Basal Inferior Research Articles

Left ventricular mechanics before and after myectomy in patients with hypertrophic obstructive cardiomyopathy

Objectives The objective of this paper is to detect changes in left ventricular (LV) mechanics after surgical myectomy in patient with hypertrophic obstructive cardiomyopathy (HOCM). Background Septal myectomy is the gold standard method to relieve LV outflow tract pressure gradient in patients with HOCM. Myocardial mechanics are abnormal in those patients, demonstrating low longitudinal strain, high circumferential strain, and high apical rotation, compared with healthy patients. The aim of this study was to determine whether functional improvement after myectomy is associated with improved myocardial mechanics. Patients and methods A total of 15 patients (60% males and 40% female) with HOCM refractory to medical treatment were subjected to septal myectomy. Clinical data and paired echocardiographic studies before and within 6 months after myectomy were analyzed and compared. Myocardial mechanics including longitudinal and circumferential strain and rotation and LV synchronization were assessed using two-dimensional strain software (velocity vector imaging). Results Results showed significant symptomatic relief. LV outflow gradient decreased dramatically from 63.13 ± 10.25 to 9.96 ± 2.72 mmHg (P < 0.0001) and left atrial volume index decreased from 37.8 ± 5.61 to 26.38 ± 3.37 cm3/m2 (P < 0.05). E/e′ decreased from 15.23 ± 2.39 to 9.18 ± 1.42 (P < 0.05). Low longitudinal strain decreased at the myectomy site (basal septum), increased in the basal inferior segment, and remained unchanged globally − 6.43 ± 6.54 to − 8.70 ± 2.30 (P = 0.232). High circumferential strain decreased from − 28.47 ± 3.35 to − 18.26 ± 2.86 (P < 0.05). High LV twist normalized from 16.52 ± 2.25 to 14.02 ± 2.27 (P < 0.05). Conclusion Patients with HOCM show mechanical adaptations to chronic elevated afterload similar to patients with severe aortic stenosis in whom there is increased circumferential strain, increased basal and apical rotation, and LV twist. However, within 6 months after myectomy, global longitudinal strain remained unchanged, circumferential strain and rotation decreased, LV twist normalized, and LV dyssynchrony showed no significant changes. Thus, improvement of symptoms after myectomy is mainly because of improvement of the predictors of diastolic function.

Risk factors for early death in acute myocardial infarction patients complicating with ventricular septal rupture

Objective: To assess the clinical characteristics and identify the risk factors in the acute myocardial infarction (AMI) patients complicating with ventricular septal rupture (VSR). Methods: A retrospective study was performed on 96 AMI patients complicating with VSR, who were hospitalized in the Second Xiangya Hospital of Central South University, Hunan Provincial Peoples' Hospital, the First Affiliated Hospital of University of South China, the Second Affiliated hospital of University of south China, Xiangtan Central Hospital from December 2007 to May 2017. There were 46 females and the age was (66.2±10.7) years (from 43 to 90 years). Patients were divided into in-hospital survival group (n=64) and in-hospital death group (n=32). The 96 patients were also divided into the early death group (survived ≤2 weeks after admission, n=50) and non-early death group (survived>2 weeks after admission, n=46). Multivariate logistic regression was used to analyze the independent risk factors of the early death. Results: Location of VSR was available in 71 patients, VSR was located at the apical or anterior septum near the apical region in 64.0% (32/50) patients with the anterior AMI, VSR was located at the posterior wall and basal inferior segment in 57.1% (12/21) patients with non-anterior AMI. Compared to the in-hospital survival group, patients in the in-hospital death group were older ((69.6±11.3) years vs. (64.6±10.1) years, P=0.031), incidence of non-ventricular aneurysm (71.9% (23/32) vs. 37.5% (24/64), P=0.001) and anterior AMI (84.4%(27/32) vs. 62.5%(40/64), P=0.028) was significantly higher in the in-hospital death group than in the in-hospital survival group. The comparison between the early death group and non-early death group showed that older age, female, no history of angina or myocardial infarction, Killip grade>Ⅲ, and non-ventricular aneurysm were related to increased risk of the early mortality in this patient cohort. Logistic regression analysis revealed that female (OR=5.109,95%CI 1.19-22.00, P=0.012), no history of angina or myocardial infarction (OR=23.34, 95%CI 3.44-158.37, P=0.001), Killip grade>Ⅲ(OR=5.35, 95%CI 1.26-22.66, P=0.019) and non-ventricular aneurysm (OR=6.30,95%CI 1.67-23.73, P=0.005) were independent risk factors for early death in this patient cohort. Conclusion: The risk factors of in-hospital death include older age, non-ventricular aneurysm and anterior AMI. Female, no history of angina or myocardial infarction, Killip grade>Ⅲ and non-ventricular aneurysm are independent risk factors for the early death of AMI patients complicating VSR.

METHYLENETETRAHYDROFOLATE REDUCTASE POLYMORPHISM AND PREMATURE CORONARY ARTERY DISEASE

SESSION TITLE: Cardiovascular Disease 1 SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: 10/09/2018 01:15 PM - 02:15 PM INTRODUCTION: Methylenetetrahydrofolate reductase (MTHFR) catalyzes the conversion of 5,10-methylenetetrahydrofolate to 5-methyltetrahydrofolate, a co-substrate for homocysteine remethylation to methionine. Its deficiency leads to increased homocysteine levels. Elevated serum levels of homocysteine have been associated with premature coronary artery disease (CAD). we present a case of recurrent acute coronary syndrome in patient with heterozygote mutation for methylenetetrahydrofolate reductase (MTHFR) with normal homocysteine level. CASE PRESENTATION: A 23 year-old man with history of MTHFR polymorphism and anterior wall ST segment elevation myocardial infarction requiring drug eluting stent (DES) in the left anterior descending artery (LAD) presented to the emergency department with substernal chest pain, T wave inversions in inferior leads on his ECG and elevated troponin levels. Coronary angiography demonstrated an acute occlusion of the proximal right coronary artery (RCA) and a chronic total occlusion of the proximal LAD with collaterals from the circumflex territory. Aspiration thrombectomy of the RCA lesion was partially successful and required continuous infusion of unfractionated heparin and tirofiban for 48 hours in addition to aspirin and ticagrelor. He underwent a successful deployment of 3 DES to his RCA. His left ventriculogram showed a mildly reduced left ventricular ejection fraction of 45 % with hypokinesis of the basal inferior wall segment. DISCUSSION: Hypercoagulability workup was unrevealing. Homocysteine levels were normal at the time of his first myocardial infarction two years prior. Repeat homocysteine level was 11.7 mg/dl (n <11.2mg/dl). His total cholesterol was 153mg/dl, LDL 80mg/dl, Apo lipoprotein B was 67 (n 52-109mg/dl), Lp(a) <10(n <75nmol/L). He was then discharge on folic acid. He was brought back to the cardiac catheterization laboratory a month later to reassess the LAD lesion but the angiogram showed complete re-occlusion of RCA. The patient was referred for coronary artery bypass surgery. CONCLUSIONS: This case demonstrates the association of MTHFR polymorphism with premature CAD and myocardial infarction despite normal homocysteine levels. Screening for MTHFR polymorphisms in addition to homocysteine levels should be considered for patients presenting with premature CAD and a normal lipid profile. Aggressive risk reduction with lifestyle modification, guideline-driven medical therapy and folic acid might be necessary for secondary cardiovascular disease prevention until more specific therapeutic options are available for this subgroup of patients. Reference #1: Frosst P, Blom HJ, Milos R, et al. A candidate genetic risk factor for vasculardisease: a common mutation in methylenetetrahydrofolate reductase. Nat Genet.1995; 10: 111–113 Reference #3: DISCLOSURES: No relevant relationships by Corina Iorgoveanu, source=Web Response No relevant relationships by Ahmed Zaghloul, source=Web Response

PREPHENOTYPIC MYOCARDIAL CRYPT MORPHOLOGY IN HYPERTROPHIC CARDIOMYOPATHY

SESSION TITLE: Cardiovascular Disease 2 SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: 10/09/2018 01:15 PM - 02:15 PM INTRODUCTION: Hypertrophic cardiomyopathy (HCM) is a genetic heart disease first described over 50 years ago. More recently, cardiovascular magnetic resonance imaging has advanced our understanding of the phenotypic heterogeneity of the disease. CASE PRESENTATION: A 21-year-old man presented after a syncopal episode while playing soccer. He reported two prior similar events that occurred ten years ago. Family history further revealed a father who was diagnosed with non-obstructive hypertrophic cardiomyopathy at a young age. Electrocardiogram showed normal sinus rhythm. Transthoracic echocardiogram identified mild concentric left ventricular hypertrophy with preserved left ventricular ejection fraction and an interventricular septal end diastolic diameter estimated at 11-millimeters. Cardiac magnetic resonance imaging (CMR) was done, which revealed a maximal wall thickness of 13-millimeters in the basal septum. There was no systolic motion of the mitral valve or evidence of flow acceleration of left ventricular outflow tract. However, myocardial crypts were noted in the basal inferior wall. These findings represent a distinctive, but unclear morphology of hypertrophic cardiomyopathy currently thought to be more prevalent in phenotype-negative patients. A four generation family pedigree of the patient was obtained. His paternal family history was notable for ischemic cardiac disease in several members but only his father had an established diagnosis of hypertrophic cardiomyopathy. Maternal family history was unremarkable for any cardiovascular disease. Father underwent genetic testing, which revealed that he was heterozygous for the p.R502W pathogenic mutation in the myosin binding protein gene (MYBPC3). Patient was then discharged home on a Life Vest with a plan for genetic testing as outpatient. Genetic testing was also offered to the other family members. DISCUSSION: HCM is an autosomal dominant genetic cardiomyopathy with most mutations having a high penetrance. In HCM, the common phenotypes encountered on Echo or Cardiac MRI are unexplained left ventricular hypertrophy, especially asymmetric, involving the septum/anterolateral wall, increased LV outflow tract gradient and systolic anterior motion of the mitral valve leaflets. Left ventricular myocardial crypts found on cardiac MRI can serve as a good ‘pre-phenotypic’ imaging marker of HCM that can help identify family members of HCM affected families to undergo genetic testing. They occur with variable frequency, but represent a distinctive morphological expression of HCM. CONCLUSIONS: Myocardial crypt identification by cardiac magnetic resonance is emerging as a potential marker for earlier recognition of genotype positive patients at risk of developing clinical hypertrophic cardiomyopathy. This case emphasizes this clinical implication and reinforces the importance of careful history taking in diagnostic decision making. Reference #1: Maron MS, Rowin EJ, Lin D et al. Prevalence and clinical profile of myocardial crypts in hypertrophic cardiomyopathy. Circ Cardiovasc Imaging 2012;5:441-7. Reference #2: Rowin EJ, Maron MS. Myocardial crypts in hypertrophic cardiomyopathy: the new gang in town. Eur Heart J Cardiovasc Imaging 2012;13:281-3. DISCLOSURES: no disclosure on file for Shantal Gupta; No relevant relationships by Sharana Hegde, source=Web Response No relevant relationships by Jae Kim, source=Web Response No relevant relationships by Anupama Rao, source=Web Response

MULTIVESSEL CORONARY ARTERY ANEURYSMS PRESENTING AS MYOCARDIAL ISCHEMIA

SESSION TITLE: Cardiovascular Disease SESSION TYPE: Med Student/Res Case Report PRESENTED ON: 10/09/2018 07:30 AM - 08:30 AM INTRODUCTION: Aneurysmal disease of the coronary artery tree (CAA) is a rare condition with an incidence of 0.3-4.9% of patients undergoing coronary angiography. The majority of cases occur in the proximal segments of the epicardial arteries and typically involve only one artery [1]. Involvement of three coronary vessels or the left main coronary artery is particularly rare, found in only 3.5% of CAA patients [2]. Multi-vessel CAA can present as an ischemic coronary syndrome, and can be challenging to manage. CASE PRESENTATION: A 48 year old African American non-smoking female with history of Parry Romberg syndrome, hypertension, obesity, and chronic kidney disease presented with progressive, intermittent, non-exertional chest pain. EKG showed voltage criteria for left ventricular hypertrophy (LVH). Bedside echocardiogram showed moderate LVH and akinesis of the basal inferior myocardial segment. Initial troponin I was 0.7ng/mL, and rose to peak of 6.16ng/mL. She was given aspirin, clopidogrel, and intravenous heparin drip. Coronary angiography showed aneurysmal disease of the left main, left anterior descending, left circumflex, and right coronary arteries, without evidence of thrombus angiographically. There were diffuse mild luminal irregularities, and a discrete 90% stenosis of the proximal right posterior descending artery. Percutaneous intervention was not performed. The patient denied history of Kawasaki’s disease. Subsequent vascular evaluation included an MR angiogram of the head, chest, abdomen and pelvis which were negative. Antinuclear antibodies, rheumatoid factor, and antineutrophil cytoplasmic antibodies were all negative. C-reactive protein and erythrocyte sedimentation rate were mildly elevated (1.01mg/dL and 32mm/Hr respectively). Her lipid profile demonstrated LDL 114mg/dL. She was discharged with dual antiplatelet therapy and high intensity statin. At 3 month follow up, she reported occasional palpitations with no chest pain, and at one year follow up she reported no symptoms. DISCUSSION: CAA is typically atherosclerotic in origin, as in our patient, although other causes exist. Previously it was believed that atherosclerosis caused CAA by increased pressure and shear stress due to luminal narrowing; however, it is now postulated that it may be due to generalized endovascular inflammation [2]. There is no known association between Parry Romberg syndrome and atherosclerosis or CAA. Medical management of CAA is limited to anticoagulant, antiplatelet, and anti-atherosclerotic therapy. Consensus Indications for percutaneous or surgical interventions are limited given the rarity of the disease; however, they are typically reserved for symptomatic flow limiting disease or if there is high risk of rupture. CONCLUSIONS: CAA is a rare condition that may mimic myocardial ischemia on presentation. Treatment options for multi-vessel CAA are limited given the paucity of data on the disease. Reference #1: 1. Abou Sherif, S. et al. “Coronary Artery Aneurysms: A Review of the Epidemiology, Pathophysiology, Diagnosis, and Treatment.” Frontiers in Cardiovascular Medicine 4 (2017): 24. PMC. 17 Feb. 2018. Reference #2: 2. Mata, Karina M. et al. “Coronary Artery Aneurysms: An Update.” Novel Strategies in Ischemic Heart Disease, 2017. Dr.Umashankar Lakshmanadoss (Ed.) DISCLOSURES: No relevant relationships by Michael Berlowitz, source=Web Response No relevant relationships by Andrew Mehlman, source=Web Response

Case report: Posterior myocardial infarction in presence of right bundle branch block: an old concept with new findings

BackgroundThe diagnosis of acute ischaemic coronary syndromes in presence of an intra-ventricular conduction disturbance represents a clinical challenge. In the cardiac segmentation model the posterior wall is replaced by the basal inferior segment. However, in the clinical scenario of acute coronary syndrome the concept of posterior myocardial infarction (PMI) endures. The association of a PMI and right bundle branch block (RBBB) is a rare condition characterised by broad R waves and ventricular repolarization disorders in right precordial leads in both entities, which could lead to misinterpretation and delay in reperfusion therapy.Case SummaryWe describe a case report of a 74-year-old man with acute chest pain and an electrocardiogram with broad R waves, a 4 mm ST-segment downsloping (excessively discordant) in right precordial leads, RBBB, and ST-segment elevation in posterior leads. There was resolution of ST-segment downsloping in right precordial leads after percutaneous coronary intervention and stenting of the circumflex artery, with disturbance of the repolarization process only attributable to RBBB.DiscussionPatients with acute chest pain with RBBB and a ST segment with an excessive downsloping (out of proportion of what is expected in isolated RBBB) suggest PMI with occlusion of the circumflex coronary artery.

Evaluation of Early Left Ventricular Dysfunction in Patients with Duchenne Muscular Dystrophy Using Two-Dimensional Speckle Tracking Echocardiography and Tissue Doppler Imaging.

Although progressive cardiac dysfunction is the leading cause of death in patients with Duchenne muscular dystrophy (DMD), their cardiac function measured by conventional echocardiography has been generally interpreted as normal at a young age. We aimed to determine whether two-dimensional speckle tracking echocardiography (STE) or tissue Doppler imaging (TDI) could be used for early identification and detection of cardiac dysfunction in young patients with DMD. Thirteen pediatric patients (mean age, 9.69 ± 2.2years) with DMD and 26 age-matched healthy children (mean age, 9.65 ± 2.2years) were included in the study. All patients were examined via conventional echocardiography, TDI, and STE. Standard echocardiographic measurements of left ventricular (LV) systolic and diastolic function were obtained. Myocardial velocities including peak-systolic and early- and late-diastolic myocardial velocities were calculated in longitudinal direction in the interventricular septum, using TDI. Speckle tracking analyses were performed by acquiring apical four-, three-, and two-chamber views with the highest possible frame rates. Conventional parameters were similar between the two groups, but heart rates were higher in patients with DMD than in controls. The results of LV diastolic function evaluated using TDI showed that annular peak velocity during early diastole (e'; 10.9 ± 1.7 vs. 14.6 ± 1.7cm/s), e'/a' ratio (2.0 ± 0.5 vs. 3.0 ± 0.5), E/e' ratio (9.4 ± 1.4 vs. 7.3 ± 0.8), and myocardial performance index (0.46 ± 0.05 vs. 0.36 ± 0.06) of the mitral septal annulus among patients with DMD differed significantly from those of healthy children. A significant decrease in global longitudinal systolic strain was found in patients with DMD (- 16.6 ± 3.7 vs. - 21.2 ± 2.1), with a marked decrease in the LV basal inferolateral and basal inferior walls. In young patients with DMD who have global normal systolic function, reductions in systolic deformation parameters as well as reduced early diastolic myocardial velocities can be detected particularly in the basal inferolateral LV walls. The prognostic significance of these findings warrants further longitudinal follow-up.

Role of contact force in ischemic scar-related ventricular tachycardia ablation; optimal force required and impact of left ventricular access route.

Contact force-sensing technology has become a widely used addition to catheter ablation procedures. Neither the optimal contact force required to achieve adequate lesion formation in the ventricle, nor the impact of left ventricular access route on contact force has been fully clarified. Consecutive patients (n = 24) with ischemic cardiomyopathy who underwent ablation for scar-related ventricular tachycardia were included in the study. All ablations (n = 25) were performed using irrigated contact force-sensing catheters (Smart Touch, Biosense Webster). Effective lesion formation was defined as electrical unexcitability post ablation at sites which were electrically excitable prior to ablation (unipolar pacing at 10mA, 2ms pulse width). We explored the contact force which achieved effective lesion formation and the impact of left ventricular access route (retrograde aortic or transseptal) on the contact force achieved in various segments of the left ventricle. Scar zone was defined as bipolar signal amplitude < 0.5mV. Among 427 ablation points, effective lesion formation was achieved at 201 points (47.1%). Contact force did not predict effective lesion formation in the overall group. However, within the scar zone, mean contact force ≥ 10g was significantly associated with effective lesion formation [OR 3.21 (1.43, 7.19) P = 0.005]. In the 12-segment model of the left ventricle, the retrograde approach was associated with higher median contact force in the apical anterior segment (31 vs 19g; P = 0.045) while transseptal approach had higher median force in the basal inferior segment (25 vs 15g; P = 0.021). In the 4-segment model, the retrograde approach had higher force in the anterior wall (28 vs 16g; P = 0.004) while the transseptal approach had higher force in the lateral wall (21 vs 18g; P = 0.032). There was a trend towards higher force in the inferior wall with the transseptal approach, but this was not statistically significant (20 vs 15g; P = 0.063). In patients with ischemic cardiomyopathy, a mean contact force of 10g or more within the scar zone had the best correlation with electrical unexcitability post ablation in our study. The retrograde aortic approach was associated with better contact force over the anterior wall while use of a transseptal approach had better contact force over the lateral wall.

PP-308 - Pneumomediastinum After Epicardial Ventricular Tachycardia Ablation

A 77-year-old male with ventricular tachycardia storm, converted by multiple anti-tachycardia pacing and shock attempts was referred to our arrhythmia center. During electrophysiologic study clinical ventricular tachycardia with pseudo-delta waves was induced. Epicardial activation and voltage mappings using Carto-3 system were obtained via subxiphoid route. Critical isthmus was detected at basal inferior right ventricular epicardium near the atrioventricular groove and radiofrequency ablation immediately stopped the tachycardia. No recurrence was seen with control stimulations. Severe retrosternal pain occurred during catheter manipulations. Transthoracic echo showed no remarkable pericardial effusion. Chest computed tomography demonstrated air localized in the periaortic area compatible with pneumomediastinum without additional complication (Figure 1, white stars). Chest-surgeon advised conservative follow-up and the patient was discharged with pain relief on the fifth postoperative day.

Correlation of ST changes in leads V4–V6 to area of ischemia by CMR in inferior STEMI

Objective. We aim to determine the correlation between ST-segment changes in leads V4–V6 and the extent of myocardial injury by cardiac magnetic resonance (CMR) in patients with inferior ST elevation (STE) myocardial infarction (iSTEMI). Design. Admission electrocardiogram and CMR data from the MITOCARE trial were used. Differences in mean myocardium at risk, infarct size, ejection fraction and myocardial segment involvement by CMR were compared in patients with first iSTEMI with STE, ST depression (STD) or no ST changes (NST) in V4–V6. Myocardial segment involvement was further evaluated by comparing proportion of patients in each group with ≥25% and ≥50% segment involvement. Results. Fifty-four patients were included. Patients with STE (n = 22) and STD (n = 16) in V4–V6 had significantly lower ejection fraction compared to NST (n = 16) (48% vs 48% vs 54%, p = .02). STE showed more apical, apical lateral and mid-inferolateral involvement but less basal inferior involvement than NST. STD exhibited greater basal inferoseptal involvement compared to STE. There were more patients with STE that had ≥25% and ≥50% apical lateral involvement compared with STD and NST groups. Patients with STD were more likely to have ≥25% and ≥50% basal inferoseptal involvement compared with STE and NST groups.Conclusion. Our study suggests that in iSTEMI, ST changes in the precordial leads V4–V6 correlates with greater myocardial injury and distribution of myocardium at risk.

Utility of Two-Dimensional Speckle Tracking Echocardiography in Understanding of Inferior ST Segment Depression in the Setting of Acute Anterior Myocardial Infarction

Background: A patient suffering from an anterior ST segment elevation myocardial infarction (STEMI) will frequently demonstrate ST segment depression (STD) in the inferior leads (II, III, and aVF). The aim of this study was to determine the meaning of STD in the early stages of an acute anterior MI, and whether they represent remote ischemia or reflect an electrical mechanism by using speckle-tracking echocardiography. Methods: Fifty patients suffering from acute anterior STEMI were enrolled in this prospective study. The patients were classified into two groups each one included 25 patients. Group 1 included patients who had STD in the inferior leads and group 2 included patients who had not. All of the patients were evaluated with a standard 12-lead electrocardiography (ECG), two dimensional echocardiography, speckle-tracking echocardiography, and coronary angiography. Results: The average global longitudinal peak systolic strain (Avg_GLPS%) was - 9.8 ± 2.4% in group 1 versus -10.7 ± 2.3 in group 2 (p=0.188). The longitudinal strains of the basal inferior segments were -13.6 ± 2.8% in group 1 versus -15.8 ± 3.7% in group 2 (p=0.026), and the longitudinal strains of mid inferior segments were -13 ± 3.2 in group 1 versus -15.1 ± 2.7% in group 2 (p=0.019). Group 1 had higher frequency of multivessel disease, right coronary artery (RCA) and left circumflex coronary artery (LCX) stenosis than group 2. Conclusion: This study supports the belief that inferior STD on an ECG during an acute anterior STEMI is a sign of ischemia that often involves the right coronary artery.

Quantification of Cardiac Subvolume Dosimetry in Breast Cancer Patients Receiving Tangential Beam Radiation Therapy

Studies have demonstrated left ventricle (LV) strain abnormalities in patients receiving tangential radiation (RT) for left-sided breast cancer. Currently, Quantitative Analysis of Normal Tissue Effects in the Clinic (QUANTEC) constraints for cardiac structures are coarse and limited to mean heart dose and V25. This study aims to document radiation dosimetry to cardiac subvolumes including individual chambers, valves, coronary arteries, and LV, based on the American Heart Association (AHA) 17 segment model. Ten breast cancer patients receiving left-sided tangential RT (50Gy in 25 (n=2) or 42.4Gy in 16 daily fractions (n=8) were prospectively recruited from October 2015 to October 2016. Non-contrast, non-ECG gated planning CTs were acquired (2 mm slice thickness). Deep Inspiratory Breath Hold was not used. Cardiac subvolumes were contoured in the cardiac short axis, 2 and 4 chamber views in Oncentra Brachytherapy Planning Software, audited by a cardiologist, and transferred to Pinnacle Treatment Planning System v9.10. Maximum, minimum and mean doses were calculated for all structures, with dose metrics including V5, V25 and V30 evaluated. Mean heart dose was 2.32Gy(1.38-3.45), V5=6.79% (3.23-10.01), V25=2.15%(0.41-3.93) and V30=1.66% (0.01-2.5). The anterior wall comprising segments 1, 7 and 13 received a maximum dose of 4.04Gy (2.59-6.08), 23.79Gy (9.59-41.03), and 43.43Gy (36.09-45.44) respectively. The apical segments 14, 15 and 16, and apex (segment 17) received maximum doses of 34.46Gy (17.97-42.25),17.73Gy (4.66-39.32),17.73Gy (4.66-39.32) and 40.87Gy (36.44-43.22) respectively. The mid and basal inferior LV walls corresponding to segments 3, 4, 5, 9, 10, 11 received less than 3.8Gy (1.6-3.79).Tabled 1Abstract 2076; Table 1Cardiac SubvolumeMaximum (Gy)Mean (Gy)Heart (whole)42.17 (36.3-46.22)2.32 (1.38-3.45)Left Anterior Descending Artery39.03 (33.01-42.93)18.51 (8.98-29.01)Left Coronary Artery1.71 (1.16-2.48)0.96 (0.37-1.55)Right Coronary Artery1.7 (1.16-2.33)0.64 (0.26-1.22)Aortic Valve1.73 (1.39-2.48)0.76 (0.34-1.28)Mitral Valve1.32 (0.93-1.7)0.51 (0.16-1.2)Pulmonary Valve7.79 (2.55-18.71)2.13 (1.21-3.81)Tricuspid Valve2.02 (1.39-3.03)0.9 (0.29-1.24)Right Atria1.54 (0.93-2.07)0.54 (0.05-0.93)Left Atria1.19 (0.69-1.56)0.31 (0.01-0.73)Left Ventricle42.11 (38.63-45.19)4.61 (2.84-6.52)Right Ventricle29.9 (16.68-42.11)2.83 (1.61-4.7) Open table in a new tab There are substantial RT dose variations in cardiac tissue exposure including within specific LV segments. This is one of few studies providing detailed radiation dosimetry to cardiac subvolumes which will aid in understanding the correlation of breast RT toxicity to specific cardiac structures.

Infective Endocarditis of the Mitral Valve in a Patient with Congenital RCA to LV Fistula

A 26-year-old female recent nursing graduate from the Philippines presented to the Emergency Department with 4-week history of intermittent fevers. This occurred following dental root canal and filling 5 months earlier. Physical examination revealed a pansystolic murmur in the left sternal edge. Blood cultures were positive for Streptococcus anginosus (one of the Milleri group Streptococci) with penicillin MIC of 0.125. Transthoracic echocardiography (TTE) demonstrated markedly dilated right coronary artery (RCA) with RCA fistula noted between the distal RCA and entering the basal inferior LV wall. Left ventricle (LV) was mildly dilated with normal systolic function (EF 58%). A transoesophageal echocardiogram revealed a strand-like echodensity (3.3 mm length) associated with the posterior mitral valve leaflet tip. There was significant dilation of the RCA (ostial RCA 1.5 cm) visualised traversing over the RV outflow tract and connecting into the basal inferior LV cavity. High turbulent diastolic flow was demonstrated consistent with RCA to LV fistula. Cardiac MRI revealed RCA to LV fistula flow representing 28% of aortic flow. A partial anomalous pulmonary venous drainage of the right upper lobe to the superior vena cava was detected. The patient was treated with 42 days of intravenous penicillin. Repeat TTE showed mild posterior mitral valve leaflet thickening with grade 0-1/4 mitral regurgitation. A 3D printed model (Fig. 1) was presented at a multidisciplinary team meeting. As LV fistulae pose a risk for rupture, a decision was made for elective percutaneous closure six months after demonstration of clearance from infection and normal inflammatory markers.

Factors associated with stroke in patients with paroxysmal atrial fibrillation beyond CHADS2 score.

This study was conducted to investigate factors associated with stroke in pa-tients with paroxysmal atrial fibrillation (PAF) beyond CHADS2 score in terms of left ventricular (LV) diastolic function or left atrial (LA) function. One hundred and sixty-one patients with PAF and age less than 75 (mean age 61 ± 10; 69 male) who underwent transthoracic echocardiography were investigated. Patients were divided into two groups according to the stroke status (group 1 - no stroke vs. group 2 - presence of stroke). Baseline echocardiographic parameters and LA segmental (4 segments: basal septal, lateral, inferior, and anterior) strain rate (SR) during normal sinus rhythm were analyzed. CHAD score (except S2) was similar between the two groups (0.6 ± 0.7 vs. 0.9 ± 0.7, p = 0.125). Patients with stroke had slightly lower body mass index (24.5 ± 2.7 vs. 23.4 ± ± 2.4, p = 0.052). Echocardiographic parameters did not show any differences in both systolic and diastolic functions between the two groups, however elevated E/E' ratio was noted (9.5 ± ± 3.8 vs. 11.6 ± 3.9, p = 0.010) due to higher E velocity (63.5 ± 15.9 vs. 70.9 ± 16.0 cm/s, p = 0.046). In the analysis of LA SR, there are no differences of SR among the 4 segments. However, standard deviations (SD) of time to peak SR (SD of tA-SR) of the 4 segments were higher in patients with stroke (10.9 ± 9.9 vs. 22.1 ± 18.1 ms, p = 0.009) which indicates dyssynchronous contraction of LA. In multivariate analysis, SD of tA-SR (OR 1.074, CI 1.024-1.128, p = 0.004) and elevated E/E' (OR 1.189, CI 1.006-1.406, p = 0.048) were independently associated with stroke in patients with PAF. Elevated E velocity, E/E' and SD of tA-SR were associated with occurrence of stroke in patients with PAF even with similar CHAD scores. Increased SD of tA-SR and E/E' were independently associated with stroke in patients with PAF. (.

Multicenter Experience With Catheter Ablation for Ventricular Tachycardia in Lamin A/C Cardiomyopathy.

Lamin A/C (LMNA) cardiomyopathy is a genetic disease with a proclivity for ventricular arrhythmias. We describe the multicenter experience with percutaneous catheter ablation of sustained monomorphic ventricular tachycardia (VT) in LMNA cardiomyopathy. Twenty-five consecutive LMNA mutation patients from 4 centers were included (mean age, 55±9 years; ejection fraction, 34±12%; VT storm in 36%). Complete atrioventricular block was present in 11 patients; 3 patients were on mechanical circulatory support for severe heart failure. A median of 3 VTs were inducible per patient; in 82%, mapping was consistent with origin from scar in the basal left ventricle, particularly the septum, but also basal inferior wall and subaortic mitral continuity. After multiple procedures (median 2/patient; transcoronary alcohol in 6 and surgical cryoablation in 2 patients), acute success (noninducibility of any VT) was achieved in only 25% of patients. Partial success (inducibility of a nonclinical VT only: 50%) and failure (persistent inducibility of clinical VT: 12.5%) was attributed to intramural septal substrate in 13 of 18 patients (72%). Complications occurred in 25% of patients. After a median follow-up of 7 months after the last procedure, 91% experienced ≥1 VT recurrence, 44% received or were awaiting mechanical circulatory support or transplant for end-stage heart failure, and 26% died. Catheter ablation of VT associated with LMNA cardiomyopathy is associated with poor outcomes including high rate of arrhythmia recurrence, progression to end-stage heart failure, and high mortality. Basal septal scar and intramural VT origin makes VT ablation challenging in this population.

0178 : Global and regional echocardiographic strain to assess early phase of hypertrophic cardiomyopathy due to sarcomeric mutations

Hypertrophic cardiomyopathy (HCM) is a genetic disease with delayed cardiac expression. Our objective was to characterize global and regional LV myocardial strain by two-dimensional imaging in sarcomeric HCM families and hypothesized that early systolic dysfunction, before hypertrophic stage, may be diagnosed by this technique. We analyzed 79 adults: HCM patients with LV hypertrophy (LVH+, n=38), mutation carriers without LV hypertrophy (LVH-/G+, n=20), and normal control subjects (n=21). We calculated global longitudinal strain (GLS) and regional peak longitudinal strain. Age, sex ratio and body surface area were not significantly different between groups. Maximal 2D wall thickness of left ventricle was 10.1±1.6 mm in LVH-/G+ and not different from controls (9.9 ±1.2 mm). We observed that LV GLS was not different in LVH-/G+ as compared to controls (–20.6% IQ:–24.2/– 8.3 vs –22.9% IQ:-26.8/-20.9) but was reduced in HCM patients (–14.1% IQ:–18.5/–11.8) although a normal ejection fraction. Interestingly, regional peak longitudinal strain was similar in LVH-/G+ and controls except in four segments: basal anteroseptal (BAS) wall (–16% vs –19%, p=0.018), basal inferoseptal wall (–16.0% vs –19.0%, p=0.047), basal inferior wall (–21.0% vs –24.0%, p=0.006) and mid anteroseptal wall (–21.0% vs –22.5%, p=0.022). Regional BAS strain <-16.5% yielded a sensitivity of 57% and a specificity of 90% to differentiate LVH-/G+ patients from controls. We also evaluated accuracy of ratio between normal and abnormal segments. Septo-basal/Latero-basal strain ratio <0.76 yielded a sensitivity of 73% and a specificity of 92% to differentiate LVH-/G+ patients from controls. Regional longitudinal strain but not global strain, was significantly reduced at early stage of HCM before development of LVH. This suggests the integration of myocardial deformation in the evaluation of HCM relatives to identify better mutation carriers and early LV abnormalities. The author hereby declares no conflict of interest

Brain Natriuretic Peptide and Particular Left Ventricle Segment Asynergy Associated with Cardioembolic Stroke from Old Myocardial Infarction

It is important to determine the usage of anticoagulants by defining the actual risk of cardioembolic stroke in patients with old myocardial infarction. In the present study, we aimed to more precisely evaluate the risks of each segment associated with cardioembolic stroke using a 16-segment model. The usage of the plasma brain natriuretic peptide (BNP) associated with cardioembolic stroke was also evaluated in comparison with a left ventricle ejection fraction less than 40%. There were a total of 190 ischemic stroke patients who had premorbid myocardial infarction. The study included a total of 143 ischemic stroke patients with old myocardial infarction who were available for evaluation and excluded patients with atrial fibrillation or acute myocardial infarction. Their left ventricle wall motion abnormality and the level of plasma BNP at their admission were analyzed. Hypertension and a plasma BNP level of 206.9 pg/mL or higher, determined from the receiver operating characteristic curve, were independently associated with cardioembolic stroke (χ(2) = 35.6, R(2) = .30, P < .001). Adjusting for these factors, statistically independent high risk was observed at the basal-inferior, basal-inferolateral, mid-anterior, mid-anteroseptal, apical-anterior, and apical-septal left ventricles. High plasma BNP levels and left ventricular wall motion abnormalities in the segments perfused with left anterior descending coronary artery or right coronary artery show a high risk for cardioembolic stroke in patients with old myocardial infarction. Considering these factors, it could be possible to more precisely define the risk of cardioembolic stroke and to perform appropriate antithrombotic treatments in old myocardial infarction patients.

Carvedilol Administration Can Prevent Doxorubicin-Induced Cardiotoxicity: A Double-Blind Randomized Trial

Objective: The aim of this study is to evaluate the preventive effects of carvedilol on doxorubicin-induced cardiotoxicity. Methods: In this trial, 70 female patients with breast cancer who were candidates to receive doxorubicin were enrolled, from which 30 were selected randomly to receive carvedilol 6.25 mg daily during chemotherapy, with the rest receiving placebo as the control group. Both groups were evaluated 1 week before and 1 week after chemotherapy by measuring the left ventricular ejection fraction and strain/strain rate. Results: Data analysis showed that the case group presented no significant reduction in strain and strain-rate parameters after intervention, while there was a significant reduction in these parameters in the control group (all p values <0.001). Also, the mean differences of strain parameters in the case group were significantly less than in the control group in all evaluated heart walls (basal septal strain, p = 0.005, basal lateral strain, p = 0.001, basal inferior strain, p < 0.001, and basal anterior strain, p < 0.001); the same was true for the strain-rate parameters (the p values for basal septal, basal lateral, basal inferior and basal anterior strain rate were 0.037, 0.037, 0.002 and <0.001, respectively). Conclusion: This study shows that carvedilol can prevent doxorubicin-induced cardiotoxicity. Whether this prophylaxis should be considered as the preferred method needs further investigation.

Association of Late Gadolinium Enhancement and Degree of Left Ventricular Hypertrophy Assessed on Cardiac Magnetic Resonance Imaging With Ventricular Tachycardia in Children With Hypertrophic Cardiomyopathy

There are limited data on the clinical significance of left ventricular (LV) mass and late gadolinium enhancement (LGE) in pediatric hypertrophic cardiomyopathy (HC). We reviewed cardiovascular magnetic resonance (CMR) studies of children with HC to investigate the associations between the extent and distribution of LGE and LV mass with ventricular tachycardia (VT) in children with HC. A blinded observer reviewed CMR studies for the presence and distribution of LV hypertrophy and LGE using a 17-segment model. The primary outcome was VT. LGE was present 17 of 33 subjects (52%). VT was present on outpatient Holter monitor or exercise stress test in 7 patients, of which 5 patients (71%) had LGE. Each additional segment of LGE was associated with an increase in the odds of VT (odds ratio [OR] 1.4, 95% CI 1.1 to 1.9) and fewer than 5 segments with LGE had 93% specificity for the presence or absence of VT (OR 0.06, 95% CI 0.01 to 0.5). VT was more common in patients with LGE in the apical septal (p= 0.03), basal inferoseptal (p<0.01), and basal inferior (p= 0.04) segments, whereas LGE in more commonly involved segments (midanteroseptal and midinferoseptal) was not associated with VT (p= 0.13, 0.26). Patients with VT had greater LV mass index (76.4 ± 40.4g/m(2.7) vs 50.9 ± 24.3g/m(2.7); p= 0.03). Each centimeter of increased maximum LV thickness was associated with increased likelihood of VT (OR 2.9, 95% CI 1.2 to 6.8). In conclusion, in pediatric HC, CMR to evaluate the extent and pattern of LGE, LV mass index, and maximum LV thickness may help to identify children with HC at risk of VT.

Anomalous Origin of the Right Coronary Artery with Inter-Aorto-Pulmonary Course Highlighted by ECG-gated Cardiac CT Angiography

Case presentation: A 46-year-old male was referred to the echo laboratory for further investigations of a 6-months history with typical chest pain that is predictably exertional. His past medical history was largely unremarkable and so was his cardiac physical examination. Electrocardiogram showed sinus rhythm, poor R wave progression in anterior precordial leads and small Q waves with isoelectric T waves in inferior leads (Figure 1). Transthoracic echocardiography revealed prominent basal inferior and mid inferior hypokinesis with reduced regional myocardial longitudinal strain (-9% and -11% respectively) (Figure 2A). Left ventricular ejection fraction was estimated to be 50%. Myocardial perfusion scintigraphy was positive for a significant reversible stress-induced ischemia of the inferior wall. Coronary angiography showed normal left coronary system and anomalous origin of the right coronary artery (RCA). For further assessment, ECG-gated cardiac CT angiography (CTCA) was done and revealed RCA arising from left aortic sinus separately of left coronary artery, with inter-aorto-pulmonary course and ostial-post-ostial part severe luminal narrowing at the takeoff portion (Figures 2B-2F), coronary artery calcifications of the mid-RCA without significant stenosis (Figures 2B and 2C) and no significant atherosclerotic disease of left coronary system. Surgical treatment was required. In fact, aggressive surgical management is often recommended to avoid sudden cardiac death, especially in documented coronary ischemia as a result of a coronary compression when coursing between the great arteries. The CTCA has an incontestable place as a first imaging modality tool for the assessment of the origin and course of coronary arteries and the detection of inter-aortopulmonary course that implies an appropriate surgical management.