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Case Presentation 69-year-old male with chronic HFrEF and VHD secondary to infective endocarditis in 1981; severe AR with SAVR in 2016 (Bioprosthetic Edwards Perimount size #25) who presented with worsening shortness of breath. Initial assessment with hypotension and crescendo-decrescendo holosystolic murmur (Grade V/VI). Shortly after admission, he had one episode of pulseless monomorphic VT. Laboratory showed NT Pro-BNP at 2,780 pg/mL. TTE: LVEF of 25% and severe AS (peak gradient 75 mmHg, mean gradient 47 mmHg, and dimensionless valve index: 0.16 cm/m 2 ) (A). TEE confirmed severity of AS caused by prosthetic valve thickening and calcification (B-C). A post-SAVR TTE in 2017 showed normal EF and valve gradients. Right heart catheterization was significant for a peak gradient: 61 mmHg, mean gradient: 45 mmHg, and aortic valve area of 0.59 cm 2 . After multidisciplinary evaluation our patient underwent a valve-in-valve (ViV) TAVR (Evolut Pro Plus prosthetic valve, size #29) and ICD implantation for secondary prevention. Post-procedure TTE showed normal bioprosthetic valve function with dimensionless valve index of 0.4 cm/m 2 . Rest of hospital stay was uneventful with rapid resolution of symptoms Discussion Prosthetic valve restenosis is a common complication of aortic valve repair but this is expected to develop at around 10-15 years following implant, early bioprostetic valve dysfunction is commonly related to valve thrombosis, in this case a TEE and pre-operative CT failed to showed findings of thrombosis. Patient was deemed high risk for a repeat SAVR based on comorbidities and hemodynamic instability at presentation (STS risk stratification: 7.4% risk of mortality). A ViV TAVR was considered as a viable option, with a pre-procedural gated CTA showing favorable valve morphology (D)

Wellens' syndrome is a pattern of electrocardiographic T-wave changes that is associated with critical left anterior descending artery (LAD) stenosis. This syndrome continues to be under-recognized by clinicians and carries a significant risk of mortality if not intervened timely. We describe the case of an elderly Chinese woman who initially presented to the outpatient clinic with atypical chest pain. A routine EKG obtained in the office was documented as non-ischemic and was sent for a dobutamine stress echocardiogram. Pretest two-dimensional (2D) echocardiogram demonstrated akinesis and aneurysmal deformity of the entire apical myocardium and upon review of the previous EKG, Type 1 Wellens' sign was noted prompting emergent coronary angiogram, which revealed critical LAD stenosis (99%). She underwent successful percutaneous coronary intervention (PCI) with drug-eluting stents.

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