ABSTRACT Vasospastic angina can cause myocardial infarction and malignant ventricular arrhythmias, but a persistent coronary occlusion in a patient with established vasospasm creates an acute diagnostic and procedural dilemma. A man with recurrent troponin‐positive presentations and prior non‐obstructive coronary angiography developed 99% mid‐left anterior descending artery narrowing in 2024 that markedly regressed after intracoronary nitrate; ergonovine provocation was subsequently positive. In April 2026, at age 42, he presented with anterior ST‐segment elevation myocardial infarction after irregular use of vasodilator therapy. Angiography showed total occlusion of the left anterior descending artery at the previously nitrate‐responsive segment. Intracoronary nitrate did not restore flow, and ventricular fibrillation occurred during the procedure. Bailout drug‐eluting stent implantation restored flow. A proximal right coronary artery occlusion was also identified during the same procedure and treated with stenting. In June 2026, angiographically confirmed stent thrombosis required repeat percutaneous coronary intervention; an implantable cardioverter‐defibrillator was subsequently implanted after multidisciplinary review. This case highlights the need to consider superimposed thrombotic or structural mechanisms when coronary occlusion in a patient with established vasospastic angina does not resolve after intracoronary nitrate. Bailout revascularization may be necessary when flow cannot be restored in a hemodynamically unstable patient, but it does not eliminate the underlying vasomotor disorder.
ABSTRACT Coronary obstruction is a rare but catastrophic complication of transcatheter aortic valve implantation (TAVI) associated with high mortality. While acute and delayed presentations have distinct pathophysiological mechanisms, their occurrence in the same patient is exceedingly rare. We present a unique case of a 91‐year‐old female who developed acute left main coronary artery (LMCA) obstruction immediately following native TAVI using a balloon‐expandable valve, which was successfully treated with bail‐out percutaneous coronary intervention (PCI). Three months later (> 60 days, classified as “Very Late” coronary obstruction), she presented with severe angina and heart failure. Intravascular ultrasound (IVUS) revealed extrinsic compression of the previously implanted coronary stent caused by a localized aortic wall hematoma. A repeat PCI with a stent‐in‐stent technique restored coronary flow, leading to complete clinical recovery. This case expands the known mechanical spectrum of very late coronary obstruction according to recent classification frameworks and highlights the vital role of intravascular imaging and multimodality assessment in diagnosis and management.
ABSTRACT RotaWire delivery can be challenging in severely calcified device‐uncrossable coronary lesions when conventional wire exchange through a microcatheter is not feasible. We report a 76‐year‐old man with a severely calcified mid‐left anterior descending coronary artery (LAD) lesion in which neither a microcatheter nor a 0.75 mm balloon could cross. A second channel was created using a penetration wire through a dual‐lumen microcatheter, allowing direct RotaWire crossing. However, the RotaWire could not be advanced sufficiently into the distal LAD. After intentional proximal pullback of the dual‐lumen microcatheter, the microcatheter and RotaWire were held together and advanced as a single unit, enabling adequate distal RotaWire positioning and successful rotational atherectomy. This case highlights a distinct challenge after successful direct RotaWire crossing and demonstrates coupled advancement with a dual‐lumen microcatheter as a potential bailout technique when distal RotaWire advancement remains difficult.
ABSTRACT Background Left ventricular outflow tract obstruction (LVOTO) is a rare but potentially life‐threatening complication of transcatheter mitral valve replacement (TMVR). Mitral valve‐in‐valve procedures are generally associated with a lower risk of LVOTO because of the predictable geometry provided by the surgical bioprosthesis, yet severe obstruction may still occur and precipitate abrupt hemodynamic collapse. Case A 79‐year‐old woman with a degenerated 27‐mm Carpentier‐Edwards Perimount mitral bioprosthesis presented with acute decompensated heart failure due to severe bioprosthetic mitral stenosis. Following multidisciplinary Heart Team evaluation, she was considered not a candidate for redo mitral valve surgery and underwent urgent transseptal valve‐in‐valve TMVR with a 26‐mm balloon‐expandable SAPIEN valve. Intervention Immediately after valve deployment, severe LVOTO developed, with an invasive peak‐to‐peak LV‐aortic gradient of 120 mmHg. A mechanism‐guided percutaneous rescue strategy was undertaken. Correction of the structural component of obstruction reduced the gradient to 60 mmHg. Persistent obstruction suggested a significant dynamic contribution, prompting selective septal branch coil embolization, which further reduced the gradient to 20 mmHg and resulted in immediate hemodynamic stabilization. Conclusion Severe LVOTO after valve‐in‐valve TMVR may reflect both structural and dynamic mechanisms. Persistence of significant obstruction after structural correction should prompt consideration of a dynamic component and may guide effective rescue therapy.
