Cardiac Necrosis Markers Research Articles

Remotely Triggered LAD Occlusion Using a Balloon Catheter in Spontaneously Breathing Mice.

Acute myocardial infarction (AMI) is a prevalent and high-mortality cardiovascular condition. Despite advancements in revascularization strategies for AMI, it frequently leads to myocardial ischemia-reperfusion injury (IRI), amplifying cardiac damage. Murine models serve as vital tools for investigating both acute injury and chronic myocardial remodeling in vivo. This study presents a unique closed-chest technique for remotely inducing myocardial IRI in mice, enabling the investigation of the very early phase of occlusion and reperfusion using in-vivo imaging such as MRI or PET. The protocol utilizes a remote occlusion method, allowing precise control over ischemia initiation after chest closure. It reduces surgical trauma, enables spontaneous breathing, and enhances experimental consistency. What sets this technique apart is its potential for simultaneous noninvasive imaging, including ultrasound and magnetic resonance imaging (MRI), during occlusion and reperfusion events. It offers a unique opportunity to analyze tissue responses in almost real-time, providing critical insights into processes during ischemia and reperfusion. Extensive systematic testing of this innovative approach was conducted, measuring cardiac necrosis markers for infarction, assessing the area at risk using contrast-enhanced MRI, and staining infarcts at the scar maturation stage. Through these investigations, emphasis was placed on the value of the proposed tool in advancing research approaches to myocardial ischemia-reperfusion injury and accelerating the development of targeted interventions. Preliminary findings demonstrating the feasibility of combining the proposed innovative experimental protocol with noninvasive imaging techniques are presented herein. These initial results highlight the benefit of utilizing the purpose-built animal cradle to remotely induce myocardial ischemia while simultaneously conducting MRI scans.

Serial measurements of protein and microRNA biomarkers to specify myocardial infarction subtypes.

BackgroundWhile cardiac-specific troponin (cTn) allows for rapid diagnosis of acute type 1 myocardial infarction (T1MI), its performance to differentiate acute myocardial injury (AI) or type 2 myocardial infarction (T2MI) is limited. The objective was to combine biomarkers to improve discrimination of different myocardial infarction (MI) aetiologies.MethodsWe determined levels of cardiac troponin T and I (cTnT, cTnI), cardiac myosin-binding protein C (cMyBP-C), NT-proBNP and ten miRNAs, known to be associated with cardiac pathology in a total of n = 495 serial plasma samples at three time points (on admission, after 1 h and 3 h) from 57 NSTEMI (non-ST-elevation myocardial infarction), 18 AI, and 31 STEMI patients, as defined by fourth universal definition of MI (UDMI4) and 59 control individuals. We then applied linear mixed effects model to compare the kinetics of all molecules in these MI sub-types.ResultsEstablished (cTnT, cTnI) and novel (cMyBP-C) cardiac necrosis markers failed in differentiating T1MI vs T2MI at early time points. All cardiac necrosis markers were higher in T1MI than in T2MI at 3 h after admission. Muscle-enriched miRNAs (miR-1 and miR-133a) were correlated with cardiac necrosis protein markers and did not offer better discrimination. Established cardiac strain marker NT-proBNP differentiated AI and T1MI at all time points but failed to discriminate T2MI from T1MI. However, the combination of NT-proBNP and cTnT along with age returned an overall AUC of 0.76 [95 % CI 0.67–0.84] for differentiating T1MI, T2MI and AI.ConclusionsRather than using single biomarkers of myocardial necrosis, a combination of clinical biomarkers for cardiac necrosis (troponin) and cardiac strain (NT-proBNP) might aid in differentiating T1MI, T2MI and AI.

Relationship of Troponin I with Neutrophil Lymphocyte Ratio and Serum Amyloid A in Acute Coronary Syndrome

Abstract
 Introduction: Acute coronary syndrome (ACS) is the leading cause of death in the world. Acute myocardial infarction can initiate an acute inflammatory process by inducing pro-inflammatory cytokines at the cellular level measured by NLR, at the biomolecular level characterized by SAA production in liver. The relationship of elevated troponin I levels as a marker of myocardial necrosis with NLR and SAA as inflammatory markers need further discussion. The purpose of this study was to determine the relationship between cardiac necrosis markers and inflammatory parameters in ACS.
 Methods: An analytic observational study with a cross-sectional approach was conducted from March to May 2019. This study involved 32 patients with ACS at the Emergency Department of Dr.Kariadi Hospital, with the onset of attacks of 4-6 hours which met the inclusion and exclusion criteria. Examination of troponin I level was done using the ELFA method, NLR value was measured using a hematology analyzer, and SAA level was measured using the ELISA method. Statistical test was done using Spearman correlation. Value of p < 0.05 was considered significant.
 Results: The median (min-max) of troponin I, NLR, and SAA values were 0.617 (0.001-40,000) μg/L, 4.92 (1.38-18.16) and 40.454 (5.879-66.059) μg/ml, respectively. The correlation of troponin I level with NLR and SAA were r=0.180, p=0.243 and r=0.655, p=0.000.
 Conclusions: There was a significant positive moderate relationship between troponin I level and SAA which could be used as a marker of acute inflammation in ACS, whereas cell inflammation marker of NLR did not provide a significant meaning.
 Keywords: ACS, NLR, SAA, troponin

Association of Plasma Methylglyoxal Increase after Myocardial Infarction and the Left Ventricular Ejection Fraction.

Background: Preclinical studies suggest that methylglyoxal (MG) increases within the myocardium upon acute myocardial infarction (AMI) and thereafter contributes to adverse postinfarct remodeling. The aims of this study were to test whether MG increases in plasma of humans after AMI and whether this increase is related to the left ventricular ejection fraction (LVEF). Methods: The plasma samples of 37 patients with ST elevation AMI undergoing primary percutaneous coronary intervention (pPCI) acquired in a previously conducted randomized controlled trial testing remote ischemic conditioning (RIC) were analyzed by means of high-performance liquid chromatography. Time courses of the variables were analyzed by means of mixed linear models. Multiple regression analyses served to explore the relationship between MG levels and the LVEF. Results: Compared to the MG levels upon admission due to AMI, the levels were increased 2.4-fold (95% CI, 1.6–3.6) 0.5 h after reperfusion facilitated by pPCI, 2.6-fold (1.7–4.0) after 24 h and largely returned to the baseline after 30 d (1.1-fold, 0.8–1.5). The magnitude of the MG increase was largely independent of that of cardiac necrosis markers. Overall, the highest MG values within 24 h after AMI were associated with the lowest LVEF after 4 d. While markers of myocardial necrosis and stretch quantified within the first 24 h explained 52% of the variance of the LVEF, MG explained additional 23% of the variance (p < 0.001). Conclusions: Considering these observational data, it is plausible that the preclinical finding of MG generation after AMI negatively affecting the LVEF also applies to humans. Inhibition of MG generation or MG scavenging might provide a novel therapeutic strategy to target post-AMI myocardial remodeling and dysfunction.

Sex differences in patients with takotsubo syndrome

Abstract Funding Acknowledgements Type of funding sources: None. OnBehalf Pol-tako Introduction Takotsubo syndrome (TTS) is an acute revesible left ventricular dysfunction which occurs mainly in postmenopausal women. Despite the fact that the most patients with TTS are postmenopausal women and the possible patomechanism is related to female hormones, including estrogens, men also suffer from TTS. Objectives The goal of this study was to compare course of disease and prognoses in male and female patients with TTS. Patients and Methods The analysis included 210 patients (192 women and 18 men) hospitalized at the academic hospital from the year 2006 to 2020. Results Physical stress was trigger of TTS more often in men than women (50 vs. 38%). There were no differences in the frequency of risk factors and comorbidities, with the exception of higher prevalence of smoking in men. Markers of cardiac necrosis were similar in both groups. At admission and peak NTproBNP levels were significantly more elevated in women (1527 vs. 3152 and 3752 vs. 5079pg/ml, respectively). ST depression was found more frequently in men than in women (22 vs. 5%). Ejection fraction was lower among male patients at discharge (50 vs. 60%), despite the same length of hospitalization. Beta-adrenolytics and statins were more frequently prescribed for women than for men (90 vs 78% and 68 vs. 31%) whereas ACEI was prescribed in 96% men and 79% women. Moreover, there was P2Y12 inhibitors were more often used in men (33 vs 10.4%). In-hospital complications (arrhytmias, mechanical complications, cardiogenic shock) were similar in both groups. However, mortality rate was higher in women (3 vs. 0%). Conclusions Clinical course in patients with TTS is similar in women and men. However, in-hospital mortality was higher in women.

Biomarkers of Inflammation and Oxidative stress in the Prediction and Management of Acute Coronary Syndrome

The assessment of patients presenting with chest pain or symptoms indicative of cardiac ischemia remains a diagnostic challenge. Many types of research have focused on the search for ideal biological markers for the rapid detection of cardiac cell injuries. Markers of inflammation and oxidative stress are the way forward. At present, the biomarker most widely used for diagnosing acute coronary syndrome is cardiac troponin though it has some limitations. Apart from cardiac troponin, several other biomarkers, especially inflammation and oxidative stress markers in acute coronary syndrome, have been investigated. However, most of them still require validation in further studies. As markers of inflammation and oxidative stress address a particular aspect of the pathophysiology of acute coronary syndrome, these biomarkers may provide unique information to the managing clinician separate from that of markers of myocyte necrosis. Serum markers of inflammation and oxidative stress appear before cardiac necrosis markers and are valuable targets for early and timely diagnosis of an acute cardiac event. Using these markers in combination with biomarkers of plaque formation, unstable plaque development, plaque rupture, thrombosis, and myocardial necrosis (multimarker approach) could increase their diagnostic and prognostic value.

Planned delivery to improve postpartum cardiac function in women with preterm pre-eclampsia: the PHOEBE mechanisms of action study within the PHOENIX RCT

Background Women whose pregnancies are affected by hypertensive disorders of pregnancy, in particular preterm pre-eclampsia, are at increased risk of long-term cardiovascular morbidity and mortality. Objectives To investigate the hypothesis that prolongation of a pregnancy affected by preterm pre-eclampsia managed by expectant management compared with planned early delivery would result in worse cardiovascular function 6 months postpartum. Design A randomised controlled trial. Setting 28 maternity hospitals in England and Wales. Participants Women who were eligible for the Pre-eclampsia in HOspital: Early iNductIon or eXpectant management (PHOENIX) study were approached and recruited for the PHOEBE study. The PHOENIX (Pre-eclampsia in HOspital: Early iNductIon or eXpectant management) study was a parallel-group, non-masked, multicentre, randomised controlled trial that was carried out in 46 maternity units across England and Wales. This study compared planned early delivery with expectant management (usual care) with individual randomisation in women with late preterm pre-eclampsia who were 34 weeks’ gestation to less than 37 weeks’ gestation and having a singleton or dichorionic diamniotic twin pregnancy. Interventions Postpartum follow-up included medical history, blood pressure assessment and echocardiography. All women had blood sampling performed on at least two time points from recruitment to the 6-month follow-up for assessment of cardiac necrosis markers. Main outcome measures Primary outcome was a composite of systolic and/or diastolic dysfunction (originally by 2009 guidelines then updated by 2016 guidelines, with an amended definition of diastolic dysfunction). Analyses were by intention to treat, together with a per-protocol analysis for the primary and secondary outcomes. Results Between 27 April 2016 and 30 November 2018, 623 women were found to be eligible, of whom 420 (67%) were recruited across 28 maternity units in England and Wales. A total of 133 women were allocated to planned delivery, 137 women were allocated to expectant management and a further 150 received non-randomised expectant management within usual care. The mean time from enrolment to delivery was 2.5 (standard deviation 1.9) days in the planned delivery group compared with 6.8 (standard deviation 5.3) days in the expectant management group. There were no differences in the primary outcome between women in the planned delivery group and those in the expectant management group using either the 2009 (risk ratio 1.06, 95% confidence interval 0.80 to 1.40) or the 2016 definition (risk ratio 0.78, 95% confidence interval 0.33 to 1.86). Overall, 10% (31/321) of women had a left ventricular ejection fraction &lt; 55% and 71% of the cohort remained hypertensive at 6 months postpartum. No differences were observed between groups in cardiorespiratory outcomes prior to discharge from hospital or in systolic or diastolic blood pressure measurements. Variables associated with the primary outcome (2009 definition) at 6 months postpartum were maternal body mass index (adjusted odds ratio 1.33 per 5 kg/m2, 95% confidence interval 1.12 to 1.59 per 5 kg/m2) and maternal age (adjusted odds ratio 2.16, 95% confidence interval 1.44 to 3.22 per 10 years). Limitations include changing definitions regarding systolic and/or diastolic dysfunction. Conclusions Preterm pre-eclampsia results in persistence of hypertension in the majority of women with late preterm pre-eclampsia at 6 months postpartum and systolic dysfunction in 10%. Pre-eclampsia should not be considered a self-limiting disease of pregnancy alone. Future work Interventions aimed at reducing cardiovascular dysfunction. Trial registration Current Controlled Trials ISRCTN01879376. Funding This project was funded by the Efficacy and Mechanism Evaluation (EME) programme, a Medical Research Council and National Institute for Health Research (NIHR) partnership. This will be published in full in Efficacy and Mechanism Evaluation; Vol. 8, No. 12. See the NIHR Journals Library website for further project information.

The prognosis of myocardial infarction (STEMI &amp; NSTEMI) in patients with metabolic syndrom

A recent review of insulin resistance syndrome (IRS) revealed a rapid escalation of metabolic syndrome among Indians and that the prevalence of predominant component of metabolic syndrome varied from region to region in Indians. Studies on the pathophysiology of this syndrome revealed close to a six-fold increase in cardiovascular mortality. Standardized definition of MI and clinical outcome will be used. A final diagnosis of MI will be made in the presence of serial increases in serum biochemical markers of cardiac necrosis, associated with typical electrocardiographic changes and/or typical symptoms. 27.27% (20) of patients of MI with METS were obese (BMI ≥ 30kg/m2) compared to 2.74% (2) of the patients of MI without METS, which was statistically significant (p value

Association between Biomarkers of Oxidative Stress and Inflammation with Cardiac Necrosis and Heart Failure in Non-ST Segment Elevation Myocardial Infarction Patients and Various Degrees of Kidney Function.

The aim of this study was to explore the possible association between markers of inflammation and oxidative stress (OS) and markers of cardiac function and necrosis in 100 NSTEMI (non-ST-elevation myocardial infarction) patients with various degrees of kidney dysfunction. At admission, ejection fraction (EF), brain natriuretic peptide (BNP), troponin (TnI), creatinine phosphokinase (CPK), alanine transaminase (ALT), aspartate transaminase (AST), high-sensitive C-reactive protein (hs-CRP), interleukins 6 and 10 (IL-6, IL10), myeloperoxidase (MPO), transforming growth factor beta (TGF-β1), glomerular filtration rate (GFR), and albuminuria were assessed. Study participants were divided into 2 subgroups based on the median level of EF. Compared to the high, patients in the low EF group had higher GFR, BNP, CPK, hs-CRP, IL-10, IL-6, and MPO values and lower albuminuria levels. The levels of EF decreased in parallel with the progression of CKD, whereas the levels of BNP, IL-6, and TGF-β were significantly higher in late stages of CKD. Spearman's rho correlation analysis showed that EF was inversely correlated with MPO (r = −0.20, p = 0.05) BNP (r = −0.30, p = 0.002), hs-CRP (r = −0.38, p < 0.0001), IL-10 (r = −0.30, p = 0.003), and IL-6 (r = −0.24, p = 0.02) and positively with GFR (r = 0.27, p = 0.008). TnI was correlated with CPK (r = 0.44, p < 0.0001), CPK-MB (r = 0.31, p = 0.002), ALT (r = 0.50, p < 0.0001), AST (r = 0.29, p = 0.004), IL-10 (r = 0.22, p = 0.03), and MPO (r = −0.28, p = 0.006). In multivariate regression analysis, only BNP (β = −0.011, p = 0.004), hs-CRP (β = −0.11, p = 0.001), and GFR (β = 0.12, p = 0.0029) were independent determinants of EF. Similarly, MPO (β = −1.69, p = 0.02), IL-10 (β = 0.15, p = 0.006), and AST (β = 0.04, p = 0.001) were the 3 major determinants of TnI. Based on these associations, we built a predictive model including markers of inflammation and OS (MPO, IL-10, and hs-CRP) to identify patients with the most severe cardiac injury (combined EF below median and troponin above median values). Receiver-operator characteristic (ROC) analysis showed that the area under the ROC curve of this model to detect patients with low EF and high TnI was 0.67 (p = 0.015, 95%confidence interval = 0.53‐0.81).

Evaluation of profilin 1 as a biomarker in myocardial infarction.

Profilin 1 (Pfn1) is likely to be involved in atherogenesis and myocardial infarction (MI). Clinical data on this subject are very limited. The aim of this study was to search for associations between serum Pfn1 and a number of parameters in MI patients: symptom onset to PCI time (OPT), myocardial necrosis markers, thrombolysis in myocardial infarction (TIMI) flow, antiplatelet drugs, heparin administration and typical atherosclerosis risk factors. We included patients with type 1 MI (according to the Third Universal Definition of Myocardial Infarction) who were able to precisely determine the time of symptom onset. Exclusion criteria involved conditions potentially altering platelet function. We screened 114 patients and included 65. We assessed serum Pfn1 in three time points: on admission (Pfn1_0), 24 hours post PCI (Pfn1_24) and 48 hours post PCI (Pfn1_48) and correlated it with OPT, cardiac necrosis markers (troponin T, CK, CKMB), TIMI flow in the infarct-related artery, pre-hospital P2Y12-antagonist and heparin administration and known atherosclerosis risk factors. Patients with a shorter OPT had higher Pfn1_0 (838.5 vs. 687.1 pg/ml, p=0.007). Patients with impaired coronary flow post PCI had lower Pfn1_24 (748.2 vs. 925.2 pg/ml, p=0.017) and Pfn1_48 (744.5 vs. 879.8, p=0.031. Pfn1_24 and Pfn1_48 were lower in patients who received a P2Y12 antagonist prior to hospital admission. Diabetic patients presented with lower Pfn1_0 concentrations. This is the first study assessing Pfn1 in type 1 MI patients in relation to the chosen parameters. Pfn1 may be a biochemical tool to objectify information on OPT in MI patients. We found an association between Pfn1 and post-PCI TIMI flow, antiplatelet drug administration and diabetes mellitus.

Type 2 myocardial infarction: is it a geriatric syndrome?

Type 2 myocardial infarctions (T2-MI) is a type of necrosis that results from reduced oxygen supply and/or increased demand secondary to other causes unrelated to acute coronary atherothrombosis. The development and implementation of sensitive and high-sensitivity cardiac necrosis marker and the age-related increase of comorbidity lead to a boost of the frequency of T2-MI. T2-MI is often a complication of a high degree of clinical frailty in older adults, emerging as a "geriatric syndrome". Age-related non-cardiovascular causes may be the triggering factors and are strongly associated with the diagnosis, treatment, and prognosis of T2-MI. To date, there are no guidelines on management of this pathology in advancing age. Patient-centered approach and comprehensive geriatric assessment play a key role in the diagnosis, therapy and prognosis of geriatric patients with T2-MI.

1639 Echocardiographic photorealistic imaging of leiomyomatosis intravascularis

Abstract 39-years old female patient was admitted to the Department of Cardiac Surgery because of the suspicion of additional mass in the right atrium (RA). She had no symptoms. Two weeks before she underwent surgery because of the tumours of the uterus and the bladder. Moreover, she was treated for papillary thyroid carcinoma 1 year before. D-dimer levels, NTproBNP and markers of cardiac necrosis weren’t elevated. In histopathological examination leiomyomatosis intravascularis was diagnosed. In the transthoracic echocardiography (TTE) we confirmed the presence of additional inhomogeneous, mobile mass in the RA with morphology corresponding to thrombus. Moreover the inferior vena cava (IVC) was also involved. We decided to perform transesophageal echocardiography (TEE). Bicaval view showed that the structure enters through the IVC to the RA and protrude across the tricuspid valve throughout the cardiac cycle. In the photorealistic imaging we could exactly see huge mass that was elongated, mobile, inhomogeneous, had no adhesion with the wall of heart and vein and waved along with the heartbeat (figure 1 A,B). The surgery was performed through median sternotomy. A huge mass with about 30cm length was excised through RA oblique incision, on beating heart with cardiopulmonary bypass (figure 1C). Abstract 1639 Figure. Leiomyomatosis intravascularis

Effect of Pretreatment with Omega-3 Supplement on Cardiac Necrosis Markers in Chronic Kidney Disease Patients Undergoing Elective Percutaneous Coronary Intervention.

Objective:Studies have demonstrated the direct relation between elevation in cardiac necrosis markers and increased risk of cardiovascular complications after percutaneous coronary intervention (PCI) in chronic kidney disease (CKD) patients. In this study, we sought to evaluate the effect of omega-3 on creatine kinase-MB (CK-MB) and troponin-I in CKD patients undergoing elective PCI.Methods:Eighty CKD patients, candidate for elective PCI, were randomly assigned into two groups: Group A – receiving omega-3 (2.5 g, 12 h before PCI) plus standard treatment (n = 37) and Group B – control group, receiving only standard therapy (aspirin 325 mg and clopidogrel 600 mg loading dose and weight-adjusted intravenous heparin) (n = 43). Blood samples were collected before and 24 h after PCI for measuring CK-MB and troponin-I. The primary endpoint was considered to be postprocedural variations of CK-MB and troponin-I levels in both groups. The secondary endpoint was the percentage of pre-procedural myocardial infarction (PMI) occurrence, defined as the elevation of post-PCI troponin-I, between study groups.Findings:Both the baseline and 24-h CK-MB were significantly higher in omega-3 group. Although 24-h troponin-I increased less in omega-3-treated arm compared to the control group, no statistically significant variation was observed between the two groups. With regard to PMI occurrence, no significant difference was detected among study groups.Conclusion:Despite the beneficial but nonsignificant effects of omega-3 on decreasing post-PCI elevation of troponin-I and PMI occurrence, further investigations with bigger study population, higher doses of omega-3 and longer duration of treatment, and long-term follow-up of patients are required to better test the potential effects of omega-3 in improving clinical outcomes in CKD patients undergoing PCI.

To Be or Not to Be … Acute Coronary Syndrome

Abstract Introduction: The association between ST segment abnormalities, elevated cardiac enzymes, and chest pain is usually a marker of acute coronary injury. However, certain other pathologies can sometimes mimic acute coronary syndromes. Case report: A 40-year-old Caucasian male, former smoker, with no other cardiovascular risk factors, presented to the Emergency Department for typical ischemic, prolonged chest pain. The ECG demonstrated inverted T waves in leads I, II, aVL, and V3 to V6. The patient presented high cardiac necrosis markers (troponin I 2.65 ng/ml). Based on these findings, the case was interpreted as non-ST segment elevation myocardial infarction, but coronary angiography excluded the presence of significant coronary lesions. The ventriculography showed an efficient left ventricle, with mild hypokinesia of the two apical thirds of the anterior left ventricular wall. Cardiac magnetic resonance imaging demonstrated areas of hypersignal on the T2-weighted imaging sequence in the left ventricular myocardium, suggestive for acute myocarditis. The patient was started on antiplatelet, beta-blocker, and angiotensin converting enzyme inhibitor, with favorable evolution. Conclusion: This case underlines the polymorphic appearance of acute myocarditis, which can often mimic an acute coronary event.

Asymptomatic Myocardial Injury in a Low Level of Carbon Monoxide Poisoning

Carbon monoxide (CO) poisoning is an important cause of mortality and morbidity. Although measured in CO levels are not always correlated with clinical symptoms, neurological symptoms may present in lower CO levels, and cardiac signs and symptoms may occur in high CO levels. Low levels of CO exposure are very rare causes of myocardial injury. In this case presentation, we aimed to report on a patient who had a 20% level of CO and high troponin level without cardiac signs and symptoms. A 26-year-old male presented to the emergency department with headache, nausea, and vomiting. The initial electrocardiogram showed ST-segment depression of 1 mm in Lead II(II)-Lead III(III) Lead augmented vector foot (aVF) and ST-segment elevation in Lead I(I)Lead augmented vector left (aVL). The patient’s laboratory values were as follows: troponin I: 1.5 ng/mL and FCOHb: 20.7%. The first echocardiogram of the patient demonstrated global hypokinesia of the left ventricle. The coronary angiogram of the patient was normal. All patients considered to have CO poisoning should be evaluated with electrocardiograms, cardiac necrosis marker measurements, and an echocardiogram for myocardial injury regardless of the level of CO or the absence of cardiac symptoms and signs. (JAEM 2015; 14: 91-3)

Tako-tsubo Cardiomyopathy on the First Day After Renal Transplantation — Case Report and Literature Review

BackgroundThe etiology of tako-tsubo cardiomyopathy, defined as a transient left ventricular dysfunction in the absence of significant coronary artery stenosis, still remains unclear. This syndrome mainly occurs in postmenopausal women and is often associated with emotional stress or miscellaneous diagnostic and therapeutic procedures. Estimated prevalence of tako-tsubo cardiomyopathy is found in 1% to 2% of patients presenting with suspected acute coronary syndrome. So far there has been only one case report of tako-tsubo cardiomyopathy in a renal transplant recipient. Case reportWe describe the case of a 68-year-old woman with a history of coronary artery disease and coronary artery bypass grafting in whom unspecific transient chest pain and hypotension were observed on the first day after renal transplantation. After transplantation, the patient was anuric with pulmonary congestion and toxic tacrolimus concentrations were observed. Electrocardiogram showed sinus rhythm with left bundle branch block (LBBB) that has not been described before. Plasma cardiac necrosis markers troponin I and creatine kinase MB were mildly elevated. Echocardiography showed severe left ventricular function impairment with characteristic shape of left ventricle. Subsequent cardiac catheterization revealed the absence of angiographic evidence of acute plaque rupture within both coronary arteries and bypass grafts. During the next few days there was marked clinical improvement with resolution of LBBB and full recovery of all biochemical parameters. On discharge, full functional recovery of the left ventricle in echocardiography was observed. Postulated mechanisms of tako-tsubo cardiomyopathy include catecholamine excess, coronary artery spasm, and microvascular dysfunction. On the other hand calcineurin inhibitors are known factors causing coronary epicardial endothelial dysfunction and negatively affecting vasomotor function. ConclusionsTako-tsubo cardiomyopathy in patients after renal transplantation may be at least in part a manifestation of calcineurin inhibitor cardiotoxicity.

Primary Angioplasty in Patient with St-Segment Elevation Myocardial Infarction in the Setting of Intentional Carbon Monoxide Poisoning

BackgroundST-segment elevation myocardial infarction (STEMI) due to coronary artery occlusion in the setting of acute carbon monoxide (CO) poisoning is a very rare presentation. ObjectiveOur aim was to report on the use of primary angioplasty in a patient with STEMI in the setting of CO poisoning. Case ReportA 36-year-old man with retrosternal chest pain was admitted after exposure to CO. The initial electrocardiogram (ECG) showed ST depression in I, aVL, and V3−V4 with slight ST elevation in II, III, aVF leads. Toxic carboxyhemoglobin level of 22% and troponin I of 2.19 μg/L were confirmed. After oxygen therapy the chest pain diminished, but after about 15 h it returned. The repeat ECG revealed normalization of previous ST depression with persistent ST elevation in II, III, aVF leads. The troponin I concentration was 5.94 μg/L. An echocardiogram demonstrated an apex hypokinesia involving the adjacent segments of the anterior and lateral wall. On the coronary angiogram, an acute occlusion of the distal left anterior descending coronary artery was confirmed. Primary percutaneous coronary intervention (PCI) of the infarct-related artery was performed. After PCI, the patient was symptom free and had partial ST-segment elevation resolution. The patient was discharged home after 7 days, with persistent ST-T changes and mild hypokinesia of the apex suggesting myocardial injury. ConclusionsPatients with toxic CO exposure who have symptoms of STEMI should be carefully evaluated with serial ECG, cardiac necrosis marker measurements, and an echocardiogram. When there is evidence of myocardial injury, a wider use of coronary angiography can identify patients who could benefit from PCI.

Ventricular septal rupture after blunt chest trauma

Ventricular septal rupture (VSR) is a rare complication of blunt chest trauma. The commonest effect of this non-penetrating injury of the thorax is pulmonary and myocardial contusion. We present the case of a 30-year-old man with post-traumatic ventricular septal rupture. Two days earlier he fell from a roof (about 4 m high) and was admitted to the emergency department of the regional hospital. On admission, he was fully conscious and by virtue of his left forearm being broken he was referred to the surgical department, where his left radius bone was attended to. Several hours later, the patient’s general clinical condition started gradually worsening. Symptoms of progressive pulmonary failure were observed, and eventually he was intubated and mechanically ventilated. Moreover, due to cardiac status deterioration, an echocardiographic examination was performed urgently and muscular VSR with left-to-right flow was visualised (Fig. 1). After this diagnosis was established, the patient was referred emergently to our Cardiosurgical Department. On admission he was mechanically ventilated and deeply unconscious with no reaction to pain. At that time no sedation was employed. Moreover, he required marked doses of positive inotropic agents (dobutamine and dopamine). By virtue of serious neurological status, he was disqualified from salvage cardiac surgical procedure. In transthoracic echocardiographic examination, a rupture in the middle, muscular part of the ventricular septum, about 10–12 mm in diameter, 40 mm from the mitral annulus and 30 mm from the apex, with accompanying left-right flow velocity of approximately 2.0 m/s was visualised. In the meantime, computed tomo graphy (CT) angiography was performed, which revealed normal thoracic aorta. Abdomen ultrasonography did not reveal serious abnormalities. Hypotonia (RR 70/40 mm Hg) was observed from the beginning and it was accompanied by high fever (up to 40°C). Several laboratory cardiac necrosis marker tests, such as cardiac troponin I, and creatinine kinase MB isoenzyme confirmed cardiac injury. Soon after admission, an intra-aortic balloon pump (IABP) was inserted through the puncture of the right femoral artery and continuous veno-venous haemofiltration (CVVH) was initiated due to renal failure with oliguria. In spite of the aggressive treatment with IABP and CVVH, the patient developed multi-organ failure including liver (alanine aminotransferase activity increased up to 8,328 IU/L and asparagine aminotransferase to 2,406 IU/L). A head CT (Fig. 2) revealed diffuse axonal injury, extensive post-traumatic changes in the form of significant swelling of the brain, overall tightening of the subarachnoid space in the third and fourth ventricles and also in the lateral ventricles. Disseminated air zones were found in the subcortical white matter. Small haemorrhagic changes were revealed in the right cerebellar hemisphere and single small (4 mm) changes were present in the frontal lobes. On the basis of the patient’s general status, and the results of imaging studies, the patient was disqualified from invasive treatment of VSR. On the seventh day of hospitalisation in the Department, the patient’s general condition rapidly worsened, hypotension non-responsive to increased doses of catecholamines appeared, and the patient developed coagulopathy. One day later, the patient developed progressive bradycardia and hypotension. Eventually, in spite of pharmacological resuscitation, he did not respond and he died.

Stress echocardiography in the ED: diagnostic performance in high-risk subgroups

PurposeTo assess stress-echo (SE) diagnostic performance in patients presenting to the emergency department (ED) with spontaneous chest pain, especially in subgroups in which exercise ECG diagnostic performance has been questioned (women, elderly, history of coronary artery disease). MethodsBetween June 2008 and May 2011, 474 patients with an episode of spontaneous chest pain, non-diagnostic electrocardiogram and negative cardiac necrosis markers underwent SE. Patients with inducible ischemia (Isch) were asked to undergo coronary angiography. Patients with negative SE were discharged and contacted by telephone at least 6 months after discharge, to ascertain the occurrence of new cardiac events. Main findingsExercise stress-echo (ESE) was employed in 270 patients and dobutamine (DSE) in 218 (including 14 with inconclusive ESE); a diagnosis of coronary artery disease (CAD) was confirmed or excluded in 434 (92%) patients. SE was negative for Isch in 318 patients (206 ESE and 112 DSE) and positive in 132. During follow-up, patients with negative SE had 4 cardiac events. SE showed: sensitivity 90%, specificity 92%, positive predictive value 78% and negative predictive value 97%. Sensitivity was comparable between patients aged < or ≥70 years (84 vs 94%) and between gender (89 vs 96%), but lower in patients with known CAD (88 vs 94%, P < .05); specificity was comparable regardless of age (94 vs 99%) and presence of CAD (97 vs 91%), but was lower among women (87 vs 96%, P < .05). ConclusionsSE had a very good diagnostic performance in ED patients with suspected Isch, both overall and in selected high-risk groups.

Macrophage Migration Inhibitory Factor Is Enhanced in Acute Coronary Syndromes and Is Associated with the Inflammatory Response

BackgroundChronic inflammation promotes atherosclerosis in cardiovascular disease and is a major prognostic factor for patients undergoing percutaneous coronary intervention (PCI). Macrophage migration inhibitory factor (MIF) is involved in the progress of atherosclerosis and plaque destabilization and plays a pivotal role in the development of acute coronary syndromes (ACS). Little is known to date about the clinical impact of MIF in patients with symptomatic coronary artery disease (CAD).Methods and ResultsIn a pilot study, 286 patients with symptomatic CAD (n = 119 ACS, n = 167 stable CAD) undergoing PCI were consecutively evaluated. 25 healthy volunteers served as control. Expression of MIF was consecutively measured in patients at the time of PCI. Baseline levels of interleukin 6 (IL-6), “regulated upon activation, normal T-cell expressed, and secreted” (RANTES) and monocyte chemoattractant protein-1 (MCP-1) were measured by Bio-Plex Cytokine assay. C-reactive protein (CRP) was determined by Immunoassay. Patients with ACS showed higher plasma levels of MIF compared to patients with stable CAD and control subjects (median 2.85 ng/mL, interquartile range (IQR) 3.52 versus median 1.22 ng/mL, IQR 2.99, versus median 0.1, IQR 0.09, p<0.001). Increased MIF levels were associated with CRP and IL-6 levels and correlated with troponin I (TnI) release (spearman rank coefficient: 0.31, p<0.001). Patients with ACS due to plaque rupture showed significantly higher plasma levels of MIF than patients with flow limiting stenotic lesions (p = 0.002).ConclusionTo our knowledge this is the first study, demonstrating enhanced expression of MIF in ACS. It is associated with established inflammatory markers, correlates with the extent of cardiac necrosis marker release after PCI and is significantly increased in ACS patients with “culprit” lesions. Further attempts should be undertaken to characterize the role of MIF for risk assessment in the setting of ACS.