion. He had been diagnosed as having hiatus hernia 2 years previously and was taking proton-pump inhibitors as necessary. He had a family history of ischemic heart disease and subarachnoid hemorrhage. INVESTIGATIONS: Physical examination, electrocardiography, echocardiography, cardiopulmonary exercise testing, coronary angiography, transoesophageal echocardiography, stress echocardiography. DIAGNOSIS: Provokable left ventricular outflow tract obstruction without electrocardiographic abnormalities or left ventricular hypertrophy on echocardiography. MANAGEMENT: Pharmacological therapy (atenolol 50 mg daily, disopyramide 250 mg twice daily), dual-chamber pacemaker implantation.

Nifekalant and disopyramide in a patient with short QT syndrome: evaluation of pharmacological effects and electrophysiological properties.

We assessed several pharmacological effects on electrocardiogram parameters and effective refractory period (ERP) in a patient with a short QT syndrome (SQTS). Pharmacological challenge tests revealed that disopyramide and selective I(kr) blocker, nifekalant normalized QT interval, and ERP of the atrial and ventricular myocardium. This study suggested that disopyramide and nifekalant should be feasible for the drug treatment of the SQTS. Moreover, QT interval was paradoxically prolonged at higher heart rates induced with isoproterenol infusion or an exercise test, although the mechanism of this QT prolongation remains to be investigated.

Oral disopyramide for the acute treatment of severe outflow obstruction in hypertrophic cardiomyopathy in the ICU setting.

When severe COPD and obstructive hypertrophic cardiomyopathy (HCM) coexist, management is challenging and complex. Drug contraindications limit pharmacologic options. Patients may not be candidates for surgical septal myectomy due to severe pulmonary disease. We describe a case of an elderly woman with severe reactive COPD who presented with an infectious exacerbation and dyspnea that progressed to near intubation due to heart failure from coexistent obstructive HCM. Transthoracic echocardiography revealed massive asymmetric septal hypertrophy and a diffusely hyperkinetic left ventricle with a left ventricular outflow tract (LVOT) gradient of 92 mm Hg. Two and a half hours after oral administration of disopyramide, LVOT gradient had decreased to 25 mm Hg with a corresponding immediate improvement in symptoms.

Pathophysiology of hypertrophic cardiomyopathy determines its medical treatment.

Physicians treating hypertrophic cardiomyopathy (HCM) are faced with unique management challenges. Understanding pathophysiology and overall good prognosis forms the basis for medical treatment. Treatment is tailored by the presence or absence of outflow tract gradient and individual symptoms. In all patients, formal stratification for sudden death risk is necessary, with consideration of defibrillator implantation in patients deemed to be at high risk. In patients with no or only mild symptoms the approach of watchful waiting is often appropriate. For symptomatic patients with non-obstructed disease medical treatment with calcium channel blockers and beta-blockers is aimed to improve heart failure symptoms, and ischemia. Verapamil is the most often used, with likely benefit of relieving ischemia. Obstruction, most commonly due to systolic anterior motion of the mitral valve (SAM) and mitral-septal contact, occurs in >/=50% of all HCM patients, worsening symptoms and increasing mortality. Successful medical treatment of obstruction with negative inotropes slows acceleration of left ventricular ejection with delay in SAM, ultimately yielding a lower pressure gradient. Beta -blockers are the first line treatment in obstructive HCM predominantly by mitigating provocable gradients. The magnitude of symptom relief with verapamil is similar to the effect of beta -blockade. Disopyramide combined with beta -blockade is thought by some to be the most effective medical treatment of obstruction, and has been shown to be safe and not pro-arrhythmic. Most symptomatic HCM patients with significant obstruction at rest or provocation can be successfully managed with long-term medication alone.

Heart rate variability is a useful parameter for evaluation of anticholinergic effect associated with inducibility of atrial fibrillation.

BACKGROUND: Disopyramide is thought to have an advantageous effect for atrial fibrillation (AF) associated with vagal activity because of its anticholinergic effect. METHOD: We used a canine vagal nerve stimulation (VNS) model. The monophasic action potential (MAP) duration at 90% repolarization (MAP(90)), the intraatrial conduction time, the induciblity of AF by electrical stimulation, and the amplitude of high-frequency component (HF-amp) of the heart rate variability (HRV) were evaluated before and after the administration of disopyramide (1 mg/kg) (group D, n = 8) or pilsicainide (1 mg/kg) (group P, n = 5). RESULTS: In group D, HF-amp decreased in the baseline condition from 1.1 +/- 0.6 to 0.6 +/- 0.4 ms and the degree of VNS-induced augmentation of HF-amp was attenuated from +492% to +127%. VNS-induced shortening of MAP(90) was also attenuated in the right atrium (from -30 +/- 15% to -10 +/- 6%) and in the left atrium (from -15 +/- 9% to -6 +/- 6%). In group P, little effect was shown in these parameters. The vagotonic AF became noninducible in all eight experiments in group D, while in only one of five in group P. CONCLUSION: The beneficial effect of disopyramide for vagotonic AF is based on the decrease of basal vagal tone and attenuation of the effect of vagal stimulation in the atrial myocardium. HRV is a useful parameter for evaluation of the effect of antiarrhythmic drugs on the autonomic nerve system, and the evaluation of variability may be useful for testing drug efficacy for arrhythmias.

Multicenter study of the efficacy and safety of disopyramide in obstructive hypertrophic cardiomyopathy.

OBJECTIVES: In this study we assessed the long-term efficacy and safety of disopyramide for patients with obstructive hypertrophic cardiomyopathy (HCM). BACKGROUND: It has been reported that disopyramide may reduce left ventricular outflow gradient and improve symptoms in patients with HCM. However, long-term efficacy and safety of disopyramide has not been shown in a large cohort. METHODS: Clinical and echocardiographic data were evaluated in 118 obstructive HCM patients treated with disopyramide at 4 HCM treatment centers. Mortality in the disopyramide-treated patients was compared with 373 obstructive HCM patients not treated with disopyramide. RESULTS: Patients were followed with disopyramide for 3.1 +/- 2.6 years; dose 432 +/- 181 mg/day (97% also received beta-blockers). Seventy-eight patients (66%) were maintained with disopyramide without the necessity for major non-pharmacologic intervention with surgical myectomy, alcohol ablation, or pacing; outflow gradient at rest decreased from 75 +/- 33 to 40 +/- 32 mm Hg (p < 0.0001) and mean New York Heart Association functional class from 2.3 +/- 0.7 to 1.7 +/- 0.6 (p < 0.0001). Forty other patients (34%) could not be satisfactorily managed with disopyramide and required major invasive interventions because of inadequate symptom and gradient control or vagolytic side effects. All-cause annual cardiac death rate between disopyramide and non-disopyramide-treated patients did not differ significantly, 1.4% versus 2.6%/year (p = 0.07). There was also no difference in sudden death rate, 1.0%/year versus 1.8%/year (p = 0.08). CONCLUSIONS: Two-thirds of obstructed HCM patients treated with disopyramide could be managed medically with amelioration of symptoms and about 50% reduction in subaortic gradient over >/=3 years. Disopyramide therapy does not appear to be proarrhythmic in HCM and should be considered before proceeding to surgical myectomy or alternate strategies.

Effects of antiarrhythmic agents on left ventricular function during exercise in patients with chronic left ventricular dysfunction.

This study was designed to determine the effects of antiarrhythmic agents on global left ventricular (LV) function during exercise in patients with chronic LV dysfunction. Thirty-five patients with LV dysfunction [LV ejection fraction (LVEF) < 45%] and ventricular arrhythmias were studied. They were randomly classified into 3 groups: patients who received a single oral dose of 6 mg/kg disopyramide phosphate (n = 12), those who received a single oral dose of 4 mg/kg mexiletine hydrochloride (n = 12), and those who received a single oral dose of 4 mg/kg pilsicainide hydrochloride (n = 11). First, all patients were subjected to baseline rest and peak exercise, equilibrium-gated cardiac-pool scintigraphy with 99mTc-human serous albumin of 740 MBq (baseline data). Second, on a separate day, they were given drugs once, and were subsequently subjected to rest and peak exercise equilibrium-gated cardiac-pool scintigraphy. Exercise LVEF and peak ejection rate (PER) after administration were significantly lower in the disopyramide and pilsicainide groups than in the mexiletine group (p < 0.05, respectively). The changes in LVEF and PER from rest to peak exercise after administration were significantly less than the baseline changes in those in the disopyramide and pilsicainide groups (p < 0.05, respectively). However, no significant changes in functional parameters were recognized in the mexiletine group. Due care should be taken when disopyramide and pilsicainide are administered to patients with chronic LV dysfunction since they reduce systolic LV function during exercise.

Effective disopyramide treatment in a boy with mid-ventricular hypertrophic obstructive cardiomyopathy.

A 14-year-old boy with mid-ventricular hypertrophic obstructive cardiomyopathy (MVHOCM) first presented at the age of 10 years with severe chest pain. Two-dimensional echocardiography disclosed marked hypertrophy at the mid-portion of the ventricular septum, and left ventriculography showed an hourglass appearance at systole. He was initially treated with propranolol, but the chest pain and dyspnea on exertion worsened at the age of 12 years. After disopyramide was started, the chest pain disappeared and the degree of the pressure gradient at the mid-ventricular level was reduced. There was also significant improvement on a 123I beta-methyliodophenyl pentadecaonic acid (BMIPP) myocardial scintigram.

An intraoperative diagnosis of dynamic left ventricular outflow tract obstruction using transesophageal echocardiography leads to the treatment with intravenous disopyramide.

UNLABELLED: Hypertrophic obstructive cardiomyopathy (HOCM) is an uncommon familial disorder, traditionally characterized by asymmetric septal hypertrophy and left ventricular outflow tract (LVOT) obstruction (1). It is now recognized that HOCM may also include those patients with secondary left ventricular hypertrophy (LVH) and dynamic LVOT obstruction. In particular, a syndrome with similar clinical and echocardiographic findings has been identified in elderly patients exhibiting concentric LVH with chronic hypertension, aortic stenosis, or sigmoid-shaped septum (2). IMPLICATIONS: During surgery, dynamic left ventricular outflow obstruction (LVOT) can potentially occur frequently, but diagnosis may be less frequent. When circulatory disturbance occurs with suspicion of LVOT obstruction, transesophageal echocardiography can provide exact proof of diagnosis and basis for immediate treatment.