Early mechanical reperfusion of the epicardial coronary artery by primary percutaneous coronary intervention (PCI) is the guideline-recommended treatment for ST-elevation myocardial infarction (STEMI). Successful restoration of epicardial coronary blood flow can be achieved in over 95% of PCI procedures. However, despite angiographically complete epicardial coronary artery patency, in about half of the patients perfusion to the distal coronary microvasculature is not fully restored, which is associated with increased morbidity and mortality. The exact pathophysiological mechanism of post-ischaemic coronary microvascular dysfunction (CMD) is still debated. Therefore, the current review discusses invasive and non-invasive techniques for the diagnosis and quantification of CMD in STEMI in the clinical setting as well as results from experimental in vitro and in vivo models focusing on ischaemic-, reperfusion-, and inflammatory damage to the coronary microvascular endothelial cells. Finally, we discuss future opportunities to prevent or treat CMD in STEMI patients.

The microvascular resistance reserve (MRR) was introduced as a means to characterize the vasodilator reserve capacity of the coronary microcirculation while accounting for the influence of concomitant epicardial disease and the impact of administration of potent vasodilators on aortic pressure. This study aimed to evaluate the diagnostic and prognostic performance of MRR. A total of 1481 patients with stable symptoms and a clinical indication for coronary angiography were included from the global ILIAS Registry. MRR was derived as a function of the coronary flow reserve (CFR) divided by the fractional flow reserve (FFR) and corrected for driving pressure. The median MRR was 2.97 [Q1–Q3: 2.32–3.86] and the overall relationship between MRR and CFR was good [correlation coefficient (R_s) = 0.88, P < 0.005]. The difference between CFR and MRR increased with decreasing FFR [coefficient of determination (R²) = 0.34; Coef.—2.88, 95% confidence interval (CI): -3.05–−2.73; P < 0.005]. MRR was independently associated with major adverse cardiac events (MACE) at 5-year follow-up [hazard ratio (HR) 0.78; 95% CI 0.63–0.95; P = 0.024] and with target vessel failure (TVF) at 5-year follow-up (HR 0.83; 95% CI 0.76–0.97; P = 0.047). The optimal cut-off value of MRR was 3.0. Based on this cut-off value, only abnormal MRR was significantly associated with MACE and TVF at 5-year follow-up in vessels with functionally significant epicardial disease (FFR <0.75). MRR seems a robust indicator of the microvascular vasodilator reserve capacity. Moreover, in line with its theoretical background, this study suggests a diagnostic advantage of MRR over other indices of vasodilatory capacity in patients with hemodynamically significant epicardial coronary artery disease. Diagnostic and prognostic value of the microvascular resistance reserve (MRR).The MRR is a novel index of the coronary vasodilatory capacity. The MMR is an index that corrects the assessment of the vasodilatory capacity for concomitant epicardial disease and the administration of vasodilatory indices. The MRR shows an excellent correlation with the coronary flow reserve (CFR), which decreases with decreasing fractional flow reserve (FFR) values. The MRR is an independent and significant predictor of both major adverse cardiac events (MACE) and target vessel failure (TVF) at 5-year follow-up.

Patients with suspected non-ST-segment elevation acute coronary syndrome (NSTE-ACS) are routinely transferred to the emergency department (ED). A clinical risk score with point-of-care (POC) troponin measurement might enable ambulance paramedics to identify low-risk patients in whom ED evaluation is unnecessary. The aim was to assess safety and healthcare costs of a pre-hospital rule-out strategy using a POC troponin measurement in low-risk suspected NSTE-ACS patients. This investigator-initiated, randomized clinical trial was conducted in five ambulance regions in the Netherlands. Suspected NSTE-ACS patients with HEAR (History, ECG, Age, Risk factors) score ≤3 were randomized to pre-hospital rule-out with POC troponin measurement or direct transfer to the ED. The sample size calculation was based on the primary outcome of 30-day healthcare costs. Secondary outcome was safety, defined as 30-day major adverse cardiac events (MACE), consisting of ACS, unplanned revascularization or all-cause death. : A total of 863 participants were randomized. Healthcare costs were significantly lower in the pre-hospital strategy (€1349 ± €2051 vs. €1960 ± €1808) with a mean difference of €611 [95% confidence interval (CI): 353–869; P < 0.001]. In the total population, MACE were comparable between groups [3.9% (17/434) in pre-hospital strategy vs. 3.7% (16/429) in ED strategy; P = 0.89]. In the ruled-out ACS population, MACE were very low [0.5% (2/419) vs. 1.0% (4/417)], with a risk difference of −0.5% (95% CI −1.6%–0.7%; P = 0.41) in favour of the pre-hospital strategy. Pre-hospital rule-out of ACS with a POC troponin measurement in low-risk patients significantly reduces healthcare costs while incidence of MACE was low in both strategies. Clinicaltrials.gov identifier NCT05466591 and International Clinical Trials Registry Platform id NTR 7346. ACS, acute coronary syndrome; CI, confidence interval; ED, emergency department; MACE, major adverse cardiac events; NSTE-ACS, non-ST-elevation acute coronary syndrome; POC, point-of-care

Calcific aortic valve disease (CAVD) is the most common valvular disease in the developed world with currently no effective pharmacological treatment available. CAVD results from a complex, multifactorial process, in which valvular inflammation and fibro-calcific remodelling lead to valve thickening and cardiac outflow obstruction. The exact underlying pathophysiology of CAVD is still not fully understood, yet the development of CAVD shows many similarities with the pathophysiology of atherosclerotic cardiovascular disease (ASCVD), such as coronary artery disease. Innate immune cells play a crucial role in ASCVD and might also play a pivotal role in the development of CAVD. This review summarizes the current knowledge on the role of innate immune cells, both in the circulation and in the aortic valve, in the development of CAVD and the similarities and differences with ASCVD. Trained immunity and clonal haematopoiesis of indeterminate potential are proposed as novel immunological mechanisms that possibly contribute to the pathophysiology of CAVD and new possible treatment targets are discussed.

Background—: The palmar arches serve as the most important conduits for digital blood supply, and incompleteness may lead to digital ischemia when the radial artery becomes obstructed after cardiac catheterization. The rate of palmar arch incompleteness and the clinical consequences after transradial access are currently unknown. Methods and Results—: The vascular anatomy of the hand was documented by angiography in 234 patients undergoing transradial cardiac catheterization. In all patients, a preprocedural modified Allen test and Barbeau test were performed. Upper-extremity function was assessed at baseline and 2-year follow-up by the QuickDASH. Incompleteness of the superficial palmar arch (SPA) was present in 46%, the deep palmar arch was complete in all patients. Modified Allen test and Barbeau test results were associated with incompleteness of the SPA ( P =0.001 and P =0.001). The modified Allen test had a 33% sensitivity and 86% specificity for SPA incompleteness with a cutoff value of >10 seconds and a 59% sensitivity and 60% specificity with a cutoff value of >5 seconds. The Barbeau test had a 7% sensitivity and 98% specificity for type D and a 21% sensitivity and 93% specificity for types C and D combined. Upper-extremity dysfunction was not associated with SPA incompleteness ( P =0.77). Conclusions—: Although incompleteness of the SPA is common, digital blood supply is always preserved by a complete deep palmar arch. Preprocedural patency tests have thus no added benefit to prevent ischemic complications of the hand. Finally, incompleteness of the SPA is not associated with a loss of upper-extremity function after transradial catheterization.