Basal Anterior Wall Research Articles

MYOCARDITIS, CORONARY ARTERY DISSECTION OR BOTH: A JUVENILE ENIGMA

Abstract A 26–year–old man was admitted to the Coronary Care Unit for severe, non–irradiated, oppressive anterothoracic pain. He had no relevant pathological history, but reported an episode of gastroenteritis the week before. EKG showed sinus rhythm and accelerated idioventricular rhythm phases. Blood pressure and 2D echo were normal. Inflammation indeces were negative, hsTnT reached a peak of 2026 ng/L. Despite the absence of inflammation signs, our first guess was myocarditis. Cardiac magnetic resonance (CMR) was performed: T2w–STIR images showed edema of the middle inferior wall and of the mid–basal anterior and anterolateral wall, while T1–weighted post gadolinium images showed transmural enhancement of the mid–basal anterior, antero lateral and inferior walls with a dubious origin from the sub endocardium in the anterior and anterolateral segments; LVEF was 55%. Invasive coronary angiography (ICA) was performed to rule out ischemic etiology: LAD showed a very thin lumen in its periphery and two obtuse marginal branches had an amputated appearance: it made us think of healing dissections. Then it turned out that the patient have been working out with heavy weights the day before: we therefore considered spontaneous coronary artery dissection. Such hypothesis was consistent with the absence of inflammations indices, but didn’t explain the basal and middle inferior involvement that CMR had shown. On the other hand, the angiographic finding may be consistent with peripheral vascular suffering linked to myocarditis induced inflammation. To date, we haven’t found univocal interpretation. Anti–remodeling therapy with IACE and beta blockers was administered, in addition to acetylsalicylic acid. CMR will be performed in two months and may provide further results once the edema will be reabsorbed. ICA will be repeated to make sure that distal coronary blood flow is improved. Take Home Messages Myocarditis can also occur with no signs of inflammation. In myocarditis it has been demonstrated that slower distal coronary blood flow may occur, due to the increase in peripheral vascular resistance linked to the presence of edema. In the acute phase, especially if CMR is performed very early, the large amount of edema can make the enhancement transmural, masking the site of origin of the damage.

Identification of Circulating Plasma Proteins as a Mediator of Hypertension-Driven Cardiac Remodeling: A Mediation Mendelian Randomization Study.

This study focused on circulating plasma protein profiles to identify mediators of hypertension-driven myocardial remodeling and heart failure. A Mendelian randomization design was used to investigate the causal impact of systolic blood pressure (SBP), diastolic blood pressure (DBP), and pulse pressure on 82 cardiac magnetic resonance traits and heart failure risk. Mediation analyses were also conducted to identify potential plasma proteins mediating these effects. Genetically proxied higher SBP, DBP, and pulse pressure were causally associated with increased left ventricular myocardial mass and alterations in global myocardial wall thickness at end diastole. Elevated SBP and DBP were linked to increased regional myocardial radial strain of the left ventricle (basal anterior, mid, and apical walls), while higher SBP was associated with reduced circumferential strain in specific left ventricular segments (apical, mid-anteroseptal, mid-inferoseptal, and mid-inferolateral walls). Specific plasma proteins mediated the impact of blood pressure on cardiac remodeling, with FGF5 (fibroblast growth factor 5) contributing 2.96% (P=0.024) and 4.15% (P=0.046) to the total effect of SBP and DBP on myocardial wall thickness at end diastole in the apical anterior segment and leptin explaining 15.21% (P=0.042) and 23.24% (P=0.022) of the total effect of SBP and DBP on radial strain in the mid-anteroseptal segment. Additionally, FGF5 was the only mediator, explaining 4.19% (P=0.013) and 4.54% (P=0.032) of the total effect of SBP and DBP on heart failure susceptibility. This mediation Mendelian randomization study provides evidence supporting specific circulating plasma proteins as mediators of hypertension-driven cardiac remodeling and heart failure.

Left ventricular electrical potential measured by the NOGA XP electromechanical mapping method as a predictor of response to cardiac resynchronization therapy.

The aim of the study was to determine whether left ventricular electrical potential measured by electromechanical mapping with the NOGA XP system has predictive value for response to CRT. Approximately 30% of patients who undergo cardiac resynchronization therapy do not see the expected effects. The group of 38 patients qualified for CRT implantation were included in the study, of which 33 patients were analyzed. A 15% reduction in ESV after 6 months of pacing was used as a criterion for a positive response to CRT. The mean value and sum of unipolar and bipolar potentials obtained by mapping with the NOGA XP system and their predictive value in relation to the effect of CRT were analyzed using a bulls-eye projection at three levels: 1) the global value of the left ventricular (LV) potentials, 2) the potentials of the individual LV walls and 3) the mean value of the potentials of the individual segments (basal and middle) of the individual LV walls. 24 patients met the criterion of a positive response to CRT vs. 9 non-responders. At the global analysis stage, the independent predictors of favorable response to CRT were the sum of the unipolar potential and bipolar mean potential. In the analysis of individual left ventricular walls, the mean bipolar potential of the anterior and posterior wall and in the unipolar system, mean septal potential was found to be an independent predictor of favorable response to CRT. In the detailed segmental analysis, the independent predictors were the bipolar potential of the mid-posterior wall segment and the basal anterior wall segment. Measurement of bipolar and unipolar electrical potentials with the NOGA XP system is a valuable method for predicting a favorable response to CRT.

P299 CONDUCTION DISORDERS AS THE FIRST HALLMARK OF ISOLATED CARDIAC SARCOIDOSIS IN A HIGHLY ACTIVE INDIVIDUAL: A CASE REPORT

Abstract A 45–year–old highly active Caucasian individual was admitted to the emergency department complaining of slightly reduced physical performances: he reported a lack of increase of heart rate beyond 80–100 bpm at fitness tracker monitoring during physical activity during the previous week. He used to train 3–4 times/week. He had no previous medical concerns and he didn’t take any medication. Basal electrocardiogram (ECG) showed 2:1 atrioventricular block (AVB) and left axis deviation, with the exception of his 2:1 AVB, the other features on the ECG are common training related changes. Transthoracic echocardiogram was normal. Treadmill exercise test revealed paroxysmal 2:1 AVB and Mobitz I AVB at peak effort, then first degree AVB and isolated and coupled right infundibular premature ventricular complexes (PVC) in the recovery phase: exercise related AV–conduction improvement suggested supra–nodal AVB. Cardiac magnetic resonance (CMR) imaging reported two areas of late gadolinium enhancement (LGE) with midwall/subepicardial distribution: the first one in the basal anterior septal wall extending to basal anterior wall and the second one involving the basal and medium segment of inferior septum and inferior wall. LGE quantification was 6.0 g/m2 (9.5%). Short tau inversion recovery (STIR) acquisitions were negative for oedema (Figure 1). Subsequent FDG–PET imaging confirmed high uptake in the basal anterior septal wall, the anterior wall and in the basal inferior septal area (Figure 2). No other organ involvement was detected. Considering the FDG–PET, LGE and AV–conduction abnormalities, the patient was clinically diagnosed with symptomatic isolated CS. However, a definitive histologic diagnosis was not possible as no myocardial biopsy was performed. High dose corticosteroid therapy was startedand after few days of treatment ECG monitoring revealed an imrovement of cardiac conduction. The treadmill test was repeated and showed conduction improvement during effort, however the test was suspended due to the occurrence of ventricular couples and ventricular bigeminy during effort. For arrhythmic risk assessment, electrophysiological study (EPS) was performed and no arrhythmias were induced. We decided to defer ICD implantation. However, a loop–recorder for continuous arrhythmias monitoring was implanted. At three months, a new CMR was performed and was identical to the previous one, with no significant LGE reduction or increase detected.

P78 AN ANTEGRADE RECANALIZATION OF LEFT ANTERIOR DESCENDING CHRONIC TOTAL OCCLUSION WITH ORBITAL ATHERECTOMY IN PATIENT WITH SEVER LEFT VENTRICULAR DISFUNCTION

Abstract We share the case of a 71–year old man, affected by hypertension, presented in Emergency Room (ER) with chest pain. No clinical evidence of heart failure. EKG showed fast atrial fibrillation with QS complex and ST elevation in precordial leads. Echocardiogram confirmed sept and apex akinesia. Troponin I peak was 72pg/ml. In ER electrical cardioversion was efficacy performed. He was referred for invasive coronary angiography, that showed a left anterior descending (LAD) chronic total occlusion (CTO), with Rentrop grade 2 collaterals providing retrograde flow from the right coronary artery (RCA), a severe stenosis of ramus intermedius (RI) and a moderate stenosis of circumflex. A stress–echocardiogram demonstrated vitality of medio–basal anterior wall. Subsequent, recanalization procedure of LAD CTO was planned. J–CTO score was 1 (tapered calcific, lesion, <20mm). double radial access and ante grade approach was chosen. An EBU3.5 guiding catheter was engaged in the left coronary artery, and 8000 units of heparin administered. The iFR of Cx was 0.99, indicative of non significant myocardial ischemia. During hemodynamic evaluation of RI, a ventricular fibrillation occurred, treated by DC–SHOCK and PCI with stenting with no polymer, eluted with Biolimus A9 (3.0x24mm) with good result. The occlusion was crossed via an antegrade approach with an Asahi Gaia II wire and with microcatheter support. Gaia II was changed in favor of Asai Sion blu, and the IVUS catheter was enable of cross the lesion. Efficacy orbital atherectomy with Diamondback 260 was performed (5 ante and retro grade run at 80Krpm and a retro grade run at 120 Krpm. Ivus was able to cross the lesion. Efficacy pre–dilatation with semi and non compliant balloon (2.5–3.5mm) was performed and then stented with a 3.0 × 36 mm Bioloimu A9–eluting stent. Finally, IVUS confirmed correct stent expansion, achieving an excellent angiographic result. Patient was discharged with triple anti–thrombotic therapy, with indication to “life jacket” till the assessment at 1 month.

Linear late gadolinium enhancement in the basal anterior septum and lateral wall may represent the contrast enhancement of vessels: A CMR and CCTA comparison study

BackgroundThe purpose of this paper was to verify that the linear high-intensity signal on late gadolinium enhancement-cardiac magnetic resonance (LGE-CMR) may represent the contrast enhancement of vessels rather than scars or fibrosis, and to assess whether this linear high-intensity signal will affect the quantification of myocardial fibrosis in patients with hypertrophic cardiomyopathy (HCM). MethodsA total of 58 patients who underwent both coronary computed tomography angiography (CCTA) and LGE-CMR in our hospital were ultimately enrolled. The definitions of positive linear LGE (LLGE+) were as follows: (1) LLGE in the basal anterior septum or lateral wall, and (2) LLGE observable at 10 mm or more. All other patients were regarded as negative LLGE (LLGE-). In LLGE+ patients, the length of the LLGE located in the anterior septum and lateral wall was compared with the length of the septal perforator artery and the circumflex artery on CCTA, respectively. For nine patients with HCM, the LGE% was measured before and after removal of LLGE. ResultsAmong the 58 patients, 40 showed LLGE+ and 18 showed LLGE-. For patients with LLGE in the anterior septum, there was a strong correlation between LLGE and anterior septal perforator arteries in length (r=0.887, p<0.001). For patients with LLGE in the lateral wall, LLGE also correlated well with the circumflex arteries in length (r=0.962, p<0.001). In nine patients with HCM, the LGE% decreased significantly after the removal of LLGE [9.50 (7.70 – 17.35)% vs. 8.80 (6.20 – 15.55)%, p<0.05]. ConclusionsThe LLGE in the anterior septum and lateral wall may represent contrast enhancement of the anterior septal perforator artery and the circumflex artery, respectively. This LLGE may overestimate the extent of myocardial fibrosis in patients with HCM.

Differences in left ventricular mass and morphology and right ventricular function differentiate phenotype-negative sarcomere gene mutation carriers from healthy volunteers

Abstract Funding Acknowledgements Type of funding sources: None. Carriers of pathogenic DNA variants (G+) causing hypertrophic cardiomyopathy (HCM) can be identified by genetic testing, before manifestation of left ventricular hypertrophy (LVH). These G+/LVH- subjects are routinely monitored for phenotypic expression, which, alongside LVH, can include other HCM-related abnormalities, including crypts and myocardial fibrosis. Cardiovascular magnetic resonance (CMR) imaging has emerged as a valuable technique in diagnosing and follow-up of HCM. In this study, we identified clinical features of subclinical HCM in a G+/LVH- population compared to healthy subjects. We studied 33 G+ subjects with CMR and a maximal wall thickness (MWT) &amp;lt;13mm, and compared them to an age- and gender-matched group of 35 healthy controls (44 ± 14 vs 48 ± 10 y, p = 0.17; 11 (33%) vs 12 (34%) men, p = 0.93). The CMR imaging protocol consisted of 1) steady state free procession cine imaging, 2) 2-dimensional late gadolinium enhancement (LGE) images in the G+ patients and 3) pre-contrast T1 mapping using a modified look-locker inverse recovery sequence. We assessed CMR examinations for features of HCM. Forward logistic regression analysis was performed to determine which of the CMR characteristics were predictive of G+ status. G+ subjects had a higher MWT (10.9 ± 1.6 vs 10.2 ± 1.3 mm, p = 0.04), a similar interventricular septal wall (IVS) thickness (8.8 ± 1.6 vs 8.7 ± 1.6 mm, p = 0.85), a smaller posterior wall (PW) and a higher IVS/PW ratio (6.6 ± 1.2 vs 7.7 ± 1.3mm, p &amp;lt; 0.001; 1.4 ± 0.3 vs 1.1 ± 0.2, p = 0.001). Indexed left ventricular (LV) mass was significantly lower in the G+ group (Table). LV function was similar (63 ± 6 vs. 61 ± 5%, p = 0.12), but right ventricular (RV) function was higher in the G+ group. They often had a characteristic hook-shaped thickening of the basal anterior wall (7 (21%) vs 0, p &amp;lt; 0.004; Figure) and more frequently exhibited myocardial crypts. Midwall LGE was present in 3 (9%) G+ subjects. Native septal T1 values were elevated in G+ patients compared to controls, although mostly within the normal range (986 ± 31 vs 963 ± 28 ms, p &amp;lt; 0.01). Crypts, indexed LV mass and RV ejection fraction were significant predictors of G+ status in logistic regression analysis (Table). CMR demonstrates significant morphological differences between the G+/LVH- population and healthy controls. Further studies are needed to assess the prognostic significance of these morphological features. Predictors of genotype-positive status Variables G+ subjects (n = 33) Controls (n = 35) P value OR for G+ status P value Left ventricular mass/BSA (g/m&amp;sup2;) 45 ± 7.4 53 ± 7.9 &amp;lt;0.001 0.86 [0.78-0.95] 0.003 Right ventricular ejection fraction (%) 58 ± 6 53 ± 4 &amp;lt;0.001 1.15 [1.00-1.32] 0.047 Crypts 17 (55%) 4 (11%) &amp;lt;0.001 9.62 [1.93-48.00] 0.006 G+: genotype-positive, OR: odds ratio Abstract Figure. CMR findings

Incremental value of cardiovascular magnetic resonance imaging in family screening for hypertrophic cardiomyopathy

Abstract Funding Acknowledgements Type of funding sources: None. Genetic testing in relatives of hypertrophic cardiomyopathy (HCM) patients can lead to early identification of carriers of pathogenic DNA variants (G+), before onset of left ventricular hypertrophy (LVH). Repeated evaluation by electrocardiography (ECG) and transthoracic echocardiography (TTE) is recommended to detect HCM during follow-up. Cardiovascular magnetic resonance (CMR) imaging has become valuable in the work-up of HCM, although its role in G+ subjects has not been extensively evaluated. In this study, we investigated the value of CMR in the G+/LVH- population. We included 55 G+ subjects who underwent CMR in addition to ECG and TTE, with a maximal wall thickness (MWT) &amp;lt;15mm on TTE. The CMR imaging protocol consisted at least of steady state free procession imaging and 2-dimensional late gadolinium enhancement (LGE) images. ECGs were considered abnormal in case of pathologic Q waves, T wave inversion or signs of LVH (by voltage criteria including Sokolow-Lyon and a Romhilt-Estes score ≥4). TTEs were abnormal in case of LVH (defined as MWT≥10mm). For both modalities, the diagnosis of HCM was based on a MWT≥13mm. The yield of CMR relative to ECG/TTE was assessed by comparing the proportion of HCM diagnoses and the presence of other phenotypic features. Forward step logistic regression was used to assess whether the presence of TTE/ECG abnormalities could predict reclassifications or abnormalities (crypts and LGE) on CMR. An overview of ECG/TTE and CMR findings is shown in the Figure. Two of 16 (13%) subjects diagnosed with HCM on TTE were reclassified as having no HCM on CMR, and 8 of 39 (21%) subjects without HCM on TTE were reclassified as HCM on CMR. These 8 subjects had a mean MWT of 15.4 ± 2.6 mm on CMR and a mean MWT difference of 4.5 ± 2.9 mm (range 1.7-9.4) compared to TTE, which in 3 cases was explained by a hook-shaped thickening of the basal anterior wall in the 2 chamber view, not visible on TTE. Compared to subjects without HCM on both modalities, the reclassified group had a significantly higher QRS duration (104 ± 14 vs 93 ± 11 ms, p = 0.03) and anterior mitral valve leaflet length (30 ± 4 vs 26 ± 3 mm, p = 0.01). Of the 13 subjects with normal ECG/TTE results, none were reclassified as HCM using CMR. The proportion of additional CMR abnormalities was large in subjects with and without abnormal ECG/TTE results (57% vs 38%, p = 0.24). Subjects with poor TTE image quality were equally likely to be reclassified compared to those with sufficient image quality (10% vs 24%, p = 0.19). Logistic regression demonstrated that the presence of TTE/ECG abnormalities (odds ratio [OR] 8.7 [1.3-59.0], p = 0.03) and age (OR 1.1 [1.0-1.2], p &amp;lt; 0.01) independently predicted reclassifications or presence of abnormalities using CMR. Additional CMR imaging reclassifies 18% of subjects. Subjects with normal ECG and TTE results are not diagnosed as HCM on CMR, but the prevalence of HCM-related abnormalities on CMR was high in subjects with and without ECG/TTE abnormalities. Abstract Figure. Diagnostic approach and CMR findings

Use of echocardiography to monitor myocardial damage during anthracycline chemotherapy.

Anthracycline-related cardiotoxicity has a poor prognosis; therefore, early detection of any change in LV function is critical. The aim of this study was to evaluate the two-dimensional speckle tracking technique for the early detection of cardiac toxicity after low-dose anthracycline chemotherapy in the Chinese population. Forty breast cancer patients were treated by chemotherapy using anthracycline for 4-6 cycles. Patients were examined by echocardiography before chemotherapy (T0) and after the second (T2), fourth (T4), and sixth (T6) cycle. LV ejection fraction (LVEF), LV global longitudinal strain (GLS) and endocardium, mid-myocardium, and epicardium global longitudinal strain (GLS-Endo, GLS-Mid, and GLS-Epi). Additionally, global circumferential strain (GCS), RV global longitudinal strain (RVGLS), and LA global longitudinal strain (LAGLS) were evaluated. Left ventricular ejection fraction was significantly reduced at T4 (P<0.05). Compared with T0, GLS, GLS-Endo, GLS-Mid, and GLS-Epi were significantly reduced at T2, T4, and T6 (P<0.05 for all), the apical septum wall (AS) was also reduced significantly at T2 (P<0.05), and the apical anterior wall (AA) and the basal anterior wall (BA) longitudinal strains were significantly reduced at T4 (P<0.05). GCS, RVGLS, and LAGLS were not significantly changed after treatment (P>0.05). LV stratified strains and strain of the segments supplied by the left anterior descending coronary artery are more sensitive to the cardiac toxicity of anthracycline.

Acute Haemodynamic and Echocardiographic Effects of Multiple Configurations of Left Ventricular Pacing Sites in Acute Myocardial Infarction: Experimental Study.

Left ventricular (LV) pacing is unsuccessful in a significant number of patients, mainly due to sub-optimal LV pacing location. Nevertheless, data about the impact of different pacing sites on LV function in ischaemic myocardium are scarce. The purpose of this study was to investigate the effect of combinations of alternative LV pacing sites on LV mechanics after experimental acute anterior myocardial infarction (AMI), in order to define the optimal configuration. Atrioventricular epicardial pacing at alternative pacing sites was performed in 16 healthy pigs simultaneously, after experimental AMI. Standard right ventricular (RV) apical pacing was combined with: i) LV apex lateral wall; ii) LV basal posterior wall; iii) LV basal anterior wall, and; iv) LV basal anterior wall + LV basal posterior wall. Moreover the pacing configurations of, v) LV basal posterior wall + LV apex lateral wall; vi) LV basal posterior wall + LV basal anterior wall, and; vii) LV basal anterior wall + LV apex lateral wall were also investigated. Haemodynamic parameters, together with classic and novel echocardiographic indices were used, to evaluate the effect of each pacing combination. A speckle tracking technique using EchoPAC software was used. After AMI, the pacing combination of LV apex lateral wall and LV basal posterior wall had the most favourable effect on LV function, leading to similar haemodynamic and torsional effects with sinus rhythm (all variables p>0.05). In pig hearts after AMI, the combination of pacing LV apex lateral wall and LV basal posterior wall managed to maintain the LV function at a level comparable to the sinus rhythm.

Calcified nodule as a cause of myocardial infarction with non-obstructive coronary artery disease

Introduction: In patients presenting with myocardial infarction (MI), angiography most often reveals obstructive coronary artery disease (cAD) but 5-20% of patients with MI have non- obstructive cAD (MINOcA) at angiography. calcified nodule has been identified as a cause of MI with obstructive cAD but to date has not been reported as a cause of MINOcA. Intravascular ultrasound (IVUs) may find an underlying cause of MINOcA but has limited sensitivity for calcified nodule. We report a case of calcified nodule in a patient with MINOcA diagnosed by optical coherence tomography (Oct). case report: the patient was a 60-year-old male former smoker with cAD risk factors who presented with one hour of mid-sternal chest pain. troponin peaked at 1.28 ng/ml. Electrocardiogram of the patient was normal. coronary angiography showed minimal luminal irregularities. the patient underwent intracoronary Oct. On Oct, thrombus was identified overlying a calcified plaque with protrusion into the right coronary artery lumen. the appearance was characteristic of calcified nodule. cardiac MrI scan showed hypokinesis in the basal inferoseptal and basal anterior walls without late gadolinium enhancement. the patient was treated with dual antiplatelet therapy (aspirin and clopidogrel) and a high intensity statin. conclusion: these combined clinical, Oct and cMr findings confirm that calcified nodule is a cause of MINOcA and underscore the utility of intracoronary imaging to determine the pathophysiology of MINOcA. Even without intracoronary imaging, plaque disruption (e.g. plaque rupture, erosion, or calcified nodule) should be considered in cases of MINOcA based on prevalence of at least 35-40% in prior studies.

Abstract 13804: Correlation between Electrocardiographic Features and Local Activation Pattern in Arrhythmogenic Right Ventricular Dysplasia

Background: Depolarization abnormalities in the terminal portion of the QRS are frequently seen in Arrhythmogenic Right Ventricular Dysplasia/Cardiomyopathy (ARVD/C). The purpose of this study was to correlate the electroanatomic activation pattern of the RV endocardium and epicardium to the surface ECG. Methods: Thirty consecutive ARVD/C patients (Mean age 33.1 +/- 11.2 years, 16 (53%) men) underwent detailed endocardial and epicardial electroanatomical mapping (EAM). Local sinus rhythm activation was annotated at the sharpest intrinsic deflection of the bipolar electrogram, including late potentials. ECG features were classified into 5 major patterns; 1. Normal QRS (12 patients) 2. Epsilon wave (5 patients) 3. Incomplete RBBB (5 patients) 4. Atypical complete RBBB (6 patients) and 5. Prolonged terminal activation duration (TAD) (2 patients) Results: The earliest endocardial and epicardial RV activation occurred on the mid anteroseptal wall on all ECG patterns. Figure 1 represented activation area (purple) after the QRS or during the delayed depolarization phase. Nearly all endocardial and epicardial RV was activated well within the QRS duration in patients with normal QRS but was activated during R’ in patients with CRBBB. The delayed activation during Epsilon wave consistently occurred in basal anterior wall and basal angle of RV. In patients with TAD, the activation of RVOT and basal angle RV represented slurred S wave. Conclusion: ECG features in ARVD/C are correlated with late activation in specific regions of RV and total endocardial activation time. The delay activation of basal anterior wall and basal angle of RV represents the Epsilon wave in the right precordial ECG.

IPSC-derived human mesenchymal stem cells improve myocardial strain of infarcted myocardium.

We investigated global and regional effects of myocardial transplantation of human induced pluripotent stem cell (iPSC)-derived mesenchymal stem cells (iMSCs) in infarcted myocardium. Acute myocardial infarction (MI) was induced by ligation of left coronary artery of severe combined immunodeficient mice before 2 × 105 iMSCs or cell-free saline were injected into peri-infarcted anterior free wall. Sham-operated animals received no injection. Global and regional myocardial function was assessed serially at 1-week and 8-week by segmental strain analysis by using two dimensional (2D) speckle tracking echocardiography. Early myocardial remodelling was observed at 1-week and persisted to 8-week with global contractility of ejection fraction and fractional area change in saline- (32.96 ± 14.23%; 21.50 ± 10.07%) and iMSC-injected (32.95 ± 10.31%; 21.00 ± 7.11%) groups significantly depressed as compared to sham control (51.17 ± 11.69%, P < 0.05; 34.86 ± 9.82%, P < 0.05). However, myocardial dilatation was observed in saline-injected animals (4.40 ± 0.62 mm, P < 0.05), but not iMSCs (4.29 ± 0.57 mm), when compared to sham control (3.74 ± 0.32 mm). Furthermore, strain analysis showed significant improved basal anterior wall strain (28.86 ± 8.16%, P < 0.05) in the iMSC group, but not saline-injected (15.81 ± 13.92%), when compared to sham control (22.18 ± 4.13%). This was corroborated by multi-segments deterioration of radial strain only in saline-injected (21.50 ± 5.31%, P < 0.05), but not iMSC (25.67 ± 12.53%), when compared to sham control (34.88 ± 5.77%). Improvements of the myocardial strain coincided with the presence of interconnecting telocytes in interstitial space of the infarcted anterior segment of the heart. Our results show that localized injection of iMSCs alleviates ventricular remodelling, sustains global and regional myocardial strain by paracrine-driven effect on neoangiogenesis and myocardial deformation/compliance via parenchymal and interstitial cell interactions in the infarcted myocardium.

Effect of Microembolization on Left Ventricular Systolic Wall Motion and Dyssynchrony Using Dipyridamole Stress Two-dimensional Speckle Tracking Imaging: An Experimental Study

To investigate whether subtle myocardial injury caused by coronary microembolization (CME) can induce left ventricular contractile dysfunction or dyssynchrony on swine models. CME swine models were constructed by the injection of 150,000 microspheres into the left coronary artery compared with the control group. The peak systolic values of longitudinal strain (LS), radial strain (RS), and circumferential strain (CS) by two-dimensional speckle tracking imaging (2D-STI) were measured under resting stage and dipyridamole stress prior to, 6 hours after, and 1 week after CME. The mean standard deviation of 12 segmental time-to-peak longitudinal strain (Tls-12SD), radial strain (Trs-12SD), and circumferential strain (Tcs-12SD) of the left ventricle were calculated as the dyssynchrony index. Postmortem analysis demonstrated 29.76% of the left ventricular segments manifested myocardial necrosis in MCE group compared with the control group (0%, p < 0.01). Left ventricular ejection fraction had no significant differences throughout the entire study ( p > 0.05). In the CME group, compared with the baseline, LS on the basal anterior wall deteriorated from −9.72 ± 4.96 % to −6.35 ± 3.75 % ( p < 0.05) and Tcs-12SD was prolonged from 85.00 ± 35.74 ms to 151.30 ± 75.14 ms at 1 week ( p < 0.01) under resting stage. After dipyridamole infusing, a further decrease of contractility on all CME-related segments occurred at 6 hours and/or 1 week ( p < 0.05–0.01). The deterioration of Tls-12SD achieved statistical significance at 1 week (157.66 ± 78.25 ms vs. 112.54 ± 62.52 ms, p < 0.05). Furthermore, Tcs-12SD was progressively delayed from 6 hours to 1 week (148.30 ± 45.53 ms and 162.45 ± 51.67 ms vs. 78.00 ± 40.17 ms, all p < 0.01). Subtle cardiac systolic dysfunction as well as dyssynchrony caused by CME can be detected using dipyridamole stress 2D-STI sensitively. Moreover, left ventricular dyssynchrony could be affected even by slight myocardial injury.

Cardiac MRI in the Assessment of Cardiac Injury and Toxicity From Cancer Chemotherapy

During the past 30 years, there has been a significant decrease in cancer mortality rates, predominantly attributable to improvements in treatment options.1 However, survivors are at increased risk of premature cardiac disease,2 both because of the overlap in risk factors for cancer and cardiovascular disease3 and the cardiotoxic effects of cancer chemotherapy. Two chemotherapeutic agent classes that are commonly associated with cardiotoxicity are the anthracyclines and tyrosine kinase inhibitors, both of which can cause left ventricular (LV) dysfunction and heart failure (HF).4,5 Mechanisms of cardiac injury from cancer therapy have been summarized elsewhere.4,6 Briefly, anthracycline cardiotoxicity has been attributed to reactive oxygen species formation, transcriptional changes in intracellular adenosine triphosphate production in cardiac myocytes, and, more recently, through interaction with cardiac topoisomerase IIβ.4,6 Trastuzumab cardiotoxicity seems to be because of inhibition of cardiomyocyte human epidermal growth factor receptor 2, resulting in ATP depletion and contractile dysfunction.4 Other proposed mechanisms include immune-mediated destruction of cardiomyocytes.4,6 At the tissue level, early anthracycline toxicity has been associated with myocardial inflammation,7–9 vacuolization,9–12 and cell swelling/edema.11,13 These changes seem to occur before myocardial functional abnormalities.11,13 Later stages of toxicity are associated with myocardial fibrosis.14,15 Unfortunately, the use of myocardial biopsy is not feasible for diagnostic purposes in this setting. However, once HF manifests, the 2-year mortality can be as high as 60%.16 This emphasizes the importance of early recognition of cardiac injury and institution of cardioprotective therapy in an effort to prevent development of HF and allow uninterrupted completion of cancer therapy.17 Thus, the diagnosis is dependent on either direct evidence of myocardial damage or functional disturbance. Either signal may be identified …

Peripartum Cardiomyopathy Associated With Left Ventricular Noncompaction Phenotype and Reversible Rigid Body Rotation

A 30-year-old woman presented 1-month postpartum with new-onset biventricular heart failure for which no other contributing cause could be found clinically or on laboratory investigations. Her 2 previous pregnancies were uncomplicated. She was HIV-positive for the preceding 3 years, but had never been on antiretroviral therapy. Initial echocardiography revealed a left ventricular (LV) end-diastolic diameter of 59 mm and LV ejection fraction of 32% (online-only Data Supplement Movies 1 and 2). There was evidence of LV noncompaction involving the apex and midinferior and midlateral walls of the LV that satisfied the Jenni criteria (Figure 1). There was no echocardiographic evidence of other congenital or organic valvular disease. Speckle tracking revealed rigid body rotation (ie, rotation at both the basal and apical levels of the LV occurred in a counterclockwise direction during systole; Figure 2). The patient was treated with furosemide, carvedilol, an angiotensin-converting enzyme inhibitor, and spironolactone. On reevaluation 6 months later, her functional status was New York Heart Association Class 1. Echocardiography revealed that LV ejection fraction was now 48% …

Mutation‐Positive Arrhythmogenic Right Ventricular Dysplasia/Cardiomyopathy: The Triangle of Dysplasia Displaced

The traditional description of the Triangle of Dysplasia in Arrhythmogenic Right Ventricular Dysplasia/Cardiomyopathy (ARVD/C) predates genetic testing and excludes biventricular phenotypes. We analyzed Cardiac Magnetic Resonance (CMR) studies of 74 mutation-positive ARVD/C patients for regional abnormalities on a 5-segment RV and 17-segment LV model. The location of electroanatomic endo- and epicardial scar and site of successful VT ablation was recorded in 11 ARVD/C subjects. Among 54/74 (73%) subjects with abnormal CMR, the RV was abnormal in almost all (96%), and 52% had biventricular involvement. Isolated LV abnormalities were uncommon (4%). Dyskinetic basal inferior wall (94%) was the most prevalent RV abnormality, followed by basal anterior wall (87%) dyskinesis. Subepicardial fat infiltration in the posterolateral LV (80%) was the most frequent LV abnormality. Similar to CMR data, voltage maps revealed scar (<0.5 mV) in the RV basal inferior wall (100%), followed by the RV basal anterior wall (64%) and LV posterolateral wall (45%). All 16 RV VTs originated from the basal inferior wall (50%) or basal anterior wall (50%). Of 3 LV VTs, 2 localized to the posterolateral wall. In both modalities, RV apical involvement never occurred in isolation. Mutation-positive ARVD/C exhibits a previously unrecognized characteristic pattern of disease involving the basal inferior and anterior RV, and the posterolateral LV. The RV apex is only involved in advanced ARVD/C, typically as a part of global RV involvement. These results displace the RV apex from the Triangle of Dysplasia, and provide insights into the pathophysiology of ARVD/C.

A misplaced and entrapped pulmonary artery catheter

A misplaced and entrapped pulmonary artery catheter

Successful Ablation for the Ventricular Tachycardia Storm Arising from the Peri-Aortomitral Continuity in a Patient with Ischemic Cardiomyopathy

Ventricular tachycardia arising from the peri-aortomitral continuity (peri-AMC) region in structural heart disease is uncommon. A 70-year-old of post-CABG patient with biventricular ICD was admitted for drug-resistant VT storm. Four inducible VTs (VT1–4) demonstrated RBBB morphology with inferior axis. Mechanism of VT was reentry based on the entrainment study but the identification of circuit was difficult. Pacemapping suggested that the exit of VT1 and 2 be in the vicinity of the peri-AMC but perfect pacemaps were not gained, whereas perfect pacemaps for VT3 and 4 were yielded at the LV basal-anterior wall where the islet of low voltage area (LVA) was elucidated with substrate mapping. In order to confine the putative origins of VT1 and 2, radiofrequency applications were given along the peri-AMC to the anterior mitral annulus (AMA). Subsequently, the linear lesion was made from the AMA to the septal LVA across the LVA-islet of basal-anterior wall. After the procedure, no VT could be induced and demonstrated. Interestingly, origins of VT1 and 2 were concentrated nearby the peri-AMC in which did not correspond to the ischemic area. We suppose that the arrhythmogenicity in the peri-AMC contributed to the VT storm in conjunction with the ischemic scars. The substrate modification of the peri-AMC was effective for the bail-out of VT storm.

An Incidental Discovery or an Impending Disaster in a Patient With Coronary Artery Disease?

A 52-year-old Native American man with a history of hypertension, hyperlipidemia, and tobacco abuse presented with C6-7 myelopathy for cervical fusion. A review of systems revealed a history of chest tightness with exertion for which he underwent a preoperative cardiac evaluation. A nuclear stress test revealed a subtle reversible defect in the basal anterior wall of the left ventricle (LV) and a moderate-sized fixed defect in the basal and midinferior walls of the LV, with a possible localized pericardial or pleural effusion.