Inferior Wall Research Articles

Semiquantitative evaluation of 68Ga-DOTANOC uptake in the normal myocardium: establishment of reference values

BackgroundTo ascertain presence of physiological uptake and derive standardized uptake values (SUV) of 68Ga-DOTANOC in normal myocardium and establish reference values. Methods and resultsDedicated cardiac 68Ga-DOTANOC PET/CT studies of patients referred for evaluation of cardiac sarcoidosis (CS) or myocarditis and found to be normal on visual assessment and on cardiac MRI were analyzed semiquantitatively. The studies were acquired 45-60 minutes after intravenous injection of 111-185 MBq of 68Ga-DOTANOC. Myocardial SUVmax normalized to lean body mass (SUVmax_lbm) values for septum, anterior wall, proximal lateral wall, distal lateral wall, inferior wall, and apical region were 1.12 ± .39, 1.09 ± .42, 1.26 ± .49, 1.16 ± .40, 1.23 ± .39, and 1.05 ± .40, respectively. Myocardial SUVmax_lbm-to-blood pool SUVmean_lbm ratios were calculated for each region and 95th percentile values of these ratios were considered the upper limit of normal. 95th percentile values of myocardial SUVmax_lbm-to-blood pool SUVmean_lbm ratio for the corresponding regions were 1.70, 1.70, 2.00 1.95, 2.05, and 1.70, respectively. ConclusionThere can be physiological uptake of 68Ga-DOTANOC in normal myocardium and the reference values of semiquantitative parameters established in this study may be employed as a corroborative tool for visual assessment in patients undergoing 68Ga-DOTANOC PET/CT for suspected CS or myocarditis.

Evaluating Middle Cerebral Artery Plaque Characteristics and Lenticulostriate Artery Morphology Associated With Subcortical Infarctions at 7T MRI.

Lenticulostriate artery (LSA) obstruction is a potential cause of subcortical infarcts. However, MRI LSA evaluation at 3T is challenging. To investigate middle cerebral artery (MCA) plaque characteristics and LSA morphology associated with subcortical infarctions in LSA territories using 7-T vessel wall MRI (VW-MRI) and time-of-flight MR angiography (TOF-MRA). Prospective. Sixty patients with 80 MCA atherosclerotic plaques (37 culprit and 43 non-culprit). 7-T with 3D TOF-MRA and T1-weighted 3D sampling perfection with application-optimized contrast using different flip angle evolutions (SPACE) sequences. Plaque distribution (superior, inferior, ventral, or dorsal walls), LSA origin involvement, LSA morphology (numbers of stems, branches, and length), and plaque characteristics (normalized wall index, maximal wall thickness, plaque length, remodeling index, intraplaque hemorrhage, and plaque surface morphology (regular or irregular)) were assessed. Least absolute shrinkage and selection operator regression, generalized estimating equations regression, receiver operating characteristic curve, independent t-test, Mann-Whitney U test, Chi-square test, Fisher's exact test, and intra-class coefficient. A P value <0.05 was considered statistically significant. Plaque irregular surface, superior wall plaque, longer plaque length, LSA origin involvement, fewer LSA stems, and shorter total and average lengths of LSAs were significantly associated with culprit plaques. Multivariable logistic analysis confirmed that LSA origin involvement (OR, 28.51; 95% CI, 6.34-181.02) and plaque irregular surface (OR, 8.32; 95% CI, 1.41-64.73) were independent predictors in differentiating culprit from non-culprit plaques. A combination of LSA origin involvement and plaque irregular surface (area under curve = 0.92; [95% CI, 0.86-0.98]) showed good performance in identifying culprit plaques, with sensitivity and specificity of 86.5% and 86.0%, respectively. 7-T VW-MRI and TOF-MRA can demonstrate plaque involvement with LSA origins. MCA plaque characteristics derived from 7-T VW-MRI showed good diagnostic accuracy in determining the occurrence of subcortical infarctions. 2 TECHNICAL EFFICACY: Stage 3.

Culprit Arteries in Patients with Inferior Wall Myocardial Infarction (IWMI) With St Segment Depression in Lead AVR

ACS is an imbalance between the myocardial oxygen demand and consumption of oxygen by the heart. While coronary plaque rupture, which results in STEMI, is almost always the cause of this mismatch development of thrombus blocking a coronary artery. Objective: To determine the frequency of culprit arteries in patients with inferior wall myocardial infarction (IWMI) with ST Segment depression in Lead AVR. Methods: This cross sectional study was conducted at Department of Adult Cardiology, NICVD, Karachi, Pakistan from November 4, 2020 to May 3, 2021. All patients who fulfilled the inclusion criteria were enrolled and consent was taken. All patients were initially stabilized and then were prepared for coronary angiography. Interpretation of coronary angiogram was done to assess the culprit arteries i.e. LCX, RCA. Data were collected in proforma. Results. Out of 317 patients, 233 (73.5%) were male while 84 (26.5%) were female with mean age of 51.4±12.4 years. Left circumflex coronary artery was found in 184 (58%) patients. Right coronary artery was found in 133 (42%) patients. Conclusions: This study concludes that LCX artery is more likely to be culprit in patients with inferior wall myocardial infarction and ST-segment depression in lead AVR. STEMI patients with IWMI should be worked up for the presence of culprit arteries to ensure adequate treatment

A Long-Term Survival Case of Coronary Artery Intimal Sarcoma.

Primary cardiac sarcomas are rare diseases with very poor prognoses. In this report, we present a case of coronary artery intimal sarcoma in a patient who survived for a long time after diagnosis. A 57-year-old female underwent percutaneous coronary intervention of the right coronary artery due to acute myocardial infarction caused by thrombotic occlusion and was diagnosed as having coronary artery intimal sarcoma. She underwent surgical resection and coronary artery bypass surgery of the artery, cryothermy coagulation, and postoperative adjuvant chemotherapy for 1 year. After 3 years, focal recurrence was detected in the caudal region of the left ventricular inferior wall. Radiotherapy was performed. The tumor shrank significantly after radiotherapy. Four years later, there was no significant abnormal uptake on positron-emission tomography/computed tomography. At 7 years after diagnosis, when this case report was submitted, the patient was alive and her performance had maintained a good status. Intimal sarcoma occurring in a coronary artery is extremely rare. The efficacy of treatments for cardiac intimal sarcoma, which include surgical resection, chemotherapy and radiotherapy, has been reported to be limited. To the best of our knowledge, this is the first report of a case of coronary artery intimal sarcoma with long-term survival after comprehensive therapies including surgical resection and radiotherapy.

Spatial Multiplexed Protein Profiling of Cardiac Ischemia-Reperfusion Injury.

Reperfusion therapy is critical to myocardial salvage in the event of a myocardial infarction but is complicated by ischemia-reperfusion injury (IRI). Limited understanding of the spatial organization of cardiac cells, which governs cellular interaction and function, has hindered the search for targeted interventions minimizing the deleterious effects of IRI. We used imaging mass cytometry to characterize the spatial distribution and dynamics of cell phenotypes and communities in the mouse left ventricle following IRI. Heart sections were collected from 12 cardiac segments (basal, mid-cavity, apical, and apex of the anterior, lateral, and inferior wall) and 8 time points (before ischemia [I-0H], and postreperfusion [R-0H, R-2H, R-6H, R-12H, R-1D, R-3D, R-7D]), and stained with 29 metal-isotope-tagged antibodies. Cell community analysis was performed on reconstructed images, and the most disease-relevant cell type and target protein were selected for intervention of IRI. We obtained a total of 251 multiplexed images, and identified 197 063 single cells, which were grouped into 23 distinct cell communities based on the structure of cellular neighborhoods. The cellular architecture was heterogeneous throughout the ventricular wall and exhibited swift changes following IRI. Analysis of proteins with posttranslational modifications in single cells unveiled 13 posttranslational modification intensity clusters and highlighted increased H3K9me3 (tri-methylated lysine 9 of histone H3) as a key regulatory response in endothelial cells during the middle stage of IRI. Erasing H3K9 methylation, by silencing its methyltransferase Suv39h1 or overexpressing its demethylase Kdm4d in isolated endothelial cells, attenuated cardiac dysfunction and pathological remodeling following IRI. in vitro, H3K9me3 binding significantly increased at endothelial cell function-related genes upon hypoxia, suppressing tube formation, which was rescued by inhibiting H3K9me3. We mapped the spatiotemporal heterogeneity of cellular phenotypes in the adult heart upon IRI, and uncovered H3K9me3 in endothelial cells as a potential therapeutic target for alleviating pathological remodeling of the heart following myocardial IRI.

Characterization of right ventricular low voltage areas in patients with arrhythmogenic right ventricular cardiomyopathy

Abstract Funding Acknowledgements Type of funding sources: None. Background Arrhythmogenic right ventricular cardiomyopathy (ARVC) is characterized by fibrofatty replacement in the myocardium progressing from the epicardium towards the endocardium and affecting primarily the right ventricle (RV). Little data is available on the distribution of RV electrical abnormalities at the era of epicardial and high-resolution mapping. Purpose To evaluate the extent and distribution of RV epicardial and endocardial low voltage areas and their relationship with ECG abnormalities in ARVC patients. Methods Patients with a definite ARVC diagnosis according to the 2020 Task Force Criteria, who underwent ventricular tachycardia ablation between 2016 and 2022 with a high-density RV 3-dimensional electroanatomic mapping, were included. A custom RV segmentation dividing the RV into 10 segments from endocardial maps was used: anterior and lateral right ventricular outflow tract (RVOT); basal and mid inferior wall; apex; septum; basal anterolateral, basal inferolateral, mid anterolateral and mid inferolateral RV free wall (Figure). A standard definition of electrical scar was used (bipolar voltage ≤0.5 mV), and scar areas were manually delineated. Percentage of scar was defined by the ratio between scar area and the total segment area. ECG abnormal findings, such as epsilon wave and T-wave inversion in precordial leads, were measured before ablation procedure. Results Twenty-nine consecutive definite ARVC patients were included, among whose 24 had epicardial mapping in addition to endocardial mapping. When considering all segments, the epicardial scar (median:70%, interquartile range [IQR] 37-97%) was larger (p&amp;lt;0.0001) than the endocardial scar (9% [IQR] 0-32%). The higher percentage of epicardial scar was found in the basal inferolateral (100% [IQR] 73-100%), basal anterolateral (94% [IQR] 67-100%), RV free wall and lateral RVOT (89% [IQR] 48-100%) segments (Table). Transmural scar was observed mostly in basal inferolateral RV free wall (10 patients, 41%) and basal inferior wall (8 patients, 33%). Patients with major depolarization criteria had a higher percentage of epicardial and endocardial scar as compared to those with no or minor depolarization criteria (respectively 93% [IQR] 59-100% versus 62% [IQR] 28-89%, p&amp;lt;0.0001 and 17% [IQR] 0-42% versus 4% [IQR] 0-23%, p=0.001). There was no significant difference of the percentage of epicardial or endocardial scar in patients with and without major repolarization criteria (respectively 90% [IQR] 49-98% versus 84% [IQR] 43-100%, p=0.91 and 14% [IQR] 11-35% versus 16% [IQR] 0-41%, p=0.73). Conclusion In ARVC, the electrical abnormalities predominate in the basal epicardium. Patients with major depolarization criteria had a higher extent of epicardial and endocardial scar, but there was an association between scar extent and repolarization abnormalities.

Usefulness of simultaneous isolation of the coronary sinus and the left atrial inferior wall for persistent atrial fibrillation refractory to box isolation

Abstract Funding Acknowledgements Type of funding sources: None. Background In patients who are refractory to box isolation (BoxI) and have atrial fibrillation (AF) substrate in left atrial inferior wall (LAIW), LAIW isolation is effective, but the procedure is highly difficult because the connection between LAIW and coronary sinus (CS) is dense. In this study, we report four cases of persistent AF in which simultaneous isolation of LAIW and CS was so effective. Methods and Results Case 1 is a 76-year-old female with persistent AF who had undergone BoxI and failed mitral isthmus block (MIB) creation. However, AF and atrial tachycardia (AT) persisted. In the 4th session, chemical ablation of Marshall vein was performed, and AF/AT was terminated, and MIB was created. Thereafter, multiple ATs were still inducible by rapid atrial pacing. Because AT substrate seemed to be confined to LAIW, we attempted to isolate LAIW by performing linear ablation between the right inferior pulmonary vein (RIPV) and posteroseptal mitral annulus (MA) near CS ostium, and linear ablation parallel to CS along posterior MA. However, LAIW isolation could not be achieved. Finally, CS ostial ablation from right atrium (RA) succeeded in simultaneous isolation of LAIW and CS. CS burst pacing could induce AT confined to LAIW and CS although RA maintained sinus rhythm (SR). Rapid RA pacing could not induce AT/AF. Case 2 is a 78-year-old female with persistent AF who completed BoxI and MIB creation. Raid RA pacing induced AF. Because cycle length of LAIW was apparently shorter than RA, we attempted to isolate LAIW. Firstly, we performed linear ablation from RIPV ostium to posterior MA. During linear ablation, AF converted to AT, and finally RA returned to SR while AT was still sustained within LAIW and CS. This tachycardia was a reentrant tachycardia circling LAIW and CS. After this AT returned to SR by linear ablation within LAIW, LAIW and CS were not isolated during SR. CS ostial ablation from RA succeeded in simultaneous LAIW and CS isolation. Case 3 is a 74-year-old female with persistent AF refractory to BoxI. Although non-pulmonary vein (non-PV) trigger was documented in LAIW, the precise origin of non-PV trigger could not be identified due to infrequency. Case 4 is a 64-year-old male with persistent AF refractory to BoxI. He had undergone catheter ablation three times. Fractionation map showed that AF substrate was likely located in LAIW. Therefore, we attempted to isolate LAIW in Case 3 and 4. We performed MI ablation, linear ablation between RIPV ostium and posteroseptal MA, and CS ostial ablation from RA, which succeeded in simultaneous isolation of LAIW and CS in both cases. AF has never recurred in Case 1 and 2. SR could be maintained with antiarrhythmics in Case 3 and 4. Conclusions In patients with persistent AF refractory to BoxI, if LAIW has AF/AT substrate or non-PV triggers, simultaneous isolation of LAIW and CS may be a new therapeutic strategy. Simultaneous isolation of LAIW and CS requires ablation at CSos from RA.

The novel left atrial anterior 'seatbelt' line reduces sustained atrial arrhythmia by 72% compared to pulmonary vein isolation alone in a cohort of 400 virtual atria models

Abstract Funding Acknowledgements Type of funding sources: Public grant(s) – EU funding. Main funding source(s): European Union’s Horizon 2020 research and innovation programme under the Marie Skłodowska-Curie grant agreement No.860974. Background The success-rate of pulmonary vein isolation (PVI) is modest in persistent atrial fibrillation (AF), but additional empirical ablation, such as posterior wall isolation (PWI), has not been shown to reduce the rate of AF recurrence. The "seatbelt", an anterior linear ablation lesion connecting the right superior pulmonary vein to the mitral annulus, is a novel substrate modification approach that is yet to be tested in a large-scale randomised clinical trial. Purpose To use in-silico trials with human-based modelling and simulation to compare the efficacy of (i) PVI alone, (ii) PVI and PWI (PVI+PWI), or (iii) PVI and seatbelt (PVI+SB) for the prevention of atrial arrhythmia in large populations of virtual patient models. Methods AF was simulated in a cohort of 400 virtual atrial models with anatomical and electrophysiological variability, with AF persisting for &amp;gt;7 seconds defined as sustained. Models which sustained AF were each independently subjected to all three ablation approaches before repeating the AF induction protocol. Results Three hundred forty-four (86%) atrial models developed sustained AF at baseline. After applying the ablation lesions, substantially fewer models sustained atrial arrhythmias in the PVI+SB group (50 [14%] vs. 134 [39%] with PVI+PWI vs. 172 [50%] with PVI). PVI+SB was more effective than PVI and PVI+PWI in preventing both AF and atrial flutter (i.e., presence of a single rotor), since PVI and PVI+PWI led to the formation of anatomical re-entries around the rings of the pulmonary veins and the posterior wall of the left atrium, respectively (Figure). Therefore, PVI+SB restricted atrial flutter mainly to the right atrium (either anatomical, around the inferior cava vein, or functional, meandering throughout the venous portion of the right atrium, Figure). Importantly, in all three ablation strategies, the likelihood of AF recurrence was directly proportional to the surface area of the right atrium (AF probability increased 0.95%/cm², 0.88%/cm² and 0.56%/cm² after PVI+SB, PVI+PWI and PVI, respectively). The role of the right atrial size was less accentuated for PVI alone, since after the ablation the entire left atrial body was still available for rotor anchoring. Moreover, an enlarged left atrium enabled the appearance of micro-re-entries in the anterior and inferior wall of the left atrium, even after applying floor and roof lines. One atrial model additionally presented a rotor in the posterior wall of the left atrium after completely isolating it from the left atrial body. Conclusion(s) In a cohort of 400 virtual atrial models, PVI+SB reduced sustained atrial arrhythmias by 72% compared to PVI alone and by 64% to PVI+PWI, but AF could still originate in an enlarged right atrium.

Crypt of the left ventricular apex.

A 61-year-old Japanese woman was introduced our hospital because of abnormality in electrocardiography (ECG). She had no symptom, and no past and family history. Three years ago, ECG showed sinus rhythm, negative T waves in I, aVL, V2 to V6 leads, and no left ventricular hypertrophy (Panel A). Echocardiography showed normokinesis (ejection fraction, 64%). Contrast enhanced computed tomography (CECT) showed normal coronary arteries but crypts (arrows) at left ventricular apex with mild hypertrophy (Panel B, C). At this time, ECG showed new negative T waves in II and aVF in addition to progression of negative T waves in I, aVL, V2 to V6 leads (Panel D). CECT showed almost disappearing crypt (arrow) due to progression of apical hypertrophy (Panel E, F). Left ventricular crypts are congenital fissure-like protrusion penetrating more than 50% of the thickness of adjoining compacted myocardium. They are commonly seen in the basal inferior wall of left ventricle and interventricular septum in hypertrophic cardiomyopathy (HCM) and HCM carriers who have not yet hypertrophy. Apical crypt may be one of the markers of progression to apical HCM that is more seen in Japanese.

P224 THE SHARK–FIN THAT EMERGES AND IMMERGES: A CASE REPORT OF TRANSIENT AND REPETITIVE TRIANGULAR QRS–ST–T

Abstract Introduction Shark fin sign, also known as triangular QRS–ST–T waveform (TW), is characterized by a giant R wave (amplitude ≥ 1 mV) resulting from the fusion of the QRS complex, the ST–segment and the T wave and showing triangular morphology. TW pattern is quite uncommon and reveals a life–threatening condition that needs aggressive management. Case presentation: A 45–year–old black man with history of arterial hypertension and without known comorbidities arrived at our emergency department (ED) with out–of–hospital cardiac arrest (OHCA). Return of spontaneous circulation occurred after 11 minutes and 2 direct current shocks. At arrival in the ED, he was hemodynamically stable, electrocardiogram showed atrial fibrillation without repolarization abnormalities, and echocardiogram revealed left ventricular hypertrophy and hypokinesia of the mid–basal inferior wall. Plasma level of electrolytes and high–sensitivity troponin were in range. Sedation in the ED was needed due to psychomotor agitation. He was transferred to the cardiac intensive care unit; no arrhythmias were noted. During the night, electrocardiogram monitoring revealed a progressive ST segment elevation in inferior leads up to a triangular QRS–ST–T giant waveform (“Shark fin sign”), confirmed at 12–lead electrocardiogram. After 3 minutes the electrocardiogram showed a progressive and complete resolution of ST–elevation. Akinesia of the inferior wall was confirmed at echocardiogram. The episode repeated 5 more times in the following 40 minutes, while waiting for the arrival of the Cath lab personnel. Coronary angiography revealed a sub–occlusive mid right coronary artery (RCA) stenosis. Percutaneous coronary intervention with the implantation of one drug eluting stent was performed. After the procedure the patient was hemodynamically stable, and the ECG did not show any other abnormality and no episodes of recurrent ST–elevation occurred. Conclusion The shark fin sign refers to the abrupt total deprivation of blood flow in large areas of myocardium that are seen during coronary thrombotic occlusion or vasospasm. In our case we assisted to transient but repetitive inferior triangular ST–elevation, probably the expression of RCA plaque coronary vasospasm that cause the ECG shark fin sign and OHCA. This sign correlates with high risk of cardiogenic shock, electrical instability, and cardiac arrest, thus requiring prompt and aggressive management.

P324 LEFT VENTRICULAR ISOLATED CARDIOMYOPATHY OR DILATED CARDIOMYOPATHY: THE ROLE OF GENETIC ANALYSIS

Abstract Introduction arrhytmogenic cardiomyopathy (ACM) is a genetic heart muscle disease caracterized by substitution of the ventricular myocardium with fibrofatty tissue. The disease was originally termed “arrhytmogenic right ventricular (dysplasia)/cardiomyopathy” to define a condition which distinctively affected the right ventricle and predisposed to fatal ventricular arrhythmias. New insights led to comprehending that the left ventricle is also frequently affected. Clinical case 62 yo, male, no cardiovascular risk factors, positive history for frequent ventricular premature beats treated with Sotalol 40 mg twice a day. No other previous cardiological events. Accesses the ER with suddenly occured dyspnea for minimal exertion, without palpitation, chest discomfort or loss of consciousness. EKG: synus rhythm, low voltages, negative V4–V6 T waves, fragmented QRS. Blood testing: TnI 0,532 ng/ml (n.v. 0–0.034) NTproBNP 3840. Echocardiography: dilated left ventricle. 20% EF due to infero–lateral wall akynesia. Coronary angiography was performed and showed no coronary stenosis. Considered the frequent NSVTs showed by the telemetry, he was admitted to ICU and treated with Amiodarone, Atenolol 100 mg, Sacubistril/Valsartan 24/26 mg, diuretic therapy showing good control of major arrhytmic events. To evaluate characterize heart tissue, a magnetic resonance was performed, which showed: scalloping of the mid and apical left ventricular lateral wall, with fibrofatty substitution. Subepicardial, mid–wall and transmural LGE of the LV anterior, lateral and inferior walls. No RV abnormalities. Considered the reduced EF and the presence of arrhytmic substratum, an ICD was implanted. Finally, a genetic evaluation was discussed with the patient, but was declined. Discussion in patients presenting with typical LV abnormalities, without RV involvement, the phenotipic Padua criterias are not enough for a certain diagnosis. This is because of the phenotipic overlap between ACM and other diseases, such as dilated cardiomyopathy, myocarditis and cardiac sarcoidosis. In the presence of LV involvement, consistent with ACM, the evidence of a pathogenetic mutation is key for the diagnosis.

P249 INTRAMYOCARDIAL HAEMATOMA AS A COMPLICATION OF ACUTE MYOCARDIAL INFARCTION

Abstract A 72–year–old overweight man, with known hypertension and dyslipidaemia, had an episode of high intensity chest pain, which appeared at rest and lasted for several hours. A few days later, he underwent a cardiological examination and the electrocardiogram showed normofrequent sinus rhythm, ST elevation of 3 mm and Q waves formed in the anterior and lateral wall leads. The patient was diagnosed with late ST elevation myocardial infarction and was transported to our emergency department. On blood test, troponin levels were significantly elevated. He was treated with dual antiplatelet therapy (DAPT, aspirin and ticagrelor) and then underwent percutaneous coronary intervention (PCI). The mid segment of the LAD was suboccluded and two drug eluting stent (DES) were implanted. The right coronary artery also had a critical stenosis at the second segment treated with implantation of a DES. Final angiographic result was good (TIMI 3). The patient was admitted to our coronary unit where he continued to receive DAPT. During hospitalization a routine transthoracic echocardiogram (TTE) was performed which showed dilated left ventricle with a–dyskinesis of the apex and middle segment of the septum and the anterior wall and reduced ejection fraction (FE 35%). Within the apical segment of the septum and inferior wall, was noted an area of 40x14 mm with different echogenicity, probably referable to intramyocardial haematoma (IH) of the ventricular wall or a stratified thrombus. Both Colour Doppler and echo–contrast, using Sonovue, did not show a continuity between the suspected IH and one of the ventricular cavities. On cardiac MRI, this finding was considered of uncertain interpretation (whether IH or non–protundant mural thrombus). Late transmural enhancement was also observed at the same echocardiographic sites with subendocardial hypointensity bands consistent with areas of no–reflow. As the patient was clinically stable and TTE monitoring showed no progression of IH, a joint decision was made by cardiologists and cardiac surgeon to continue conservative management with DAPT without initiating anticoagulant therapy. At 1 month follow–up, TTE showed a reduction of the IH and an improvement of the EF to 45%. IH is a rare complication of myocardial infarction and revascularization treatments. The incidence is not well documented and the finding is usually occasional by TTE. Appropriate management is still controversial and a personalised approach is recommended.

C76 FINDING OF MYOCARDIAL CRYPTS IN SUDDEN CARDIAC ARREST PATIENTS: TWO CASE REPORT

Abstract Left ventricular myocardial crypts are definined as deep blood–filled invaginations trasversing &amp;gt; 50% of the myocardial wall and are located predominantly at the mid–basal segment of inferoseptal wall or at the apical segment. To date the incidence of crypts is 9.1% of patients undergoing cardiac CT and are not associated with intermediate–term major adverse cardiovascular events. However several studies have suggested that the presence of crypts is a marker of myocardial disease that should warrant clinical follow–up prior to the potential development of left ventricular hypertrophy and occurrence of serious cardiovascular events, such as heart failure or death. A lot of publications demonstrate that ventricular crypts could be a pre–phenotypic marker of hypertrophic cardiomyopathy (HCM). HCM is a genetic ereditary cardiomyopathy which is associated with fatal ventricular arrhytmias. We present the case of two patients who had a sudden cardiac arrest resuscitated with cardiac defibrillation. These are two males, 59 and 53 years old respectively, without cardiovascular risk factor and with familiarity for HCM. The first patient had a sudden cardiac arrest during exercise and was resuscitated with early cardiac defibrillation. The second patient had ventricular fibrillation after otolaryngology surgery treated with single defibrillator shock. Coronary arteries were free from atherosclerotic lesions at the angiografy study and no other reversible causes of cardiac arrest were identified. CMR showed normal biventricular funtion and ruled out signs of myocardial oedema or fibrosis. The only morphological finding was the detection of single left ventricular myocardial crypt at the CMR study in both patients: in one patient the crypt was located at the inferior wall while in the other at the level of the septum in the mid–apical segment. Ultimately both patients underwent genetic testing for cardiomyopathy. These findings may be a pre–phenotypic markers of HCM in patients who don’t present a clear expression of the pathology but may be a correlation with sudden cardiac arrest. The rarity of their finding in patient who have had sudden cardiac arrest can be explained by the small survival rate in patients with sudden cardiac arrest. Future studies and the increasingly simple access to advanced imaging methods like CMR and CT will allow us to clarify the role of these myocardial anomalies in the risk of developing fatal arrhythmic events.

P119 WHEN THE ELECTROCARDIOGRAM CHANGES YOUR DIAGNOSIS

Abstract Sarcomeric hypertrophic cardiomyopathy is among the most common genetic cardiovascular diseases.Clinical,electrocardiographic and echocardiographic evaluation plays a crucial role in the diagnosis and initial framing of the hypertrophic phenotype. A 51–year–old Caucasian man with multiple myeloma,previous autologous transplant,undergoing chemotherapy for disease recurrence,without cardiovascular risk factors or family history of MCV or MCI came to our outpatient clinic for a follow–up visit.At another center,cardiac amyloidosis was diagnosed due to the echocardiogram finding of concentric left ventricular hypertrophy. Patient asymptomatic for angor,NYHAI dyspnea,heart palpitation,syncope,presented with rhythmic cardiac action,2/6 systolic murmur at centrum and tip,no central or peripheral stasis.On ecg sinus bradycardia at fc57 bpm,PR202 msec,high QRS V4–V6 voltages with negative T waves in infero–lateral site,suggestive for left ventricular hypertrophy. On echocardiogram:concentric left ventricular hypertrophy with posterolateral papillary hypertrophy,preserved contractile function,FE 62%,grade I diastolic dysfunction,no signs of elevated filling pressures,left atrium and right ventricle in normal range;tripartite aortic valve in absence of gradients,prolapse of the LAM(A1–A2)with mild grade insufficiency,mild tricuspid insufficiency. At cardiac MRI:non–dilated left ventricle with concentric hypertrophy,maximum thickness 16mm at basal SIV level,apical inferior wall,15mm anterior wall,anterolateral media,apex systolic obliteration 14mm,FE 64%.Right ventricle and atria in normal.T2–STIR sequences tenuous hyperintensity at infero–lateral media wall,inferior apical wall and lateral,increased T2 mapping in relation to myocardial edema. Subendocardial LGE of middle infero–lateral,apical lateral and postero–medial papillary wall,slight increase in native T1 mapping,ECV 27%,picture of sarcomeric hypertrophic heart disease.Holter ecg showed no arrhythmias;at HCM score low risk,no indication for ICD implantation. The patient was undergoing genetic screening test for HCM.The presence of left ventricular hypertrophy may mimic different forms of hypertrophic cardiomyopathy,leading to misdiagnosis or delayed diagnosis.Differential diagnosis,ecg and specific use of imaging tests are of paramount importance.

P236 THE EARLY USE OF A PARTICULAR HEMODIALYTIC FILTER DURING SCA–STEMI COMPLICATED BY MULTIORGAN FAILURE

Abstract A 66–year–old man, hypertensive, obese and avid smoker, in apparent good health until, due to the onset of typical chest pain associated with vomiting and algid sweating, he went to the PS where a diagnosis of acute coronary syndrome with ST–segment elevation was made. As per the guidelines, antithrombotic therapy was administered and transfer to the HUB center was arranged to perform urgent coronarography; thrombotic occlusion of the I M.O. branch was revealed and treated with angioplasty and drug–eluting stent implantation. On admission to the NICU, the patient presented hypotensive, tachycardic and with repeated episodes of rectorrhagia and vomiting intermingled with blood. Cardiac echocolorDoppler showed mild reduction in global kinesthesia (FE 45%) with hypo–akinesis of the inferior and lateral walls, circumferential pericardial effusion that was not hemodynamically significant, dilated and fixed inferior vena cava with mild increase in systolic pulmonary artery pressure. On suspicion of gastro–intestinal ischemic damage, supported by the clinical and laboratory findings (creatinine increase with anuria for more than 12 hours and severe signs of hepato–pancreatic insufficiency) CT scan with mdc was performed showing hepato–renal hypoperfusion. Therefore, on suspicion of multi–organ dysfunction syndrome, renal replacement therapy was started in CVVHD mode with filter for clearance of medium molecular weight molecules (cut–off 40 kDa) to reduce possible cytokine and myoglobin damage. Already from the first hours of treatment, there was a rapid and exponential improvement in clinical–laboratory parameters with resumption of diuresis. During hospitalization, two episodes of paroxysmal atrial fibrillation treated with electrical and pharmacological cardioversion were detected; given a CHA2DS2VASc score 3 and a HAS–BLED score 2, triple antithrombotic therapy was initiated. At follow–up, there was improvement in echocardiographic parameters (minimal residual pericardial dislodgement and inferior vena cava of normal caliber and respiratory collapsibility) and clinical–laboratory.

P403 MITRAL VALVE PROLAPSE AND RISK OF SUDDEN CARDIAC DEATH IN A PATIENT WITH VENTRICULAR ARRHYTHMIAS: THE PROGNOSTIC ROLE OF CARDIAC MAGNETIC RESONANCE IMAGING

Abstract Introduction in most cases mitral valve prolapse is a benign condition, however in 2% of cases it has been associated with the risk of sudden cardiac death (SCD). Basso et al have demonstrated papillary muscle’s and left ventricle’s inferolateral wall fibrosis on cardiac magnetic resonance imaging (MRI), in patients who died from SCD with mitral valve prolapse. Clinical case A 59–year–old patient was admitted to the Cardiology Department of Pertini Hospital (Rome, Italy) for episodes of vertigo and not sustained ventricular tachycardia in two morphologies at 24–hour ECG monitoring. The patient had negative history for cardiovascular risk factors, but an echocardiogram had demonstrated a moderate mitral valve regurgitation, secondary to valve prolapse with mitral annular disjunction (MAD) (Fig.1). Considering patient‘s age associated with low pre–test probability of coronary artery disease, the patient underwent coronary CT that showed a coronary artery tree free from injury. Cardiac MRI showed increased volumes in the left ventricle and slightly reduced systolic function and valve prolapse of both mitral leaflets determining moderate regurgitation. In addition, intra–myocardial Late Gadolinium Enhancement (LGE) showed fibrosis of the inferior and inferolateral wall with extension to the proximal portion of the inferior papillary muscle (Fig.2). Considering such findings, an intracavitary electrophysiological study (EPS) was performed for an evaluation of the arhythmic burden, by administrating the patient a double extra stimulus from the outflow tract of the right ventricle; the treatment induced a polymorphic ventricular tachycardia, starting from the inferior papillary muscle and degenerating into ventricular fibrillation (Fig.3). Discussion considering all the above findings, a mitral valve prolapse at high risk of malignant arrhythmias has been diagnosed and a subcutaneous cardiac defibrillator was implanted. Conclusions in mitral valve prolapse associated with complex ventricular arrhythmias, evaluation with cardiac MRI increasingly plays a crucial role in prognostic stratification for defibrillator implantation in primary prevention.

P456 SUBACUTE STEMI AND ISCHEMIC STROKE DURING SARS–COV2 INFECTION: A CASE REPORT

Abstract A 71–year–old woman arrived in the ER for left hemiparesis and dysarthria. The Patient was oriented, collaborative. Stable hemodynamics. Left hemiparesis. Dysarthria. NIHSS 8, Ranking 2. Blood tests, EGA, swab for SARS–Cov2 were performed (hsTnI 9433 ng, PCR 15.6 mg/dl, Sars–Cov2 positive test). ECG showed evidence of inferolateral ST–segment elevation with Q waves in the inferior site and negative T waves in the inferolateral leads. An episode of chest pain radiating to the left upper limb two days ago was reported. The echocardiography showed non–dilated left ventricle with global systolic function at the lower limits. Inferior, infero–lateral and medio–basal akinesia with hyper–refractive wall and preserved thicknesses were found. Moreover, a slight layer of circumferential pericardial effusion, without any hemodynamic importance was showed. In order to exclude an aortic syndrome, a CT angiography of the brain, neck and chest was performed for recent lesions, with negative result. Angiography showed the left vertebral artery up to the V3 segment, suspected by dissection. Recommendations on performing fibrinolysis in adults, with concurrent ischemic stroke and subacute STEMI, are conflicting: according to ASA/AHA guidelines in recent 3–month infarction, treatment is reasonable if the inferior or right wall is involved. According to ESO guidelines, fibrinolysis is not recommended if the subacute STEMI is seven days old. The Italian guidelines consider the treatment of acute stroke with r–TPA with subsequent PTCA, with possible stent, and recognize a very low risk of consequent hemopericardium. Depending on the timing of the anginal symptoms, the presence of Q waves on the ECG and the echocardiographic alterations, the AMI was considered subacute with no indication for urgent coronary angiography. For the patient of this case report, a conservative attitude for both pathologies was decided, performing an antiplatelet therapy with ASA and continuous ECG monitoring. Despite the treatment, the patient suffered heart failure and exitus after 10 days hospitalization. The lack of unequivocal guidelines on the treatment of patients with simultaneous ischemic stroke and subacute STEMI, require careful evaluation of the individual case, searching for possible predisposing factors of a poor prognosis.

C62 CHALLENGING DIAGNOSIS OF A TRIPLE CARDIAC PATHOLOGY: TRANSTHYRETIN AMYLOIDOSIS WITH ASPECTS OF HYPERTROPHIC OBSTRUCTIVE CARDIOMYOPATHY AND ANOMALOUS CORONARY ARTERY

Abstract A 70 years–old man with a history of systemic hypertension and surgically treated bilateral carpal tunnel was referred for dyspnea on exertion for few months. At physical examination a systolic heart murmur exacerbated by Valsalva maneuver was appreciated; no signs of heart failure. EKG with low–voltage QRS is shown in Fig.1A. Blood tests showed elevated NT–proBNP (1434 pg/ml). Transthoracic echo (ETT) revealed hyperdynamic left ventricle (LV) with severe asymmetric hypertrophy (interventricular septum 23 mm, posterior wall 17 mm), ‘granular sparkling’ appearance of myocardium, grade 2 diastolic dysfunction and ‘apical sparing’ pattern at global longitudinal strain (GLS, Fig.1B). Moreover, elongated mitral leaflets, anomalies of mitral sub–valvular apparatus with apically displaced papillary muscles and systolic anterior motion of the mitral valve (SAM) with dynamic outflow tract obstruction (20 mmHg at rest and 90–100 mmHg with Valsalva maneuver) were seen (Fig. 2A–B–C). For ETT suspicion of a coronary artery anomaly (Fig.3A), the patient underwent coronary CT angiography that confirmed a separate origin of left anterior descending artery (LAD) from right coronary sinus with a long mid–proximal intramyocardial bridge (Fig.3B–C). As a part of evaluation of the hypertrophic phenotype, a 99mTC–HDP bone scintigraphy was performed with high–grade of cardiac uptake (Perugini Score 2, Fig.1C). Screening for monoclonal gammopathy and genetic testing for hereditary amyloidosis resulted negative. Cardiac MRI revealed late gadolinium enhancement (LGE) in midwall septum, diffuse endocardial LGE in the LV basal inferior and posterolateral walls (Fig.1D), elevated T1 mapping and ECV (40–42%) and confirmed the asymmetric hypertrophy with apically displaced papillary muscles (Fig.2D) and SAM. These clinical, EKG and imaging features led to a non–invasive diagnosis of wild–type transthyretin cardiac amyloidosis (ATTRwt) with aspects of hypertrophic obstructive cardiomyopathy (HOCM). The patient started a disease–modifying therapy with Tafamidis and, cautiously, Metoprolol tartrate, with good tolerance and relevant reduction of LVOT obstruction at follow–up. Genetic testing for HCM was also performed. In conclusion, in rare cases hypertrophic phenotype may be challenging, showing features overlap between ATTR and HOCM. Multimodality evaluation is crucial for a correct diagnosis, thus identifying the most effective target–therapy for the underlying hypertrophic phenotype.

P155 CT EVIDENCE OF PARTIAL ISCHEMIC PAPILLARY MUSCLE RUPTURE

Abstract A 77–year–old man was referred for coronary CT following an episode of prolonged chest pain that occurred about 30 days earlier, with subsequent onset of dyspnea on moderate exertion. Coronary CT demonstrated right dominance, occlusion of the right coronary artery, as well as severe stenosis of the distal segment of the left anterior descending artery and of the first obtuse marginal branch. CT scan also showed an intraventricular image consistent with partial rupture of the posteromedial papillary muscle (Figure 1). The patient was transferred to the emergency department. An ECG showed signs of inferolateral necrosis. Transthoracic echocardiography confirmed akinesia of the inferior and inferolateral walls and of the basal segment of the inferior septum, with severe mitral valve insufficiency from anterior leaflet prolapse (A3 scallop) from partial rupture of the posteromedial papillary muscle (Figure 2). Transesophageal echocardiography confirmed the diagnosis (Figure 3). The patient was admitted to the CCU and underwent coronarography, which confirmed the severe triple vessel coronary artery disease with occlusion of the right coronary artery, and then urgent mitral valve replacement with bioprosthesis and aortocoronary bypass with saphenous vein grafting to the posterior descending artery. The postoperative course was uneventful. Ischemic papillary muscle rupture is a rare cause of mitral insufficiency. Papillary rupture typically occurs within 5 days of an acute myocardial infarction, and causes mitral insufficiency by prolapse and flail of one or, more rarely, both mitral valve leaflets. The posteromedial papillary muscle is most commonly affected, since the anterolateral papillary muscle has dual supply from the anterior interventricular artery and the circumflex artery. Papillary muscle rupture can be total or partial; however, most cases of partial rupture progress to complete rupture and therefore require urgent surgical treatment. The peculiarity of this case lies in the fact that it is the first case described in the literature of a papillary muscle rupture documented on CT.

P282 PAUCISYMPTOMATIC POST–COVID MYOCARDITIS IN A YOUNG ATHLETE DURING THE DIAGNOSTIC INVESTIGATIONS BEFORE RETURNING TO COMPETITIVE PRACTICE, POSSIBLE USEFULNESS OF THE GLS ANALYSIS

Abstract It is now known that the Covid19 infection can cause myocardial inflammatory damage. Several studies have shown that the echocardiographic parameter of the global longitudinal strain (GLS) was reduced compared to the general population even in paucisymptomatic patients. A young competitive athlete came to our observation for the diagnostic investigations before returning to competitive practice (return to play protocol) after Sars–Cov2 infection. The electrocardiogram did not show significant abnormalities as well as spirometry examination. Negative inflammation indexes and markers of myocardial damage were observed. The cycloergometer test showed no signs of myocardial distress, rapid chronotropic increase and dyspnea at 100W work load. HolterECG was performed showing 830 isolated ventricular ectopic beats. Echocardiographic examination showed preserved left ventricular systolic function (FEVS 59% – Simpson method) with a moderate reduction of GLS parameter –16,9%. The cardiopulmonary exercise test (CPET) showed an early anaerobic threshold and a normal pVO2max but not in line with the presumed range for a top–level athlete. Putting together the symptoms described, the CPET data and GLS parameter, despite the negative first–level investigations he underwent MRI that documented a myocardial edema in the mid–basal region of inferior and inferolateral walls of the left ventricle. Suitability for competitive practice was blocked, a gradual physical readaptation path was started and therapy with low–dose bisoprolol was set. An important clinical improvement is reported at the 6–month follow–up with evidence of normalization of the GLS parameter –23%. The CPET howed a realignment of the HR/VCO2 curve with a late threshold and increment of pVO2max. The 6–month control MRI examination showed almost no signs of myocardial inflammation and so the patient was made suitable for returning to competitive sport. In our case first–level investigations did not support any hypothesis of myocardial inflammation. The presence of stress symptoms confirmed by CPET data but especially the reduction of GLS parameter led to a deepening investigation with MRI that confirmed the presence of myocardial inflammatory lesion. Our case suggests that within a “return to play” protocol for athletes with recent SarsCov2 infection, the analysis of left ventricular systolic function by GLS may represent an additional useful element to be considered in support of standard investigations.