Although the widespread adoption of timely invasive reperfusion strategies over the last two decades has significantly improved the prognosis of patients with ST-segment elevation myocardial infarction (STEMI), up to half of patients after angiographically successful primary percutaneous coronary intervention (PCI) still have signs of inadequate reperfusion at the level of coronary microcirculation. This phenomenon, termed coronary microvascular dysfunction (CMD), has been associated with impaired prognosis. The aim of the present review is to describe the collected evidence on the occurrence of CMD following primary PCI, means of assessment and its association with the infarct size and clinical outcomes. Therefore, the practical role of invasive assessment of CMD in the catheterization laboratory, at the end of primary PCI, is emphasized, with an overview of available technologies including thermodilution- and Doppler-based methods, as well as recently developing functional coronary angiography. In this regard, we review the conceptual background and the prognostic value of coronary flow reserve (CFR), index of microcirculatory resistance (IMR), hyperemic microvascular resistance (HMR), pressure at zero flow (PzF) and angiography-derived IMR. Finally, the so-far investigated therapeutic strategies targeting coronary microcirculation after STEMI are revisited.

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.

Background: Aortic stenosis (AS) is a common valve disease and atrial fibrillation (AF) is the most common cardiac arrhythmia, frequently associated with AS. This study aimed to evaluate the impact of AF on mortality in patients with moderate and severe AS. Methods: We retrospectively analyzed 1070 consecutive moderate and severe AS patients (57% were male, age was 69 ± 10, severe AS 22.5%), who underwent transthoracic echocardiography from March 2018 to November 2021. AS severity was defined by specific threshold values with severe AS being defined by a peak velocity > 4 m/s, an MPG > 40 mmHg, and an AVA < 1 cm² and moderated by a peak velocity of 3–4 m/s, an MPG 20–40 mmHg and an AVA 1–1.5 cm. Patients with AF were defined as those having a history of AF when AS was found on the index echocardiography. The follow-up assessment in December 2023 ascertained vital status and data on aortic valve replacement (AVR). Results: 790 (73.8%) patients were with sinus rhythm (SR) and 280 (26.2%) patients with AF. Mortality was higher in patients with AF than in those with SR (46% vs. 36.2% HR 1.424, 95% CI 1.121–1.809, p = 0.004). After adjusting for clinical confounders, mortality risk in AF relative to SR remained significant (HR 1.284, 95% CI 1.03–1.643, p = 0.047). Patients with AF demonstrated high mortality risk in the moderate aortic stenosis stratum (HR 1.376, 95% CI 1.059–1.788, p = 0.017), with even greater risk in the severe AS stratum (HR 1.644, 95% CI 1.038–2.603, p = 0.034) with significant interaction (p = 0.007). In patients with AF AVR demonstrated a protective effect on survival (HR 0.365, 95% CI 0.202–0.627, p < 0.001), but to a lesser degree than in patients with sinus rhythm (HR 0.376, 95% CI 0.250–0.561, p < 0.001) without significant interaction (p = 0.278). In patients with AF mortality risk was high in the conservative treatment stratum (HR 1.361, 95% CI 1.066–1.739, p = 0.014), in the AVR stratum mortality risk was higher but did not reach statistical significance (HR 1.823, 95% CI 0.973–3.414, p = 0.061). However, when corrected for echocardiographic variables strongly correlated with AF, AF was no longer independently associated with all-cause mortality. (HR 0.97 95% CI 0.709–1.323, p = 0.84). Conclusions: Patients with moderate and severe AS and AF have worse prognosis than patients with SR which can be explained by cardiac damage. AVR improves survival in patients with AF and with SR.

Background Long-term stent healing after primary PCI of culprit unprotected left main (ULM) lesions is insufficiently explored. In this setting, large vessel size and bifurcation anatomy may limit angiographic stent optimisation and contribute to persistent strut malapposition and incomplete coverage. Objectives To identify OCT-derived geometric and healing parameters associated with long-term strut coverage and malapposition after angiography-guided primary PCI of culprit ULM lesions. Methods This single-center exploratory study included 30 patients with long-term OCT follow-up after angiography-guided primary PCI of culprit ULM lesions. OCT analysis was performed separately in three prespecified subsegments: the left main (LM), polygon of confluence (POC), and distal main branch (dMB). Five predefined strut-level healing outcomes were analysed: covered struts, malapposed struts, malapposed and uncovered struts, significantly malapposed struts (>400 μm), and significantly malapposed and uncovered struts. Associations between patient-level healing outcomes and OCT-derived measures of lumen geometry, stent dimensions, neointimal response, and an exploratory lumen–stent mismatch variable were assessed using univariable and multivariable linear regression. Results A total of 31,703 struts were analysed. Overall strut coverage was 90.7 ± 6.6%. Compared with the dMB, proximal ULM segments (LM and POC) showed lower strut coverage (82.8% and 84.2% vs. 93.9%, p< 0.001) and higher malapposition rates (17.4% and 14.2% vs. 0.4%, p< 0.001). In regression analysis, larger native lumen dimensions were associated with lower strut coverage and higher malapposition, whereas larger achieved stent area was associated with better strut healing. The exploratory lumen–stent mismatch variable was independently associated with all five healing outcomes in multivariable models (all p < 0.01). Conclusions After angiography-guided primary PCI of culprit unprotected left main lesions, long-term strut healing was significantly influenced by the mismatch between native reference lumen area and the achieved minimum stent area. Whether intravascular imaging–guided optimization of stent sizing and expansion in large-calibre left main anatomy improves strut healing requires further investigation.

Background: Long-term stent healing after primary PCI of culprit unprotected left main (ULM) lesions is insufficiently explored. In this setting, large vessel size and bifurcation anatomy may limit angiographic stent optimization and contribute to persistent strut malapposition and incomplete coverage. Objectives: To identify OCT-derived geometric and healing parameters associated with long-term strut coverage and malapposition after angiography-guided primary PCI of culprit ULM lesions. Methods: This single-center exploratory study included 30 patients with long-term OCT follow-up after angiography-guided primary PCI of culprit ULM lesions. OCT analysis was performed separately in three prespecified subsegments: the left main (LM), polygon of confluence (POC), and distal main branch (dMB). Five predefined strut-level healing outcomes were analysed: covered struts, malapposed struts, malapposed and uncovered struts, significantly malapposed struts (>400 μm), and significantly malapposed and uncovered struts. Associations between patient-level healing outcomes and OCT-derived measures of lumen geometry, stent dimensions, neointimal response, and an exploratory lumen–stent mismatch variable were assessed using univariable and multivariable linear regression. Results: A total of 31,703 struts were analysed. Overall strut coverage was 90.7 ± 6.6%. Compared with the dMB, proximal ULM segments (LM and POC) showed lower strut coverage (82.8% and 84.2% vs. 93.9%, p < 0.001) and higher malapposition rates (17.4% and 14.2% vs. 0.4%, p < 0.001). In regression analysis, larger native lumen dimensions were associated with lower strut coverage and higher malapposition, whereas larger achieved stent area was associated with better strut healing. The exploratory lumen–stent mismatch variable in multivariable models with all five healing outcomes in multivariable models (all p < 0.01). Conclusions: After angiography-guided primary PCI of culprit unprotected left main lesions, long-term strut healing was significantly influenced by the mismatch between native reference lumen area and the achieved mean stent area. Whether intravascular imaging–guided optimization of stent sizing and expansion in large-calibre left main anatomy improves strut healing requires further investigation.