We conducted a nationwide retrospective survey on the impact of COVID-19 on the diagnosis and treatment of acute cornary syndrome (ACS) from 2 to 29 March in Austria.

Medial vascular calcification, associated with enhanced mortality in chronic kidney disease (CKD), is fostered by osteo-/chondrogenic transdifferentiation of vascular smooth muscle cells (VSMCs). Here, we describe that serum- and glucocorticoid-inducible kinase 1 (SGK1) was upregulated in VSMCs under calcifying conditions. In primary human aortic VSMCs, overexpression of constitutively active SGK1^S422D, but not inactive SGK1^K127N, upregulated osteo-/chondrogenic marker expression and activity, effects pointing to increased osteo-/chondrogenic transdifferentiation. SGK1^S422D induced nuclear translocation and increased transcriptional activity of NF-κB. Silencing or pharmacological inhibition of IKK abrogated the osteoinductive effects of SGK1^S422D. Genetic deficiency, silencing, and pharmacological inhibition of SGK1 dissipated phosphate-induced calcification and osteo-/chondrogenic transdifferentiation of VSMCs. Aortic calcification, stiffness, and osteo-/chondrogenic transdifferentiation in mice following cholecalciferol overload were strongly reduced by genetic knockout or pharmacological inhibition of Sgk1 by EMD638683. Similarly, Sgk1 deficiency blunted vascular calcification in apolipoprotein E–deficient mice after subtotal nephrectomy. Treatment of human aortic smooth muscle cells with serum from uremic patients induced osteo-/chondrogenic transdifferentiation, effects ameliorated by EMD638683. These observations identified SGK1 as a key regulator of vascular calcification. SGK1 promoted vascular calcification, at least partly, via NF-κB activation. Inhibition of SGK1 may, thus, reduce the burden of vascular calcification in CKD.

Late gadolinium enhancement (LGE) cardiovascular magnetic resonance (CMR) using magnitude inversion recovery (IR) or phase sensitive inversion recovery (PSIR) has become clinical standard for assessment of myocardial infarction (MI). However, there is no clinical standard for quantification of MI even though multiple methods have been proposed. Simple thresholds have yielded varying results and advanced algorithms have only been validated in single center studies. Therefore, the aim of this study was to develop an automatic algorithm for MI quantification in IR and PSIR LGE images and to validate the new algorithm experimentally and compare it to expert delineations in multi-center, multi-vendor patient data. The new automatic algorithm, EWA (Expectation Maximization, weighted intensity, a priori information), was implemented using an intensity threshold by Expectation Maximization (EM) and a weighted summation to account for partial volume effects. The EWA algorithm was validated in-vivo against triphenyltetrazolium-chloride (TTC) staining (n = 7 pigs with paired IR and PSIR images) and against ex-vivo high resolution T1-weighted images (n = 23 IR and n = 13 PSIR images). The EWA algorithm was also compared to expert delineation in 124 patients from multi-center, multi-vendor clinical trials 2–6 days following first time ST-elevation myocardial infarction (STEMI) treated with percutaneous coronary intervention (PCI) (n = 124 IR and n = 49 PSIR images). Infarct size by the EWA algorithm in vivo in pigs showed a bias to ex-vivo TTC of −1 ± 4%LVM (R = 0.84) in IR and −2 ± 3%LVM (R = 0.92) in PSIR images and a bias to ex-vivo T1-weighted images of 0 ± 4%LVM (R = 0.94) in IR and 0 ± 5%LVM (R = 0.79) in PSIR images. In multi-center patient studies, infarct size by the EWA algorithm showed a bias to expert delineation of −2 ± 6 %LVM (R = 0.81) in IR images (n = 124) and 0 ± 5%LVM (R = 0.89) in PSIR images (n = 49). The EWA algorithm was validated experimentally and in patient data with a low bias in both IR and PSIR LGE images. Thus, the use of EM and a weighted intensity as in the EWA algorithm, may serve as a clinical standard for the quantification of myocardial infarction in LGE CMR images. CHILL-MI: NCT01379261 . MITOCARE: NCT01374321 .

Cardiac magnetic resonance (CMR) is the gold-standard modality for the assessment of left ventricular (LV) remodeling in ST-elevation myocardial infarction (STEMI) patients. However, the commonly used remodeling criteria have never been validated for hard clinical events. We therefore aimed to define clear CMR criteria of LV remodeling following STEMI with proven prognostic impact.

In patients with acute ST-elevation myocardial infarction (STEMI), elevated concentrations of inflammatory markers are correlated with worse clinical outcome. The aim of this study was comprehensively to investigate the relationship of circulating markers of inflammation with myocardial and microvascular damage after STEMI. In 111 consecutive STEMI patients, blood samples were obtained on admission and from day 1 to day 4 after primary percutaneous coronary intervention and analysed for high-sensitivity C-reactive protein (hs-CRP), white blood cell count and fibrinogen. Cardiac magnetic resonance imaging was performed within the first week and 4 months after primary percutaneous coronary intervention. Peak concentrations of hs-CRP (20.5 (9.6–44.4) mg/L), white blood cell count (12.4 (10.5–15.3) G/L) and fibrinogen (3640 (3150–4550) mg/L) showed significant correlations with both infarct size (r=0.31 to 0.41; P<0.01) and left ventricular ejection fraction (r=−0.29 to −0.39; P8% of left ventricular myocardial mass) were moderate without significant differences (area under the curve: hs-CRP 0.73 (95% confidence interval (CI) 0.63–0.82), white blood cell count 0.67 (95% CI 0.56–0.78) and fibrinogen 0.69 (95% CI 0.59–0.79); all P>0.12). Combination of inflammatory markers did not significantly increase the area under the curve (P>0.05). In reperfused STEMI patients, increased levels of hs-CRP, white blood cell count and fibrinogen are associated with decreased left ventricular function and more pronounced myocardial damage at baseline and 4 months after infarction.

Background: Microvascular injury ( MVI ) after primary percutaneous coronary intervention for ST ‐elevation myocardial infarction ( STEMI ) is a major determinant of adverse clinical outcome. Experimental data indicate an impact of hypercholesterolemia on MVI ; however, there is a lack of clinical studies confirming this relation. We aimed to investigate the association of cholesterol concentrations on admission with MVI visualized by cardiac magnetic resonance imaging and clinical outcome in STEMI patients treated by primary percutaneous coronary intervention. Methods and Results: In this prospective, observational study, we included 235 consecutive revascularized STEMI patients. Cholesterol (total cholesterol, low‐density lipoprotein [ LDL ], and high‐density lipoprotein cholesterol) and triglyceride concentrations were determined at presentation. Cardiac magnetic resonance scans were performed 2 (2–4) days after infarction to assess infarct characteristics, including MVI . Clinical end point was the occurrence of major adverse cardiac events ( MACE ) comprising all‐cause mortality, nonfatal reinfarction, and new congestive heart failure. Patients with MVI (n=129; 55%) showed higher levels of total cholesterol (204 [172–226] versus 185 [168–212] mg/dL; P =0.01) and LDL cholesterol (142 [113–166] versus 118 [103–149] mg/dL; P =0.001), whereas high‐density lipoprotein cholesterol and triglycerides did not differ significantly. In multivariable analysis, including all significant clinical and cardiac magnetic resonance determinants of MVI , LDL concentration emerged as an independent predictor of MVI (odds ratio, 1.02 [95% confidence interval, 1.01–1.02]; P =0.002). Furthermore, increased LDL cholesterol (>150 mg/dL) significantly predicted the occurrence of major adverse cardiac events (hazard ratio, 3.09 [95% confidence interval, 1.22–7.87]; P =0.01). Conclusions: In STEMI patients undergoing primary percutaneous coronary intervention, baseline LDL cholesterol concentrations were independently associated with MVI , revealing a clinically relevant link between LDL metabolism and MVI in acute STEMI .