Septal Branch Research Articles

Iatrogenic coronary artery injuries during non-coronary artery adult cardiac surgery

: The close adjacency of the coronary ostia to the aortic valve, the left circumflex artery to the posterior mitral valve annulus, the right coronary artery to the tricuspid valve, and the septal branch of the left anterior descending artery to the pulmonary valve make them injury prone during surgical interventions on these valves. Iatrogenic coronary artery injuries during non-coronary artery adult cardiac surgery can endanger the myocardium and result in a substantial risk of morbidity and mortality. The clinical presentation of iatrogenic coronary injury is determined by the nature of injury. Acute injuries usually become apparent intraoperatively or immediately postoperatively. Chronic injuries mostly manifest within the first 6 postprocedural months, but they may occur as late as 30 months postoperatively. Prompt diagnosis and timely intervention can salvage the myocardium and improve the prognosis. Intraoperative detection of iatrogenic coronary artery injuries requires a high index of suspicion. The choice of therapeutic strategy, percutaneous coronary intervention or coronary artery bypass grafting, is dictated by the timing of detection as well as the clinical condition of the patient. This review article provides an overview of the incidence, mechanisms, diagnosis and therapeutic strategies to treat iatrogenic coronary artery injuries during non-coronary artery valvular surgery in adults.

C1 COMPLETE HEART BLOCK AS A RARE MANIFESTATION OF GRANULOMATOSIS WITH POLYANGITIS: A CASE REPORT

Abstract A 42–year–old male with prior smoking habit presented at our emergency department after atraumatic syncope preceded by severe pain in the left lower limb. One month prior to presentation, due to persistence of nonproductive cough he underwent a chest computed tomography (CT), which showed 2 pulmonary nodules with hypercaptation at PET performed later (figure 1). The 12–lead electrocardiogram showed sinus rhythm with complete atrioventricular block and ventricular escape rhythm at 40 bpm (figura 1). Ecofast revealed a mildly impaired left ventricular systolic function (left ventricular ejection fraction [LVEF] 45%) with basal septal hypokinesis. Laboratory assessment showed leukocytosis (marked neutrophilia and eosinophilia), thrombocytosis anemia, elevated C–reactive protein (193 mg/dl), troponin I (18483 ng/L), NTproBNP (14627 ng/l) and creatinine (2.27 mg/dL) levels. The patient was transported to the catheterization laboratory for temporary pacemaker insertion and coronary angiography, which depicted distal occlusion of the first septal branch (Figure 2A), the first diagonal branch (Figure 2B) and the obtuse marginal branch (Figure 2C). After the procedure due to persistent ischemia of the left lower limb, several unsuccessful procedures to restore limb vascularization by means of locoregional thrombolysis and percutaneous angioplasty were attempted, but a leg amputation above the knee was eventually performed after few days. Neoplastic markers, blood cultures and urine cultures resulted negative, urine sediment examination showed cylinders, leucocytes and microhematuria. A brain/facial bones CT scan was performed, showing left maxillary sinusitis (figure 1). A rheumatologic screening was also performed, showing high titer of cANCA(125 UI/ml) hinting at a systemic vasculitis. The histopathological results of the amputated limb depicted marked necrotizing vasculitis with extensive involvement of small–medium caliber and larger caliber arterial vessels (figure 2). Based on these clinical and laboratory findings, a diagnosis of granulomatosis with polyangiitis (GPA) was made. The patients was treated with ev methylprednisolone and rituximab. After the induction therapy, chest CT scan showed a marked reduction of the size of the pulmonary nodule (Figure 3); renal function progressively improved and physiological atrioventricular conduction being restored

CE-454610-3 VT STORM DUE TO HYPERTROPHIC CARDIOMYOPATHY TREATED WITH ALCOHOL SEPTAL ABLATION

Radiofrequency (RF) ablation is a guideline-recommended therapy for ventricular tachycardia (VT). However, certain locations can be inaccessible through endocardial or epicardial approach. There are several documented unconventional techniques in these cases where VT is either treatment-refractory to RF ablation, or ablation is unlikely to be successful due to deep intramural substrate. N/A N/A A 66-year-old gentleman with a history of coronary artery disease (CAD) presents with four days of palpitations and lightheadedness to the emergency department. An ECG was performed which showed monomorphic VT from a basal septal focus. He was hemodynamically stable and thus started on a lidocaine drip and intermittent metoprolol IV pushes with conversion to sinus rhythm. Given the history of CAD, primary differential concerns were ischemia-mediated or scar-mediated VT. Thus, the patient underwent a coronary angiogram which revealed stable non-obstructive CAD. The patient then underwent a cardiac MRI which revealed severe asymmetric left ventricular hypertrophy measuring up to 18 mm in the mid-basal interventricular septum with mid-myocardial late gadolinium enhancement in the same area. This was most consistent with hypertrophic cardiomyopathy (HCM) as the etiology for the patient’s VT. As the patient continued to have significant ventricular ectopy and recurrent bouts of sustained VT on medical management, options for VT ablation were discussed. Overall, given the deep intramural location of the suspected VT substrate, endocardial and epicardial approaches were thought to have a low probability of success. Transarterial coronary ethanol ablation (TCEA) of the septum was thought to have the highest likelihood of success at controlling the patient’s VT in the setting of HCM. The patient underwent successful TTE guided TCEA of the first septal branch. Left ventricular outflow tract (LVOT) gradient improved from 45 to 17 mmHg. The patient was observed for 24 hours without evidence of VT. An ICD was subsequently implanted for secondary prevention. The patient was discharged in stable condition on an oral beta blocker without any additional anti-arrhythmic medications. In patients with VT due to HCM where there is a deep intramural substrate not amenable to traditional RF catheter ablation, TCEA is a reasonable approach. We describe a case of successful TCEA in both decreasing a patient’s LVOT gradient as well as cessation of the patient’s treatment refractory VT.

PO-04-201 A CASE OF PVC OCCURRING RIGHT BUNDLE BRANCH BLOCK AND PR INTERVAL PROLONGED DURING ETHANOL ABLATION VIA THE CORONARY VENOUS SYSTEM

Ethanol ablation via the coronary venous system (CVS) has been reported to be effective and safe as a novel therapy for ventricular arrhythmias, especially for the epicardial and intramural origin sites. Previous studies reported no heart block complications during retrograde coronary venous ethanol ablation, neither atrioventricular block (AVB) nor other types of conductive system block. N/A A 67-year-old female with symptomatic and drug-refractory premature ventricular contractions (PVCs) was admitted for ablation therapy. The PVC burden was 31.7%. The 12-lead ECG showed a PVC with LBBB, inferior axis with a precordial transition in lead V3, and QS pattern in lead I. The QRS duration of PVC was 143ms. The Q-wave ratio of lead aVL/aVR was 1.47. Endocardial mapping was performed using a 3.5mm open-irrigated-tip catheter (ThermoCool, Biosense Webster, CA, USA). The earliest activation time was -8ms and -10ms pre-QRS at the septal aspect of right ventricular outflow tract (RVOT) and the left coronary sinus (LCC), respectively (Fig 1A). Ablation with 35-40W, 45-50°C was attempted but no response. We considered it might be an intramural origin site. The CVS angiography was performed and the ablation catheter was positioned in LCC for reference (Fig 1B). The earliest activation time (-27ms) was mapped in a septal branch of the anterior interventricular vein (AIV) with a 3.3F quadripolar catheter and local pace mapping matched well. Selective angiography confirmed the quadripolar catheter was in the septal branch rather than AIV (Fig 1C-D). A balloon was used to deliver ethanal and prevent its backflow to AIV. 1ml 96% ethanol was infused slowly (Fig 1E-F). PVC was eliminated immediately as soon as the ethanol infusion. But we noticed the PR interval prolonged from 178 to 190ms. More ethanol was injected carefully to consolidate the effect but we stopped infusion after a total of 2.5ml ethanol because the ECG showed complete RBBB and PR interval prolonged further to 202ms. RBBB and I° AVB were persistent during the whole hospitalization for 3 days. However, at 1-month follow-up, the QRS morphology returned to normal and the PR interval shortened to 172ms (Fig 1G). 24-hour Holter showed no recurrence. Ethanol ablation via the CVS also might induce heart block complications due to the adjacent anatomical position with the conductive system, even though it might be reversible. Operators should be cognizant of the potential risk.

PO-03-219 ANGIOGRAPHIC ASSESSMENT OF CORONARY VENOUS SYSTEM FOR CANNULATION: LESSONS FROM HIGH-SPEED ROTATIONAL RETROGRADE ANGIOGRAPHY

Venous ethanol ablation (VEA) is a novel effective therapy method for radiofrequency ablation refractory ventricular arrhythmias, especially the epicardial or intramural origin sites. Multielectrode catheters and balloons are usually used for mapping and VEA. However, there is limited data on the size and the collateral condition of the main tributaries of coronary venous system (CVS) in non-heart failure patients. To evaluate the size of the main tributaries of CVS for making better cannulation strategies via rotational retrograde angiography. We measured and analyzed the size of the great cardiac vein (GCV), the anterior ventricular vein (AIV) (including the first septal branch of AIV), and the main tributaries draining the posterior and lateral wall of the left ventricle in patients undergoing electrophysiology study. The diameters of the main tributaries of CVS were measured in the view that offered the least foreshortening and covering. High-speed rotational CVS angiography was performed on 60 patients. The diameter of GCV at the level of Vieussens valve (the “ostium” of GCV) and the distal end of GCV (junction of GCV-AIV) was larger in males than females (6.6±1.2 vs. 5.6±1.3mm, p=0.005; 5.1±0.9 vs. 4.6±0.8, p=0.045, respectively) while other tributaries showed no difference on genders. The diameter of middle cardiac vein (MCV), posterior vein (PV), lateral vein (LV), anterior ventricular vein and the first septal vein was 4.9±1.3, 3.0±1.0, 2.9±1.0, 4.4±1.0 and 1.4±0.7, respectively). 96% patients had collateral between main tributaries. Over half of them (62.5%) had collateral between MCV and AIV. We provide a systematic description and size measurement of CVS. Rotational angiography could be useful for the comprehensive assessment of CVS before ethanol ablation.

PO-05-007 CORONARY VENOUS ETHANOL ABLATION OF SUBEPICARDIAL SUBSTRATE IN PATIENTS WITH VENTRICULAR TACHYCARDIA AND LEFT VENTRICULAR ASSIST DEVICE.

Patients with a left ventricular assist device (LVAD) and ventricular tachycardia (VT) often have subepicardial substrate, which may not be amenable to epicardial ablation due to sternotomy-related adhesions and the LVAD itself. As an alternative approach, coronary venous ethanol ablation (VEA) can be used to ablate VT substrates without needing pericardial access. To assess the feasibility and acute safety of VEA in patients with LVAD and VT. We retrospectively studied patients with LVAD who underwent VT ablation using VEA between 8/2015 – 11/2022 at a tertiary referral medical center. Baseline patient and procedural characteristics were obtained. Of the 10 patients included, 7 presented with VT storm, 5 had prior VT ablation, 3 had multiple prior sternotomies, all were on amiodarone, 8 were on 2 or more antiarrhythmic drugs in the prior year, all had prior defibrillator implants, and 9 had shocks in the prior year. Across the cohort, 4 different vein territories were targeted for VEA, including the middle cardiac vein, posterolateral branch vein, anterolateral branch vein, and septal branch of the anterior interventricular vein. In 4 cases, 2 separate vein territories were targeted. An average of 17 ± 10 cc of ethanol was used per case. Concomitant radiofrequency ablation was used in all 10 patients. Procedure and fluoroscopy times were 290 ± 56 minutes, and 32 ± 15 minutes, respectively. Acute procedural success, defined as no inducible VT, was achieved in 9 cases. There was 1 complication, which was transiently increased threshold on the LV pacing lead and RV failure necessitating prolonged inotropic support. All the patients survived to hospital discharge. In an inherently high-risk LVAD population with VT, VEA can be used as an alternative approach to target subepicardial substrate that would otherwise be inaccessible via standard percutaneous access of the pericardial space. Acute procedural success was high in this limited cohort. Further study with larger numbers of cases and longer follow up is warranted.

Bridge of the left anterior descending artery revealed by syncope: a case report.

The myocardial bridge is a congenital coronary anomaly defined as the presence of a region of myocardium overlying an epicardial coronary artery. This is a 51-year-old patient, diabetic for 4 years on oral hypoglycemic, has had stress angina for 4 years, neglected by the patient. The current history goes back to 2 months by the installation of an episode of syncope occurring with the effort, then of a second episode the day of its admission. Electrocardiogram on admission showed complete atrioventricular block with an heart rate of 32 beats per minute, the patient spontaneously recovered sinus rhythm with a heart rate of 88 beats per minute and a PR interval of 200ms, coronary angiography was performed showing coronary arteries without stenosis with an intramyocardial bridge of the left anterior descending artery. During exercise and in the presence of a myocardial bridge on the left anterior descending artery, systolic compression leads to a decrease in flow to the septal branches, which is responsible for an alteration of the vascularization of the sub-nodal tissue with paroxysmal conduction disorders leading to syncope. Conduction disorders of ischemic origin are not always associated with atherosclerotic or thromboembolic lesions, but may also be secondary to myocardial bridges.

Misplacement in myocardial contrast echo during alcohol septal ablation in hypertrophic obstructive cardiomyopathy indicates intraseptal collateralization.

A 42-year-old patient with HOCM was submitted for percutaneous transluminal septal myocardial ablation (PTSMA). Coronary angiography (Panel A) identified the first septal branch (SB) (yellow arrow) as estimated target vessel and a second SB (white arrow). Compared with intraprocedural baseline transthoracic echocardiography (TTE) (Panel B), myocardial contrast echocardiography (MCE) with injection of 1.5 mL cold gelafundin 4% through an inflated over the wire balloon catheter (OTW-BC) in the first SB (Panel C) identified a correct septal depot (orange arrow), but also opacification at the left ventricle apex (dotted orange arrow). Contrast dye injection through the OTW-BC (dotted yellow arrow) showed collateralization from the first (yellow arrow) into the second SB (yellow arrow) and drainage into the left anterior descending (LAD) (red arrow) as reason for the misplacement (Panel D). We placed a second OTW-BC in the collateralized second SB (dotted white arrow; Panel E). Contrast injection through both inflated OTW-BC showed only distal first (yellow arrow) and second SB (white arrow) without further collaterals and without drainage into the—in the meantime wired—LAD (red arrow). MCE (Panel E) showed only opacification of the targeted septal area (orange arrow) as TTE (Panel F) does after injection 1.5 cc of alcohol through each balloon. After deflation and retraction of the BCs, 10 min after alcohol injection, haemodynamic measurements ensured elimination of resting and provocable gradients. Final coronary angiography (Panel G) showed occluded SBs (arrows) and unchanged LAD.

Use of Echocardiography to Diagnose Obstructive Hypertrophic Cardiomyopathy

Fabian Knebel, Sana Klinikum, Berlin, Germany, and Department of Cardiology and Angiology, Charité Campus Mitte, Berlin, Germany, opened the podcast with a definition of hypertrophic cardiomyopathy (HCM), which is characterised by left ventricular hypertrophy. Knebel then described the symptoms of the condition, such as shortness of breath and syncope after physical exertion. Up to one in 400 persons carry the genetic mutations that can lead to HCM, which is a dangerous condition if left undiagnosed, potentially leading to ventricular tachyarrhythmias and sudden cardiac death, or end-stage heart failure. HCM is a genetic condition, and genetic testing should be performed in cases of unexplained death so that families can be tested if HCM is diagnosed. Echocardiography is the first imaging method of choice for patients with HCM due to its relatively low cost and wide availability, but cardiac MRI may also be performed to measure left ventricular wall thickness, fibrosis, and left ventricular outflow tract (LVOT) obstruction, and to evaluate the success of therapies such as septal myectomy. When using echocardiography, the first obvious finding to indicate HCM is a thickened left ventricular wall, usually in the interventricular septum. European and American guidelines agree that an end-diastolic left ventricular wall thickness of ≥15 mm should be considered HCM. Knebel provided advice on how to effectively perform echocardiography, including using apical cut planes, and measuring the pressure gradient in the LVOT during the Valsalva manoeuvre. A case study was presented of a patient presenting with signs and symptoms suggestive of myocardial infarction, demonstrating the potential complexity of diagnosing HCM. Knebel concluded with a summary of current therapeutic options, such as septal reduction surgery and septal branch ablation, and pointed out that in the near future there will be medications to reduce LVOT obstruction and alleviate symptoms.

Left bundle branch area pacing: How to prevent a coronary venous fistula.

Left bundle branch area pacing: How to prevent a coronary venous fistula.

Multi-vessel giant coronary artery aneurysms: An unusual cause of chest pain

We describe an unusual case of multi-vessel giant coronary artery aneurysms complicated by acute coronary syndrome despite escalation of therapy. A 65-year-old man with hypertension and hypercholesterolemia presented to clinic with atypical chest pain over 4 months. Outpatient computed tomography coronary angiography (CTCA) demonstrated giant coronary aneurysms involving all 3 major coronary arteries. Outpatient coronary angiogram findings were in concordance with the CTCA with no definite obstructive coronary disease. Myocardial perfusion imaging was normal. He was commenced on dual antiplatelet therapy (DAPT). At 6 months, he presented with chest pain and non-ST-elevation myocardial infarction. Repeat coronary angiogram demonstrated occluded first septal LAD branch which previously had aneurysmal dilatation. DAPT was changed to long-term oral anticoagulation. He remains well at 18 months. This case highlights the importance of multi-modality imaging in the diagnosis and workup of coronary artery aneurysms and challenges in management; an individualized approach is required.

The sphenopalatine vein: anatomical study of a rarely described structure.

Although in counterpart, the sphenopalatine artery (SPA), has been well described in the medical literature, the sphenopalatine vein (SPV) has received scant attention. Therefore, the present anatomical study was performed. Additionally, we discuss the variations, embryology, and clinical significance of the SPV. Adult cadaveric specimens underwent dissection of the SPV. In addition, some specimens were submitted for histological analysis of this structure. The SPV was found to drain from the sphenoidal sinus and nasal septum. Small tributaries traveled through the nasal septum with the posterior septal branches of the SPA and nasopalatine nerve. The SPA and SPV were found to travel through the sphenopalatine foramen and another tributary was found to perforate the medial plate of the pterygoid process and to connect to the pterygoid venous plexus which traveled lateral to the medial plate of the pterygoid process. The vein traveled through the posterior part of the lateral wall of the nasal cavity with the posterior lateral nasal branches of the SPA and the lateral superior posterior nasal branches of the maxillary nerve. To our knowledge, this is the first anatomical study on the SPV in humans. Data on the SPV provides an improved anatomical understanding of the vascular network of the nasal cavity. Developing a more complete picture of the nasal cavity and its venous supply might help surgeons and clinicians better manage clinical entities such as posterior epistaxis, cavernous sinus infections, and perform endoscopic surgery with fewer complications.

362 COMPLETE HEART BLOCK AS A RARE MANIFESTATION OF GRANULOMATOSIS WITH POLYANGIITIS: A CASE REPORT

Abstract A 42-year-old male with prior smoking habit presented at our emergency department after atraumatic syncope preceded by severe pain in the left lower limb. He had no past relevant medical history until one month prior to presentation, when the onset and persistence of nonproductive cough deemed the performance of a chest computed tomography (CT), which showed a 28 mm pulmonary nodule. A positron emission tomography-CT scan performed thereafter showed hypercaptation of the apical pulmonary nodule (SUV 6.87), and hypercaptation of the left nasal cavities. He was not on daily medications. On presentation the patient complained of dyspnoea at rest with no chest pain. On physical examination the left foot was cold and numb with no pedidial pulses. Laboratory assessment showed leukocytosis, thrombocytosis, anemia and elevated C-reactive protein, troponin I, NTproBNP and creatinine levels. The 12-lead electrocardiogram showed sinus rhythm with complete atrioventricular block and ventricular escape rhythm at 40 bpm; the transthoracic echocardiography revealed a mildly impaired left ventricular systolic function with basal septal hypokinesis; a chest-CT scan confirmed the stability of the aforementioned pulmonary lesions. The patient was transported to the catheterization laboratory for temporary pacemaker insertion and coronary angiography, which depicted distal occlusion of the first septal branch, the first diagonal branch and the obtuse marginal branch; no percutaneous coronary intervention was performed. The patient was then transferred to our Coronary Intensive Care Unit: due to persistent ischemia of the left lower limb, and several unsuccessful procedures to restore limb vascularization, a leg amputation above the knee was performed on day 2 of hospitalization. Meanwhile, the patient also developed fever, epididymitis, digital infarcts with bilateral hand purpura, upper and lower extremities paresthesia, worsening renal failure, persistent anemia and leukocytosis with eosinophilia. Neoplastic markers, blood cultures and urine cultures resulted negative; urine sediment examination showed cylinders, leucocytes and severe dysmorphic microhematuria suggestive of glomerulonephritis; bronchoalveolar lavage showed inflammatory cells. A rheumatologic screening was also performed, showing high titer of cANCA (125 UI/ml) hinting at a systemic vasculitis. The histopathological results of the amputated limb depicting marked necrotizing vasculitis with extensive involvement of small-medium caliber and larger caliber arterial vessels. Based on these clinical and laboratory findings, a diagnosis of granulomatosis with polyangiitis (GPA) with myocardial infarction due to coronary involvement and subsequent atrioventricular block was made on day 4 of hospitalization. Daily 500 mg boluses of intravenous methylprednisolone were administered for three days since day 4 of hospitalization, followed by high dose oral glucocorticoids (prednisone 1 mg/kg/day) and subsequent remission induction therapy with rituximab 375 mg/m2 weekly. Renal function progressively improved; heart conduction abnormalities gradually recovered and there was a marked reduction of the size of the pulmonary nodule. GPA presents remains one of the most challenging diagnostic dilemmas in clinical medicine. Despite we performed a prompt diagnosis, a leg amputation had to be done due to the common rapid progression of the disease. Clinicians should be aware of the various manifestations of GPA and bear in mind the possibility of coronary vasculitis.

His bundle combined with deep septal left bundle branch area pacing for atrial fibrillation prior to atrioventricular node ablation.

To mitigate the risk of dyssynchrony-induced cardiomyopathy, international guidelines advocate His bundle pacing (HBP) with a ventricular backup lead prior to atrioventricular node ablation in treatment-refractory atrial fibrillation and normal left ventricular ejection fraction. As a result of concerns with long-term pacing parameters associated with HBP, this case series reports an adopted strategy of HBP combined with deep septal left bundle branch area pacing (dsLBBAP) in this patient cohort, enabling intrapatient comparison of the two pacing methods. Eight patients aged 72 ± 10 years (left ventricular ejection fraction 53 ± 4%) underwent successful combined HBP and dsLBBAP implant prior to AV node ablation. Intrinsic QRS duration was 118 ± 46 ms. When compared to dsLBBAP, HBP had lower sensed ventricular amplitude (2.4± 1.1 vs. 15 ± 5.3V, p= .001) and lower lead impedance (522 ± 57 vs. 814 ± 171ohms, p= .02), but shorter paced QRS duration (101 ± 20 vs. 119 ± 17 ms, p= .02). HBP pacing threshold was 1.0± 0.6V at 1ms pulse width, and dsLBBAP pacing threshold was 0.5± 0.2V at 0.4ms pulse width. Five patients underwent cardiac CT showing adequate dsLBBAP ventricular septal penetration (8.6± 1.3 mm depth, 2.4± 0.5 mm distance from left ventricular septal wall). No complications occurred during a mean follow-up duration of 121 ± 92 days. Combined HBP and dsLBBAP pacing is a feasible approach as a pace and ablate strategy for atrial fibrillation refractory to medical therapy.

Abstract 12162: Acute Myocardial Infarction Caused by Spontaneous Coronary Artery Dissection of the First Septal Perforator

A 68 year old female with hyperlipidemia and tobacco use presented with acute, substernal, chest pressure that occurred during yard work. She had no prior history of coronary artery disease or stable angina. Electrocardiograms (ECG) did not have ischemic changes but high sensitivity troponin was elevated at 285 ng/L and peaked at 1308 ng/L. Therapy was started for acute coronary syndrome and nitroglycerin drip for continued discomfort. Echocardiogram showed ejection fraction of 61% and akinesis of the infero-septum at the mid-ventricle. Coronary angiogram showed diffuse narrowing of the large first septal branch artery (S1) concerning for coronary intramural hematoma. No other significant coronary artery disease was present. Cardiac magnetic resonance (CMR) confirmed hypokinesis of the septum and subendocardial delayed enhancement in the interventricular septum at the mid ventricle suggestive of an isolated septal perforator infarct. She was conservatively managed and discharged 48 hours later. Four days later she had recurrent chest pressure and was re-admitted. Her ECG showed J-point elevation in the anteroseptal leads. Repeat coronary angiogram showed unchanged type 2 spontaneous coronary artery dissection of S1 and a small coronary cameral fistula between the distal septal branch and the right ventricle. The diagnosis of spontaneous coronary artery dissection of the first septal branch is rare and may be missed on angiogram. CMR in addition to invasive coronary angiography aides in the evaluation of this rare cause of acute myocardial infarction and changes clinical management decisions including observation time and evaluation for fibromuscular dysplasia.

Abstract 14188: An Unexpected Cause of Anterior ST Segment Elevation After Coronary Intervention

Background: ST elevation (STE) in V1 to V3 is traditionally labeled as anteroseptal infarction due to occlusion of the LAD proximal to the septal branches. An important and uncommon cause for similar ECG findings is an isolated RV myocardial infarction due to occlusion of the proximal RCA and/or its branches. We present a case of anteroseptal ST elevation after jailing of a conus branch during percutaneous coronary intervention (PCI) to the RCA. CASE: 89-year-old female with history of moderate aortic stenosis (AS), hypertension, hypercholesterolemia, and prior stroke presented with progressive dyspnea on exertion and 3 days of chest tightness. Initial echocardiogram showed an EF of 64% and severe AS with peak velocity of 4.27 m/s, mean gradient of 45 mmHg and aortic valve area of 0.43 cm 2 . Coronary angiography showed severe stenosis of the proximal RCA successfully treated with intravascular lithotripsy and drug-eluting stent deployment with jailing of the conus branch. The LAD and LCX had mild nonobstructive disease. Patient developed chest pain after the procedure with new STE in V1 to V3. She was taken for emergent cardiac angiogram due to suspected occlusion of the LAD however this showed unchanged anatomy with patent stent in the RCA and no new severe stenosis or occlusion of the left coronary arteries. There was no flow in the jailed conus branch that was not intervened on due to small vessel size. A repeat echocardiogram showed new mild RV dilatation with unchanged EF and normal LV wall motion. Patient had resolution of the chest pain and STE within 2 hours and was discharged home in stable condition. Conclusion: Occlusion of a conus branch artery with associated isolated RV myocardial infarction is an uncommon cause of STE in anteroseptal leads. High index of suspicion is important to anticipate and manage potential complications like ventricular arrhythmias and RV failure.

Clinical utility of a new protocol of cardiac computed tomography in dogs.

The characteristics of non-electrocardiography- and electrocardiography-gated multidetector computed tomography have not been extensively studied in veterinary clinics but it can be useful for cardiac imaging. This study aimed to ascertain the differences between non-electrocardiography and electrocardiography gating methods and to establish their clinical utility based on patient history. Six client-owned dogs (two with patent ductus arteriosus, two with heart base tumour, one with pericardial mesothelioma, and one with normal health) were included in this study. All the dogs were examined using a non-electrocardiography-gated scan, followed by a retrospective electrocardiography-gated scan. Images were reviewed to determine the optimal scan timing and R-R interval in non-electrocardiography- and electrocardiography-gated images, respectively, for detailed coronary artery imaging, diagnostic quality of the best coronary artery visualisation in non-electrocardiography- and electrocardiography-gated images through visual assessment of the main coronary artery branches, and branching patterns of the left coronary artery. Further, we compared the size and margin demarcation of the heart or pericardial lesions in non-electrocardiography- and electrocardiography-gated images obtained from patients with heart or pericardial tumours. The optimal scan timing and R-R interval were the second-scan timing and end-diastole (70%-90%), respectively. Second-scan non-electrocardiography-gated images allowed coronary artery evaluation, indicating high-grade quality in visual assessment, except for the septal branch. Electrocardiography-gated images, but not non-ECG-gated images, clearly revealed pericardial nodules in two dogs. Our findings suggest the respective clinical utilities of non-electrocardiography- or electrocardiography-gated imaging using high-slice cardiac computed tomography based on patient history.

Alcohol Septal Ablation for Hypertrophic Obstructive Cardiomyopathy: A case Report

Alcohol septal ablation (ASA) has shown to be a safe and effective procedure for treatment of symptomatic hypertrophic obstructive cardiomyopathy (HOCM) for more than 20 years with results similar to those of surgical myectomy. The first septal branch of the left anterior descending artery (LAD) is located and 96% alcohol is instilled to induce an artificial myocardial infarction and necrosis at the base of the hypertrophied septum. Now we present our first experience of a patient with HOCM with a very high left ventricular outflow tract gradient who had successful alcohol septal ablation. Cardiovasc j 2022; 15(1): 95-99

An Acute Anterior Reinfarction Complicating with Transient Symptomatic Total Atrioventricular Block

Abstract
 Background
 Acute stent thrombosis is a frequent cause of myocardial infarct (MI) after stent placement. Total atrioventricular (AV) block is frequently become the conductive disturbance complication of acute reinfarct. Inferior MI has Low long-term mortality and greater reversibility than anterior MI which has higher in-hospital and long-term mortality.
 
 Case Illustration 
 44 years man, came to emergency department Cardiovascular Centre Harapan Kita with altered mental status since 12 hours ago. PPCI stenting at proximal LAD of his acute anterior MI 2 days ago. Patient had acute stent thrombosis then underwent urgent PCI at referring hospital. Patient present with blood pressure 57/30, heart rate 20 -30 with TAVB rhythm. Laboratory showed increased serum lactate level 5.2. Patient was diagnosed with Total AV block caused by MI. Patient was planned for emergency temporary pacemaker (TPM) implantation. After 24 hours close monitoring, the patient intrinsic rhythm resolved with spontaneous recovery. Patient was hemodynamically stable until discharge.
 
 Discussion 
 Stent thrombosis of proximal stent of LAD will cause TAVB because of the source of the distal portion of the AV node is originating from septal branch of LAD. It is caused by extensive necrosis with higher in-hospital and long-term mortality, often culminated in permanent pacemaker. However, spontaneous recovery of TAVB into sinus rhythm take place. This could be caused by transient reversible ischemia of infra nodal region of AV node which supplied by septal perforator branch
 
 Conclusion 
 This case reporting a complete atrioventricular block during the course of acute anterior reinfarct and had spontaneous resolution of the AV block. Mechanisms of spontaneous resolution of complete AV block in the setting of acute MI is associated transient ischemia after occlusion of proximal LAD.
 
 Keyword: Reinfarct, Stent Thrombosis, Total AV Block

Intramyocardial mapping of ventricular premature depolarizations via septal venous perforators: Differentiating the superior intraseptal region from left ventricular summit origins

The intramyocardial aspect of the left ventricular summit (LVS) can be mapped by advancing a unipolar guidewire into septal perforator branches of the anterior interventricular vein. The purpose of this study was to differentiate between ventricular premature depolarizations (VPDs) with a basal superior intraseptal (SIS) site of origin and those originating from the epicardial LVS using septal intramyocardial mapping. A retrospective cohort of patients with suspected LVS VPDs who underwent SIS unipolar mapping were reviewed for their clinical characteristics, mapping findings, and procedural outcomes. SIS mapping was successful in 44 of 47 cases (93.6%). VPD origin was SIS (defined as earliest activation from the intraseptal wire) in 20 patients (45.5%; median 23 ms pre-QRS). Procedure success was similar in patients with (group 1) and without (group 2) SIS origin (84% vs 87.5%, respectively; P = .842). Of the 10 patients in group 1 without presystolic endocardial activation, 5 (11.3% of all 44 cases) were successfully ablated from the left ventricular endocardium by using an anatomical approach targeting the endocardium closest to the earliest intraseptal activation site. A significant proportion (45.5%) of VPDs that appear to arise from the left ventricular summit can be demonstrated to have a SIS origin using septal perforator venous mapping. A significant minority (11.3%) of these can be ablated from the endocardium by targeting from an anatomic vantage point closest to the earliest intraseptal activation site. The described strategy may help differentiate true LVS VPDs from those with SIS sites of origin.