key: cord-0794392-nxpb102e authors: nan title: Full Issue PDF date: 2020-08-31 journal: JACC: Case Reports DOI: 10.1016/s2666-0849(20)30980-3 sha: 7f47a21a4717e180dae5179417a603912f723071 doc_id: 794392 cord_uid: nxpb102e nan to the hospital via ambulance, she was reportedly in atrial fibrillation. She was hemodynamically stable on arrival with a blood pressure of 107/71 mm Hg, a heart rate of 80 beats/min, and an oxygen saturation of 99% on room air. Cardiac, respiratory, and pulse examinations were unremarkable. Although she cited work-related stressors, there were no clear physical or emotional triggers preceding presentation. She additionally denied any antecedent infectious symptoms. SCAD is a common etiology of ACS in young women and can result in significant morbidity and mortality if not recognized in a timely manner. Repeat angiography should be pursued in individuals if clinical suspicion exists for worsening ischemia in the context of myocardial infarction with nonobstructive coronary arteries without clear etiology. Although there may be a potential association between SCAD and TTC, SCAD should be carefully excluded when the diagnosis of TTC is entertained because the management strategy may be different. CMR can be very valuable in characterizing the myocardial pathology. Before presentation, the patient reported good health with satisfactory employmentmandated routine physical examinations. She denied a history of smoking, alcohol, or illicit drug use. She had never been pregnant and was not on hormone supplementation. A wide differential was considered by the admitting team, including pulmonary embolism, acute coronary syndrome (ACS), and pericarditis/myocarditis. At this stage, her presentation was suspicious for myocardial infarction with nonobstructive coronary arteries with coronary thrombosis/emboli highest on the differential. The electrocardiogram revealed evidence of repolarization abnormalities consistent with anterolateral injury. She was started on metoprolol. Her blood pressure did not tolerate further neurohormonal blockade. Unfractionated heparin was started on arrival given the reported atrial fibrillation in the ambulance and was continued because of the concern for potential embolic MI. Ultimately, these ECG strips were obtained, and no atrial fibrillation was noted. A transesophageal echocardiogram did not reveal an embolic source or patent foramen ovale, and unfractionated heparin was promptly discontinued. Four days into hospitalization, she developed arm numbness, mild chest discomfort, and emesis. An RENT CASE CHALLENGING? The case was challenging in light of her fairly unremarkable coronary angiogram relative to her dramatic presentation. After her initial angiogram, which did not demonstrate an obstructive coronary lesion, concern remained high for TTC or missed SCAD. Given the small caliber of the abnormal diagonal branch, intravascular imaging was not feasible for further investigation of the abnormal coronary segment. Repeat angiography, although initially considered, has associated risk if SCAD is on the differential diagnosis, given the possibility of propagating dissection with coronary instrumentation. Cardiac imaging in this case, namely with CMR, helped to narrow the differential diagnosis (see later), and recurrence of ischemia drove the decision for repeat angiography, which ultimately confirmed the diagnosis. SCAD and TTC has been previously described (4) . It is hypothesized that an acute adrenergic rise in TTC may potentiate coronary artery sheer stress and SCAD or that stress associated with SCAD may theoretically manifest as TTC (3, 5) . Interestingly, in 2 series of patients originally diagnosed with TTC, re-review of angiograms revealed the presence of previously unrecognized SCAD in up to 9% (6, 7) . The persistent clinical syndrome, discordantly elevated troponin peak, ECG evolution, and presence of LGE in a single coronary territory played a critical role in differentiating our case from TTC and prompting the team to evaluate for alternative diagnoses. Furthermore, in TTC, the wall motion abnormalities typically extend beyond territories supplied directly by the LAD, including the inferior, posterior, and lateral territories, which were not noted in this case. Although routine follow-up angiography is not often pursued, there is a role for repeat testing in cases with diagnostic uncertainty or ongoing ischemia. Therefore, this case underscores the importance of avoiding committing to a single diagnosis when discordant clinical and investigational findings develop. Our case additionally highlights the utility of CMR in delineating myocardial pathology and the various etiologies of myocardial infarction with nonobstructive coronary arteries (MINOCA) through the identification of LGE, myocardial edema, and wall motion abnormalities (8) . TERRITORIES? The LAD is the most commonly affected coronary artery, with multivessel involvement in less than one-fourth of cases (3, 9) . WHY IS REVASCULARIZATION UNCOMMONLY PUR-SUED? The mainstay of management for most SCAD is medical therapy due to spontaneous healing over time in the majority of cases, the risk of propagating dissection with repeat invasive evaluation, and poor long-term patency of grafts; however, revascularization with CABG is considered in very select situations after comprehensive clinical decision making, including in cases with LM or proximal coronary involvement, ongoing ischemia despite conservative measures, or cardiogenic shock (9, 10) . In these scenarios, it is critical for the surgeon to differentiate a false versus a true lumen to provide the highest likelihood of graft patency. The patient recovered well post-CABG and will be returning to her hometown (internationally) where she will undergo evaluation for fibromuscular dysplasia and connective tissue disorders. SCAD can have a challenging clinical and angiographic presentation. As such, clinical familiarity with this entity is integral to prevent associated morbidity and mortality. Although there may be an association or overlap between SCAD and TTC, careful consideration with various imaging modalities, including intravascular or magnetic resonance imaging as well as a detailed review of coronary angiography, may be integral in delineating etiology and guiding further management. To discuss the potential long-term cardiorespiratory sequelae of mediastinal radiation. To understand the technical challenges to valve intervention imposed by extensive calcific valve disease, particularly involving the aortomitral continuity. To understand the potential role of preprocedural modeling informed by multimodality imaging to mitigate these hazards and plan transcatheter interventions. aortomitral continuity with severely calcified aortic valve leaflets and circumferential mitral annular calcification ( Figures 1A to 1C ). Coronary angiography indicated eccentric, angiographically mild, biostial left main stem and right coronary artery disease, likely reflecting the underlying radiationinduced pathology. Despite relatively low perioperative risk scores (European System for Cardiac Operative Risk Evaluation II ¼ 1.8% and Society of Thoracic Surgeons score ¼ 3.6%), the extensively calcified anatomy posed high surgical risk. The consensus across heart teams in multiple international centers was that conventional dual-valve replacement was not technically feasible, and they proposed the "Commando" procedure to reconstruct the aortomitral continuity after mitral annular decalcification in conjunction with mitral and aortic valve replacement (1) . The patient declined, citing unacceptable operative risk, thereby prompting consideration of transcatheter options. Radiation-induced, severe calcific valve disease; Degenerative valve disease; Noncardiac dyspnea (e.g., pulmonary fibrosis). Hemodynamics improved dramatically, and the patient has remained well. Depending on the precise definition used, clinically significant calcific valve disease may develop in up to 37% of patients after mediastinal radiation (5, 6) . The incidence is dose dependent, and, as in this case, extensive field radiation (e.g., Mantle) and co-administration of chemotherapeutic agents are recognized risk factors (7) . Moreover, as survival from malignancies such as Hodgkin lymphoma continues to improve (20- year survival now >80%), the incidence of remote cardiac complications is expected to increase (8) . Patients with radiation-induced valve disease undergoing conventional cardiac surgery are at increased risk of perioperative complications in a manner not reflected in traditional risk stratification models. The potential sequelae of radiation exposure including mediastinal fibrosis/adhesions; pulmonary fibrosis; pericardial constriction; and coronary, cardiac, and aortic calcification confer an increased risk of perioperative bleeding, cardiorespiratory failure, rhythm disturbance, embolic stroke, and death (9, 10) . As present in this case, extensive calcification of the aortomitral continuity presents a particularly formidable surgical challenge, with the attendant risks of intractable hemorrhage, atrioventricular complications, and operative mortality (>10%) still relatively high, even in experienced hands (11) . In the face of prohibitive or unacceptable surgical risk, transcatheter techniques may offer an alternative, although the treatment of dual radiation-induced valve pathology demonstrated here has not previously been systematically described (12) (13) (14) . In particular, complex, calcified mitral valve anatomy poses numerous challenges to treatment with a round THV without an anchoring mechanism, with potential complications including paravalvular regurgitation, valve migration, and principally LVOT obstruction through distortion of the subvalvular apparatus. Thus, despite technical advancements, 30-day mortality for transcatheter valve in mitral annular calcification remains unacceptably high (25% to 30%) (15, 16) . Appropriate patient selection is key to minimizing risk, with cardiac computed tomography to measure the expected neo-LVOT area considered mandatory. However, this approach does not permit modeling of the dynamic interaction of the valve with the host and vice versa (e.g., mitral annulus calcification deformation under conditions of radial stress). As such, the evaluation based on geometric measurements alone is likely insufficient to accurately predict outcome. We selected a balloon-expandable prosthesis for the mitral position, reflecting the majority of experience worldwide in this setting (15) . We also opted for The prevalence of valvulopathies after RT ranges from 2% to 37% (2), of which approximately 17% develop moderate to severe stenosis or regurgitation (3) . Although the physiopathology is not widely known, it seems that radiation activates fibrogenic growth factors (4) and induces valve interstitial cell differentiation to an osteogenic phenotype (5) . These facts could explain the severe valve thickening and calcification present in these patients. Multivalvular heart disease is a growing condition against which we must make decisions based on expert opinions or previous clinical experiences (6) . RT-induced valvulopathies are associated with cardiopulmonary disorders such as mediastinal and pulmonary fibrosis, constrictive pericarditis, coronary disease, porcelain aorta, and extensive valve calcification which incurs an elevated surgical risk that is not predicted by standard surgical risk scoring systems (7) . Likewise, the effects of RT on valves are usually extensive, and adjacent structures, such as subvalvular apparatus, annulus, and especially the aortomitral curtain (7), are commonly involved, and higher thickening is a robust predictor of mortality (8) . Mitral The second concern is neo-LVOT obstruction. During mitral prosthesis implantation, the anterior mitral leaflet is shifted anteriorly toward the basal septum creating a so-called neo-LVOT (16) that is likely to be obstructive depending on valve sizing, basal septum anatomy, and mitroaortic angle. Guerrero et al. (17) reported an incidence of neo-LVOT obstruction of 9.3% with poor outcomes. A neo-LVOT cross-sectional minimal area cutoff of 1.7 cm 2 has been described to rule out a significant neo-LVOT obstruction (18) . Nevertheless, this has theoretical limitation because in the neo-LVOT 3D configuration, neither flow is taken into account. Interestingly authors have used the 3D biomodel to evaluate the physiological response in terms of gradients and pressures especially within the neo-LVOT, using computational fluid dynamic systems. Finally, A woman in her 50s presented to the emergency room because of chest pain lasting for 90 min. Twenty years before this presentation, she had myocardial infarction (MI) with atrioventricular (AV) branch lesion of the right coronary artery (RCA), which was treated medically, and renal artery stenosis, which was treated with angioplasty. Initial blood pressure was 138/80 mm Hg, heart rate was 70 beats/min, and respiratory rate was 30/min. Electrocardiogram (ECG) revealed marked down sloping ST-segment depression in V 2 to V 4 and mild STsegment elevation in lead I and aVL ( Figure 1A) . Her next ECG, taken 39 min later during coronary angiography (CAG), revealed typical de Winter pattern with ST-segment depression in V 2 to V 5 and peaked T-wave in V 3 to V 5 ( Figure 1B) . Emergency CAG revealed high-grade abrupt tapering at the diagonal branch, which distributed parallel to the normal left anterior descending (LAD) artery ( Figures 1D and 1E , Videos 1 and 2). There was no significant stenosis at the RCA ( Figure 1F , Video 3). Because there was a Thrombolysis In Myocardial Infarction (TIMI) flow grade 3, and the morphology of the stenosis was consistent with type 2 spontaneous coronary artery dissection (SCAD), coronary intervention was deferred (1) . Moreover, the history of renal artery stenosis (fibromuscular dysplasia) and complete resolution of AV branch lesion were also consistent with SCAD. The ECG change resolved in 2 h ( Figure 1C) , and her clinical course was stable. Repeat CAG 9 months later showed normalized diagonal lesion (Video 4). The de Winter ECG pattern is usually caused by occlusion of the proximal LAD artery (2) . de Winter ECG patterns caused by non-LAD artery lesion have been seldom reported. Montero Cabezas reported a case in which occlusion of the diagonal branch was the cause (3). The diagonal branch was large and distributed parallel to the LAD artery, as in the current case. Another important point learned from this case is that de Winter ECG pattern may reflect 1 frame of a dynamic ECG change, as shown in LVAD outflow obstruction is usually caused by external compression from mediastinal tissue, twisting or kinking of the outflow graft, or accumulation of gelatinous protein matrix or biodebris (1, 2) . The outflow graft may be subject to twisting and kinking, resulting in decreased flow and hemodynamic instability, especially during surgical manipulation, as noted in our case. Multimodality imaging should be considered, including chest radiography and echocardiogram to assess biventricular function and size and cannula flow velocities, and, if results are equivocal, computed tomography angiography to delineate possible mechanical complications of LVAD ( Figure 1D) (3). In our case, pathological examination of the explanted pump revealed fragments of thrombus on the inflow stator region, indicating that our patient had both pump thrombosis and outflow cannula obstruction as causes of the lowflow, high-power alarms. Extra attention during cardiac surgical interventions is needed to avoid outflow cannula mechanical obstruction. To understand the pathophysiology and clinical manifestation of DRESS-associated eosinophilic myocarditis. To review the mechanism of tofacitinib and understand its potential role in treatment of DRESS myocarditis. The patient has a history of acne vulgaris. bars reveal when therapy was stopped and dosing decreased. All 3 times, reintroduction of tofacitinib led to rapid recovery. Due to her continued off-label use, the patient had insurance denial for tofacitinib. She was unable to afford the out-of-pocket cost of therapy, was forced to self-discontinue tofacitinib for 2 weeks, and was readmitted with profound cardiogenic shock requiring inotropes and IABP. A repeat TTE showed Patients with X-linked CGD, gp91 phox deficiency phenotype X91 0 , and without NAPDH oxidase activity in leukocytes had very low levels of circulating oxidative stress markers and very high responses of flow-mediated vasodilation. Superoxide generated by leukocyte NADPH oxidase plays an important role in endothelial function even under a normal condition without cardiovascular risk factors. endothelium-dependent vasodilation in patients with X-linked CGD by increasing oxidative stress. We present flow-mediated vasodilation (FMD) and oxidative stress markers before and after BMT in 2 patients with X-linked CGD who had gp91 phox deficiency phenotype X91 0 . In the following 2 years from the age of 7 years, he had fistulized infections by a fungus in the skin. The number of episodes of infection (e.g., lung, liver, brain, skin, and bone) that required hospitalization was 8 before BMT. Cytochrome b558 protein, gp91phox, NADPH oxidase activity, and superoxide generation in activated leukocytes were totally absent ( Figure 1A ). The mutation in Case 2 was identified as a deletion of the nucleotides TTTGGTACACA-CATCATCT in base 614 in exon 6, resulting in a frameshift and formation of a stop codon ( Figure 1B) . We confirmed that the mutation in Case 2 was de novo in accordance with previous studies (5) and the CYBB gene database. This de novo mutation was localized in the transmembrane region ( Figure 1B) . The phenotype of X-linked CGD was X91 0 . Table 1 . BMT was performed in Cases 1 and 2 as previously described (6) . FMD was measured before and after BMT as described previously (7). Table 2 ). Table 2 ). Endothelial dysfunction is the initial step in the Figure 1C ) and heart block and recovery of sinus rhythm ( Figure 1D ). The present case is unique because the patient was much older than the average age of GCM patients (1). Although GCM is widely reported to affect middleaged adults, the medical literature suggests that this is due to an underdiagnosis, with many patients being diagnosed at autopsy. A U G U S T 2 0 2 0 : 1 4 8 patients may be overlooked if genetic testing or a histological evaluation is not performed. Here, we report a patient who has survived for more than 56 months with medical therapy including key agents that potentially modified the severity of pulmonary vascular disease or lowered pulmonary artery pressure. Table 1 . is surrounded by an adjacent bronchial venule (d, misaligned pulmonary vein) and bronchiole (e). In both images, the capillary bed is diminished, and there is heterogeneous alveolar septal thickening. The lack of homogenous septal thickening demonstrates a milder pattern in this disease process. J A C C : C A S E R E P O R T S V O L . 2 , N O . 1 0 , 2 0 2 0 ª 2 0 2 0 T H E A U T H O R S . P U B L I S H E D B Y E L S E V I E R O N B E H A L F O F T H E A M E R I C A N C O L L E G E O F C A R D I O L O G Y F O U N D A T I O N . T H I S I S A N O P E N A C C E S S A R T I C L E U N D E R T H E C C B Y -N C -N D L I C E N S E ( To recognize chronic lead exposure as one of the causes of cardiomyopathy and myocarditis. To understand that, with early diagnosis and management, there can be a potential improvement in ejection fraction. To understand the spectrum of cardiovascular effects of chronic lead exposure. This temporal association strongly suggested the possibility of direct lead toxicity as the cause of a drop in his cardiac contractility. The exact association between LVEF and lead is unknown. Animal experiments have indicated that the cardiotoxic effects of lead are likely related to its interference with calcium-dependent cellular processes (6) . There is also a suggestion that depressed myocardial contractility may be due to impaired phosphorylation of the myocardial contractile proteins (7). These findings have yet to be confirmed. Finally, BLL is reported to significantly affect LV mass, LV end-diastolic dimension, and relative wall thickness. In a study conducted in Poland, Kasperczyk et al. (4) compared a group of individuals exposed to lead in lead factories with a control group of administrative workers, who were not exposed to lead and found that the LV end-diastolic dimension was 6% higher and there was an 11% increase in LV mass index in the group with lead exposure (4). That study did not eliminate the confounding factor of blood pressure. A study by Schwartz (8) Myocarditis due to lead toxicity is a rare condition. It is a very challenging to diagnose because the possibility of coincidental viral myocarditis cannot be ruled out. Nevertheless, the diagnosis of lead cardiomyopathy was more likely in this patient with no viral prodromes in preceding months, and the temporal association of his BLL with his LV function and LV mass. In a review of the medical literature, 3 other cases of myocarditis due to chronic lead exposure in adults (9,12,13) were found. To the best of these authors' knowledge, this case is the fourth reported case of lead myocarditis and second reported case in an adult male. The development of cardiomyopathy due to chronic lead exposure is most likely secondary to its direct toxic effect on the myocardium. More experimental Based on patient presentation, the differential diag- trials (NCT02643212, NCT03193502) that will study the effects of rivaroxaban in patients with liver cirrhosis. Perhaps these studies will help to establish the patient population with liver cirrhosis and LV thrombus that will benefit from DOACs and the correct drug dosage. Patients with a history of LV thrombus and liver cirrhosis should be treated with warfarin or low- A 75-year-old man with a 20-year history of diabetes underwent percutaneous coronary intervention for angina. Cardiac enzyme levels were elevated, and minor electrocardiographic abnormalities were observed although the patient was asymptomatic during follow-up. We suspected myocardial ischemia and performed coronary computed tomography angiography (CCTA) because the patient was unable to exercise. His vital signs were: blood pressure, 130/ 80 mm Hg; heart rate, 66 beats/min; respiratory rate, 12 breaths/min; and temperature, 36.0 C. Physical examination results were unremarkable. CCTA revealed no significant coronary artery stenosis, but pericardial masses were detected incidentally. We also noted multiple visceral pericardial nodules adjacent to epicardial fat, concurrent with localized pericardial thickening and pericardial and paraphrenic lymph node enlargement ( Figures 1A and 1B) . The patient had a history of diabetes mellitus, dementia, and angina. Differential diagnoses based on cardiac magnetic resonance (CMR) findings include metastatic The pericardium was diffusely reddish. The resected Conversely, nonsteroidal anti-inflammatory drugs plus colchicine is the first-line therapy for chronic pericarditis of idiopathic or viral origin (10) . Whether these drugs show similar beneficial effects on IgG4related pericarditis remains unclear; however, these were not useful in IgG4-related pericarditis according to a case report (5) . The future challenge is to establish site-specific diagnostic and therapeutic methods for IgG4-related pericarditis. J A C C : C A S E R E P O R T S V O L . 2 , N O . 1 0 , 2 0 2 0 ª 2 0 2 0 T H E A U T H O R S . P U B L I S H E D B Y E L S E V I E R O N B E H A L F O F T H E A M E R I C A N C O L L E G E O F C A R D I O L O G Y F O U N D A T I O N . T H I S I S A N O P E N A C C E S S A R T I C L E U N D E R The patient remains symptom-free during the followup examinations. Herein, we describe a case of biopsy-proven early- Abdominal examination exhibited no palpable masses. Distal pulses were 2þ throughout. Past medical history includes only hypertension. An unknown antihypertensive medication was initiated 2 years prior but had elapsed several months ago. Acute-onset, severe chest pain with associated dyspnea is especially concerning for life-threatening conditions including acute coronary syndrome, acute aortic dissection (AoD), pulmonary embolism, tension pneumothorax, esophageal rupture, and cardiac tamponade. Markedly elevated BP at his age raised concern for secondary hypertension. Severe To recognize and adequately triage chest pain representing AoD. To acknowledge a comprehensive diagnostic work-up of secondary hypertension. To distinguish between PCCs and PGLs. To recognize critical pharmacological and surgical strategy in functional PGL-induced AoD. Eventually, BP was controlled, and secondary surgical Chest radiograph demonstrating no acute cardiopulmonary process. Computed tomography of the abdomen-pelvis revealing a 5.8cm left pararenal mass (orange arrow). Computed tomography angiography revealing aortic dissection involving the ascending thoracic aorta (orange arrow). The patient tolerated both procedures very well. Once the PGL was removed, improvement in BP was significant, and he was eventually weaned off all antihypertensive medications. Plasma free metanephrines, drawn 8 weeks post-extraction normalized to 48 pg/ml (reference range, <57 pg/ml). His The patient's medical history included PAD, venous insufficiency with prior venous stent placement, tobacco use (60 pack-year history), COPD, rheumatoid arthritis, and type 2 diabetes. It is unclear if the patient's development of a foot ulcer, worsening LE edema, and progressive dyspnea To present a patient with critical limb ischemia, venous insufficiency, and PH. To discuss the pathophysiology and differential diagnosis in a patient with cor pulmonale. To review the complications of venous stent placement. To discuss management for a high-flow AV fistula. The patient's complete blood cell count and chemistry panels were normal. Renal function was normal, and rheumatologic evaluation was unremarkable. High-flow fistulas often present with a high-output state, and previous case reports have described fistulas between the common iliac artery and ipsilateral vein with similar but varying presentations (2,4). More frequently seen and well-described phenomena are the high-output state and distal hypoperfusion Endovascular therapy is a proven and safe treatment for AV fistulas with high success rates and low rates of complications (7) . AV fistulas are a rare finding; however, fistulas of this size may present with the temporal development of limb ischemia, venous insufficiency, and PH. A U G U S T 2 0 2 0 : 1 5 1 5 -9 A 72-year-old woman presented to her primary care physician with symptoms of coughing and shortness of breath for the past 2 weeks. Heart rate, blood pressure, and respiratory rate were 58 beats/min, 128/75 mm Hg, and 26 breaths/min, respectively. Pulse oximetry done in the office showed 90% oxygen saturation on room air. The patient had a history of hypertension, hyperlipidemia, and alcohol consumption. The patient's presenting symptoms were nonspecific and suggestive of either primary cardiac or pulmonary disease. Initial chest radiograph was performed ( Figure 1 ) and she was admitted to the hospital for further work-up. The patient had an 11-year history of RP and coarctation of the descending thoracic aorta requiring percutaneous stenting 1 year before presentation. He initially presented with nasal and auricular chondritis, inflammatory arthritis, and aortitis. He was started on azathioprine, but it was discontinued due to pancreatitis. He was transitioned to prednisone and methotrexate, which was tapered 3 weeks before presentation. To broaden the differential for etiologies of ST-segment elevation myocardial infarction/ non-ST-segment elevation myocardial infarction. To recognize aortic insufficiency and ostial coronary artery disease as a rare cardiac complication of RP. Fulminant aortitis with involvement of the coronary arteries was our initial concern, as the patient's symptoms coincided with recent taper of immunosuppression, and diagnostic testing (electrocardiography [ECG] and troponin levels) was concerning for coronary ischemia. Aortic dissection, a severe complication of aortitis, was also considered. Vasculitis of the coronary arteries, plaque rupture, spontaneous coronary artery dissection, and coronary artery embolism are in the differential diagnosis for a patient with vasculitis and hypercoagulability. The first 12-lead ECG revealed no significant STsegment changes ( Figure 1A) . One hour later, the patient's chest pain acutely worsened. A repeat ECG revealed diffuse ST-segment depressions ( Figure 1B) . To recognize pulmonary artery sarcomas on imaging and understand their presentation, epidemiology, workup, treatment, and prognosis. To recognize the large spectrum of clinal presentations of Addisonian crisis and prompt diagnosis of this rare but lifethreatening situation. To emphasize the need of a broader etiological study in incessant pericarditis with cardiac tamponade, particularly in younger age. To highlight the role of multidisciplinary and multimodality imaging in management of pericardial diseases. noradrenaline the next day and progressive resolution of the effusion. He had childhood asthma, nonallergic rhinitis, and an idiopathic episcleritis, controlled with topical corticosteroids. One month earlier, he had been admitted to an intensive care unit due to septic shock complicating tonsillitis. A pericardial friction rub in the presence of retrosternal pleuritic chest pain in a young man is highly suggestive of acute pericarditis. However, other diagnoses as myocarditis, pulmonary embolism, pneumoniae, asthma exacerbation, and pneumothorax also should be considered. Streptococcus mitis was isolated in the pericardial fluid and ceftriaxone was initiated. At this point, the echocardiogram showed constrictive-effusive physiology (Figures 2 to 4, Videos 1 and 2) . Although the autoimmunity workup was pendent, the patient was discharged on colchicine 0.5 mg every day (q.d.), The etiologic study performed so far ( Table 1 ) was inconclusive and the patient was discharged with a higher dose of methylprednisolone (32 mg q.d.). Despite the gradual corticosteroid tapering, symptoms recurred whenever the dose was lowered to Further evaluation for autoimmune diseases showed the presence of anti-intrinsic factor autoantibodies and primary hypogonadism was further found. Marinho et al. Echocardiography revealed the following: calcified pericardium that was approximately 11 mm thick; septal bounce; medial and lateral mitral eʹ velocity of 12 and 7 cm/s, respectively; more than 25% variation in mitral inflow velocity with respiratory movements ( Figure 1A) ; a dilated inferior vena cava; and expiratory diastolic flow reversal in hepatic veins ( Figure 1B) . Fluoroscopy revealed dense circumferential pericardial calcification ( Figure 1C , Video 1), and computed tomography demonstrated classic "eggshell" calcification encircling the heart ( Figures 1D and 1E ). Constrictive physiology was further confirmed on cardiac catheterization, which revealed elevated and equalization of all pressures including mean right atrial pressure, pulmonary capillary wedge pressure, right ventricular pressure, and left ventricular end-diastolic pressure (i.e., 30 mm Hg). Biventricular pressure tracings showed a typical "dip-and-plateau" configuration, as well as ventricular discordance ( Figure 1F , white arrow) suggestive of CCP. The initial tracing ( Figure 1F ) also showed ventricular concordance suggestive of underlying myocardial involvement (restrictive physiology) associated with extensive pericardial calcification. Surgical pericardiectomy was performed through a median thoracotomy. The calcified, firmly adherent pericardium was resected from the anterior and left lateral aspect of the heart. The patient had uneventful recovery. Histopathologic examination of resected pericardial tissue revealed extensive fibrosis, hyalinization, and calcification, without any granulomatous or giant cell inflammation. CCP manifests as right-sided heart failure. The dyspnea on exertion results from raised filling pressures, whereas easy fatigability is caused by decreased cardiac output. The most common type of CCP is idiopathic (1), as in the index case, followed by CCP caused by infections, post-cardiac surgery status, radiation therapy. Although mild calcification is common in pericarditis, extensive calcification as seen in the index case is extremely rare in CCP (2). The discomfort completely resolved. Upon arrival to the emergency department, his blood pressure was 117/84 mm Hg, heart rate was 80 beats/ min, respiratory rate was 16/min, and oxygen saturation was 97% on 2 l via nasal cannula. The patient denied chest discomfort or dyspnea, was in no distress, and was lying flat for examination. Neither the ED physician nor cardiologist reported jugular venous distension, murmurs, gallops, or rales. The patient reported gastroesophageal reflux disease, hypertension, diabetes, and hypercholesterolemia. He was taking esomeprazole, ranitidine, metoprolol, metformin, and simvastatin. He had never smoked. Besides transient cardiac ischemia, the differential diagnosis included esophageal disease, B-lines can be detected by a brief POCUS lung examination, are a finding of interstitial pulmonary edema, and have been associated with a worse prognosis in acute coronary syndromes. Detectable by POCUS, "flash" interstitial pulmonary edema can be an early presentation of life-threatening global LV ischemia and occur with minimal or no symptoms. musculoskeletal discomfort, and-unlikelyaortic dissection, pericarditis, or pulmonary embolism. Pocket-sized devices promote convenient ultrasound application as ultrasound stethoscopes, A U G U S T 2 0 2 0 : 1 5 5 3 -7 The scans show the qualitative and quantitative response of cardiac sarcoidosis (CS) to escalating anti-inflammatory therapies. Max SUV liver values show standardization of the background glucose uptake. Max ¼ maximum; SUV ¼ standardized uptake value; other abbreviations as in Figure 1 . The images show gradual improvement and finally complete resolution of cardiac inflammation. Abbreviations as in Figure 1 . A 79-year-old man with a history of recurrent rightsided loculated pleural effusion presented with progressive dyspnea and was found to be in acute heart failure. Two months before admission he underwent video-assisted thoracoscopic surgery with pleural biopsy and mediastinoscopy with lymph node biopsy. Lymph node biopsy revealed a collagenized granu- (Figures 1A and 1B) . On this current presentation to the emergency department, he was afebrile, his heart rate was 96 beats/min, blood pressure was 117/76 mm Hg, and oxygen saturation was 94% on 3 l of oxygen through a To understand the physiology, pathology, and hemodynamics of CP. To recognize IgG4-RD as a possible cause of CP and understand management options. The patient had a pleural effusion that was thought to be related to IgG4-RD, as well as chronic diastolic heart failure. The differential diagnosis included constrictive pericarditis (CP) related to IgG4-RD, CP related to alternative causes (viral, idiopathic), chronic diastolic heart failure, and pulmonary hypertension. A U G U S T 2 0 2 0 : The patient had a history of Miller Fisher syndrome, hypertension, and dyslipidemia. Given the findings of severe central chest pain and ST-segment elevation, the most likely differential To recognize that, in patients presenting with myocardial infarction with nonobstructive coronary arteries, an exhaustive search for the underlying cause should be undertaken, as per the 2019 AHA Scientific Statement. To recognize that early CMR is a key investigation in patients with MINOCA. To be aware that RV microvascular obstruction is a rare complication of RV myocardial infarction and can be misinterpreted as normal myocardium. To recognize that repeat CMR examination in the chronic phase can be helpful in selected high-risk patients in whom initial diagnostic tests have been unsatisfactory. To recognize that comprehensive intracoronary imaging is recommended in cases of suspected MINOCA. diagnosis was ST-segment elevation myocardial infarction (STEMI). Other important differentials considered were myocarditis, pericarditis, pulmonary embolus, and bowel ischemia. Initial high-sensitivity troponin T level was 50 ng/l, which peaked at 1,229 ng/l (normal range <14 ng/l). Cardiac magnetic resonance (CMR) was performed 1 day following the presentation ( Figure 3 ). This revealed normal LV systolic function with no regional wall abnormalities. However, there was marked systolic flattening of the interventricular septum, and the RV was mildly dilated with impaired ejection fraction (EF) (49%) and severe hypokinesia/ akinesia of the mid to apical RV free wall. T2-short tau inversion recovery (STIR) imaging was normal, and there was no late gadolinium enhancement (LGE) to suggest any acute edema or acute MI. In addition, the Mild diffuse disease of the right coronary artery (A to C) and the mild-to-moderate plaque disease in the left coronary system (D to F). Williams et al. MVO is seen following coronary reperfusion in patients who have had significant periods of ischemia. Its appearances on CMR are caused by the inability of gadolinium contrast material to pass through the myocardial microvasculature, as reperfused myocytes become edematous because of osmotic overload and occlude the capillaries (9) . This leads to a focal, welldefined area of absent signal within an area of highsignal infarction or acute ischemia (8) . Myocardium with microvascular obstruction is less likely to regain function and leads to ventricular wall scarring and remodeling when compared with patients who have no microvascular obstruction (10) . The presence of microvascular obstruction is associated with higher rates of cardiovascular events in the first 2 years following an MI and a poorer prognosis. Our final diagnosis was a transmural, nonviable, RV MI. The patient was contacted to explain the diagnosis and was restarted on aspirin 75 mg, clopidogrel 75 mg, and appropriate secondary prevention. The presumed culprit lesion was an ostial RV branch occlusion, which could not be identified on angiography. Subsequent ECGs (Supplemental Figures 1 and 2 ) demonstrated findings consistent with a transmural infarction. The role of antiplatelet therapy in MINOCA is controversial. In our case, we thought that the most likely underlying pathophysiology was an ostial plaque rupture event, and so we decided to treat the patient as a nonreperfused STEMI, as per the 2017 ESC guidelines (11) . A 63-year-old asymptomatic woman with visceral inversion, rheumatoid arthritis, and scleroderma treated with prednisolone 9 mg/day and methotrexate 16 mg/week was admitted for management of an intracardiac mass incidentally found on computed tomography (CT). Although visceral inversion was detected on CT when the patient was in her thirties, the intracardiac mass was not identified at the time. On admission, her blood pressure was 124/75 mm Hg and pulse rate 88 beats/min. Clinical examination revealed no heart murmur. CT revealed a 3-cm low-density mass with mean CT value of -40 HU in the apical anterior wall of the left ventricle; it infiltrated the muscle layer and showed no contrast enhancement ( Figure 1A) . Echocardiography revealed protrusion of a slightly mobile mass into the left ventricular (LV) cavity (Video 1). Although thrombosis after myocardial infarction must be considered for a mass in the LV apex, LV wall motion did not suggest myocardial infarction. 18F-fluoro-deoxyglucose positron emission tomography-CT showed no significant focal uptake in the mass ( Figure 1B) , suggesting low probability of malignancy. Cardiac magnetic resonance imaging (MRI) showed a high intensity on T1-and T2-weighted images with fat suppression without contrast enhancement ( Figure 1C to 1F, Videos 2 and 3). Based on these findings, benign cardiac lipoma was suspected. Owing to the high surgical risk for histological diagnosis and absence of tumor-related symptoms, careful follow-up was planned. Follow-up CT after 6 months showed no change in the size of the mass and no tumor-associated symptoms on follow-up for 9 months. Cardiac lipomas represent 8.4% of primary cardiac tumors (1), most commonly originating in the subendocardium (50%), followed by the myocardium (25%) and subepicardium (25%); typical locations include the right atrium and the left ventricle (1). The degree of symptoms depends on the location and size of the tumors. Notably, cardiac lipoma complicating visceral inversion has never been reported. Visceral inversion is associated with genetic mechanisms but not with the development of cardiac tumors (2) . Despite reports of concurrent development of visceral inversion and digestive system neoplasms, the presence of cardiac lipoma and visceral inversion could be incidental. Accordingly, the clinical manifestation of this case is rare. In conclusion, we report the first case of cardiac lipoma with intramyocardial invasion complicating visceral inversion. Multiple imaging enabled noninvasive differential diagnosis and management of the cardiac tumor. blood cell count (14,600/ml) and serum C-reactive protein (7.9 mg/dl), 3 sets of blood cultures were all negative. He was initially diagnosed with community-acquired pneumonia, which responded well to intravenous ceftriaxone. On hospital day 19, he developed sudden-onset dyspnea; chest radiography revealed bilateral pulmonary congestion ( Figure 1A) . Vital sign measurements showed a blood pressure of 140/81 mm Hg, heart rate of 98 beats/min, and oxygen saturation of 88% (room). Chest auscultation was remarkable for bilateral coarse crackles and a holosystolic murmur (4/6 intensity), maximal at the apex radiating to the axilla. TTE Figures 1B to 1D, Videos 1 and 2) . Although percutaneous valve-in-valve implantation was considered a promising option (1), this procedure is not fully reimbursed for clinical use in Japan. On hospital day 23, after multidisciplinary discussion between the cardiology and cardiothoracic surgery departments, the failed valve was surgically replaced with a 29-mm St. Jude Medical mechanical valve (St. Jude Medical, Inc., St. Paul, Minnesota), which was selected based on several factors: valve durability, re-intervention risks, the need for Bioprosthetic Mitral Valve Failure long-term anticoagulation, and patient preference as per international guidelines (2) . The patient was uneventfully discharged on postoperative day 33. Pathologic examination revealed a slit-like leaflet tear along one side of the stent post with no significant calcification, pannus formation, or valve thrombosis (Figures 1E and 1F) . Histologically, no sutures were detected at the affected side of the stent post, although they were clearly present along the opposite side of the valve ( Figure 1G) . Microscopic examination revealed no significant inflammation, fibrosis, calcification, or myxomatous degeneration that may contribute to a leaflet tear of this nature (3) . Accordingly, we concluded that the missing sutures most likely played a pivotal role in promoting acute prosthetic valve dysfunction, although we do not know whether the sutures were absent initially or became unfastened over the years of image the propagation of regional myocardial contraction in both ventricles (1, 2) . Recently, the authors developed an activation imaging system that can visualize images integrating both ventricular contractions. Then, they used the modality in assessing the effect of CRT in a patient with ACHD. A 24-year-old man with tetralogy of Fallot had a history of intracardiac repair that was performed when he was 3 years of age and elimination of remaining right ventricular (RV) outflow obstruction that was performed when he was 8 years of age. During the second operation with a monocusp transannular patch, the complete atrioventricular block was caused, and epicardial DDD pacemaker implantation was performed, and the RV lead was located at RV outflow (Supplemental Figure 1 ). When he was 21 years old, he presented with left ventricular (LV) systolic dysfunction with 28% LV ejection fraction (EF) and was treated with enalapril and carvedilol, which could not improve LV systolic function. Also, severe pulmonary regurgitation PR was concomitant. Because magnetic resonance imaging was not available due to the magnetic resonance imaging nonconditional pacemaker, 3D-STE was used in assessing both ventricular functions and revealed that LVEF was 30% and RVEF was 42%. Besides, the activation imaging system allowed us to visualize the intraventricular and interventricular dyssynchrony ( Figure 1, Videos 1, 2, 3, and 4) . Despite the presence of severe pulmonary regurgitation, it was apparent that his critical issue was LV dysfunction caused by pacemaker-induced LV dyssynchrony. Then, CRT was performed when he was 22 years old, and intraventricular and interventricular dyssynchrony was dramatically resynchronized (Figure 1) . At 1 year after CRT, LV reverse remodeling was obtained (LV end-systolic volume, 113 to 90 ml, 20% reduction, LVEF 30% to 42%). In contrast, despite RV resynchronization, RVEF was reduced from 42% to 38%. The residual significant pulmonary insufficiency may be related to the nonresponded RV function after CRT. Because of the large variability of electromechanical sequences with very different structures, patients with ACHD require tailor-made therapy for each case. The integrated activation imaging of both ventricles may be helpful in assessing the pathophysiology and be a guide for a strategy using cardiac implantable electronic devices in patients with ACHD. In the present case, we used the 3D-STE, which is derived from the cubic pattern-matching technology using the cube-shaped template in a 3D echocardiography volume dataset (3). 3D-STE is better than 2-dimensional (2D)-STE in the following points. First, 3D-STE is not affected by the 3D movement of the heart. In the setting of 2D echocardiography, the heart moves through the 2D plane of interest, and, in fact, different myocardium appear in the 2D image frame by frame (4). This is called "through plane or out of the plane phenomenon." Second, for RV, 2D assessment has drawbacks related to the intrinsic complexity in its anatomy and deformation pattern. As a result, this may cause no negligible effects on the accuracy of tissue tracking in 2D images. In contrast, 3D full-volume LV and RV data overcome the limitation of the plane-dependency of the 2D image (5). We presented this case with the development of pacemaker-induced dyssynchrony in congenital heart disease, which is a critical sequela in ACHD care with the previous implantation of a pacemaker at childhood. The initial pacemaker ventricular lead was on the RV outflow region, which is an uncommon site for epicardial pacing. According to the multicenter study by Janou sek et al. (6) , epicardial pacing lead site is rarely at RV outflow tract (n ¼ 8 of 178; 5%), and they concluded that the pacing from the RV outflow tract/lateral RV was related to significantly decreased LV function. AMTV is a rare congenital anomaly consisting of an endocardial cushion that typically arises from the anterior mitral leaflet and often a cause of LVOT obstruction. Patients with AMVT may have an asymptomatic murmur or present with chest pain, palpitations related to arrhythmia, congestive heart failure, cerebrovascular events, fatigue, or syncope. Echocardiography is pivotal for diagnosis and follow-up. Surgical resection is recommended in symptomatic patients and patients with significant LVOT obstruction. the gradient with a Valsalva maneuver. There was no prior TTE for comparison. He had a history of hypertension and left bundle branch block that was seen on prior electrocardiograms. He had no prior workup for his left bundle branch block. Identification of a mobile structure in the LVOT raises concerns for vegetation, subaortic membrane, redundant mitral valve chordae, primary or secondary cardiac tumors, and accessory mitral valve tissue (AcMVT). Because his TTE was nondiagnostic, transesophageal echocardiography (TEE) was pursued to better define the ill-defined structure in the LVOT. On the standard mid-esophageal 4-chamber TEE view there was a parachute-like subaortic structure prolapsing into the LVOT, consistent with an AcMVT (Videos 1 and 2) . As the aortic valve opened, the parachute-like structure was noted to prolapse in a "peek-a-boo" manner to- (Figures 2 to 5) . His perioperative period was uncomplicated, and he was discharged to cardiac rehabilitation on goal-directed heart failure therapy for his depressed left ventricular ejection fraction. AcMVT is a rare congenital anomaly of the endocardial cushion that typically arises from the anterior mitral Surgical resection is recommended for patients with a significant LVOT obstruction mean gradient of >25 mm Hg and for those undergoing cardiac surgery for other cardiac pathology (6) . There are no clear guidelines for management of asymptomatic patients (7) . At his 2 weeks follow-up, this patient was completely asymptomatic. Repeated TTE 1 month after surgery showed resolution of LVOT obstruction but We describe a rare case of SAM associated with severe mitral regurgitation (MR) complicating the early post-operative period after treatment of type A Precise and prompt recognition of this potentially lethal association is vital to provide adequate clinical and interventional management. MitraClip can be an effective and lifesaving alternative to manage SAM associated with severe MR in patients with high surgical risk or a contraindication to conventional cardiac surgery. acute aortic dissection (AAD), which was successfully managed with a MitraClip intervention. A 64-year-old man was admitted to the emergency department with a sudden onset of retrosternal discomfort radiating to the back and superior abdomen associated with weakness in the right arm. On emergency department arrival, vital signs were as follows: noninvasive blood pressure 134/100 mm Hg, heart rate 86 beats/min, oxygen saturation level 98%, Glasgow Coma Scale score 15. The right lower limb was colder than the left, and he had no palpable pulse. His showed mild to moderate AV regurgitation, mild MR, and posterior leaflet prolapse. The chest radiograph showed mediastinal widening, the electrocardiogram was normal, and chest computed tomography revealed a Stanford type A AAD involving the entire ascending, descending, and abdominal aorta, with no pericardial or pleural effusion. A transesophageal echocardiogram (TEE) showed a tricuspid AV with moderate regurgitation, moderate MR, and nonsignificant SAM ( Figures 1A and 1B, Video 1) . Left ventricular ejection fraction was 60%. This case shows that, in selected patients, Mitra-Clip use can be a feasible alternative to address refractory MR and SAM, with excellent safety profile and hemodynamic outcomes. Doppler imaging ( Figure 1E ). Pulsed wave Doppler imaging of mitral inflow revealed a short E-wave deceleration time and DMR after the E-wave ( Figure 1F) . DMR is not a common phenomenon. For it to occur, 1 of 2 conditions must be present. First, DMR occurs whenever there is a reversal of the atrioventricular pressure gradient, as in severe AR (1) or dilated cardiomyopathy (2). Second, DMR results from the absence or delay of effective LV contraction essential to mitral valve closure, as in atrioventricular block (3) and atrial tachyarrhythmias (2) . Acute AR is classically associated with end-DMR (1). In our patient, DMR was observed in mid-diastole, immediately after the E-wave. This finding suggests that DMR was generated directly by overshoot backward aortic flow to the left atrium, instead of the very typical high diastolic LV pressure. Mid-DMR in atrioventricular block is reported (2) . It is believed that DMR is not hemodynamically significant. In addition, because of its relatively low velocity, DMR may be difficult to diagnose noninvasively (2) . imagers, however, have not universally adopted this schema, despite the fact that recent guidelines (2) do recommend the use of this system to classify the causes of AR. Accordingly, the purpose of this series was to encourage imagers to assess the cause of AR as they do MR by using the Carpentier classification system ( Table 1) . A 38-year-old man with a history of poorly controlled hypertension, end-stage renal disease on dialysis, and pulmonary embolism taking warfarin therapy was admitted with congestive heart failure. Transthoracic echocardiography (TTE) performed on hospitalization day 3 showed moderate concentric left ventricular (LV) hypertrophy with an LV ejection fraction (LVEF) of 35%. There was moderate to severe AR with normal leaflet morphology (Figure 1, far left) . To recognize the importance of measuring the ventriculoaortic junction, sinus of Valsalva, and sinotubular junction in every patient with significant AR. To be able to use the Carpentier classification system to stipulate the cause of AR. To appreciate the value of 3D echocardiography in the assessment of the cause of AR. ventriculoaortic junction (VAJ) were normal in size ( Figures 1A and 1B, Video 1) . The sinotubular junction (SJ) was enlarged and effaced with dilation of the ascending aorta (AAo) (Figures 1A and 1B) and central AR ( Figures 1C and 1D) . Given the normal aortic cusp motion and the presence of SJ and AAo dilation, this patient's AR was classified as Type Ia. Figures 4C and 4D, blue arrows, Video 3) . This was seen on the 2-dimensional (2D) mid-esophageal short-axis view of the AV (Figures 4E and 4F , blue arrow), on the 3D narrow-angle imaging captured in end-systole ( Figure 4G , blue arrow), and on 3D color Doppler imaging, also captured in end-systole ( Figure 4H , blue arrow). Figure 5D ). The predominant cause of AR was right coronary cusp prolapse (Type II) with associated Type I disease. CASE 6. A 67-year-old healthy man with asymptomatic chronic moderate AR was being followed on a regular basis until he developed a drop in LVEF on TTE. A TEE was ordered to better assess AR severity. The TEE revealed Type III severe AR ( Figure 6 , far left). The SoV was mildly dilated. The SJ and VAJ were normal in size ( Figure 6A ). The AAo was 42 mm (mildly dilated). The AV leaflets were thickened and restricted on 2D imaging ( Figure 6B ), resulting in malcoaptation and AR ( Figure 6C ). The leaflet thickening and restriction was clearly observed on the 3D narrow-angle image taken in end-diastole ( Figure 6D ). color Doppler from the aortic perspective ( Figure 6G ). All 3D narrow-angle datasets ( Figures 6D to 6F , A U G U S T 2 0 2 0 : 1 5 8 9 -9 4 Mechanisms of Aortic Regurgitation translucent and were seen in their entirety on 3D imaging due to the abnormal thickening. A 3D color Doppler confirmed the fact that the origin of the AR was the area of malcoaptation ( Figure 6G) , which seems to be in the middle of all 3 leaflets. The AV is part of the aortic root ( Figure 7) . The VAJ forms the basal attachment of the AV cusps and denotes the aortic annulus. The SJ forms the proximal A 62-year-old woman with hypertension and advanced multiple sclerosis developed substernal chest pain 4 days before her presentation, associated Her COVID-19 test done in the ED returned negative. The cardiovascular community has made significant progress toward reducing cardiovascular morbidity and mortality in the past decades (5) . The fear of contracting COVID-19 infection, although justified, will likely result in an increase in non-COVID morbidity and mortality caused by avoidance of the medical system. A significant increase in 911 calls and cardiac arrest at home was noted in areas highly affected by COVID-19 (6) . We suspect many of these deaths are related to untreated cardiovascular emergencies, as illustrated by our 2 cases. The total effect will be difficult to measure until after the pandemic, but in the meantime, it is imperative to educate the public and develop systems of care that minimize delays and maintain high quality. Rapid testing and wider availability of personal protective equipment may facilitate achievement of these goals. Patient-based anxiety and concerns of contracting COVID-19 in the hospital is delaying as well as decreasing the timely presentation and interventions for emergencies such as ST-segment elevation myocardial infarction. Delayed presentations of ST-segment elevation myocardial infarction such as a ventricular septal rupture is a very rare presenting encounter, but in the current era of the COVID-19 pandemic, the incidence of this catastrophic complication as a delayed presenting complaint may increase. 7 days before admission, which resolved after he stopped. He was reluctant to visit the hospital and getting exposed to the ongoing viral pandemic, hence stayed at home, and the pain abated on its own. Family history was also remarkable for heart disease in both parents in their 50s. Differential diagnosis incudes ST-segment elevation myocardial infarction (STEMI), takotsubo cardiomyopathy, acute pericarditis/myocarditis, hyperkalemia, pulmonary embolism, and Prinzmetal's angina. Repeat ECG revealed persistence of ST-segment elevation with Q waves in leads II, III, and aVF. Complete blood count and basic metabolic panel were unremarkable. N-terminal pro-B-type natriuretic peptide was elevated to 3,231 pg/ml (normal <125 pg/ml). Creatine kinase and creatine kinasemyocardial band fractions were within normal limits, and troponin T was elevated to 1.2 ng/ml (normal 0 to 0.029 ng/ml) and trended downward on repeat testing. Coronavirus testing via nasopharyngeal swab was negative. Left heart catheterization revealed a completely occluded right coronary artery (RCA) at the midsegment (Video 1). Because no antiplatelet agents were administered before the catheterization, the patient was maintained on a bivalirudin drip. The RCA lesion was difficult to cross because the lesion appeared hard and fibrotic, but eventually, the lesion was hemodynamically stable with no hypotension, chest pain, arrhythmias, or heart block. The electrocardiogram on presentation shows ST-segment elevation in leads II, III, and aVF with small Q waves. Table 1) . The case was concluded, the PA catheter was VSR is a devastating complication following acute MI, and its incidence has decreased from 1% to 3% following STEMI in the pre-reperfusion era to 0.17% to 0.31% following primary percutaneous coronary (6). The patient was transferred to the cardiac intensive care unit, and an intra-aortic balloon pump was . At first contact, his blood pressure was 85/ 50 mm Hg, and his heart rate 100 beats/min. Examinations of his heart and lungs were unremarkable. The patient had no cardiovascular risk factors, no individual history, and no family history of cardiovascular disease, and was not taking any medications or drugs. No other diagnosis was possible, as the presentation was clearly an ST-segment elevation myocardial infarction (STEMI). COVID-19 may contribute to delayed presentations of acute myocardial infarction. Delayed presentation with late reperfusion is associated with an increased risk of LVFWR. When a high suspicion arises for an impending LVFWR in a patient recovering from extensive anterolateral transmural myocardial infarction, an early diagnosis and surgical repair initiated promptly can make a substantial difference in the outcome of this sometimes fatal complication. The first contact electrocardiogram (ECG) was indicative of an extensive anterolateral STEMI ( Figure 1A) , therefore the patient was brought to the hospital to perform a primary percutaneous coronary intervention (PCI). Pertinent laboratory findings on admission and in the next 4 days are shown on Table 1 . Figure 3A ) and the remaining coronary arteries were normal. Primary PCI was performed. After manual thrombectomy, a stent was implanted at the LAD ostium with good final result ( Figure 3B , Video 2). After PCI, the patient became asymptomatic. He remained asymptomatic, hemodynamically stable, with normal blood pressure and regular heart rate for the next 4 days, Anzai et al. (7) found C-reactive protein levels >20 mg/dl to be an independent predictor of cardiac rupture after the first STEMI (7). Pieck et al. (8) evaluated the levels of neutrophil and lymphocyte, 2 independent markers of inflammation, and showed that STEMI patients with LVFWR had increased N/L ratios. The use of these inflammatory markers has been proposed for predicting postinfarction LVFWR (8) . Thus, STEMI patients with a disproportionate elevation of C-reactive protein levels >20 mg/dl and/or an elevated N/L ratio >3.7 should be followed more closely in terms of mechanical complications. In the present patient, the suspicion of impending LVFWR was reinforced by the angiographic presence of a The suspicion of LVFWR was finally confirmed by cardiac CT that detected an intramyocardial dissecting hematoma (2) . In a percentage of STEMI patients, LVFWR does not occur as a sudden, explosive, and fatal episode but as an insidious, progressive entity. This "subacute" rupture, classified as an "oozing" type, is characterized by a small rupture or leakage through a friable aneurysm that may leak blood into the LV wall creating a subepicardial hematoma before massive rupture ensues (3) . In this particular subgroup of patients, when diagnosis is suspected, surgical treatment is possible and must be initiated promptly to be lifesaving (3) . In this patient, in whom the impending LVFWR was diagnosed on day 5 but To recognize the re-emergence of rare complications of MI delayed presentation and management during the COVID-19 pandemic. To acknowledge patient fears of acquiring SARS CoV-2 infection and subsequent delay in seeking timely medical care for MI. and 2). Although the present authors were able to wire past the lesion, balloon angioplasty was unsuccessful due to extensive thrombus burden. An intra-aortic balloon pump was inserted, and he was The incidence of MI-related complications increases with delayed presentation and management (7) . In addition to the common sequalae of MI (i.e., arrhythmia and heart failure), rare complications such as papillary muscle rupture, ventricular septal rupture, and pericarditis can develop from delayed management (8) . Streptokinase trials from the early 1990s revealed that the incidence of early post- On presentation to the hospital, he was found to be in respiratory distress. The patient had a history of hypertension and was taking lisinopril, 20 mg daily, and hydrochlorothiazide, 12.5 mg daily. He had a 40-pack-year smoking history. He worked in different restaurants and had exposure to a large number of people. The differential diagnosis included the following: acute coronary syndrome; an infectious or inflammatory process, including coronavirus disease-2019 (COVID-19); acute respiratory distress syndrome; and pulmonary embolism. In the COVID-19 era, vigilance for timely diagnosis, isolation, and treatment of COVID-19 patients is imperative. However, fear should not deter us from recognizing common disorders. The chest radiograph showed diffuse patchy airspace opacities throughout the lungs (Figure 1) . Arterial The electrocardiogram at presentation shows sinus tachycardia and a left bundle branch block. The previous electrocardiogram shows normal sinus rhythm and an incomplete right bundle branch block. Recently, the neurology community released a plea to the public not to ignore symptoms of a stroke. We also send out a plea to the cardiology community to do the same and to be vigilant about the common cardiac-related diagnosis that we may mislabel in the COVID-19 era. Because the patient had completed the LAD artery infarct (Figure 8) , the decision was made against LAD artery revascularization. The patient was taken to the operating room, an Impella 5.5 device (Abiomed, Danvers, Massachusetts) was placed through the axillary artery, and the patient was weaned from ECMO successfully. Currently, he remains in the intensive care unit and is recuperating from an arduous journey to be able to be considered for options of potential revascularization (after proven viability) or LV assist device placement (if he cannot be weaned from the Impella device) versus cardiac recovery (if he is able to be weaned from the Impella device successfully). We have presented the case of a 56-year-old man with risk factors for coronary artery disease who presented with STEMI. In the COIVD-19 era, the diagnosis was diverted toward COVID-19, and STEMI was missed. Echocardiographic still image of an apical 2-chamber view with contrast. The dramatic presentation of acute MI in these patients, as well as the permanent sequelae they will carry along, might have been reduced by an earlier referral to emergency medical services (EMS The patient had hypertension, dyslipidemia, and coronary artery disease (CAD) with prior PCI with stents to the right coronary artery (RCA) in 2002. The differential diagnosis includes inferior myocar- Right heart catheterization demonstrated a mean pulmonary capillary wedge pressure of 28 mm Hg associated with significant "v" waves ( Figure 5) Given concern for hypoxia, fevers, and cough, the (Figures 3 and 4) . The incidence of papillary muscle rupture has decreased dramatically following the widespread The patient had a history of hyperlipidemia, prediabetes, gout, and well-controlled hypertension. Given the patient's severe respiratory distress, electrocardiographic abnormalities, and his occupa- To diagnose ruptured papillary muscle in the cardiac catheterization laboratory. To understand the pathophysiology of acute MR and understand noninvasive and invasive therapies for stabilization of hemodynamics. The chest radiogram showed a diffuse interstitial abnormality suggestive of pulmonary edema ( Figure 2 Another option for hemodynamic support is the TandemHeart (LivaNova, London, United Kingdom) left ventricular assist device that serves to decompress the left atrium and left ventricle and improve The arrow shows the occlusion. AMI complicated by acute severe MR portends a very poor prognosis with in-hospital mortality approaching 70% when surgery is not performed (7) . Although an initial computed tomographic scan of the head following cardiac catheterization laboratory resuscitation did not reveal ischemic brain injury, Twitter: @AurasAtreya. To understand the potential scope and adverse outcomes of late MI presentations during the pandemic due to fear of contracting infection. To institute public awareness and education regarding the potential hazards of delayed presentation with concerning symptoms of MI. cases who are too petrified to come to the emergency department? New Jersey is the second most affected state in the The patient developed a ventricular septal rupture and complications, and death. Another very concerning aspect of our experience was that these cases were not due to patients being unable to recognize their symptoms but rather, that they were often ignoring their symptoms in the hope they would resolve, thereby avoiding any potential health care exposure risk. Although the concern of contracting SARS-CoV-2 is real for both patients and health care workers, it is important that it not be a deterrent in providing optimal treatments known to improve outcomes. Our experience demonstrates the consequences of delaying seeking medical care for patients with acute coronary syndrome. As we start to experience a second surge of the COVID-19 pandemic in the United States, it is crucial to educate the public that even during this pandemic, we continue to use the necessary measures needed to minimize exposure to SARS-CoV-2 and to therefore not disregard symptoms out of fear but rather seek prompt medical attention. Now listen, you who say, "Today or tomorrow we will go to this or that city, spend a year there, carry on business and make money." Why, you do not even know what will happen tomorrow. What is your life? You are a mist that appears for a little while and then vanishes. Instead, you ought to say, "If it is the Lord's will, we will live and do this or that" (1). "Back to the Future" for STEMI? The COVID-19 Experience pandemic (8, 9) . Furthermore, door-to-balloon and transfer in (door-to-door-to-balloon) STEMI times for primary PCI were also prolonged due to extensive safety precautions required to protect physicians and hospital staff and limit infectious exposure (10,11). Concern over COVID-19 cardiac involvement testing coupled with concern by clinicians for infectious exposure prompted calls for thrombolytic therapy ("no touch approach") even in PCI-capable centers, despite established data that primary PCI reduced mortality associated with STEMI compared to thrombolytic therapy and current societal guidelines supporting primary PCI as the standard of care for STEMI (10, 16 Overall, we find that this challenging case was well managed by our colleagues and congratulate them for suspecting false positive cTn results before proceeding to additional investigation or interventions. Although we agree that the patient did not have an NSTEMI, hAb interference can only be considered AMA Prior Authorization (PA) Physician Survey Association of prior authorization and out-of-pocket costs with patient access to PCSK9 inhibitor therapy What does it cost physician practices to interact with health insurance plans? Putting patients first by reducing administrative tasks in health care: a position paper of the American College of Physicians Prior authorization reform for better patient care Senate Bill 129 Insurer denied needed medical tests, senate finds. 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The authors have reported that they have no relationships relevant to the contents of this paper to disclose.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, A, Liden H, Johnsson P, Hartford M, Rådegran K. Surgical repair of post Elevated pulmonary capillary wedge pressure (PCWP) with prominent "v" waves. 9