Case Presentation: A 59-year-old female with a history of hypertension was brought to a local hospital after being found unresponsive at home. Computed tomography angiography (CTA) of the chest showed type A aortic dissection (TAAD) with maximal aortic dimension of 9.0 cm. She was transferred to our center for escalation of care. She had poor neurological status but stable hemodynamic status, without malperfusion or acute cerebrovascular accident. Lab studies showed severely elevated thyroid-stimulating hormone of 80.4 mIU/ML and free thyroxine 4 (T4) less than 0.2 ng/dL, indicating severe hypothyroidism consistent with myxedema coma. Due to her low functional baseline status, surgical repair was deferred. Anti-impulse therapy was initiated with short acting beta blocker and calcium channel blocker infusion to maintain control of heart rate (HR) and blood pressure (BP). Her clinical course was complicated by pulseless electrical arrest and acute renal failure. After 100 mcg of intravenous levothyroxine, she was extubated and regained renal function. After 40 days, she was discharged to an acute rehabilitation center. 6 weeks later, she showed marked improvement in her frailty index, and medications were optimized. She underwent elective aortic repair, coronary bypass surgery, and was discharged to home. Discussion: Due to the patient’s initial neurological status, repair of her TAAD with aneurysmal degeneration was deferred. She was later diagnosed with myxedema coma and her TAAD was deemed chronic rather than acute . Surgical repair of both acute and chronic TAAD remains the gold standard; however, medical therapy with strict control of HR and BP parameters may stabilize the patient for future surgical repair. 1,2 In this case, by treating the patient’s underlying hypothyroidism and managing risk factors, her surgical risk was reduced, and she underwent successful aortic repair, reporting drastically improved functional status and quality of life.

Mrs. Z is a 56-year-old woman with a long history of symptomatic paroxysmal supraventricular tachycardia (PSVT) who presented with neck and back pain. MRI of cervical and thoracic spine revealed an abnormal signal in the right mediastinal area. A chest CT demonstrated a lobulated 5.8 x 5.5 x 3.5 cm, fluid density lesion contiguous with the pericardium adjacent to right atrium (RA) and inferior venacava (IVC) without wall thickening or solid components, consistent with a pericardial cyst (PC). A transthoracic echo (Panel B) revealed normal left ventricular size and systolic function with an EF of 66%. An echolucency adjacent to the RA and IVC consistent with a pericardial cyst was noted without any extrinsic compression. Given her asymptomatic presentation and normal cardiac imaging, a shared decision was made to conservatively manage.Two years ago, she underwent ablation for AVNRT, followed by an ablation for atrial tachycardia (AT). She continues to have short, symptomatic runs of AT ( Panel A ). A recent CMR re-demonstrated a large, septated pericardial cyst (6.2 x 5 cm) abutting the RA and IVC ( Panel C ). Given her on-going symptomatic SVT, she is referred for robotically assisted thoracoscopic surgery despite stability in size. Discussion: PCs are rare but typically benign. They are the third most common and account for 6% of mediastinal masses. They can be congenital or acquired, simple or complex, and have a predilection for R costophrenic angle (50-70%) followed by the L costophrenic angle (28-38%). Although most are asymptomatic and diagnosed incidentally, they sometimes can result in symptoms such as chest pain, dyspnea, and paroxysmal tachyarrhythmias. Large PCs can lead to tamponade. If a PC is suspected by CXR or echo, cardiac CT or CMR are used for confirmation. Periodic imaging is recommended every 1-2 yr. Most PCs resolve spontaneously. Treatment options include aspiration or surgical resection. Minimally invasive surgical options appear to be the best.

Background To date, few risk models have been validated to predict recurrent atrial fibrillation (AF) >1 year after ablation. The SCALE-CryoAF score was previously derived to predict very late return of AF (VLRAF) >1 year following cryoballoon ablation (CBA), with strong predictive ability. In this study, we aim to validate the SCALE-CryoAF score for VLRAF after CBA in a novel patient cohort. Methods Retrospective analysis of a prospectively maintained single-center database was performed. Inclusion criteria were pulmonary vein isolation using CBA 2017-2020. Exclusion criteria included prior ablation, <1-year follow-up, lack of pre-CBA echocardiogram, additional ablation lesion sets, and documented AF recurrence 90–365 days post-CBA. The area under the curve (AUC) of SCALE-CryoAF was compared to the derivation value and other established risk models. Results Among 469 CBA performed, 241 (61% male, 62.8 ±11.7 years old) cases were included in analysis. There were 37 (15.4%) patients who developed VLRAF. Patients with VLRAF had a higher SCALE-CryoAF score (VLRAF 5.4 ± 2.7; no VLRAF 3.1 ± 2.9; p <0.001). SCALE-CryoAF was linearly associated with VLRAF (y=14.35x-11.72, R 2 =0.99), and a score > 5 had a 32.7% risk of VLRAF. The SCALE-CryoAF risk model predicted VLRAF with an AUC of 0.74, which was similar to the derivation value (AUC derivation : 0.73) and statistically superior to MB-LATER, CHA2DS2-VASc, and CHADS 2 scores. Conclusions The current analysis validates the ability of SCALE-CryoAF to predict VLRAF after CBA in a novel patient cohort. Patients with a high SCALE-CryoAF score should be monitored closely for recurrent AF >1 year following CBA. Graphical abstract

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