Coronary artery calcification (CAC) develops early in the pathogenesis of atherosclerosis and is a strong and independent predictor of cardiovascular disease (CVD). Arterial calcification is caused by an imbalance in calcification regulatory mechanisms. An important inhibitor of calcification is vitamin K-dependent matrix Gla protein (MGP). Both preclinical and clinical studies have shown that inhibition of the vitamin K-cycle by vitamin K antagonists (VKA) results in elevated uncarboxylated MGP (ucMGP) and subsequently in extensive arterial calcification. This led us to hypothesize that vitamin K supplementation may slow down the progression of calcification. To test this, we designed the VitaK-CAC trial which analyses effects of menaquinone-7 (MK-7) supplementation on progression of CAC. The trial is a double-blind, randomized, placebo-controlled trial including patients with coronary artery disease (CAD). Patients with a baseline Agatston CAC-score between 50 and 400 will be randomized to an intervention-group (360 microgram MK-7) or a placebo group. Treatment duration will be 24 months. The primary endpoint is the difference in CAC-score progression between both groups. Secondary endpoints include changes in arterial structure and function, and associations with biomarkers. We hypothesize that treatment with MK-7 will slow down or arrest the progression of CAC and that this trial may lead to a treatment option for vascular calcification and subsequent CVD.

Intramyocardial dissecting hematoma is a rare complication of percutaneous coronary intervention. A 56-year-old patient underwent percutaneous coronary intervention with successful right coronary artery stenting, complicated by distal wire perforation and contrast extravasation. Although initially managed conservatively, follow-up echocardiography showed a rapidly expanding septal intramyocardial hematoma. Urgent coronary angiography demonstrated multiple sites of contrast accumulation, which progressed despite balloon inflation, but ultimately stabilized after covered stent placement. Cardiovascular magnetic resonance and computed tomography angiography confirmed the diagnosis of intramyocardial hematoma and revealed transmural myocardial infarction with microvascular obstruction. Most reports describe intramyocardial hematomas in chronic total occlusion or prior bypass surgery. In this case, multimodality imaging suggests subclinical myocardial infarction with spontaneous reperfusion, creating a vulnerable environment for rapid hematoma expansion. Covered stent placement likely prevented septal wall rupture. Multimodality imaging facilitates diagnosing intramural hematoma, a rare but potentially life-threatening complication.

Aims: Cardiovascular magnetic resonance (CMR) could be considered as first diagnostic test in patients with suspected non-ST-elevation acute coronary syndrome (NSTE-ACS), since up to one-third do not have obstructive coronary artery disease (CAD). This meta-analysis aimed to investigate (i) the diagnostic accuracy of CMR to detect obstructive CAD and NSTE-ACS, and (ii) the prognostic value of CMR in patients with suspected NSTE-ACS. Methods and results: Pubmed, Embase, and Cochrane Library were searched (30 November 2024) for eligible studies. To determine the diagnostic accuracy of CMR prior to invasive coronary angiography, sensitivity, specificity, and likelihood ratios (LR+/−) were calculated for each endpoint. Data were pooled using a bivariate random-effects model. This meta-analysis was pre-registered in PROSPERO (CRD42024625306). Sixteen studies with 1386 patients were included. The pooled sensitivity and specificity to detect obstructive CAD (eight studies) were 85% (95%CI 78–91%) and 73% (95%CI 57–85%). The pooled LR+ and LR− were 3.20 (95%CI 1.78–5.73) and 0.20 (95%CI 0.11–0.36). The pooled sensitivity and specificity to diagnose NSTE-ACS (five studies) were 83% (95%CI 73–89%) and 89% (95%CI 72–96%). The pooled LR+ and LR− were 7.45 (95%CI 2.77–20.02) and 0.20 (95%CI 0.13–0.30). Finally, the pooled sensitivity and specificity for prognosis based on ACS-related outcomes (four studies) were 98% (95%CI 42–100%) and 85% (95%CI 65–95). The pooled LR+ and LR− were 6.55 (95%CI 2.45–17.54) and 0.03 (95%CI 0–1.54). Conclusion: CMR can detect obstructive CAD and diagnose NSTE-ACS with excellent pooled sensitivity and specificity. CMR findings are strongly associated with clinical outcome in patients with suspected NSTE-ACS.

Approximately one-third of patients with suspected non-ST-elevation myocardial infarction (NSTEMI) have non-obstructive coronary artery disease. Low-risk patients might benefit from early non-invasive diagnostic testing that can appropriately select those without obstructive coronary artery disease and prevent unnecessary invasive coronary angiography (ICA). The purpose of this study is to evaluate the diagnostic value of computed tomography angiography (CTA) in suspected NSTEMI. Patients with clinically suspected type 1 NSTEMI were included. In case ICA was indicated, CTA was performed prior to ICA. The accuracy of CTA to diagnose NSTEMI, assigned by an adjudicated final diagnosis committee, was investigated. Of the 66 included patients, 40 (61%) were diagnosed with NSTEMI. CAD-RADS ≥ 3 (i.e. stenosis ≥50%) had a sensitivity of 95% (95%CI 83–99%), a specificity of 65% (95%CI 44–83%) and an overall accuracy of 83% (95%CI 72–91%). The Agatston score was significantly different between patients with and without NSTEMI (404 [IQR 132–883] and 31 [IQR 0–163], respectively, p < 0.001). Nineteen patients (29%) met the criteria of ≥2 high-risk plaque (HRP) features, which was more often present in patients with NSTEMI compared to those without NSTEMI (43% and 8%, respectively, p = 0.002). Combining all CTA parameters (CAD-RADS ≥ 3, Agatston score >1.000 and ≥2 HRP features) did not improve the diagnostic accuracy compared with CAD-RADS alone. CTA accurately diagnoses NSTEMI in patients with acute chest pain and elevated high-sensitivity cardiac troponin T levels. Patients with NSTEMI more often presented with CAD-RADS ≥ 3, Agatston score >1.000 and HRP features.

Background/Objectives: 18F-fluorocholine is a positron emission tomography (PET) tracer earlier found to be a marker of macrophage content in carotid plaques. We aimed to assess the feasibility of 18F-choline PET-MRI to non-invasively localize vulnerable coronary plaques, using optical coherence tomography (OCT) as a reference standard. Methods: Patients with recent myocardial infarction who were scheduled for a secondary angiography of a non-culprit vessel underwent 18F-fluorocholine coronary PET-MRI. Subsequently, OCT was performed during the secondary angiography. Maximum target-to-background (TBRmax) values of 18F-fluorocholine uptake were determined in two vessel sections that contained either vulnerable or stable plaques as defined by OCT. The OCT-based definition of a vulnerable plaque was a fibrous cap thickness < 70 µm. To enhance the detectability of coronary plaques using PET, three different motion-correction strategies were used: multigate respiratory gating motion correction (MRG-MOCO), extended MR-based motion correction (eMR-MOCO), and extended MR-based motion correction with ECG gating (eMR-MOCO-ECG). Results: Fifteen patients were included in this study. One patient needed to be excluded due to extravasation of the tracer. In another patient, no region with only a stable plaque could be identified. TBRmax values were as follows for three different reconstructions in vulnerable versus stable plaques: MRG-MOCO: mean TBRmax 1.45 vs. 1.35, p = 0.52 (n = 13); eMR-MOCO: mean TBRmax 1.47 vs. 1.27, p = 0.26 (n = 11); eMR-MOCO-ECG: mean TBRmax 1.49 vs. 1.26, p = 0.21 (n = 11). Conclusions: 18F-fluorocholine uptake in vulnerable atherosclerotic plaques in coronary arteries was not significantly different from uptake in stable plaques, even though advanced motion-correction methods were applied. That may be caused by multiple factors, such as small coronary plaque size, tracer biology, or remaining cardiac motion.