key: cord-0049998-nrajnf8d authors: nan title: Full Issue PDF date: 2020-09-15 journal: JACC Case Rep DOI: 10.1016/s2666-0849(20)31008-1 sha: 8a4694c0fa87b7f67ae8e3446cee30c705b9d961 doc_id: 49998 cord_uid: nrajnf8d nan The patient had undergone mechanical aortic valve replacement and had an implantable cardioverterdefibrillator. Congestive heart failure and other noncardiac causes of dyspnea and peripheral edema were included in the differential diagnosis. Serial troponin levels were within the normal range. Echocardiography demonstrated a reduced left ventricular ejection fraction at 45%. He was referred for invasive coronary angiography (ICA) to rule out an ischemic cause for the new onset cardiomyopathy. ICA was performed through a right radial approach. A 5-F Judkins right 4 (JR4) diagnostic catheter (Merit Medical Systems, South Jordan, Utah) was advanced over a 0.035-inch guidewire into the ascending aorta. Multiple attempts were made to engage the right To understand the predisposing factors and mechanisms that lead to kinking and trapping of a coronary catheter, which is an uncommon, but potentially morbid complication of left heart catheterization. To discuss strategies to kinking and trapping of a coronary catheter, as well as percutaneous approaches to retrieve a kinked coronary catheter safely. coronary artery without success because of severe tortuosity of the innominate artery (IA) and the takeoff of the coronary artery. We eventually lost the pressure waveform and, on troubleshooting, found that we could not aspirate or torque the catheter. A kink was noted in the middle portion of the catheter on fluoroscopy. The image shows our approach to retrieval of the kinked JR4 catheter by telescoping it into a retrograde 14-F sheath and stabilizing it in the sheath with a balloon. Catheter knotting during ICA is an uncommon but recognized complication, usually occurring during manipulations while intubating the right coronary artery (1) . This has been reported to be related to higher torque buildup in the proximal portion of the catheter during manipulations, compared with the distal end, in the setting of vascular tortuosity (2) . Indeed, this condition precipitated the situation in our case. Points to be kept in mind to help prevent this complication, as summarized in Table 1 , include avoidance of torquing a catheter more than 180 , being mindful of vascular tortuosity if encountered, maintaining a guidewire through the catheter, and paying attention to situations where loss of torque is observed, pressure dampening is noted, or an inability to aspirate the catheter occurs (3) . Other elements to consider are the use of long sheaths if considerable vascular tortuosity is noted and that catheters smaller than 6-F are more prone to kinking because of their thin-walled construction. Once a kink has occurred, techniques to deal with this are anecdotal, with a dearth of randomized data on this topic. A technique has been described whereby the proximal end of the knotted catheter is fixed by inflating a sphygmomanometer cuff in the ipsilateral brachial region, followed by gentle torque of the catheter in the opposite direction of the initial torque to untwist a kinked catheter (4) . Another approach involves catching the tip of the kinked catheter by using an Amplatz Goose Neck Snare (Medtronic, Dublin, Ireland) guided by a guiding catheter through the FA, followed by pulling the kinked catheter into a larger-caliber vessel and then unraveling the knot (5) . A similar approach, but with a slight modification, is the use of an EN Snare catheter (Merit Medical Systems) to capture the distal end of a kinked JR5 catheter. This is followed by gently pulling and rotating the distal end of the JR5 with the EN Snare catheter while simultaneously rotating and pulling the hub of the JR5 catheter in the opposite direction, thereby unkinking the catheter and allowing for successful retrieval through the radial artery (6) . Another report detailed a kinked JL catheter in the brachial segment that was able to be retrieved by cutting the hub of the catheter and replacing the 6-F radial sheath with a long, 5-F sheath while leaving the JL catheter in place to maintain arterial access. The long sheath was then brought to the antecubital fossa, and the kinked catheter was gently pulled back and straightened while being pulled into the long sheath and thus removed (7) . All the techniques mentioned here are summarized in Table 2 . To our knowledge, retrieval of a kinked catheter by using balloon-assisted trapping, as in our case, has not been reported before. The patient was medically managed with a plan to return in the future for ischemic evaluation. As with most issues in the cardiac catheterization laboratory, preventing a complication is often much 2. Avoid torquing catheters more than 180 . 3. Maintain a guidewire through the catheter. 4 . Pay close attention to loss of torque, pressure waveform, or an inability to aspirate a catheter. 5 . Take care when using catheters smaller than 6-F in caliber because they may be more prone to kinking. 6 . Consider using a long sheath if extensive vascular tortuosity is noted. 7. Consider a left radial artery approach because of the lower prevalence of left-sided brachiocephalic tortuosity, especially in older adults. Blood pressure cuff inflation on ipsilateral brachial region followed by gentle untwisting of catheter (4) Amplatz Goose Neck Snare (Boston Scientific, Marlborough, Massachusetts) to catch tip of catheter, followed by unraveling of knot in a large-caliber vessel (5) EN Snare catheter (Merit Medical Systems, South Jordan, Utah) to capture distal tip of kinked catheter, followed by twisting of distal and proximal ends of kinked catheter in opposite directions to unravel knot (6) Cutting hub of catheter, placing long sheath over catheter, and dragging kinked segment into the sheath to straighten (7) Balloon-assisted trapping and removal of kinked catheter through a large-bore sheath easier than managing it. Care must be taken in all aspects while manipulating the catheter, especially within tortuous vasculature. Once the complication is suspected, recognizing it early is paramount; once it has occurred, tailoring retrieval to each individual case is prudent. with a regular heart rhythm, and he had no murmurs. He had a normal jugular venous pressure with warm extremities and no peripheral edema, but he required norepinephrine to maintain adequate mean arterial pressure. To heighten awareness of various causes of coronary artery ectasia. To develop an approach to management of acute coronary syndromes in patients with coronary artery ectasia. The patient first received a diagnosis of CAE in 2004 after he presented with NSTEMI at an outside institution. Coronary angiography at the time revealed aneurysmal, ectactic coronary vasculature, concerning for vasculitis or Kawasaki disease, and he was referred to our institution. He informed us that his biological brother had also recently been given a diagnosis of CAE, and his father underwent surgery for abdominal aneurysms. The patient was subsequently evaluated for and received a diagnosis of thoracic aortic aneurysm and iliac artery aneurysms. He was transitioned to aspirin and warfarin and was referred to a geneticist. Given his family history and the distribution of In the context of known CAE and multiple previous NSTEMIs, the patient was presumed to have experienced an ischemic VT or VF arrest. However, coronary artery dissection or rupture, VT or VF related to underlying cardiomyopathy, electrolyte abnormalities, and sepsis were also considered. The admission electrocardiogram ( Figure 2B 2) thrombus formation and/or embolization; 3) concomitant atherosclerosis; and 4) microvascular dysfunction (3, 4) . Optimal management of stable CAE centers on traditional atherosclerotic risk factor modification. Nitrates, however, have been shown to exacerbate myocardial ischemia and should generally be avoided as antianginal therapy (5) . Acute coronary syndromes in patients with CAE are difficult to manage and are associated with worse outcomes when compared with patients with normal Multimodality imaging is recommended to achieve a diagnosis of post-stenting mycotic coronary pseudoaneurysm. The mortality rate of post-stenting mycotic coronary pseudoaneurysm is high despite combined medical and surgical therapy. History included hypertension, type 2 diabetes mellitus, dyslipidemia, cocaine misuse, chronic idiopathic anemia, and thrombocytopenia (60 Â 10 3 /ml, normal range, 130 to 400 Â 10 3 /ml). The differential diagnosis was acute myo-pericarditis, pneumonia, and pleurisy. Conservative antibiotic treatment was administered, but, despite an initial promising response, the patient died 3 months later due to sepsis. Bacteria, particularly S aureus, are the most common etiological agents (2) . Although mycotic coronary aneurysm onset is usually subacute, time to presentation can be extremely variable, with several cases (as in our patient) reported to occur even in the early days after PCI (3) . Diagnosis is challenging because symptoms can be subtle and there is not a "one-stop-shop" imaging test able to provide complete information to reach the diagnosis (4) . Morbidity and mortality are high, especially in the context of pseudoaneurysm, which carries an increased risk of rupture, or in the case of infectious dissemination, involving the myocardium and pericardium. Prompt treatment is required, although, to date, little evidence concerning the optimal strategy is available and the mortality rate remains high independent from the combined efforts of medical and surgical therapy (2) . In the presented case, surgical correction was excluded due to the prohibitive pre-operative mortality risk. For this reason, we decided to treat the patient percutaneously at least to minimize the risk of cPSA rupture (a wellknown fatal consequence). Antibiotic treatment was administered to control infections. However, we observed a dismal prognosis, which culminated with the patient's death. The differential diagnosis included severe sepsis due to pneumonia, acute coronary syndrome complicated by cardiogenic shock, and acute pulmonary embolism. An electrocardiogram was obtained that showed new lateral T-wave inversions and his cardiac biomarkers were elevated, diagnostic for a non-ST-segment To present the technical aspects of a challenging case involving the navigation of a dormant AV fistula, from peripheral arterial access through a venous segment and back to artery, for successful coronary angiography and LAD PCI in a patient with high-risk NSTEMI and cardiogenic shock. To discuss the limited evidence regarding the navigation of AV fistulae for interventional procedures and review the indications and pros and cons of such an approach. He was admitted to the cardiac intensive care unit (CICU) and required norepinephrine to maintain a mean arterial pressure teries that were felt to be likely to prevent crossing with a wire or catheter. Given concern regarding the feasibility of femoral access due to severe PAD and the need for continued hemodynamic monitoring via the right radial artery, the decision was made to pursue coronary angiography via left radial arterial access through the dormant AV fistula. The left radial artery was accessed using the counterpuncture approach. A 6-F Glidesheath slender (Terumo Interventional Systems, Somerset, New Jersey) could not be fully advanced into the radial artery due to extensive calcification but was able to be seated well enough to provide adequate wire and catheter support. Figure 3B ). (Figure 1 ). The patient was placed on anticoagulation with warfarin, with goal international normalized ratio of 2 Davies et al. A second challenging subset is the need to deliver IVL in multivessel calcified stenosis simultaneously. Current experience with the IVL system has proven to be safe. However, some recent reports have warned about the evidence of coronary vasoconstriction (2) and electrophysiological side effects (3). This paper describes the feasibility of IVL in 2 clinical cases highlighting potential issues that could arise. Undilatable lesions are particularly challenging and expose the patient to high risk of under-expanded stents, especially under bail-out conditions. When dealing with an acute or chronically under-expanded stent, IVL may become the standard of care if high-pressure balloons fail. Recognizing the likelihood that IVL could induce a vasoconstriction immediately after or during procedures. A 67-year-old man, hypertensive and diabetic, with angina on effort, had a chronic total occlusion of the proximal left anterior descending artery (LAD) with a heavily calcified mid-segment and a proximal blunt stump ( Figures 1A and 1B) . The setup was the left radial access for collateral opacification and the right femoral access for the target lesion. The parallel wire technique, supported Figure 1E ). Despite the fact that coronary flow was recovered, the hemodynamic status got slightly better with persisting chest pain and a faint collateral perfusion. (Figures 2A and 2B ). The LAD stenosis was dilated using a 3.0/20-mm NC balloon up to 12 atm, but incomplete balloon expansion occurred. The balloon waist resolved after 2 cycles of 10 impulses with a 3.0/12-mm balloon inflated to 6 atm of IVL delivery ( Figure 2C) . A T-andprotrusion stenting technique was then performed to treat the bifurcation lesion ( Figure 2D ). The right coronary artery issue was undertaken by the femoral access using an AL1 guiding catheter and multiple buddy wires. After pre-dilation with a standard 2.5/20-mm balloon, the IVL was easily advanced, and the complete balloon expansion (3.5/12 mm inflated to 6 atm) was achieved after 3 cycles of 10 impulses ( Figures 2E to 2G ). Multiple overlapped stents were implanted followed by high-pressure NC balloon dilation ( Figure 2H ). An optimal result was obtained with a thrombolysis in myocardial infarction flow grade III. However, in the recovery room, the patient complained of chest discomfort associated with diffuse ST-segment elevation in multiple leads without reciprocal STsegment changes ( Figures 3B and 3C) . Alternatively, the diffuse electrocardiography changes that occurred could be attributed to the capacity of coronary IVL to trigger ventricular ectopies and cellular depolarization in response to a mechanoelectrical coupling between the energy generated by the sonic pressure of the IVL and the local stretch-activated cellular ionic channels, as previous studies have reported (3) . The adoption of IVL as a bail-out procedure for underexpanded stents seems to be a promising option. (8) . The patient was transferred to intensive care unit. Chest closure occurred on post-operative day 2. She was extubated on post-operative day 3 and discharged home on post-operative day 9 without com- A 48-year-old man presented with progressively worsening exertional chest pain and dyspnea, which had been occurring predominantly at rest for the previous 2 weeks. The patient had a prior history of hypertension, myocardial infarction, and percutaneous coronary interventions in left anterior descending artery, left circumflex artery, and distal right coronary artery (RCA). The differential diagnosis for chest pain includes acute coronary syndrome, aortic dissection, pulmonary embolism, panic disorder, and gastroesophageal reflux disease. To recognize coronary perforation as potential complication associated with rotational atherectomy especially in small arteries. To understanding the acute management of Type III cavity spilling perforation. Given the worsening chest pain, decision was made to proceed with percutaneous coronary intervention. We hereby describe a case of rotational atherectomy induced Type III CS coronary perforation (CP) and its acute management. There is no consensus to manage type III CS perforations, and management of these coronary artery fistulas can be addressed with different approaches. Prolonged perfusion balloon inflation may treat some of them and previous reports have described spontaneous closure of some of these iatrogenic coronary artery fistulas. Patients with these fistulas can remain asymptomatic in 50% to 60% of cases, but can also lead to progressive development of dyspnea and heart failure symptoms when a significant amount of left to right shunt develops over time (8) . Considering a large amount of shunt, we decided to proceed with covered stent implantation to seal the perforation after prolonged balloon inflation failed to do so. We used a PK Papyrus covered stent, which provides greater flexibility and smaller crossing profile and successfully sealed the perforation (9,10). The patient was discharged home the following day after a repeat transthoracic echocardiogram showed preserved ejection fraction and no pericardial effusion. Post-percutaneous coronary intervention peak troponin was 4 ng/ml and peak creatine kinase-MB was 31 IU/l. We hereby describe a rare case of rotational CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). Consider leaking CAA as a differential diagnosis in patients with hemoptysis after DES implantation, so that proper diagnostic and management steps can be taken. In patients with CAA as a differential diagnosis, early CT coronary angiography must be planned to identify this serious complication in a timely manner. Plan early coronary angiography followed by definitive management in case of a CT angiography result indicative of leaking CAA, so that critical lifesaving time is not lost. The patient was started on intravenous antibiotics, which resulted in resolution of hemoptysis. Coronary angiography was planned; however, before the procedure, the patient had an episode of massive CAAs after PCI are rare (incidence, 0.3% to 6.0%), and most of these lesions are pseudoaneurysms (1-3). CAA after PCI has been reported with bare-metal stents (BMS), as well as with drug-eluting stents (DES) (2) . Mechanisms of CAA after PCI include coronary dissection and medial injury resulting from the use of oversized balloons or stents, high-pressure balloon inflation, atherectomy, and laser angioplasty (1-3). CAA is seen more commonly with DES as compared with BMS (2). DESs elute antiproliferative drugs to prevent restenosis; however, this may also delay coronary healing. In addition to this mechanism, medial inflammation secondary to a hypersensitivity reaction to the drug, polymer, or stent platform may also predispose patients to CAA formation after DES implantation (4) (5) (6) . This complication is more frequently seen after bailout or complex coronary procedures. In this case, a pseudoaneurysm (7, 8) , and rupture of CAAs, albeit rare, may lead to ischemia and life-threatening tamponade (7, 9, 10 OCT demonstrated the extra lumen more clearly (Video 2). Bridging collateral vessels develop in chronic total occlusions, but in this case the coronary artery was not occluded. If this channel had been caused by recanalized thrombus, the extra lumen should have been present within the coronary lumen. IVUS appeared to show that the extra lumen was outside the tunica media, but it was unclear ( Figure 1B) . OCT demonstrated that the lumen was clearly outside the tunica media ( Figure 1C ). The IVUS appearance could have been consistent with intramural hematoma ( Figure 1D ), which is occasionally observed in spontaneous coronary dissection, but we were unable to demonstrate an intimal tear with OCT ( Figure 1E ). On the basis of the OCT findings, we confirmed that the correct diagnosis was WCAA. A drug-eluting stent was implanted ( Figure 1F ), and both IVUS and OCT showed a well-deployed stent with a diminished additional lumen (Videos 3 and 4). WCAA is a very rare congenital anomaly that is usually considered benign, and accurate diagnosis is difficult to establish. IVUS and OCT are useful for the diagnosis (1,2), but few reports have used both techniques to Manuscript received May 5, 2020; revised manuscript received July 16, 2020, accepted July 27, 2020. determine which is superior for the diagnosis of WCAA. In this case report, OCT was superior to IVUS for confirming the presence of WCAA. This patient remained symptom free during 1-year follow-up. In conclusion, OCT was better for the diagnosis of WCAA when we detected an abnormal structure around a coronary artery. KEY WORDS coronary artery disease, intravascular ultrasound, optical coherence tomography, woven coronary artery anomaly APPENDIX For supplemental videos, please see the online version of this paper. Safety of IVL in thrombus-laden lesions is unknown. Insonification of platelet/fibrin-rich thrombi by shockwaves may result in thrombus degradation/embolization. Shockwaves can induce myocardial depolarization (2) . Although an R-on-T phenomenon inducing tachyarrhythmia has not been substantiated in stable coronary lesions (2), such a risk in electrically excitable myocardium during early reperfusion is unknown. Thus, "off-label" IVL use in acute STEMI is not recommended. We propose that IVL can be used in staged stenting procedure during which thrombus burden and myocardial electrical instability may be substantially less. The patient had aortic coarctation partially corrected during childhood with a bypass between the left subclavian artery and the descending thoracic aorta. He underwent reoperation with a Hemashield (Maquet, Rastatt, Germany) aortic graft implantation at 24 years of age. Follow-up cardiac magnetic resonance confirmed a good result of the aortic graft but significant stenoses at the proximal and distal To make a differential diagnosis of myocardial damage in young adults with multimodality imaging. To relate coronary anomalies with other CHD. To understand the importance of combining clinical presentation, past medical history, and clinical impact of the findings to select the best approach when high-quality published reports are lacking. Manuscript received March 25, 2020; accepted April 20, 2020. anastomosis of the subclavian-to-aortic bypass ( Figures 1A and 1B) . He was previously diagnosed with type 1 bicuspid aortic valve with normal function (Video 1). He had no known cardiovascular risk factors. In this scenario, different entities must be considered in the presence of elevated troponin, such as myocarditis or acute myocardial infarction type 1 or type 2. During hospitalization, no arrhythmias were detected in continuous ECG monitoring. In the absence of chest pain or new clinical events, the patient was considered at low risk for sudden cardiac death (SCD). He was conservatively managed and discharged to be closely followed. The therefore, the only evidence is based on case reports. In these cases, adult patients presented with resting angina, dyspnea, New York Heart Association functional class III or IV, or aborted cardiac death in shockable rhythm were surgically treated. Only 1 reported patient (9) had angina and no pathological findings on ECG or echocardiography but was surgically treated. However, most of the adults described in published reports have had no previous heart operations (3, (5) (6) (7) 9, 10) . Besides, survival depends on collateral development (5, 9) , Peak systolic velocity is 161 cm/s, and peak systolic gradient is 10 mm Hg. This outcome supports medical treatment as an option in selected scenarios. LCxPA is a rare coronary anomaly, but it has been described in association with CHD, especially aortic coarctation. Awareness of this entity will enable early Anomalous origin of circumflex coronary artery from the right pulmonary artery associated with subaortic stenosis and coarctation of the aorta. Eur J Cardiothorac Surg 1997;12:663-5. There was history of rheumatoid arthritis and an episode of pericarditis 4 years prior, with pericardial tamponade requiring a pericardial window. There were no coronary artery disease risk factors. Because of diffuse ST-segment elevations on the ECG and shock, the patient was brought emergently to the cardiac catheterization lab. Coronary angiography revealed acute total and subtotal occlusions of the left anterior descending artery, first diagonal, and 3 obtuse circumflex branches To learn about the entity of coronary compression due to focal pericardial constriction and fibrous bands. To learn the role of multimodality imaging in diagnostic dilemmas. To understand a potential late complication of pericarditis treated with partial pericardiectomy. Manuscript received November 7, 2019; revised manuscript received April 25, 2020, accepted May 6, 2020. The second cardiac catheterization performed for recurrent chest pain: stent placed to OM1 during this procedure. Narrowing can be seen in the stents to OM1, OM2, and the LAD. Asymmetric pericardial thickening seen on echocardiogram. Large pleural effusion is demonstrated. Cardiac computed tomography demonstrates inward kinking of stents. Abbreviations as in Figure 2 . matthew.schaikewitz@atlantichealth.org. Previous studies indicate a prevalence for thromboembolic events in Fontan patients of 1% to 30% (5). However, guidelines for anticoagulation in Fontan patients are evolving (5) . One study showed no significant differences in thromboembolic events for Fontan patients treated with antiplatelet therapy compared to well-regulated anticoagulation therapy (5) . American Heart Association guidelines recommend antiplatelet therapy after the Fontan procedure but anticoagulation only in high-risk patients (6). The semilunar valves were normal with a tri-leaflet Balancing potential risks and benefits, corrective heart surgery had been proposed to the patient, but was rejected in the absence of symptoms. Currently, after 3 years of follow-up, she is asymptomatic, taking bisoprolol 5 mg/die and routinely transthoracic echocardiogram has been scheduled every 6 months. Bicuspid pulmonary valve is an exceedingly rare finding usually associated with PAA that could result as the consequence of chronic stenosis of the valve. Few sporadic cases of PAA have been reported until now, especially concerning autoptic analysis, but such a giant PAA with bicuspid pulmonary valve in an asymptomatic woman has never been described. Moreover, as demonstrated here, a multimodality imaging approach was crucial to better define the morphology of the pulmonary valve, to exclude any other congenital defects, such as conotruncal anomalies, and to rule out any associated complications. Different cutoffs for PAA have been proposed, from a range of 26.9 mm in women (1) to 29 mm (2) in the general population, and an absolute diameter $55 mm has been designated for surgical intervention (3); so our case, where PAA was 64 mm, was clearly enclosed in these ranges. Overall, surgery remains the cornerstone of these pulmonary abnormalities; however, there are no clear guidelines yet on the optimal management of these patients (4). In our case, the absence of complications and symptoms has leaded the patient to give up the proposed corrective surgery, so we have planned a follow-up every 6 months. Moreover, albeit not clearly specified, a pharmacological treatment with beta-blockers has been introduced to reduce vascular wall stress, as is usually also done for the aneurisms of the aortic tract. Table 1) . A 44-year-old white woman with a history of TOF at birth underwent a left-sided Blalock-Taussig shunt in the neonatal period followed by complete repair at the age of 3 years. She presented to our community-based multidisciplinary adult congenital heart disease clinic to establish care with a local cardiologist after she was noted to have a markedly abnormal electrocardiogram and an enlarged heart on a chest radiograph during an urgent care visit for an upper respiratory infection (Figures 1 and 2) . Her cardiac examination revealed a mildly enlarged heart To recognize the importance of long-term surveillance in patients with adult congenital heart disease, such as TOF. To identify major long-term complications of TOF. To be familiar with guidelines for evaluation and management of TOF. To recognize the most common surgical procedures appropriate for management of TOF and symptomatic relief. to palpation with an RV lift. The first heart sound was normal, whereas the second heart sound had a slightly wide split. There was a grade 2/6 short, low-pitched systolic ejection murmur that was loudest at the mid-upper left sternal border with slight radiation to the posterior lung fields, as well as a grade 2/6 low-pitched diastolic murmur in the same region. The patient is an active smoker who recently relocated. She saw her adult congenital heart disease specialist 3 years earlier and needed to establish care with a local cardiologist. As a child, she was advised to avoid overexertion with physical activities and thus did not participate in competitive sports. However, she otherwise denied any limitations when playing with other children. She gave birth to 1 child without complications. The patient appeared to have rapid deterioration of her bioprosthetic valve, suspected to be secondary to thrombosis caused by a lack of compliance and a questionable coagulopathy ( Figures 4A to 4D ). Sanchez et al. Potential Complications Years After TOF Repair A findings were consistent with low-flow lowgradient aortic stenosis (Figure 1, Video 1E ). Kellett et al. Femoral artery access for transcatheter endograft was aborted because the required 16-F sheath could not traverse 3.9-mm and 1.5-mm vessels; the subclavian arteries were occluded. Patients with ACHD who present again decades after initial palliation may require unique management solutions, including establishment of sufficient vascular access to permit transcatheter therapy. We pursued alternative transcaval vascular access ( Figures 1A to 1F) . Pre-procedural comprehensive advanced imaging (including peripheral access vessels) for pediatric patients with congenital heart disease is not systematic. As our case illustrates, it should be common practice in patients with ACHD and was performed before the subsequent transcaval procedure. For better anatomic visualization and assessment of hemodynamic significance a cardiac computed tomography (CT) scan was performed. A large coronary-venous fistula (maximum diameter 8 mm) arising from the proximal circumflex artery, running between the left ventricular outflow tract and the anterior wall of the left atrium and draining into the superior vena cava, was shown (Central Illustration A, Figure 1B , Video 2). In addition, a small vessel originated from the descending aorta and bifurcated into 2 branches: 1 running superior and 1 inferior to the left pulmonary artery (Central Illustration B, Figure 1C , Video 3). The 2 branches rejoined and drained into the distal part of the coronary-venous fistula. For further spatial assessment of the complex vessel anatomy a multicolor 3-dimensional (3D) printed model, using binder-jetting technology, was created ( Figure 1D, Video 4) . This technology allows creating a multicolored 3D model, while also identifying small substructures such as the fistula origin and adjacent arteries, which would be essential for a safe interventional or surgical treatment (1). A coronary aneurysm or dilatation of right chambers, as indirect sign of hemodynamic relevance, could be excluded. Furthermore, echocardiographically, there was no evidence of an elevated pulmonary artery pressure; a cardiac magnetic resonance scan showed a pattern of acute myocarditis without evidence of myocardial infarction with normal biventricular dimensions, equal and normal biventricular stroke volumes, as well as aortic and pulmonary flow volumes. Therefore, the patient was treated conservatively. Coronary fistulae are rare, primarily congenital abnormal communications between coronary arteries and another cardiovascular structure without an interposed capillary bed ranging from 0.05% to 0.9% in several large selected series (2) . Clinically, the drainage site of a fistula is more important than its origin; coronary cameral fistulae terminate in a cardiac chamber (commonly into low-pressure right-side cardiac structures), and coronary arteriovenous fistulae terminate into a venous structure such as venae cavae, coronary sinus, bronchial veins, and pulmonary arteries (2) . imaging technologies in conjunction with a highly integrated heart team for management. The origin of the fistula may drain from a main coronary artery and is usually a dilated and tortuous artery terminating in one of the cardiac chambers or a vessel. The more proximal the origin from the main coronary artery, the more dilated it is. If the fistula drains to the right atrium with a proximally arising feeding artery, it tends to be considerably dilated but less tortuous. If there is a more distal origin, as when the fistulas originate from the left coronary artery and drain to the left ventricle, they may be very tortuous, presenting a challenge for catheter closure. However, in the less frequently encountered right coronary artery to coronary sinus, the fistula vessel may be large and very tortuous. There may be multiple feeding arteries to a single coronary arterial fistula drainage point or there may be multiple drainage sites. Fistulas originate from the right coronary artery in 52% of cases, the left anterior descending is the next most frequently involved in approximately 30% of cases, and the LCX in about 18% of cases. Over 90% of the fistulas regardless of origin egress to the right side of the heart, and the remainder drain to the left side of the heart. In the right heart, drainage occurs most frequently to the right ventricle (in about 40%), followed by the right atrium, coronary sinus, and pulmonary trunk. In adults, occasionally fistulas may be encountered that originate from both coronary arteries and drain into the pulmonary trunk. After occluding the main fistulous vessel, repeat selective coronary angiography in both coronary arteries is essential, as a second branch feeding the fistula or multiple feeding vessels may be visualized. With catheter-based closure techniques, complete occlusion of the fistula may be achieved in >95% of the patients. In the remaining patients, either further procedures may be required to close the fistulas or Figure 2) . He had developed PR prolongation, and the pre-existing LPFB was no longer evident, likely because of balanced delay in the LAF, induced by mechanical injury. On the reconstructed rhythm strip ( Figure 1A) , with sinus tachycardia (rate: 102 beats/min), the patient had primarily RBBB (QRS duration: 130 ms) with a normal PR interval (180 ms). When the RB is able to intermittently conduct, it now conducts faster than the LAF, resulting in a shorter PR interval than baseline (140 ms) and left bundle-branch block (LBBB) QRS duration 150 ms. Figure 1B Kulkarni et al. Sinus acceleration is evident as atrioventricular (AV) block develops, culminating in 6 s of ventricular asystole before AV conduction begins to resume. Even when the sinus rate (indicated by red arrows) has accelerated to 120 beats/min, AV conduction is still not 1:1. ECG, electrocardiogram. We report 2 cases of vagally mediated heart block during rapid sinus rates. In the midst of nausea, extreme diaphoresis, retching, and presyncope (all consistent with a vagally mediated syndrome), the sinus rate (indicated by red arrows) remains at approximately 100 beats/min although atrioventricular (AV) node block occurs culminating in significant ventricular asystole. Excessive artifact toward the end of the recording does not allow accurate assessment of sinus cycle length. Suggs et al. The first case is unusual in that vagal activation during colonic insufflation resulted in AV block during on-going sinus tachycardia without sinus slowing; in fact, the sinus node accelerated, seemingly a "disconnect" between vagal influence on the 2 nodes. The second case showed continued sinus rates of 95 to 100 beats/min for the first many seconds of vagal AV block, although P waves were difficult to assess because of excessive artifact. It is known that sinus node automaticity is more powerfully influenced by vagal inhibition, whereas AV node conduction is largely controlled by sympathetic activation. Therefore, one often sees sinus slowing with continued AV conduction or sinus arrest during vagal activation, but our 2 cases showed the reverse responses. However, it must be acknowledged that vagal activation rarely occurs in isolation, and most often there is an on-going balance between sympathetic and vagal tone. H67-73. She denied any other signs or symptoms, and never experienced a syncopal episode or defibrillator shock. The patient presented to the emergency department where vitals were noted to be within normal limits and physical examination was unremarkable with the exception of a well-healing surgical wound. To raise awareness of this potentially lifethreatening interaction between magnetic components of breast tissue expanders (or other chest prostheses) and ICD function. To promote prompt recognition and rectification is necessary if this situation is encountered post-operatively. To understand that, if faced with this situation pre-operatively, clinicians should recommend use of alternative prostheses that do not have magnetic components. The differential diagnosis of a high-pitched beeping sound and vibration over her ICD included cardiac device malfunction or deactivation from a number of potential mechanisms following left chest surgery. The patient presented to our facility where ICD interrogation showed normal function and stable pacing and sensing thresholds. However, after further inquiry it was discovered that the recently implanted breast expander had a magnetic port that intermittently disabled the tachyarrhythmia detection and therapy function of the ICD 23 times over the preceding 2 days. We deduced that when the patient leaned forward or raised her left arm, the magnetic port on the breast tissue expander came into close proximity to the defibrillator, leading to inhibition of tachyarrhythmia detection and therapies. The magnetic port and defibrillator relationship can be seen on the chest radiograph in Figure 1 Given known history of CPVT, the differential diag- ICD interrogation showed the device functioning normally with appropriate settings ( Table 1) . Review of events revealed 11 recurrent episodes of VT or VF over 11.5 min, with the last episode persisting for nearly 4 min ( Table 2 ). The ventricular arrhythmias were refractory to a total of 14 antitachycardia pacing (ATP) episodes and 21 ICD discharges. In the final event, VF persisted despite maximal ICD discharge capacity, with interrogation noting "No More Therapies" (Figure 1 ). VF continued for 53 s after the last ICD shock before spontaneously converting to normal sinus rhythm (Figure 2 ). should be started on nonselective beta-blocker therapy; nadolol is preferred (5, 6) . Even with beta-blocker therapy, an ICD may be required. The rate of breakthrough arrhythmias on beta-blocker therapy ranges from 3% to 11% annually (7) . Therefore, patients should be assessed for recurrent ventricular arrhythmias even after initiation of beta-blocker therapy. The effectiveness of ICD therapy for management of CPVT depends on the mechanism of arrhythmia. Appropriate ICD shocks delivered to polymorphic or bidirectional VT often fail, but shocks delivered to VF are usually effective (8, 9) . However, inappropriate shocks are common (8, 10) . Furthermore, serial defibrillation can perpetuate enhanced adrenergic stimulation and electrical storm (10), as likely occurred in this patient and made her refractory to recurrent ICD shocks. The patient has had no further evidence of arrhythmia since cardiac transplantation. The effectiveness of radiofrequency ablation drops exponentially with distance, limiting the ablation of deep substrate arrhythmia. Direct-current ablation has been reinvestigated in animal models and has shown considerably good outcomes and safety margins with better lesion depths. Modified version of direct-current ablation using biphasic energy lowers the current density to further minimize its complications. Recently, DC ablation has been reinvestigated as an alternative source of energy in cardiac ablation with the advancement in catheter technology where the catheter can deliver relatively low energy as well as low current density without creating an arc (6) . The mechanism of DC ablation is disruption of cell membranes using electrical energy, resulting in apoptosis (7) . An animal study showed 100-to 300-J-unipolar DC ablation resulted in larger and deeper lesions (8 to 10 mm) than standard RF ablation (4 to 5 mm) (8) . Coronary luminal diameters were also unaffected by DC ablation in porcine models (9) . A 75-year-old man with symptomatic drug-refractory atrial fibrillation (AF) and with recurrent AF after previous AF ablation was admitted for repeat catheter ablation. Other than AF, the patient had no cardiac history and no coronary artery disease risk factors. He denied symptoms concerning for angina. The patient had no family history of a cardiac disorder or sudden death. The patient was brought into the electrophysiology laboratory for repeat ablation. All 4 pulmonary veins Coronary vasospasm is a rare potential complication of ethanol ablation of the VOM. Figures 2A and 2B ). The differential diagnosis of ST-segment elevation in the inferior leads during AF ablation includes air embolism, LA embolism to the right coronary artery (RCA), coronary vasospasm, and acute pericarditis. To the best of our knowledge, this is the first report of coronary arterial vasospasm after coronary venous ethanol ablation of the VOM during AF ablation. Recently, the VOM has been increasingly recognized to be a potential target site during AF ablation to achieve mitral isthmus block (1-3), vagal denervation (4), and for targeting non-PV triggers (5-7) and This case supports the notion that the full effects of ethanol ablation can take time to occur after the infusion. Figures 1A to 1C) . She was initially treated with lowdose metoprolol and amiodarone for rate control and potential suppression of episodes of atrial arrhythmia, however, this further exacerbated the symptomatic conversion pauses and episodic bradycardia. To recognize cardiac tumors as a potential cause of both tachyarrhythmias and bradyarrhythmias. To highlight cardiac vein anatomy as it relates to alternative positions for pacemaker lead placement. The patient had a medical history of hypothyroidism on levothyroxine with a family history of malignancy including lung cancer (mother) and melanoma (father). Considering that the patient was a relatively healthy middle-aged woman, the differential diagnosis of her progressive dyspnea over a 3-to 4-month period included new-onset cardiomyopathy, however, her unintentional weight loss raised suspicion for malignancy. The red arrow indicates the right atrial mass. LA ¼ left atrium; LV ¼ left ventricle; RA ¼ right atrium; RV ¼ right ventricle. The patient had been treated for several years with beta-blockers, as well as flecainide. Screening for cardiomyopathy was negative. Before the admission, a 24-h Holter showed a high PVC burden (42%) and several episodes of nonsustained VT despite antiarrhythmic therapy with metoprolol 100 mg once daily and flecainide 150 mg To use personalized 3D information from noninvasive 3D mapping and a CT roadmap that locates the origin of ventricular arrhythmias and guides the operator to find the optimal access to an ablation target. To consider ablation through the LAA to reach the epicardium of the LV summit, when endocardial ablation fails and/or an epicardial approach seems difficult. once daily. The electrocardiogram (ECG) on admission is shown in Figure 1 . In our case, 12-lead ECG morphology of the ectopic focus was suggestive of LV summit origin with a nonspecific bundle branch block morphology with The patient underwent a stress treadmill test and 24-h Holter monitoring to detect higher degrees of AV block. Holter monitoring showed the presence of firstand second-degree AV blocks, including a 2:1 AV block during sleep ( Figure 2 ) and normal AV conduction when the heart rate was higher ( Figure 3 , Table 1 ). To our surprise, there was an improvement in AV conduction during higher exercise velocity in the Ellestad protocol, a change suggesting parasympathetic behavior of the AV node. On the basis of these findings, in June 2018, we decided to perform CNA. Before CNA, we performed a basal electrophysiological study (EPS) and administered 3 g of atropine to prove that the AV conduction normalized during the drug effect. After that, we conducted a new EPS with and without atropine. Major EPS findings pre-ablation were normal. Her His-ventricle interval was normal, with no AV jump or echo beats. There was an increase in heart rate after atropine by 114%, from 56 to 103 beats/min, and there was normal AV conduction. The Wenckebach point decreased from 520 to 410 ms, and the AV refractory period decreased from 500 to 310 ms before and after atropine, respectively. Finally, at this point we started the ablation procedure. Electrical targets for ablation were high frequency, and long fractionated signals were seen in the distal and proximal catheter dipoles and at abnormal FFT signals. Heart rate increase during radiofrequency applications was higher at these sites than at other sites without these characteristics. After CNA, the final heart rate was 97 beats/min ( Figure 8) . EPS with and without atropine showed no heart rate increase, a Wenckebach point at 430 ms, and an atrial refractory period of 340 ms, thereby displaying a loss of parasympathetic behavior. Three main parasympathetic ganglia are found outside the atrial wall in paracardiac fat pads that provide innervation to the heart (2), and they are subdivided into ganglia A, B, and C. Ganglion A is located between the aorta and the superior vena cava ( Figure 7) , ganglion B is located between the right pulmonary veins and the right atrium (Figures 4 to 6) , and ganglion C is located between the inferior vena cava and at the wall between the right atrium and left atrium (Figures 4 to 6) . Ganglion A appears to be the Anatomically mediated CNA has been increasingly used to treat severe vagally related arrhythmias worldwide (1, (3) (4) (5) (6) . Although guidelines (7) Higher rate with normal atrioventricular conduction. The major explanation for this is that the atropine test is not a procedure that can be done routinely in public and private hospitals in Brazil. However, the way that we addressed the vagal ablation response, even with the residual atropine effect, is the heart rate increase during radiofrequency application. In this specific case we show the 2-year follow-up of the patient that may prove that the AV conduction was normalized and stayed normal after the procedure. Targeting all the ganglionated plexus could be a risk if continuous monitoring by extracardiac vagal stimulation is not performed because AV block can become more severe if you denervate only the sinus node with the heart rate increase. Therefore, an individualized approach to ensure the objectives and success of the CNA is mandatory. This is 1 of few reported cases of catheter ablationbased treatment to improve AV conduction to avoid pacemaker implantation. Like the case reported by Red dots indicate radiofrequency applications on the left side parasympathetic plexus (anteroposterior view). Red dots indicate radiofrequency applications on the left side parasympathetic plexus (posteroanterior view). Green dots indicate radiofrequency applications in the superior vena cava and aorta, and blue dots indicate the atrioventricular plexus (posterior coronary sinus). Vassallo et al. The patient had a history of paroxysmal atrial fibrillation and LAA closure with Watchman, hypertension, dyslipidemia, well-controlled diabetes mellitus type 2 (hemoglobin A1c 6.6%), and chronic kidney disease. Her home medications included aspirin, bisoprolol, evolocumab, ferrous sulfate, fluoxetine, gabapentin, rosuvastatin, semaglutide, and furosemide. Differential diagnoses include Watchman erosion to the pericardial and pleural spaces, Watchman-related inflammatory process, pulmonary embolism, druginduced pleural effusion, malignancy, and connective tissue disease. The Watchman device is an LAA closure device that is increasingly used to prevent stroke among patients with atrial fibrillation. Complications associated with this device include pericardial effusion, tamponade, device erosion, and embolization. Although the safety profile of this device has improved with enhanced operator technical skills, it is important to recognize rare complications that may arise from the placement of this device. In this case report, we described the clinical presentation and management of recurrent pleural effusion and pericarditis following placement of the Watchman device. Pleural effusion is a rare complication of LAA closure with the Watchman device and can be the result of an inflammatory response due to intraprocedural pericardial injury. It is important to differentiate inflammationrelated pleural effusion from bloody pleural effusion secondary to device erosion of the pericardial and pleural spaces. Conservative treatment with nonsteroidal anti-inflammatory drugs and colchicine can be successful in the treatment of post-Watchman pericarditis and exudative pleural effusion. A 39-year-old man with recurrent dizziness and syncope, but no other medical issues, was referred to the Training and Research Hospital, for permanent pacemaker implantation. Physical examination was completely normal except for an irregular heart rate. A baseline electrocardiogram (ECG) showed an atypical persistent Mobitz type I atrioventricular (AV) block (AVB) and a narrow QRS complex ( Figure 1A ). The patient had dyspnea with onset of exercise that resolved after a few minutes. He reported frequent syncopal episodes with prodromal symptoms of nausea, a sensation of warmth followed by clammy skin, blurry vision and lightheadedness since adolescence that occurred with upright posture and light activity. Holter recordings revealed frequent intermittent high-degree AVB, reaching up to 4 consecutive blocked P waves ( Figure 2 ). To differentiate among subtypes of AVB by means of functional noninvasive and invasive testing. To understand the role of CNA in the treatment of functional AVB. The differential diagnosis included functional (vagal) AVB, intrinsic (structural) AVB, and extrinsic idiopathic AVB with accompanying vasovagal syncope. To determine the nature of the AVB, an atropine response test was conducted. During the test, a stepwise increase in sinus rate from 75 to 103 beats/min was noted, and partial resolution of AVB with a 240 ms PR interval was seen after administration of 2 mg of intravenous atropine ( Figure 1B) . Intrinsic AVB is usually initiated by premature extrasystoles, and sinus rate acceleration is observed during the block (4). Conversely, AVB is often accompanied by slowing of the sinus rate in functional AVB, and progressive PR interval prolongation preceding the AVB may also be seen. To differentiate intrinsic from functional types in cases of persistent AVB, atropine response testing may be used (5, 6) . In these studies, resolution of AVB during exercise, following atropine administration and during atrial pacing, were highly suggestive of functional AVB, as in the present case. Moreover, our patient had a normal HV interval at baseline and during atrial pacing, a finding supporting a functional mechanism. Extrinsic idiopathic AVB is characterized by recurrent syncopal episodes without prodromal symptoms (7) . In the present case, the prodromal symptoms were whereas the RSGP predominantly affects the sinoatrial node. This association has not been confirmed in human subjects yet (8, 9) . In a recently published study, Bulava et al. (10) In 4 patients, it was performed only by the right atrium. All patients became asymptomatic, but 1 case (12.5%) remained with occasional nocturnal Mobitz I AV block. In the others, CNA was performed by using a biatrial approach, and no AV block was observed. CNA for the treatment of functional AV blocks is more challenging than that for other bradyarrhythmias and should be performed by using a biatrial approach; however, in addition to the technical details, it is essential to achieve total elimination of the AV block induced by left vagus nerve stimulation as the endpoint of the procedure (Figures 1 and 2) . Before the procedure, we must be sure that the AV block is functional, that the conduction system is intact, and that there is an adequate response to atropine. Due to the location, the AV node receives innervation from all ganglionic plexuses (GP), which makes it difficult to denervate. Furthermore, the procedure must be carefully performed to avoid AV node damage. Most of the innervation comes from GP2 located between the insertion of the right pulmonary veins (PVs), left atrial roof, and oval foramen, the socalled "P point" (4, 5) , from GP3, between the coro- (Figures 1 and 2 ). This approach consists of advancing a catheter through the internal jugular ( Figure 1B) up to the jugular foramen at the cranium basis (6) . In this location, due to the proximity to the vagus nerve ( Figure 1C ), ECVS is achieved even without direct contact with the nerve, using 50 Hz, 50 ms, with an amplitude of 1 V/kg of body weight up to a maximum of 70 V ( Figure 1A) . Typically, immediate asystole occurs due to the vagal effect ( Figure 1D ). However, considering that the AV node receives more innervation from the left vagus, while treating a functional AV block, we regularly perform stimulation of the left vagus during atrial pacing with 80 to 100 ppm, if necessary, to prevent bradycardia. This procedure aims to appropriately challenge the AV conduction ( Figure 2B ). The goal is to attain total disappearance of the vagal-induced AV block ( Figure 2C ) when complete AV node vagal denervation has been achieved. Thus, the AV block induced by ECVS before or during CNA ( Figure 2B ) must be completely eliminated ( Figure 2C ). The hardest endpoint is the total elimination of vagal-induced AV block with or without atrial pacing. It is essential to achieve complete abolition of the vagal effect to guarantee a safety margin to counter the natural reinnervation that may affect the long-term result. A 48-year-old woman presented with chronic leg edema and worsening exertional dyspnea. She also IDA-induced cardiomyopathy can be characterized by severe chronic anemia, significant microvascular dysfunction, and high-output HF, which is reversible if treated properly. Multi-imaging modalities such as transthoracic echocardiography, CMR, coronary angiography with hemodynamics measurements, and cardiac positron emission tomography can improve accurate diagnosis and appropriate management. The patient's medical history was unremarkable except for that she regularly smoked tobacco and consumed alcohol. The (Figures 2A and 2B) . On the seventh hospital day, coronary angiography ( Figure 2C) Figure 5) . Finally, the patient was referred to our obstetrics and gynecology department where the solid mass in her uterus was diagnosed as endometrioid cancer on histology. Frusemide and enalapril were commenced, and the patient was gradually weaned from supplemental Figures 1C and 1D ). Her LV ejection fraction improved to 69%, and LV diastolic dimension was still enlarged (54 mm) with a mildly elevated LV mass index of 111 g/m 2 ( Figure 2B ). CMR studies at the 4-month visit were repeated with the corresponding images (D to F). Concentric left ventricular (LV) hypertrophy and biventricular enlargement were visible with a reduced LV ejection fraction of 32%, which improved to 47% over 4 months with a significant drop in the LV end-diastolic volume from 184 to 96 ml. Late gadolinium enhancement was not present over the entire myocardium at both the acute (C) and follow-up phases (F). The patient had history of well-controlled hypertension and no other modifiable or nonmodifiable risk factors or clinical markers of coronary artery disease. Because of the incidental CT findings in this asymptomatic patient, the possibility of congenital versus acquired coronary aneurysm was raised. Given that the patient had not undergone any coronary interventions, the possibility of past iatrogenic causes or coronary manipulation was excluded. Subsequent coronary CT angiography (CTA) showed a giant (3.7-cm), calcified proximal LCX aneurysm with a small thromboatheroma (Figure 1 ). The incidence of coronary artery aneurysms is 0.02% to 0.04%, and these aneurysms are usually seen in the right coronary artery. To our knowledge, there has been no case reported of a patient with an LCX LCX aneurysm is an extremely rare clinical condition. Careful evaluation of the coronary anatomy is needed to identify any additional coronary anomalies in these patients. Our case represents a unique anatomy, with a giant LCX aneurysm and the distal LCX draining into a confluence receiving terminal portions of all coronary arteries and communicating with the LV through a transmural fistulous tract. Complex coronary anomalies require indepth evaluation, including multimodality imaging to assess the patients for presence of myocardial ischemia and significant leftto-right shunt. Cardiac CTA is a very helpful diagnostic tool in establishing definitive anatomy in these cases. The treatment should be individualized on the basis of the patients' symptoms, objective prediction of risk (presence of ischemia, progression of the lesion), and the presence of associated coronary and cardiac anomalies. With a careful work-up and follow-up, this coronary anomaly may have a benign shortterm clinical outcome. Giant LCX Aneurysm With Coronary-to-LV Communication other abbreviations as in Figure 1 . Touma et al. The patient underwent yearly coronary CTA for surveillance without significant change in the size of the LCX aneurysm, and he has remained without cardiac complications to date for a total of 3 years. LCX aneurysm is an extremely rare clinical condition. The content is shared by the JACC journals' formal SoMe accounts in addition to individual SoMe editors' accounts ( Figure 1 ). When studying the impact of the SoMe team in disseminating the journal's content, AAS applies certain modifiers to offset potential bias set by active "sharing" of papers by the editorial board (12) . These modifiers sometimes take into account the connection between the "tweeter"/author of SoMe post and the journal being promoted for a given paper. For Table 1) . Among the top 100 papers, 65% were case reports and 5% were clinical case series and editorial comments. In total, 16% of the papers were Voices in Cardiology used strategically allows for bite-sized discussions facilitated by content dissemination that may allow for the generation of future hypotheses and increase overall scientific collaborations and, ultimately, scientific output (13, 14) . Although case reports are seldom cited, educational discussion around high- There are several limitations to the AAS score. Although sharing of the paper by the journal or by editorial board gets less attention than someone unrelated to the journal or editorial board, a fundamental concern with AAS is the process of data collection, management, and update of SoMe impact to generate this score. Also, AAS does not provide information about the quality of the paper; on the contrary, criticism/negative attention is also counted as "attention" (16) . recording of an event, the ECG recording showed an atrioventricular block followed by an asystole. After several seconds of asystole, symptoms of hallucinations, screaming, and shaking began, followed by loss of consciousness ( Figure 1, Video 2) . The EEG showed diffuse highamplitude slow activity after which the EEG became isoelectric, a typical EEG pattern for syncope (1) . Our patient was diagnosed with syncope due to intrinsic paroxysmal atrioventricular block. After pacemaker implantation (dual chamber pacemaker), the events no longer occurred. Transient loss of consciousness is a commonly encountered symptom and may pose a clinical dilemma, as the underlying condition can be difficult to establish. The major causes are epileptic seizure, In chronological order, the figure depicts onset of atrioventricular block, screaming and shaking with motion artifact on electrocardiogram (ECG), onset of slow highamplitude electroencephalogram (EEG) activity, which is soon followed by loss of consciousness, and flattening of the EEG signal. Soon after, QRS complexes reappear on the ECG and slow EEG activity returns, the patient regains consciousness. This slow-flat-slow EEG pattern is a typical feature of syncope. (6) . Importantly, patients assigned these hallucinations to the period of unconsciousness or during the period afterward, but did not experience them before losing consciousness (6, 7) . Prodromal hallucinations would normally be suggestive for epilepsy (8, 9) . Therefore, a diagnosis of epilepsy was initially suspected in our patient, which was the reason for performing the ECG-EEG recording that established the diagnosis of cardiac syncope instead. Thus, the limb shaking, vocalizations, and hallucinations in our patient were caused by cerebral hypoperfusion. Of note, cardiac arrhythmia can occur secondary to an epileptic seizure (10), but this was ruled out with the EEG registration and further substantiated by the fact that no more events occurred after pacemaker implantation. In accordance with established guidelines, the initial diagnostic workup of a patient suspected of syncope should include a careful history taking, including the situation in which syncope occurs, the nature and duration of prodromal symptoms, bystander observations, post-event symptoms, prior medical history and medication use, and family history with emphasis on syncope and sudden unexplained death (10) . In the current case, high-risk features suggesting cardiac syncope were the presence of structural heart disease, a short history of syncope, age >60 years, very short prodromes, and syncope occurring in supine position (10) . A diagnosis of reflex syncope should be considered in case of more prolonged prodromal signs, absence of a prior history of heart disease, younger age, specific triggers (e.g., dehydration, pain, stress, micturition) and a long history of syncope (10) . Syncope occurring in the setting of positional change (supine to sitting, sitting to standing) is suggestive of orthostatic hypotension. Recommended physical examination in case of syncope includes blood pressure and heart rate and rhythm, testing for orthostatic hypotension if the patient's history is compatible with this condition, cardiac auscultation, and a basic neurological examination. Performing an ECG in syncope is recommended and performing targeted blood tests (e.g., to exclude anemia) is reasonable, whereas routine and comprehensive laboratory testing is not considered useful (10) . After pacemaker implantation, the events no longer occurred. pandemic, and many of these consequences directly impact their fellowship candidacies ( Table 1) . Fellowship program leaders face related challenges in navigating this virtual recruitment season but should also remain mindful of applicants' circumstances (Table 1) . Here, we outline the common challenges that general cardiology fellowship applicants and programs will face during the 2020 recruitment season with a focus on the virtual interview, and we offer strategies to support and guide trainees and program leaders through the virtual interview process. For the July 2020 cycle, the Electronic Residency We suspect that because applicants will not be able to meet faculty in person or visit the facilities or the city/town, they will likely have more questions than to which interviewers may be accustomed and may need more time in the interview to discuss these aspects of the training program. Interviewers should avoid scheduling interviews to overlap with clinical or administrative obligations. It remains unclear if programs will choose to structure interview days with all interviews being held over the same day for each applicant or if they will trial interviews with sessions spread over multiple days. These variations may lead to a change in the atmosphere of an "interview day." APPLICANTS. Expectations for applicants to wear professional attire will remain unchanged. Applicants should plan to hold virtual interviews in a comfort- Here in the United Kingdom, we were hit hard by the COVID-19 pandemic, during which time we encountered not only the victims but also the "hidden" victims, those patients who will need long-term support or those caregivers who have been in such emotional distress that it will be difficult for them to completely recover. I feel for my friends and colleagues in the United States and other countries, which are still undergoing the peak of the pandemic. Percutaneous technique for the reduction of knotted coronary catheters Increased coronary perforation in the new device era. 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Journal editors and altmetrics: moth to the flame? Do altmetrics correlate with the quality of papers? A large-scale empirical study based on F1000Prime data Symptoms and signs of syncope: a review of the link between physiology and clinical clues Historical criteria that distinguish syncope from seizures Seizure versus syncope Identifying cardiac syncope based on clinical history: a literature-based model tested in four independent datasets ESC Guidelines for the diagnosis and management of syncope Syncope: a videometric analysis of 56 episodes of transient cerebral hypoxia Out-of-body experience and auditory and visual hallucinations in a patient with cardiogenic syncope: crucial role of cardiac event recorder in establishing the diagnosis Syncope, seizureinduced bradycardia and asystole: two cases and review of clinical and pathophysiological features Proposal: Different types of alteration and loss of consciousness in epilepsy Guideline for the evaluation and management of patients with syncope Adapting the educational environment for cardiovascular fellows-in-training during the COVID-19 pandemic The impact of the COVID-19 pandemic on cardiovascular fellows-in-training: a national survey Reinforcing cardiology training during a pandemic: an open letter to our leaders Coalition for Physician Accountability's Work Group on Medical Students in the Class of 2021 Moving Across Institutions for Post Graduate Training. Recommendations for Away Rotations and Interviews for Graduate Medical Education Fellowship Applicants During the 2020-2021 Academic Year. Available at Association of American Medical Colleges AAMC VITA FAQ for the 2021 Application Cycle. Available at Conducting interviews during the coronavirus pandemic National Resident Matching Program. Match Communication Code of Conduct COVID-19: a lesson in humility and an opportunity for sagacity and hope Therasse 1 5530 Yvoir Belgium E-mail: pascal.reper@uclouvain Ó 2020 The Authors. Published by Elsevier on behalf of the American College of Cardiology Foundation. This is an open access article under the CC BY-NC-ND license Cardiovascular disease, drug therapy, and mortality in Covid-19 Acute myocarditis presenting as a reverse tako-tsubo syndrome in a patient with SARS-CoV-2 respiratory infection Takotsubo syndrome in the setting of COVID-19 infection International expert consensus document on takotsubo syndrome (part I): clinical characteristics, diagnostic criteria, and pathophysiology A novel clinical score (InterTAK Diagnostic Score) to differentiate takotsubo syndrome from acute coronary syndrome: results from the International Takotsubo Registry Ó 2020 The Authors. Published by Elsevier on behalf of the American College of Cardiology Foundation. This is an open access article under the CC BY-NC-ND license Hays has received support from the Magic that Matters Fund of Johns Hopkins Medicine and National Institutes of Health (NIH)/NHLBI grant 1R01HL147660. The authors attest they are in compliance with human studies committees and animal welfare regulations of the authors' institutions and Food and Drug Administration guidelines, including patient consent where appropriate. For more information Takotsubo syndrome in the setting of COVID-19 International expert consensus document on takotsubo syndrome (part II): diagnostic workup, outcome, and management points for the absence of ST-segment depression). As stated in the original description of this score, "patients with 50 points have a probability of 18%.of suffering from TTS" (2) . Although the InterTAK score may be helpful in other patients with TTS, in the case of our patient the score as calculated did not strongly support or refute a diagnosis of TTS. For our patient, the classic imaging pattern on the initial echocardiogram and the reversibility seen on a subsequent echocardiogram were more consistent with TTS, thus leading to our diagnosis. We acknowledge that this is