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Percutaneous coronary intervention (PCI) aims to relieve coronary vessel obstruction to improve coronary blood flow and relieve cardiac ischaemia. Some studies suggest little improvement in outcomes compared with medication alone, whereas others suggest that PCI is beneficial if physiologically guided. Few studies have assessed whether PCI improves coronary blood flow and how any change in flow is related to stenosis severity. We sought to determine whether fractional flow reserve (FFR), a pressure-only physiological index of stenosis severity and surrogate for ischaemia, could predict the improvement in coronary flow produced by PCI. We assessed 75 stenoses in 67 patients undergoing elective PCI. We conducted simultaneous transtenotic pressure and Doppler flow velocity measurements during adenosine-mediated hyperaemia, both before and after PCI. Flow velocity was calculated over the whole cardiac cycle. Change in flow was stratified by lesion severity, with particular interest to flow changes in stenoses with FFR more than 0·80, which is typically classed as non-ischaemic. Hyperaemic flow velocity was significantly higher after PCI than before PCI (mean 0·30 m/s [SE 0·02] vs 0·51 [0·03], p<0·001) across all stenoses. Both the absolute and relative increase in blood flow after PCI was strongly correlated to the pre-PCI FFR measurement (r=−0·65, p<0·001), with a small non-significant but detectable increase in flow when FFR was borderline (FFR 0·71–0·80: mean change from pre-PCI [Δ] 0·11 m/s [0·07], p=0·14). The greatest incremental increase was seen when FFR in stenoses was less than 0·60 (Δ 0·41 [0·05], p<0·001). By contrast, when pre-PCI FFR was more than 0·80, PCI produced little improvement in flow (0·05 m/s [0·02]) and this change was significantly less than when stenoses were classed before PCI as flow limiting (p<0·001). By removing epicardial stenoses, PCI improves hyperaemic coronary blood flow, and this increase is strongly related to the physiological significance of the stenosis before PCI. Only stenoses defined as severe by FFR, with values consistent with ischaemia, had a significant rise in flow velocity after PCI. Stenoses deemed non-significant by FFR had comparatively little improvement in flow. These findings provide a mechanistic explanation for the improved outcomes and symptomatic improvement after physiologically guided stenting, and strongly support restricting PCI to patients with truly flow-limiting coronary stenoses. UK Medical Research Council.

The introduction of wire-free microcirculatory resistance index from functional angiography (angio-IMR) promises swift detection of coronary microvascular dysfunction, however it has not been properly validated. We sought to validate angio-IMR against invasive IMR and PET derived microvascular resistance (MVR). Moreover, we studied if angio-IMR could aid in the detection of ischemia with non-obstructive coronary arteries (INOCA). In this investigator-initiated study symptomatic patients underwent [ 15 O]H 2 O positron emission tomography (PET) and invasive angiography with 3-vessel fractional flow reserve (FFR). Invasive IMR was measured in 40 patients. Angio-IMR and QFR were computed retrospectively. MVR was defined as the ratio of mean distal coronary pressure to PET derived coronary flow. PET and QFR/angio-IMR analyses were performed by blinded core labs. The right coronary artery was excluded. A total of 211 patients (mean age 61 ± 9, 148 (70%) male) with 312 vessels with successful angio-IMR analyses were included. Angio-IMR correlated moderately with invasive IMR ( r  = 0.48, p  < 0.01), whereas no correlation was found between angio-IMR and MVR ( r =-0.07, p  = 0.25). Angio-IMR did not differ for vessels without obstructive coronary artery disease (CAD) (FFR-) but with reduced stress perfusion (PET+) compared to vessels without obstructive CAD (FFR-) with normal stress perfusion (PET-) (median 28.19 IQR 20.42–38.99 vs. 31.67 IQR 23.47–40.63, p  = 0.40). Angio-IMR correlated moderately with invasively measured IMR, whereas angio-IMR did not correlate with PET derived MVR. Moreover, angio-IMR did not reliably identify patients with INOCA. Graphical Abstract

The introduction of wire-free microcirculatory resistance index from functional angiography (angio-IMR) promises swift detection of coronary microvascular dysfunction, however it has not been properly validated. We sought to validate angio-IMR against invasive IMR and PET derived microvascular resistance (MVR). Moreover, we studied if angio-IMR could aid in the detection of ischemia with non-obstructive coronary arteries (INOCA). In this investigator-initiated study symptomatic patients underwent [ O]H O positron emission tomography (PET) and invasive angiography with 3-vessel fractional flow reserve (FFR). Invasive IMR was measured in 40 patients. Angio-IMR and QFR were computed retrospectively. MVR was defined as the ratio of mean distal coronary pressure to PET derived coronary flow. PET and QFR/angio-IMR analyses were performed by blinded core labs. The right coronary artery was excluded. A total of 211 patients (mean age 61 ± 9, 148 (70%) male) with 312 vessels with successful angio-IMR analyses were included. Angio-IMR correlated moderately with invasive IMR (r = 0.48, p < 0.01), whereas no correlation was found between angio-IMR and MVR (r=-0.07, p = 0.25). Angio-IMR did not differ for vessels without obstructive coronary artery disease (CAD) (FFR-) but with reduced stress perfusion (PET+) compared to vessels without obstructive CAD (FFR-) with normal stress perfusion (PET-) (median 28.19 IQR 20.42-38.99 vs. 31.67 IQR 23.47-40.63, p = 0.40). Angio-IMR correlated moderately with invasively measured IMR, whereas angio-IMR did not correlate with PET derived MVR. Moreover, angio-IMR did not reliably identify patients with INOCA.

Background Coronary vascular dysfunction comprises VSA and/or MVA and is more common in women than in men with angina without obstructive coronary artery disease (ANOCA). Invasive coronary function testing is considered the reference test for diagnosis, but its burden on patients is large. We aimed to investigate the potential of electrocardiography (ECG) as noninvasive marker for vasospastic angina (VSA) and microvascular angina (MVA) diagnosis. Methods We systematically screened Pubmed and EMBASE databases for studies reporting on ECG characteristics in ANOCA patients with (a suspicion of) coronary vascular dysfunction. We assessed study quality using QUADAS‐2. We extracted data on diagnostic values of different ECG characteristics and analyzed whether the studies were sex‐stratified. Results Thirty publications met our criteria, 13 reported on VSA and 17 on MVA. The majority addressed repolarization‐related ECG parameters. Only 1 of the 13 VSA papers and 4 of the 17 MVA papers showed diagnostic accuracy measures of the ECG characteristics. The presence of early repolarization, T‐wave alternans, and inverted U waves showed of predictive value for VSA diagnosis. The QTc interval was predictive for MVA diagnosis in all six studies reporting on QTc interval. Sex‐stratified results were reported in only 5 of the 30 studies and 3 of those observed sex‐based differences. Conclusions ECG features are not widely evaluated in diagnostic studies for VSA and MVA. Those features predictive for VSA and MVA diagnosis mostly point to repolarization abnormalities and may contribute to noninvasive risk stratification.

Angina with nonobstructive coronary arteries (ANOCA) is a major cause of chronic coronary syndromes, affecting nearly half of patients with anginal symptoms who undergo invasive coronary angiography. ANOCA may lead to substantial symptom burden, increased risk of adverse cardiac events, increased healthcare utilization due to ongoing symptoms, repeat hospitalizations, and invasive testing. The pathophysiology of ANOCA often involves a variety of coronary disorders, such as coronary microvascular dysfunction, epicardial or microvascular vasospasm and endothelial dysfunction. While coronary function testing (CFT) can identify each of these specific endotypes, in current practice it is used as a second- or third-line diagnostic tool, delaying diagnosis which contributes to persistent symptoms and diminished quality of life. The ILIAS ANOCA clinical trial aims to enhance understanding and management of ANOCA through early routine CFT-guided management. After exclusion of obstructive coronary artery disease, eligible patients undergo comprehensive CFT, and will be randomized to blinding of the CFT results (control group) or disclosure of the CFT results combined with a tailored medical therapy escalation plan (intervention group). The control group will be unblinded after 1 year. The primary outcome is the mean difference in the within-subject change in Seattle Angina Questionnaire (SAQ) summary score between the groups at 6 months from baseline. Secondary outcomes include differences in SAQ-summary score and additional health-status and quality of life questionnaires at 12 and 24 months from baseline. International Clinical Trials Registry Platform identifier NL-OMON20739.

The coronary microcirculation plays a key role in modulating blood supply to the myocardium. Several factors like myocardial oxygen demands, endothelial and neurogenic conditions determine its function. Although there is available evidence supporting microvascular dysfunction as an important cause of myocardial ischaemia, with both prognostic and symptomatic implications, its diagnosis and management in clinical practice is still relegated to a second plane. Both diagnostic and therapeutic approaches are hampered by the broadness of the concept of microvascular dysfunction, which fails addressing the plurality of mechanisms leading to dysfunction. Normal microcirculatory function requires both structural integrity of the microcirculatory vascular network and preserved signalling pathways ensuring adequate and brisk arteriolar resistance shifts in response to myocardial oxygen demands. Pathological mechanisms affecting these requirements include structural remodelling of microvessels, intraluminal plugging, extravascular compression or vasomotor dysregulation. Importantly, not every diagnostic technique provides evidence on which of these pathophysiological mechanisms is present or predominates in the microcirculation. In this paper we discuss the mechanisms of coronary microvascular dysfunction and the intracoronary tools currently available to detect it, as well as the potential role of each one to unmask the main underlying mechanism.

Background Pulmonary embolism is an important cause of preventable mortality. Treatment strategies depend on risk stratification. High-risk patients, and some intermediate-high-risk patients, require urgent reperfusion therapy. Systemic thrombolysis (ST) is the effective first-choice treatment in these patients; however, the high risk of bleeding complications is a major drawback. In this single-centre retrospective cohort study, we report our experience with the FlowTriever thrombosuction system as an alternative or adjunct to ST in intermediate-high and high-risk pulmonary embolism. Methods Demographic and clinical data of all patients treated with the FlowTriever system from December 2021 until March 2024 were retrieved from the electronic medical records. Primary outcomes were technical success rate, 30-day all-cause mortality and major bleeding. Results Twenty-one patients were treated with the FlowTriever system, 14 of whom were considered high risk. The technical success rate was 100%. Thirty-day all-cause mortality was 29% and major bleeding was recorded in 5 patients (24%), of which one bleeding event was related to the FlowTriever procedure. A significant reduction was seen in mean pulmonary arterial pressure and right ventricular end-diastolic dimension. Conclusion In intermediate-high and high-risk pulmonary embolism patients with ST treatment failure or a contraindication for ST, the FlowTriever thrombosuction system seems to be a minimally invasive alternative treatment modality with low complication rates.

Pre‐clinical studies aimed at treating ischemic heart disease (i.e. stem cell‐ and growth factor therapy) often consider restoration of the impaired microvascular circulation as an important treatment goal. However, serial in vivo measurement hereof is often lacking. The purpose of this study was to evaluate the applicability of intracoronary pressure and flow velocity as a measure of microvascular resistance in a large animal model of chronic myocardial infarction (MI). Myocardial infarction was induced in Dalland Landrace pigs (n = 13; 68.9 ± 4.1 kg) by a 75‐min. balloon occlusion of the left circumflex artery (LCX). Intracoronary pressure and flow velocity parameters were measured simultaneously at rest and during adenosine‐induced hyperemia, using the Combowire (Volcano) before and 4 weeks after MI. Various pressure‐ and/or flow‐derived indices were evaluated. Hyperemic microvascular resistance (HMR) was significantly increased by 28% in the infarct‐related artery, based on a significantly decreased peak average peak flow velocity (pAPV) by 20% at 4 weeks post‐MI (P = 0.03). Capillary density in the infarct zone was decreased compared to the remote area (658 ± 207/mm2 versus 1650 ± 304/mm2, P = 0.017). In addition, arterioles in the infarct zone showed excessive thickening of the alpha smooth muscle actin (αSMA) positive cell layer compared to the remote area (33.55 ± 4.25 μm versus 14.64 ± 1.39 μm, P = 0.002). Intracoronary measurement of HMR successfully detected increased microvascular resistance that might be caused by the loss of capillaries and arteriolar remodelling in the chronic infarcted pig heart. Thus, HMR may serve as a novel outcome measure in pre‐clinical studies for serial assessment of microvascular circulation.

Cardiovascular disease in women has historically been underrepresented in research. In recent years, several funding bodies, including the Dutch Heart Foundation, have launched numerous research initiatives and consortia in the Netherlands to address knowledge gaps in women. This article provides an overview of the current landscape of cardiovascular disease in women and emphasizes the critical need for continued investment in this field. One area with urgent knowledge gaps is the early detection, diagnosis, therapy, and prognosis of Angina with Non-Obstructive Coronary Arteries (ANOCA) in women with persistent signs and symptoms of ischemia. In the Netherlands, in recent years, we have established a robust clinical infrastructure and a translational framework that enables us to address these challenges. Additionally, we have performed implementation studies to fast-track knowledge on ANOCA in clinical practice, giving us a unique opportunity to transform clinical care for women with signs and symptoms of ischemia. We advocate for a broad perspective that incorporates characteristics such as ethnicity, socio-economic background, and female-specific risk factors. Our goal is to provide solid evidence to ensure the best possible care for all women suffering from persistent signs and symptoms of ischemia.

Cardiac abnormalities after subarachnoid hemorrhage (SAH) such as electrocardiographic changes, echocardiographic wall motion abnormalities, and elevated troponin levels are independently associated with a poor prognosis. They are caused by catecholaminergic stress coinciding with influx of inflammatory cells into the heart. These abnormalities could be a sign of a myocarditis, potentially giving insight in pathophysiology and treatment options. These inflammatory cells are insufficiently characterized, and it is unknown whether myocarditis is associated with SAH. Myocardium of 25 patients who died of SAH and 18 controls was stained with antibodies identifying macrophages (CD68), lymphocytes (CD45), and neutrophil granulocytes (myeloperoxidase). Myocytolysis was visualized using complement staining (C3d). CD31 was used to identify putative thrombi. We used Mann-Whitney U testing for analysis. In the myocardium of SAH patients, the amount of myeloperoxidase-positive (P < .005), CD45-positive (P < .0005), and CD68-positive (P < .0005) cells was significantly higher compared to controls. Thrombi in intramyocardial arteries were found in 22 SAH patients and 1 control. Myocytolysis was found in 6 SAH patients but not in controls. Myocarditis, consisting of an influx of neutrophil granulocytes, lymphocytes, and macrophages, coinciding with myocytolysis and thrombi in intramyocardial arteries, occurs in patients with SAH but not in controls. These findings might explain the cardiac abnormalities after SAH and may have implications for treatment.