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Background: Radial (RA) instead of femoral access (FA) for coronary interventions has become a European Society of Cardiology Class-IA guideline recommendation. But when the decision on the access site is left to the discretion of the operator, differences in adverse event rates mitigate., Methods: We compared the 30-day outcome for RA and FA in all patients recruited for the observational German Austrian ABSORB Registry (GABI-R) in regard to all-cause mortality, stroke, myocardial infarction (MI), TIMI major bleedings (TMB) and quality of life (QoL). All patients were treated with a bioresorbable vascular scaffold. Access site was left to the discretion of the operator., Results: In total, 3137 patients included by 92 centers received percutaneous coronary interventions (PCI) for acute MI in 51.5% and non-acute settings in 48.5%. RA was performed in 47.8% and had a higher median radiation exposure (3896 vs. 3082 cGycm 2 , p < 0.001). There was no difference in the amount of contrast used. There was also no difference in all-cause mortality (0.53% vs. 0.49%, p = 0.86), the combination of death, MI and stroke (1.87% vs. 1.83%, p = 0.94), but a trend towards more TMB (0.47% vs. 1.04%, p = 0.07) with FA. These outcomes were consistent across the subgroups of patients with ST-elevation MI, non-ST-elevation-ACS and stable coronary artery disease. Finally, QoL did not differ between RA and FA., Conclusions: In this contemporary GABI-R cohort, in which access site was left to the discretion of the operator, both access routes were safe and equal concerning QoL (ClinicalTrials.gov; NCT02066623)., Competing Interests: Declaration of competing interest, (Copyright © 2021 Elsevier Inc. All rights reserved.)

Objective: To investigate the outcomes after bioresorbable scaffold (BRS) implantation in calcified coronary lesions. In calcified coronary lesions, durable metallic drug-eluting stent (DES) implantation is associated with worse clinical outcomes compared to noncalcified lesions. Although not recommended, BRSs were frequently implanted in calcified lesions in clinical practice. Their outcome is not well investigated., Methods: Between November 2013 and January 2016, 3326 patients were enrolled in the German-Austrian ABSORB ReglstRy (GABI-R). Lesion calcification severity was classified into no (n = 1144), mild (n = 1306), and moderate-to-severe (n = 690) calcification., Results: Patients with calcification were older (none: 59.1 ± 11.2 vs. mild: 61.6 ± 10.9 vs. moderate to severe: 62.4 ± 10.5 years, P < 0.001), had more diabetes (19.1 vs. 20.8 vs. 23.9%, P = 0.015), and more often had previous myocardial infarction (MI) (19.3 vs. 23.1 vs. 25.4%, P = 0.002). Despite a higher rate of postdilatations (P < 0.001), lesions with calcification had more residual stenosis (2.05 ± 9.36% vs. 3.11 ± 9.36% vs. 3.89 ± 9.39%, P < 0.001). Consequently, procedural success was achieved in 97.7 vs. 96.2 vs. 93.6% of cases in none, mild, and moderate-to-severe calcification (P < 0.001). At 24 months, cardiac death (0.3 vs. 0.7 vs. 1.6%, P = 0.009) was higher with increasing calcification. However, no significant between-group difference was observed in the incidence of target vessel MI, target vessel revascularization, or target lesion failure. The rate of probable scaffold thrombosis was significantly higher with increasing calcification., Conclusion: In GABI-R, ABSORB scaffolds in calcified lesions required more postdilation, led to more residual stenosis, but did not portend increased target lesion revascularization over 2 years. Nevertheless, coronary calcification severity emerged as a cardiovascular risk marker and was predictive of cardiovascular mortality. Clinicaltrial.gov NCT02066623.

Background: There is a large body of literature on acute myocardial infarction complicated by cardiogenic shock. However, very little is known about patients who are initially haemodynamically stable and develop cardiogenic shock during percutaneous coronary intervention., Methods: A total of 47,407 consecutive patients were prospectively enrolled in the PCI Registry of the Euro Heart Survey Programme. We analysed interventions with peri-procedural complications that were classified as 'shock induced by procedure' on the case report form. Clinical and procedural characteristics as well as hospital outcomes of haemodynamically stable patients who developed cardiogenic shock during percutaneous coronary intervention were evaluated. Patients with haemodynamic instability at presentation prior to intervention were excluded., Results: A total of 68 patients (0.2%) developed cardiogenic shock as a complication of percutaneous coronary intervention. The majority of cases comprised acute coronary syndrome (60.3%) with complex lesions (93.1%). Most patients had multi-vessel disease (82.1%) and an ejection fraction less than 40% (58.1%). In the multivariate analysis, left main disease (odds ratio (OR) 9.51), ST-segment elevation myocardial infarction (OR 5.31) and multi-vessel disease without left main involvement (OR 3.32) were the strongest independent predictors of peri-procedural cardiogenic shock. Among these patients procedural success was low (66.1%) and in-hospital mortality was very high (39.7%)., Conclusions: In this real-world registry the rate of haemodynamically stable patients who developed cardiogenic shock during percutaneous coronary intervention was very low. Patients at a priori high risk were more likely to be affected by this complication. The in-hospital mortality rate of these patients was very high.

Periprocedural myocardial infarction (MI), a rare complication after transcatheter aortic valve implantation (TAVI), is associated with worse outcome. According to the Valve Academic Research Consortium (VARC-2), MI is defined by an increase in cardiac troponin (cTn) and creatine kinase MB (CK-MB) levels; however, many patients show periprocedurally elevated cTn without clinical evidence of MI. The aims of this study were to establish reference values of cardiac troponin I measured with a high-sensitivity assay (hs-cTnI) and to assess the periprocedural diagnostic value of this biomarker in patients who underwent TAVI. Hs-cTnI and CK-MB levels were assessed before and up to 3 days after transfemoral (TF) or transapical (TA) TAVI in 515 patients. A high proportion (61.2%) of patients had elevated hs-cTnI at baseline. According to VARC-2 criteria, almost all TA-patients (99.5%) showed an MI based on hs-cTnI compared with 4.2% based on CK-MB. In TF-patients, 81.1% had an MI based on hs-cTnI compared with 9.0% based on CK-MB. Only 10 patients (2%), however, had a type 1 MI. The ninety-ninth percentile for hs-cTnI was 285 ng/L in the TAVI cohort. After applying a TAVI-specific cutoff the frequency of MI was lower and more realistic (TF: 5% vs 81.1%; p <0.001; TA: 22.2% vs 99.5%; p <0.001). In conclusion, the VARC-2 definition leads to an overestimation of periprocedural MI. Our new TAVI-specific reference values yield a more realistic estimation of the myocardial ischemic risk. hs-cTnI, however, does not seem to be the biomarker of choice for MI detection in this setting., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Context: Troponin T upstream open reading frame peptide (TnTuORF) may be useful as a novel biomarker in acute cardiac syndromes., Objective: The study examined the early release kinetics of TnTuORF., Materials and Methods: We analyzed the time course of the release of cardiac troponins I and T and TnTuORF in patients (n = 31) with hypertrophic obstructive cardiomyopathy undergoing transcoronary ablation of septal hypertrophy (TASH)., Results: Fifteen minutes after TASH, the levels of both troponins increased significantly (cTnT median: 18 ng/L versus 27 ng/L; cTnI median: 15 ng/L versus 25 ng/L). TnTuORF showed no variation., Discussion: We observed a significantly greater increase in cTnI compared with cTnT., Conclusion: Our results demonstrate that troponin assays allow early detection of myocardial injury, whereas TnTuORF levels remain unchanged in this setting.

Background: The signal peptide for human B-type natriuretic peptide preprohormone (BNPsp), which is released from cardiomyocytes, is increased in plasma of patients with acute myocardial infarction (AMI); however, its exact release kinetics have not been defined., Methods: We measured BNPsp and high-sensitivity cardiac troponin T (hs-cTnT) in a reference group of individuals without structural heart disease (n = 285) and determined the release kinetics of these biomarkers in patients (n = 29) with hypertrophic obstructive cardiomyopathy undergoing transcoronary ablation of septal hypertrophy (TASH), a procedure allowing exact timing of onset of iatrogenic AMI. Blood samples were collected before TASH and at numerous preselected time points after TASH., Results: The reference median BNPsp concentration was 53.4 pmol/L [interquartile range (IQR) 47.0-61.0; 95th percentile 85.9 pmol/L; 99th percentile 116.3 pmol/L]. Baseline concentrations in patients undergoing TASH were higher than in the reference group [91.9 pmol/L (IQR 62.9-116.4); P < 0.0001]. BNPsp increased significantly, peaking at 15 min after induction of AMI [149.6 pmol/L (109.5-204.9) vs baseline; P = 0.004] and declining slowly thereafter, falling below the preprocedural value after 8 h (P = 0.014). hs-cTnT increased significantly 15 min after induction of AMI [26 ng/L (19-39) vs 18 ng/L (11-29); P = 0.001] and remained high at all later time points., Conclusions: BNPsp concentrations increased immediately after AMI induction, providing early evidence of myocardial injury. The release kinetics of BNPsp differed from those of hs-cTnT. These findings provide information that should help in establishing the diagnostic value of BNPsp in the setting of early AMI., (© 2015 American Association for Clinical Chemistry.)

Background: The introduction of modern troponin assays has facilitated diagnosis of acute myocardial infarction due to improved sensitivity with corresponding loss of specificity. Atrial fibrillation (AF) is associated with elevated levels of troponin. The aim of the present study was to evaluate the diagnostic performance of troponin I in patients with suspected acute coronary syndrome and chronic AF., Methods: Contemporary sensitive troponin I was assayed in a derivation cohort of 90 patients with suspected acute coronary syndrome and chronic AF to establish diagnostic cut-offs. These thresholds were validated in an independent cohort of 314 patients with suspected myocardial infarction and AF upon presentation. Additionally, changes in troponin I concentration within 3 hours were used., Results: In the derivation cohort, optimized thresholds with respect to a rule-out strategy with high sensitivity and a rule-in strategy with high specificity were established. In the validation cohort, application of the rule-out cut-off led to a negative predictive value of 97 %. The rule-in cut-off was associated with a positive predictive value of 88 % compared with 71 % if using the 99th percentile cut-off. In patients with troponin I levels above the specificity-optimized threshold, additional use of the 3-hour change in absolute/relative concentration resulted in a further improved positive predictive value of 96 %/100 %., Conclusions: Troponin I concentration and the 3-hour change in its concentration provide valid diagnostic information in patients with suspected myocardial infarction and chronic AF. With regard to AF-associated elevation of troponin levels, application of diagnostic cut-offs other than the 99th percentile might be beneficial.

Objective: Alterations in cortisol awakening and stress responses (CAR, CSR) are sensitive markers for the basal activity and responsiveness of the hypothalamus-pituitary-adrenal axis (HPAA) in psychopathological conditions. We investigated whether patients with takotsubo cardiomyopathy (TTC) differ in these markers when compared with non-ST-segment elevation myocardial infarction (NSTEMI) patients and healthy controls., Methods: 19 female TTC patients were compared with 20 female NSTEMI patients and with 20 healthy women, matched by age and index event date. Salivary sampling indicated cortisol release, questionnaires assessed personality, life events, chronic stress and psychiatric symptoms., Results: The groups did not differ relevantly in their basal HPAA activity, psychiatric or personality profiles. Despite increased heart rates in response to stress (median difference (MDdiff)=3.5, p=0.002) and higher nervousness scores (MDdiff=-3.0, p=0.024), TTC patients revealed a blunted CSR with a medium effect compared to the controls (MDdiff=-3.2 nmol/L, p=0.022, r=0.36); even when controlled for prestress cortisol differences (p=0.044, r=0.33). In comparison with NSTEMI patients, no significant differences in CSR (MDdiff=-1.9 nmol/L, p=0.127, r=0.25) or nervousness (MDdiff=2.0, p=0.107) can be observed. Stressful life events, for example, traumatic experiences, occurred more often in TTC (42%) than in NSTEMI patients and controls (both 10%, p=0.031)., Conclusions: In this small exploratory trial, a trend for a blunted CSR and high incidences of stressful life events were observed in TTC patients. If these results can be confirmed in larger studies, chronic stress and the inhibitory influence of cortisol on catecholamine release might be significant for the pathogenesis of TTC., (Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.)

Acute myocardial infarction was one of the most common causes of death in Germany in 2011. According to the guidelines of the European Society for Cardiology, systemic fibrinolysis and primary percutaneous coronary intervention (PCI) are the methods of choice for acute treatment. Primary PCI should be given priority due to its superiority. The transradial access should be preferred due to the lower bleeding complication rate. In the selection of stents the new generation of drug-eluting stents (DES) are superior to the first generation of bare metal stents (BMS). It has now been demonstrated that the incident rates of DES (e.g. mortality, target vessel revascularization, early and late stent thrombosis and myocardial infarction) are significantly lower. For bioresorbable scaffolds (BRS) long-term results for the use in treatment of ST-elevation myocardial infarction (STEMI) are not yet available but initial results are very promising. However, the selection of a stent needs to be done on an individual basis in order to do justice to all aspects. Data with respect to thrombectomy in acute treatment are heterogeneous. Currently, a thorough consideration of all aspects is necessary because thrombus aspiration can also be associated with an increased rate of incidents. In a state of hemodynamic stability only so-called culprit lesions should currently be treated with a stent. Elective interventions on further stenoses should be carried out after consideration of individual factors and if necessary evaluation of the hemodynamic relevance.

Objective: To determine the release kinetics of different biomarkers with potential as novel early ischaemic biomarkers in patients with acute coronary syndrome (ACS); it is difficult to establish the detailed release kinetics in patients with acute myocardial infarction (AMI)., Methods: We analysed the release kinetics of soluble fms-like tyrosine kinase (sFlt-1), ischaemia modified albumin (IMA), and heart-type fatty acid binding protein (hFABP) in patients with hypertrophic obstructive cardiomyopathy who were undergoing transcoronary ablation of septal hypertrophy (TASH), a procedure mimicking AMI. Consecutive patients (n=21) undergoing TASH were included. Blood samples were collected before TASH and 15, 30, 45, 60, 75, 90, and 105 min and 2, 4, 8, and 24 h after TASH. sFlt-1 and hFABP were quantified in serum, and IMA was quantified in plasma using immunoassays., Results: sFLT-1 and hFABP increased significantly 15 min after induction of AMI vs baseline as follows: sFlt-1, 3657.5 ng/L (IQR 2302.3-4475.0) vs 76.0 ng/L (IQR 71.2-88.8) (p<0.001); hFABP, 9.0 ng/mL (IQR 7.0-15.4) vs 4.6 ng/mL (IQR 3.4-7.1) (p<0.001). sFlt-1 demonstrated a continuous decrease after the 15th min. hFABP showed a continuous increase until the 8th hour with a decline afterwards. The IMA concentrations increased significantly 30 min after induction of AMI vs baseline, with values of 26.0 U/mL (IQR 21.8-38.6) vs 15.6 U/mL (IQR 10.1-24.7) (p=0.02), and then decreased after 75 min., Conclusions: sFlt-1 and hFABP increased very early after induction of myocardial ischaemia, showing different release kinetics. The additional information provided by these findings is helpful for developing their potential combined use with cardiac troponins in patients with suspected AMI.

Diagnosis of myocardial infarction (MI) is based on ST-segment elevation on electrocardiographic evaluation and/or elevated plasma cardiac troponin (cTn) levels. However, troponins lack the sensitivity required to detect the onset of MI at its earliest stages. Therefore, to confirm its viability as an ultra-early biomarker of MI, this study investigates the release kinetics of cardiac myosin binding protein-C (cMyBP-C) in a porcine model of MI and in two human cohorts. Release kinetics of cMyBP-C were determined in a porcine model of MI (n = 6, pigs, either sex) by measuring plasma cMyBP-C level serially from 30 min to 14 days after coronary occlusion, with use of a custom-made immunoassay. cMyBP-C plasma levels were increased from baseline (76 ± 68 ng/l) at 3 h (767 ± 211 ng/l) and peaked at 6 h (2,418 ± 780 ng/l) after coronary ligation. Plasma cTnI, cTnT, and myosin light chain-3 levels were all increased 6 h after ligation. In a cohort of patients (n = 12) with hypertrophic obstructive cardiomyopathy undergoing transcoronary ablation of septal hypertrophy, cMyBP-C was significantly increased from baseline (49 ± 23 ng/l) in a time-dependent manner, peaking at 4 h (560 ± 273 ng/l). In a cohort of patients with non-ST segment elevation MI (n = 176) from the SYNERGY trial, cMyBP-C serum levels were significantly higher (7,615 ± 4,514 ng/l) than those in a control cohort (416 ± 104 ng/l; n = 153). cMyBP-C is released in the blood rapidly after cardiac damage and therefore has the potential to positively mark the onset of MI.

The value of multivessel percutaneous coronary intervention (MV-PCI) in patients with cardiogenic shock (CS) and multivessel disease (MVD) is still unclear because randomized controlled trials are missing. Therefore, we sought to evaluate the impact of MV-PCI on in-hospital outcomes of patients with MVD presenting with CS: 336 patients with acute myocardial infarction complicated by CS and ≥70% stenoses in ≥2 major epicardial vessels were included in this analysis of the Euro Heart Survey PCI registry. Patients undergoing MV-PCI (n = 82, 24%) were compared to those with single-vessel PCI (n = 254, 76%). The rate of 3-vessel disease (60% vs 57%, p = 0.63) was similar in the 2 cohorts. Presentation with resuscitation (48 vs 46%, p = 0.76) and ST-segment elevation myocardial infarction (83 vs 87%, p = 0.31) was frequent in patients with MV-PCI and single-vessel PCI. Patients with ventilation were more likely to receive MV-PCI (30% vs 19%, p = 0.05). There was a tendency toward a higher hospital mortality in patients with MV-PCI (48.8% vs 37.4%, p = 0.07). After adjustment for confounding variables, no significant difference for in-hospital mortality (odd ratio [OR] 1.28, 95% confidence interval [CI] 0.72 to 2.28) could be observed between the 2 groups. Age (OR 1.41, 95% CI 1.13 to 1.77), 3-vessel disease (OR 1.78, 95% CI 1.04 to 3.03), ventilation (OR 3.01, 95% CI 1.59 to 5.68), and previous resuscitation (OR 2.55, 95% CI 1.48 to 4.39) were independent predictors of hospital death. In conclusion, MV-PCI is currently used in only 1/4 of patients with CS and MVD. An additional nonculprit PCI was not associated with a survival benefit in these high risk patients., (Copyright © 2012 Elsevier Inc. All rights reserved.)

We present a 45-year-old patient who had to undergo aortocoronary bypass surgery after acute posterior myocardial infarction. On day twelve, the patient suddenly developed the classic signs of cardiogenic shock including angina, tachycardia, and hypotension. ECG displayed significant ST-elevations and troponin T was positive. Echocardiography suspected relevant pericardial effusion. However, the typical clinical signs of acute pericardial tamponade(distension of jugular veins, paradoxical pulse) were absent. Therefore, a computed tomography was carried out, which confirmed an isolated left ventricular tamponade resulting in severe diastolic and systolic dysfunction with profoundly impaired left ventricular filling. Immediate operative drainage was necessary since percutaneous pericardiocentesis was impossible given the untypical localization. This case demonstrates that clearcut signs of myocardial infarction can be misleading and may represent the untypical presentation of left ventricular tamponade,particularly in the setting after open-heart surgery.

Objective: The paradigm that cardiac myocytes are non-proliferating and terminally differentiated cells has recently been challenged by several studies reporting the ability of bone marrow-derived cells (BMC) to transdifferentiate into cardiomyocytes. However, these results are controversial and could not be reproduced by others. Therefore, we studied the contribution and potential transdifferentiation of BMC into different cell types during the remodelling process in mouse hearts with experimental myocardial infarction., Methods: Mice (C57BL/6J) were sublethally irradiated, and BM from enhanced green fluorescent protein (eGFP)-transgenic mice was transplanted. Coronary artery ligation was performed 3 months later. The hearts were studied 7 days (n=13) and 21 days (n=12) after infarction. Immunohistochemical staining was performed using antibodies against titin, connexin 43, vimentin, SMemb alpha-smooth muscle actin, CD45, CD34, F4/80, BS-1, CD31, and eGFP. Sections were analyzed using fluorescence and confocal laser microscopy., Results: Success of BM transplantation was confirmed by FACS analysis. Occlusion of the coronary artery resulted in infarct sizes of 41+/-6% of the left ventricle. CD45+/eGFP+ inflammatory cells were found frequently after 7 days and to a lesser degree after 21 days. In 25 examined hearts, only 3 eGFP-positive cardiomyocytes were found. However, numerous BMC-derived fibroblasts and myofibroblasts were found in the infarct area. BMC contributed to scar tissue neoangiogenesis but not to angiogenesis in the periinfarct and remote zones., Conclusion: Transdifferentiation of BMC into viable cardiomyocytes is a negligible event in normal repair processes after myocardial damage. BMC-derived fibroblasts and myofibroblasts as well as neoangiogenesis significantly contribute to post-infarction scar formation and might be important in scar tissue remodelling.

The guidelines "Akutes Koronarsyndrom" published by the German Society of Cardiology, "Management of acute myocardial infarction in patients presenting with ST-segment elevation", and "Guidelines for percutaneous coronary interventions" published by the European Society of Cardiology evaluate diagnostic tools and treatment strategies for ST segment elevation myocardial infarctions. These guidelines offer evidence-based recommendations and allow a standardized therapeutic approach thereby improving the patient's treatment and reducing the mortality. The optimal care for patients presenting with ST segment elevation myocardial infarctions consists of a prehospital phase where an immediate diagnosis should be reached by means of a twelve-channel ECG followed by basic medical treatment with administration of acetylsalicylic acid, heparin, beta-blocker, and nitrates by an emergency physician. The hospital phase can be optimized by integrated myocardial infarction networks with coronary care units offering primary percutaneous coronary interventions (PCIs) and adjuvant medical treatment including the administration of glycoprotein IIb/IIIa inhibitors. If the onset of symptoms is < 3 h and the transportation time to a coronary care unit > 90 min, the indication of primary fibrinolysis should be given by the emergency physician. If fibrinolysis fails, there is a clear indication for rescue PCI. Even with successful thrombolysis PCI should be performed within 24 h. A dual oral antithrombotic therapy starting immediately after diagnosis with a loading dose of 600 mg clopidogrel should be continued with 75 mg/d clopidogrel for 9-12 months on top of 100 mg/d acetylsalicylic acid.