Transient LV Dysfunction Research Articles

Acute myocarditis or apical balloon cardiomyopathy in a patient with systemic lupus erythematosus: The priority of common sense

Myocarditis can mimic takotsubo cardiomyopathy and via versa. We present a 70‐year‐old woman with known systemic lupus erythematous who presented to the emergency department twice during the last 2 years with chest pain, dyspnea and transient LV dysfunction. We also discuss the difficulties in differential diagnosis between lupus myocarditis and takotsubo cardiomyopathy.

Successful TAVI Despite Sudden Low Output and Ventricular Fibrillation in a Patient with Cardiac Amyloidosis

Management of patients with cardiac amyloidosis and concomitant high-grade aortic stenosis is challenging. Here, we report the case of a 79-year-old man with transcatheter aortic valve implantation (TAVI) complicated by low cardiac output during release of a Medtronic Evolut R 34 mm valve. After initiation of mechanical circulatory support, the TAVI valve was successfully implanted despite ongoing ventricular fibrillation. The ventricular fibrillation was successfully treated with injection of potassium into the aorta, with subsequent defibrillation and ventricular pacing. Moreover, pharmacological management of transient severe LV dysfunction and high-grade mitral regurgitation finally led to a favourable course.

Left ventricle dysfunction in patients with critical neonatal pulmonary stenosis: echocardiographic predictors. A single-center retrospective study.

The aim of this study is to identify echocardiographic predictors of transient left ventricle dysfunction after pulmonary valve balloon dilatation (PVBD), in neonates with pulmonary valve stenosis (PVS) and atresia with intact septum (PAIVS) at birth. The study includes patients admitted at the Bambino Gesù Children Hospital from January 2012 to January 2017. Clinical, echocardiographic and cardiac catheterization data before and after PVBD were retrospectively analyzed. Twenty-nine infants were included in the study (21 male and eight female). The median age was 5.8 ± 7.1 days. Eight patients developed transient LV dysfunction (three PAIVS and five PVS) and comparing data before and after the procedure, there was no difference in right ventricle geometrical and functional parameters except for evidence of at least moderate pulmonary valve regurgitation after PVBD. Moderate to severe degree pulmonary valve regurgitation was significant associated to LV dysfunction (p < 0.05) in PVS and PAIVS patients.

ASSOCIATION BETWEEN TAKOTSUBO CARDIOMYOPATHY AND PITUICYTOMA-INDUCED HYPOPITUITARISM

TOPIC: Cardiovascular Disease TYPE: Medical Student/Resident Case Reports INTRODUCTION: Takotsubo cardiomyopathy (TCMP) is defined by transient LV dysfunction with electrocardiographic changes and minimal myocardial enzymatic release mimicking acute myocardial infarction, but without significant coronary artery disease (1). Patients with this reversible cardiomyopathy typically suffer from preceding excess physical or emotional stress, thyrotoxicosis, and adrenal insufficiency (AI) (2). The literature for hypopituitarism causing TCMP is infrequent. Here, we report a case of TCMP caused by panhypopituitarism due to pituicytoma. CASE PRESENTATION: A 67-year-old previously healthy female presented with fatigue for one month. Her blood pressure was 88/50 mmHg, heart rate was 115 beats/min, and temperature 98.7F. She had no abnormal skin pigmentation or dysmorphic features. Laboratory data including CBC and lactic acid was unremarkable. She continued to be hypotensive after receiving IV fluids. Random cortisol and ACTH were 0.8ug/dl (normal range, >3ug/dL) and 13pg/ml (6-50 pg/mL), respectively. Cosyntropin stimulation test revealed a baseline cortisol of 0.9ug/dl, 6.9ug/dl at 30 minutes, and 10ug/dl at 60 minutes, which were diagnostic of AI. TSH of 0.05 uIU/ML (0.30-4.50 uIU/mL) with Free T4 0.8 ng/dL (0.9-1.7 ng/dL). Arginine vasopressin was 2 pmol/L (1-5 pmol/L). Sodium 152 mmol/L with glucose of 60 mg/dL. MR pituitary protocol revealed a 19 X 13 mm pituicytoma. The patient developed chest pain. Troponin was elevated to 0.026. An EKG demonstrated T wave inversion in the anterio-inferior leads. Echo revealed mildly dilated LV with an EF of 35% with severe apical hypokinesis. The patient refused emergent coronary angiography. She was placed in the ICU and treated with 300 mg/day of hydrocortisone for adrenal crisis, levothyroxine 25 mcg/day for secondary hypothyroidism, and DDAVP for diabetes insipidus. Her chest pain improved immediately and blood pressure normalized after 4 days. She was transitioned to 50mg/day of hydrocortisone and continued on DDAVP and levothyroxine. Repeat echo performed 8 days after the original study revealed normal LV with EF of 55% and no wall motion abnormalities. We concluded the patient had panhypopituitarism secondary to the pituicytoma, which led to her TCMP. DISCUSSION: Pituicytoma is a rare tumor of the sellar and suprasellar regions (5). There have been less than 100 reported cases of pituicytoma since it was first described in 1955. Only 17 percent has been associated with hypopituitarism (5). Secondary AI has been shown to cause TCMP due to nonfunctioning pituitary adenomas in one reported case. TCMP resolved after patients receive stress dose steroids (4). Our patient was found to have TCMP due to pituicytoma causing panhypopituitarism, which resolved a week after receiving corticosteroids and thyroid hormone replacement. CONCLUSIONS: Pituicytoma should be considered when patients present with panhypopituitarism and TCMP. REFERENCE #1: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3518949/pdf/CRIM.ENDOCRINOLOGY2 012-580481.pdf REFERENCE #2: https://www.jstage.jst.go.jp/article/endocrj/advpub/0/advpub_0_0707300023/_pdf REFERENCE #3: http://edelweisspublications.com/edelweiss/article/reversible-stress-induced-cardiomyopathy-in-adrenal-insufficiency-cccm-18-107.pdf DISCLOSURES: No relevant relationships by Willie Gilbert, source=Web Response No relevant relationships by Jin Lee, source=Web Response No relevant relationships by Arish Maknojia, source=Web Response

CIGARETTES THAT BROKE HER HEART: COPD-INDUCED TAKOTSUBU CARDIOMYOPATHY

SESSION TITLE: Medical Student/Resident Obstructive Lung Disease Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Takotsubo cardiomyopathy (TCM) is a form of sudden transient LV dysfunction often associated with severe emotional and physical stressors; that mimics ACS. Currently, there are limited studies showing the relationship between COPD and TCM. We present a case of Takotsubo cardiomyopathy in a post-menopausal female secondary to AECOPD. CASE PRESENTATION: A 70-year-old female with a history of COPD, HTN, and smoking presented with severe midsternal chest pain and SOB associated with increased cough and sputum production. On arrival, she was tachycardic, tachypneic, and hypoxic. She had decreased air entry in bilateral lung fields with expiratory wheeze, respiratory acidosis, and hyperinflated lungs on CXR. She received multiple Ipratropium-Albuterol nebulizations for AECOPD resulting in symptomatic improvement. Further workup revealed EKG findings of new hyperacute T waves in V3-V6, TWI in V1 and V2; and up-trending Troponin I which peaked at 7.13. She was managed as Type I NSTEMI with Aspirin, Clopidogrel & IV Heparin. Emergent LHC showed 60% occlusion of RCA. TTE revealed a hyperkinetic base with hypokinetic apical and mid anterior wall, new-onset reduced LVEF of 40 to 45%, consistent with TCM. Her noncritical coronary artery disease was not considered to be contributing to her symptom burden and did not correspond to her EKG and echocardiographic findings. Follow up TTE in 6 months revealed improvement in LVEF to 55 to 60% with a resolution of apical hypokinesis. Given the history of no further psychosocial stressors most likely etiology for her TCM was stress related to acute COPD. DISCUSSION: AECOPD related respiratory failure leading to hypoxemia and hypercapnia has been identified as a potential physical trigger of TCM. Catecholamine excess plays a central role in stress-related apical myocardial stunning and coronary vasospasm; reducing the viability of myocytes via cAMP-mediated calcium overload resulting in contraction band necrosis. Hypoxia with coexisting acidosis causes cardiomyocyte damage through activation of BCL-2 family of proapoptotic proteins leading to changes in mitochondrial permeability and DNA fragmentation. Potential mechanisms include sympathetic overstimulation due to the administration of beta-agonist in the setting of endogenous catecholamine excess from the stress of respiratory failure and concurrent administration of ipratropium resulting in inhibition of parasympathetic system, tachycardia, and rarely paradoxical bronchospasm. It is unclear whether respiratory failure from COPD leading to hypoxia and hypercapnia or repeated use of Albuterol-Ipratropium caused TCM in our patient. CONCLUSIONS: In our case, we highlight that by early recognition of COPD induced TCM; complications could be minimized by limiting the use of beta-agonists and treating ongoing cardiac dysfunction. Further studies are required to establish the exact mechanism of COPD induced TCM. Reference #1: Sharkey S, Windenburg D, et al. "Natural History and Expansive Clinical Profile of Stress (Tako-Tsubo) Cardiomyopathy.” J Am Coll Cardiol., 2010 Jan 26; 55(4):333-341. DOI: https://doi.org/10.1016/j.jacc.2009.08.057 Reference #2: Wittstein I, Thiemann D, et al. "Neurohumoral features of myocardial stunning due to sudden emotional stress.” N Engl J Med. 2005 Feb 10; 352:539-548 https://doi.org/10.1056/NEJMoa043046 Reference #3: Kubasiak, Lori A. and Hernandez, Olga M. and Bishopric, Nanette H. and Webster, Keith A., "Hypoxia and acidosis activate cardiac myocyte death through the Bcl-2 family protein BNIP3.” Proceedings of the National Academy of Science, 2002 Oct; 99(20): 12825-12830. DOI = 10.1073/pnas.202474099 DISCLOSURES: No relevant relationships by Tahreem Ahmad, source=Web Response No relevant relationships by Khubaib Ahmad, source=Web Response No relevant relationships by Waqas Ali, source=Web Response No relevant relationships by Pranali Santhoshini Pachika, source=Web Response

Donor Heart Transient Left Ventricular Dysfunction is Associated with Post-Transplant Primary Graft Dysfunction

There is a significant unmet patient need for heart transplantation, driven partly by low donor heart utilization. Donor left ventricular dysfunction (LVD) is the most common reason for non-allocation. A significant proportion of brain-dead donors will have transient LVD with subsequent recovery, and these donor hearts are considered an underutilized subset. However, their association with post-transplant outcomes, specifically primary graft dysfunction (PGD), remains unclear. This study investigates the relationship between donor clinical characteristics and post-transplant PGD. Donor and post-transplant data was obtained for all donor hearts originating from a centralized diagnostic and recovery OPO that were transplanted at a single institution between 2010-2017. Transient LVD was defined as initial LV ejection fraction (LVEF) at OPO <40% with subsequent normalization of LVEF. All donor hearts had an LVEF ≥50% at time of procurement. The primary outcome was ISHLT-defined LV PGD, and secondary outcomes included 30-day and 1-year mortality. 152 heart transplant patients were identified with corresponding donor hearts originating from the OPO, of which 32 (21%) had post-transplant PGD. PGD was not associated with donor baseline characteristics, pressor requirements, or lab values (Table 1). PGD was associated with lower donor final LVEF (57.5% vs. 60%, p<0.01). 36 (23%) donor hearts had transient LVD, while 116 (77%) did not. Among patients receiving donor hearts with transient LVD, there was a two-fold increased risk of PGD (41% vs. 19%, p=0.01, OR=2.1). Donor transient LVD was not associated with post-transplant 30-day or 1-year mortality. This study indicates that patients receiving donor hearts with transient LV dysfunction have a two-fold increased risk of PGD. Given these findings, vigilance for PGD, careful consideration regarding donor-recipient matching, and early hemodynamic support should be considered in these patients.

Kounis syndrome leading to transient LV dysfunction

Kounis syndrome leading to transient LV dysfunction

Increased Prevalence of Cardiac Allograft Donors with Improved LV Systolic Function Utilizing an Out-of-Hospital Treatment and Recovery Center

Background Published data from UNOS demonstrated that donor hearts with transient LV dysfunction can be used without increasing the risk of poor transplant outcomes, but account for less than 3% of allocated donors. Our organ procurement organization (OPO) utilizes a centralized treatment and recovery facility allowing for aggressive protocol driven management and frequent assessment of organ function early after brain death declaration. Methods We retrospectively reviewed our OPO experience with cardiac allograft donors from 2013-2017. Clinical data (patient demographics, cause of death, medical management, biomarkers, and serial echocardiographic imaging) were extracted from the OPO EMR for all 168 allocated cardiac donors during this time period. Improved LV systolic function was defined as an initial LVEF ≤40% which later improved to ≥50% consistent with the definition used in the prior UNOS analysis. Results We found that 23% (38/168) of allocated cardiac allografts from our OPO had transient LV dysfunction with an EF ≤40% on the initial echocardiogram. This rate was consistent over the years examined. Moreover 55% of donors had an initial echocardiogram with an EF of less than 50%. Comparison of donors with an initial EF ≤40% to donors with normal LV function on initial examination revealed minimal differences. There was no difference in the average age or sex between the two groups. No differences were found in the dose of vasopressors used either at the time of arrival to the facility or at organ harvest. The average amount of blood transfused was not different between the two groups. Although peak ALT was significantly higher in donors with transient LV dysfunction (402 vs 175 Units/L), there was no differences found in peak AST, troponin, lactate, or creatinine. Conclusion We found a markedly higher percentage of cardiac donors with transient LV dysfunction in allografts coming from our OPO facility compared to the UNOS database. The extent to which this reflects increased recognition versus increased organ yield is unknown at this time. These donors did not differ significantly from donors with normal LV function on initial examination. Coupled with prior data that showed equivalent outcomes in donors with recovered LV function, these data suggest that additional efforts to recover cardiac allografts initially found to have LV dysfunction could be an important means of increasing the donor pool and further work is ongoing to understand the most important factors in the recovery process.

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

Abstract 14124: A Marked Increase in Myocardial Oxidative Stress Associated With Sympathetic Hyperactivity is Related to Transient Myocardial Dysfunction in Patients With Takotsubo Cardiomyopathy

Introduction: Sympathetic hyperactivity is considered as one of the most likely pathogenic mechanism in takotsubo cardiomyopathy (TC). However, little is known about the relationship between sympathetic hyperactivity and myocardial oxidative stress (OS). Hypothesis: We hypothesized that cardiac sympathetic hyperactivity was associated with cardiac myocardial OS, and OS related to transient myocardial dysfunction in patients with TC compared with acute anteroseptal myocardial infarction (AMI). Methods: In 8 TC patients and 8 AMI patients (NYHA 3), ECG, echocardiography, cardiac catheterization and serial measurements of plasma catecholamines, urinary (U) 8-hydroxy-2’-deoxyguanosine (8-OHdG) as a marker of OS and plasma CPK were performed for two weeks from onset. Results: Blood sampling from coronary sinus (CS) and aorta (Ao) at 1st day showed that norepinephrine (NE) levels and 8-OHdG level in CS were significantly higher than those in Ao and peripheral blood, indicating that an increase in myocardial OS was associated with cardiac sympathetic hyperactivity. NE levels in peripheral blood were peaked out at 1st day and 2-times higher in TC than in AMI within a week, while the max CPK value in TC was significantly lower than that in AMI. Dual scintigraphy of 201Tl and 123I-meta-iodobenzylguanidine was performed at 7th day showed that cardiac sympathetic nervous injury was much larger than myocardial perfusion damage in all TC patients. U-8OHdG level (ng/mg Cr; normal range:&lt;10.0) in TC was elevated in parallel with the profile of plasma NE level (1st day: 65.6±24.5, 4th day: 19.1±8.3, 7th day: 16.4±9.1), while it was decreased to almost normal range after percutaneous coronary intervention for left anterior descending artery in AMI (1st day: 24.3±13.8, 4th day: 9.8±3.4, 7th day: 12.3±2.7). Interestingly, difference in serum 8-OHdG levels (CS vs Ao) in TC increased proportionally with wall motion score (WMS) as an index of LV dysfunction (R=0.93, p&lt;0.001), while difference in serum NA levels (CA vs Ao) in TC did not. U-8OHdG level in TC was positively correlated with WMS at each day (1st day, 7th day). Conclusions: These findings suggest that myocardial OS induced by cardiac sympathetic hyperactivity may play a critical role in transient LV dysfunction in TC.

0108: Specific alterations in cardiac function induced by a 300 km mountain ultra-marathon

Although popularity of ultra-long endurance races is growing, data on their consequences on cardiac function are still lacking. Thus, we aimed to assess the progressive cardiac consequences of the World's most challenging mountain ultra-marathon (Tor des Geants; Italy; 300km; 24000 m D+). Resting cardiac evaluations were conducted prior (pre-), during (mid-; km 150) and after (post-) the race on fifteen participants. Left and right ventricle (LV and RV) morphologies, functions and mechanics were assessed using standard tissue Doppler imaging and Speckle tracking echocardiography. Runners completed the race in 126±15 h. From pre- to post-, the increase in stroke volume (SV) (103±19 vs. 110±23 vs. 116±21 mL; p<0.001 from pre- to post-race) was concomitant with the increase in LV early filling (i.e. peak E; 72.9±15.7 vs. 74.6±13.1 vs. 82.1±11.5 cm.s-1; p<0.05). Heart cavity sizes were 12-19% higher at post-. Significant correlations were found between percent changes in peak E and LV end-diastolic volume (r=0.56, p<0.05) or left atrial and right ventricle diastolic areas (r=0.66, p<0.05; r=0.80, p<0.001; respectively). Resting heart rate and LV systolic strain rates demonstrated a biphasic adaptation since they were increased at mid- (55±8 vs. 72±11 bpm, p<0.001) but returned to baseline pre- values at post- (55±8 vs. 59±8 bpm, respectively). Whereas it is well-described that long duration exercise of several hours induces a transient LV dysfunction, we observed specific cardiac adaptations characterized by a progressive increase in SV and diastolic function during much longer exercise; e.g. 4-7 days of mountain running. Our data strongly support the key role of a cardiac volume overload in these alterations. The underlying mechanisms of such specific alterations after an extreme mountain ultra-marathon and their clinical implications remain challenging for the future. Abstract 0108 – Figure : LV end-diastolic volumes and LA, RA and RV end-diastolic areas at pre-, mid- and post-race. Percentage changes from baseline are presented for each size or volume cavity

SEIZURE-INDUCED MYOCARDIAL STUNNING

A transient LV dysfunction complicating subarachnoid hemorrhage, neurogenic myocardial stunning, has been well described. A similar dysfunction could complicate seizures, a much more prevalent condition, requiring early recognition to prevent complications. A 75-year-old woman was brought to the

Abstract 17826: Frequency and Pattern of Left Ventricular Dysfunction in Potential Heart Transplant Donors

Cardiac transplantation is a recognized treatment for patients with end stage cardiomyopathy. However, the scarcity of donor hearts remains a limiting factor. In addition, some potential donor hearts may be rejected due to cardiac dysfunction reported on diagnostic imaging by echocardiography or cardiac catheterization. We report a series of 34 consecutive adult organ donors whose hearts were evaluated for LV systolic function. The donors suffered acute, fatal brain injury. 11/34 (32%) had LV systolic dysfunction. Predominate apical, basal, mid-cavity, or global dysfunction patterns were characterized. Serial echocardiograms, when available, were examined. The findings are summarized in the table 1. In our series we noted that serial studies uniformly demonstrated a significant improvement in LV systolic function. Improvement appeared independent of the specific pattern in LV dysfunction or sex. In 27% systolic function completely normalized. No difference between the sex of the donor and the pattern of cardiac dysfunction was seen. In conclusion, our study noted that greater than 30% of screened potential donor hearts have systolic dysfunction. A variable pattern of dysfunction is seen with Global type noted most frequently. Even in hearts with severe initial dysfunction, considerable improvement in EF occurred. Our findings suggest that an initial examination showing LV dysfunction should not exclude a potential heart donor. Reassessment over time and possibly temporizing organ procurement to permit left ventricular function to improve could increase the pool of hearts available for transplantation. Further research into the mechanism underlying transient LV dysfunction in potential heart donor suffering acute, fatal brain injury is warranted.

Atypical presentation of "takotsubo cardiomyopathy" without ST segment elevation: a case report

Introduction"Takotsubo cardiomyopathy" is characterized by transient LV dysfunction and mimicking acute myocardial infarction.Case presentationWe reported a case with atypical presentation of "takotsubo cardiomyopathy" without ST segment elevation, but with severe transient left ventricular dysfunction.ConclusionDiagnosis of "takotsubo cardiomyopathy" should be based on typical left ventricular dysfunction without coronary artery disease.

Section 11: Evaluation and Management of Patients With Heart Failure and Preserved Left Ventricular Ejection Fraction

Section 11: Evaluation and Management of Patients With Heart Failure and Preserved Left Ventricular Ejection Fraction

Three Cases of Stress Induced Transient LV Dysfunction: Stress Induced Cardiomyopathy

Three Cases of Stress Induced Transient LV Dysfunction: Stress Induced Cardiomyopathy

Reversible Left Ventricular Dysfunction Induced by Recurrent Ventricular Tachycardia

Two cases of transient LV dysfunction associated with VT are described. Both patients had a history of palpitations of several years' duration without symptoms of congestive heart failure. The reason for presentation was an increase in frequency and duration of palpitation. Decreased LV wall motion, observed by 2DE, normalized shortly after treatment of the VT. Diffusely decreased LV wall motion is associated with frequent episodes of VT and may mimic DCM except that signs and symptoms of heart failure are absent.