Spontaneous coronary artery dissection (SCAD) is a rare but increasingly recognized cause of acute coronary syndrome (ACS) with recent advancements in cardiac imaging facilitating its identification. However, SCAD is still often misdiagnosed due to the absence of angiographic hallmarks in a significant number of cases, highlighting the importance of meticulous interpretation of angiographic findings and, when necessary, additional usage of intravascular imaging to verify changes in arterial wall integrity and identify specific pathoanatomical features associated with SCAD. Accurate diagnosis of SCAD is crucial, as the optimal management strategies for patients with SCAD differ from those with atherosclerotic coronary disease. Current treatment strategies favor a conservative approach, wherein intervention is reserved for cases with persistent ischemia, patients with high-risk coronary anatomy, or patients with hemodynamic instability. In this paper, we provide a preview of invasive imaging modalities and classical angiographic and intravascular imaging hallmarks that may facilitate proper SCAD diagnosis.

Background: Elective unprotected left main (ULM) percutaneous coronary intervention (PCI) has long-term mortality rates comparable to surgical revascularization, thanks to advances in drug-eluting stent (DES) design, improved PCI techniques, and frequent use of intravascular imaging. However, urgent PCI of ULM culprit lesions remains associated with high in-hospital mortality and unfavourable long-term outcomes, including DES restenosis and stent thrombosis (ST). This analysis aimed to examine the long-term outcomes and healing of DES implanted in ULM during primary PCI using high-resolution optical coherence tomography (OCT) imaging. Methods: A total of 15 consecutive patients undergoing long-term OCT follow-up of ULM primary PCI from a high-volume center were included in this analysis. During the index primary PCI all subjects underwent angio-guided DES implantation, and follow-up was uneventful in all but one subject who had a non-target PCI lesion. The primary endpoint was the percentage of covered, uncovered, and malappossed stent struts at long-term follow-up. Secondary endpoints included quantitative and qualitative OCT measurements. For the left main bifurcation, a separate analysis was performed for three different segments: left main (LM), polygon of confluence (POC) and distal main branch (dMB), in all cases. Results: The average follow-up interval until OCT was 1580 ± 1260 days. Despite aorto-ostial stent protrusions in 40% of patients, optimal image quality was achieved in 93.3% of cases. There were higher rates of malapposed (11.4 ± 16.6 vs. 13.1 ± 8.3 vs. 0.3 ± 0.5%; p < 0.001) and lower rates of covered struts (81.7 ± 16.8 vs. 83.7 ± 9.2 vs. 92.4 ± 6.8%; p = 0.041) observed for the LM and POC segment compared to the dMB. Significantly malapposed stent struts (>400 μm) were less likely to be covered at follow-up, than struts with a measured strut to vessel wall distance of <400 μm (15.4 ± 21.6 vs. 24.8 ± 23.9%; p = 0.011). Neoatherosclerosis was observed in 5 (33.3%) and restenotic neointimal hyperplasia (NIH) in 2 (13.3%) patients, requiring PCI in 33.3% of patients. Conclusions: Long-term OCT examination of DES implanted during primary PCI for culprit ULM lesions demonstrated high rates of incomplete strut coverage, late malapposition, and high subclinical DES failure rates. These negative OCT results highlight the need for image optimization strategies during primary PCI to improve DES-related long-term outcomes.

Spontaneous coronary artery dissection (SCAD) could be the cause of acute myocardial infarction (AMI) and sudden cardiac death. Clinical presentations can vary considerably, but the most common is the elevation of cardiac biomarkers associated with chest discomfort. Different pathological etiology in comparison with Type 1 AMI is the underlying infarct size in this population. A 42-year-old previously healthy woman presented with SCAD. Detailed diagnostical processing and treatment which were performed could not prevent myocardial injury. The catheterization laboratory was the initial place for the establishment of a diagnosis and proper management. The management process can be very fast and sometimes additional imaging methods are necessary. Finding predictors of SCAD recurrence is challenging, as well as predictors of the resulting infarct scar size. Patients with recurrent clinical symptoms of chest pain, ST elevation, and complication represent a special group of interest. Therapeutic approaches for SCAD range from the ”watch and wait” method to complete revascularization with the implantation of one or more stents or aortocoronary bypass grafting. The infarct size could be balanced through the correct therapeutical approach, and, proper multimodality imaging would be helpful in the assessment of infarct size.

Introduction/Objective. Following the failure of the single-wire technique in percutaneous coronary intervention (PCI) for chronic total occlusions (CTO), two principal antegrade escalation strategies are commonly employed: the parallel-wire technique and antegrade wire escalation (AWE). Despite their widespread use, comparative data on the procedural characteristics and long-term clinical outcomes of these strategies remain scarce. This study aims to compare the procedural parameters and long-term outcomes of the parallel-wire and AWE techniques after single-wire failure in CTO PCI. Methods. This retrospective, single-center study included patients who underwent successful CTO PCI between January 2018 and December 2023 using either the parallel-wire or AWE technique following single-wire failure. The primary endpoint was a composite of cardiac death, myocardial infarction, stroke, or target vessel revascularization (TVR). Secondary outcomes included procedure duration, fluoroscopy time, contrast volume, and total radiation dose. Median follow-up duration was 1222 days (IQR 580?1969 days). Results. Among 270 CTO PCI procedures, 112 (41.5%) required escalation: 90 with AWE and 22 with the parallel-wire technique. Baseline clinical and angiographic characteristics were comparable. The primary composite outcome occurred in 14.4% of the parallel-wire group and 9.1% of the AWE group (p = 0.73). No significant differences were observed in individual clinical events. Procedure duration was longer (95.5 ?} 43.6 vs. 77.0 ? 30.7 min; p = 0.064) and contrast volume higher (336.4 ? 113.3 vs. 271.6 ? 90.6 mL; p = 0.014) in the AWE group, with similar fluoroscopy time and radiation dose. No clinically or angiographically significant complications occurred during the periprocedural period. Conclusion. Both AWE and parallel-wire techniques demonstrate comparable safety and efficacy following single-wire failure in CTO PCI. While procedural efficiency slightly favored the parallel-wire strategy, overall outcomes support either approach, pending further prospective validation.

Background: Coronary microvascular dysfunction is associated with adverse prognosis after ST-segment elevation myocardial infarction (STEMI). We aimed to compare the invasive, Doppler wire-based coronary flow reserve (CFR) with the non-invasive transthoracic Doppler echocardiography (TTDE)-derived CFR, and their ability to predict infarct size. Methods: We included 36 patients with invasive Doppler wire assessment on days 3–7 after STEMI treated with primary percutaneous coronary intervention (PCI), of which TTDE-derived CFR was measured in 47 vessels (29 patients) within 6 h of the invasive Doppler. Infarct size was assessed by cardiac magnetic resonance at a median of 8 months. Results: The correlation between invasive and non-invasive CFR was modest in the overall cohort (rho 0.400, p = 0.005). It improved when only measurements in the LAD artery were considered (rho 0.554, p = 0.002), with no significant correlation in the RCA artery (rho −0.190, p = 0.435). Both invasive (AUC 0.888) and non-invasive (AUC 0.868) CFR, measured in the recanalized culprit artery, showed a good ability to predict infarct sizes ≥18% of the left ventricular mass, with the optimal cut off values of 1.85 and 1.80, respectively. Conclusions: In patients with STEMI, TTDE- and Doppler wire-derived CFR exhibit significant correlation, when measured in the LAD artery, and both have a similarly strong association with the final infarct size.

Myocardial bridging (MB) is a congenital coronary anomaly characterized by systolic compression of the intramyocardial arterial segment and delayed early diastolic artery relaxation, resulting in reduced vessel luminal diameter in diastole. Current evidence suggests that MB, particularly in the left anterior descending artery, may cause anginal symptoms and/or myocardial ischemia through several different pathophysiological and cellular mechanisms acting independently or synergistically: (1) delayed early diastolic relaxation of intramyocardial arterial segment; (2) impaired endothelial-dependent vasodilation with vessel smooth muscle cell hyperactivity in the coronary artery with MB, especially within the bridged segment; (3) focal (septal) ischemia due to “septal steal” phenomenon; and (4) development and progression of an atherosclerotic lesion in the coronary artery segment proximal to MB. Patients with isolated-MB may also experience anginal pain and/or myocardial ischemia due to concomitant structural and/or functional abnormalities of the coronary microcirculation. Both MB and coronary microvascular dysfunction refer to a subgroup of patients with angina and/or ischemia with non-obstructive coronary arteries (ANOCA/INOCA). Therefore, it may be challenging to determine whether MB is causing anginal pain and/or ischemia, particularly since both phenomena have also been reported without MB’s existence. Therefore, comprehensive coronary physiology testing should be encouraged in patients with this coronary anomaly to identify the underlying cause of anginal pain and/or myocardial ischemia, enabling optimal therapeutic strategies in these patients. This review is focused on different pathophysiological and cellular mechanisms of MB-related angina and/or ischemia and future perspectives in the functional assessment of MB severity, bearing in mind the complexity of coronary physiology in the presence of this anomaly.