Elevated Cardiac Enzymes Research Articles

Acute neurogenic stunned myocardium in a patient with Guillain-Barré syndrome: case report.

A 65-year-old man with GBS presented with reversible left ventricular systolic failure. On first presentation, our patient had no history or indications of heart malfunction. During the clinical manifestation of his autonomic dysfunction, he had electrocardiographic alterations, modestly increased cardiac enzymes, significant left ventricular systolic dysfunction, and segmental wall motion irregularity. Once the initial episode was over, these anomalies and his symptoms resolved quickly. We believe the reversible left ventricular dysfunction was caused by the toxic impact of elevated catecholamines as well as transiently injured sympathetic nerve endings in the myocardium, which was apparently caused by GBS. We recommend that echocardiography be performed in patients who exhibit clinical signs of autonomic dysfunction, particularly if they are associated with abnormal electrocardiographic findings, cardiac enzyme elevation, or hemodynamic instability, so that appropriate medical therapy can be instituted as soon as possible. GBS is a not a very rare situation in our context. Thus, doctors are supposed to know the life-threatening complications such as neurogenic stunned myocardium and be prepared to dodge it.

PO-02-034 PULSED-FIELD ABLATION OF ATRIAL FIBRILLATION: KINETIC OF RELEASE OF MULTIPLE CARDIAC BIOMARKERS

Different studies have showed data on the variation of cardiac biomarkers after a thermal energy approach (i.e. cryoablation or radiofrequency) for the ablation of atrial fibrillation (AF). To date, when a non-thermal energy is used, such as electroporation obtained by means of a pulsed-field ablation (PFA), the kinetic of release of multiple cardiac biomarkers has not yet been clarified. We studied the pattern of release of 6 different biomarkers prior and after PFA of AF. All consecutive patients (pts) indicated for AF ablation who received a PFA treatment with the new PFA catheter (FARAWAVE) at our center were included. PVI was obtained using 2 kV with 8 applications per vein with additional lesions delivered at the operator’s discretion. Samples of cardiac troponin I (cTnI, ng/l), creatinine kinase-MB (CK-MB, ng/dl), fibrinogen (FB, mg/dl), myoglobin (MY, ng/ml), N-terminal (NT)-pro hormone B-type natriuretic peptide (NT-ProBNP, pg/ml) and C-reactive protein (CRP, mg/dl) were collected before PFA ablation (baseline) and at 3h, 24h and 48h after ablation. Data are reported as mean±SD. We analyzed data from a total of 25 pts (64±11 years, 52% male, 68% with paroxysmal AF). A total of 36±3 PFA deliveries was required to achieve PVI. In ten cases an additional set of PFA lesions was performed (25±6 PFA deliveries). No significant differences were found between baseline and 3h, 24h and 48h for both FB and NT-ProBNP (Panel a,b). On the contrary, MY level significantly increased from baseline at 3h and decreased at 24h and restored at 48h (Panel c). CRP values remained stable at 3h and significantly increased from baseline after 24h and 48h (Panel d). Kinetics of CK-MB and cTnI were similar: they both significantly increased after 3h and decreased after 24h and 48h (Panel e,f). No correlation was found between the total number of PFA deliveries and kinetics of different biomarkers after 3h, 24h and 48h. CK-MB, cTnI, and MY increased at 3h and have a recover towards lower values already after 24h. Cardiac enzyme elevations were not correlated with the number of PFA deliveries after AF ablation.

Expanding Heart Donor Pool With a Broken Heart: Cardiac Transplant From Donor Following Circulatory Death With Takotsubo Syndrome.

Owing to the growth of patients with advanced heart failure and limited potential for donation after brain death, expanding donor source with hearts from controlled donation after circulatory death (cDCD) and meeting extended criteria are essential strategies. We present the first case of a patient who successfully underwent cardiac transplant (CT) from cDCD with Takotsubo syndrome (TTS). The donor was a 49-y-old man without risk factors for coronary artery disease (CAD) and terminal amyotrophic lateral sclerosis with respiratory failure and mechanical ventilation support. A decision was made with patient’s family to withdraw life-sustaining therapies (WLSTs). Organ donation option was presented and consented, and cDCD Maastricht Classification III1 was considered suitable. He presented normal blood tests, electrocardiogram, and echocardiogram. The cDCD process was performed using an extracorporeal membrane oxygenation circuit to perform thoracoabdominal normothermic regional perfusion.2 During intraoperative evaluation, transesophageal echocardiography revealed normal left ventricular ejection fraction (LVEF). However, after WLST, moderate dysfunction (LVEF 37%) and apical ballooning suggestive of TTS were observed (Figure 1A), continuing present after thoracoabdominal normothermic regional perfusion withdrawal and organ extraction. Epicardial coronary arteries palpation did not reveal pathology.FIGURE 1.: A, Intraoperative transesophageal echocardiography evaluation that shows the left ventricle in diastole and systole with apical akinesia and preserved contractility of basal segments. B, The 12-lead electrocardiogram reveals T wave inversion and prolonged QT interval. C, A graph of heart recovery timeline based on the high-sensitivity troponin T levels, left ventricular ejection fraction, and inotrope support, correlated with the d after cardiac transplant. D, Normal right and left coronary arteries in the post cardiac transplant protocol–based coronary angiography. LVEF, left ventricular ejection fraction.The heart recipient was a 52-y-old man with severe, irreversible ischemic cardiomyopathy and 10 d with a ventricular assist device, listed for CT after excluding severe comorbidities and a multidisciplinary team discussion. An orthotopic transplant was performed using the bicaval technique, with spontaneous heartbeat and cold ischemia time of 86 min. He required minimal vasoactive support, withdrawn 48 h after CT. The electrocardiogram showed diffuse negative T waves and prolonged QTc interval (Figure 1B), and peak level of high-sensitivity troponin T was 2115 ng/L. Six days after CT, LVEF normalized. The timeline of heart recovery is represented in Figure 1C. The coronary angiography ruled out donor CAD (Figure 1D). The patient was discharged 30 d after CT and is doing well 43 wk after. Serial echocardiograms reveal normal wall motion and function. DISCUSSION Although TTS and CT have been indirectly associated, few cases have been published on donor hearts with TTS, these with no compromised survival3; none in cDCD. Similar pathophysiological aspects, present in TTS and cDCD, could be responsible for the phenomenon that occurred during CT. In the cDCD, the heart experiences a warm ischemia period during the WLST, cardiac arrest, and CT. This implies ischemia–reperfusion injury: activation of inflammatory and coagulation cascades and release of catecholamines.4 The mechanisms behind TTS, clinical condition characterized by acute transient left ventricular dysfunction, remain unknown. The most widely accepted theory is catecholamine-induced cardiotoxicity, and growing evidence is arising for myocardial inflammation, endothelial and microcirculation dysfunction, and neurohormonal alterations.5 Because of donor’s age, low-risk profile of CAD, and echocardiographic abnormalities, TTS was suspected. The post-CT protocol–based coronary angiography ruled out obstructive CAD or atherosclerotic plaque rupture. There was a rapid normalization of LVEF, negative T waves in the electrocardiogram, and elevated cardiac enzymes. This fulfilled the most widely used TTS diagnostic criteria.5 A pre-CT coronary angiography in patients >40 y or at risk of CAD could avoid ruling out hearts with left ventricular dysfunction. CONCLUSION The pathophysiological knowledge of cDCD and TTS could increase CT rates. This first experience in cDCD should be cautiously interpreted and analyzed individually in future cases.

Neutrophil-to-lymphocyte ratio as a predictive marker for acute coronary syndrome

Abstract Introduction: Measurement of a simple inflammatory marker like neutrophil-to-lymphocyte ratio (NLR) could improve the risk stratification of patients with acute coronary syndrome (ACS), especially in a limited resource country like ours. Therefore, this study was conducted to evaluate the predictive value of NLR in determining ACS. Materials and Methods: A cross-sectional, observational study was conducted. A total of 101 patients suffering from angina/angina equivalents with electrocardiography (ECG) changes or typical elevation of cardiac enzymes (troponin T/creatinine phosphokinase-MB [CPK-MB]) who present to the hospital within 12 h of the onset of symptoms were selected and analyzed for the study. Results: The study found that NLR significantly correlated with CPK-MB and left ventricular ejection fraction (LVEF). Conclusion: It was found that NLR showed significant correlations with CPK-MB and LVEF, indicating its usefulness as a predictive factor for the severity of ACS. NLR was also not affected by the type of ACS or other comorbidities/risk factors of diabetes and hypertension, indicating its role as an independent prognostic factor in ACS.

Aortic Intramural Hematoma Mimicking Acute Coronary Syndrome

Type A Aortic intramural haematoma (IMH), a variant form of classic aortic dissection, has been accepted as an increasingly recognised and potentially fatal entity of acute aortic syndrome.It is a very dangerous, fatal, and emergency condition. It is very important to recognize the symptoms of acute aortic syndrome related to appropriate management Case Illustration A 52 year old man patient suffered from chest pain with moderate intensity while he was working at home. It was sharp , tear-like sensation, in the middle of the chest radiated to the back, accompanied with cold sweating, and did not relieve by rest. Because of this condition he brought to hospital. From examination at Emergency room, he had cardiomegaly, aortic dilatation. From the Electrocardiography an st elevation at V1-V2 and T inverted V4-V6 precordial lead,I aVL extremities lead and slightly elevated cardiac enzymes with risk factors for active smoking and uncontrolled hypertension. Initially he was suspected of having acute coronary syndrome with differential diagnose acute aortic syndrome. To exclude the diagnose he had underwent cardiac catheterization, the cardiologist in charge suspicious this patient with aortic dissection because of trapping contrast durante procedure and coronary minor disease. For a better diagnosis, transtransthoracic echocardiography and Aortic Computed Tomography angiography was performed on the patient which confirmed the evidence of dissection. After being diagnosed, we treat the patient as an acute aortic syndrome and we stabilize the patient's condition. The patient was planned for cardiac surgery Discussion Acute aortic syndrome, which includes Acute Aortic Dissection, Intramural Hematoma and penetrating aortic ulcer, is difficult to diagnosed. Aortic intramural hematoma, which is one of the acute aortic syndromes, is characterized by the presence of a hematoma in the medial layer of the aortic wall without the appearance of an intimal tear. The incidence of intramural hematoma differs slightly from that of aortic dissection syndrome. Patients with intramural hematomas often occur in older patients, more often with aortic aneurysms The patient receive treatment aggressively to control blood pressure by administering a non-dihydropyridine calcium channel blocker intravenously and then beta blocker, angiotensin II receptor blockers, was also needed. Acute aortic syndrome, where an intramural aortic hematoma can present with varying symptoms of varying severity, which can lead to misdiagnosis and delay in cases of life-threatening disease. In the case of our patient, who had strong cardiac risk factors, His initial presentation described an acute myocardial infarction; the diagnosis was made after CT scan was performed and the patient remained stable Conclussion Complaints of chest pain due to symptoms of acute aortic syndrome are very important to be recognized immediately because they need proper management. Complaints in this syndrome have similarities with complaints in acute coronary syndrome, pulmonary embolism and others. Patients with aortic intramural hematoma are at high risk for developing periaortic hematoma and hemorrhagic pericardial effusion. In patients with an intramural aortic hematoma, Stanford A, the most appropriate management is surgical technique. Initial management of blood pressure control, heart rate and anti-pain can be given. In this case, the choice of a combination of surgery with endovascular may be a logical choice of therapy

Stuttering as a signal of encephalopathy associated with toripalimab in a pancreatic ductal adenocarcinoma patient: a case report

BackgroundImmune checkpoint inhibitor (ICI) combined with chemotherapy has exhibited promising results in small sample studies of pancreatic cancer patients. The efficacy of toripalimab, a programmed cell death protein 1 (PD-1) monoclonal antibody has been explored in the previous studies and it was established that immune-related adverse events (irAEs) associated with administration of this drug deserve proper attention and adequate management.Case presentationA 43-year-old female patient with advanced pancreatic ductal adenocarcinoma (PDAC) was treated with toripalimab in combination with gemcitabine and nab-paclitaxel (T-GA) as the first-line treatment. She developed immune-related encephalopathy with stuttering as the main clinical symptom and Magnetic resonance imaging (MRI) showed multiple cerebral white matter demyelination changes, concomitant with asymptomatic cardiac enzyme elevation and hypothyroidism. The symptoms resolved after the discontinuation of toripalimab and corticosteroid treatment.ConclusionsStuttering might be an early sign of neurotoxicity which can be easily neglected during the treatment. These findings provide guidance for the identification of these rare and occult neurological irAEs (n-irAEs) in the clinical practice.

Arm Pain After Walking Up a Flight of Stairs

Acute coronary syndrome is a leading cause of mortality and morbidity worldwide, requiring emergency care and admission. Wellens syndrome is a preinfarction state that may not have the classic electrocardiographic findings expected with other forms of acute coronary syndrome or the elevated cardiac enzymes. This lack of typical changes in electrocardiography provides a clinical challenge for diagnosis. The ability to promptly identify and treat this time-sensitive state of potential myocardial infarction and death has a significant prognostic value that cannot be overstated.

Vasospastic angina following COVID-19 vaccine-related myocarditis: an underlying cause of chest pain.

We present a 13-year-old boy who had recurrent chest pain with elevated cardiac enzymes and abnormal ST segments in electrocardiogram 36 hours after the second dose of BNT162b2 vaccination. Cardiac MRI and coronary angiography with acetylcholine provocation confirmed myocarditis and vasospastic angina, respectively. Coronary vasospasm may play a pivotal role in the chest pain in COVID-19 vaccine-related myocarditis.

Calanus oil attenuates isoproterenol-induced cardiac hypertrophy by regulating myocardial remodeling and oxidative stress

ABSTRACT Calanus oil, an oil extracted from the marine crustacean Calanus finmarchicus, is one of the richest sources of omega-3 and poly-unsaturated fatty acids. Although calanus oil has been shown to have a significant anti-hypertensive, anti-inflammatory, anti-fibrotic and anti-obesity effects in various cardiovascular diseases, but little is known about its effect on pathological cardiac hypertrophy. Thus, the present study was carried out to evaluate the therapeutic effect of calanus oil on cardiac hypertrophy. Cardiac hypertrophy was induced by subcutaneous injections with isoproterenol (5 mg/kg b.w) for 14 consecutive days. Calanus oil (400 mg/kg) was given orally for 4 weeks. Cardiac pathological remodeling was evaluated by echocardiography, after which morphometric, biochemical, histological and ultrastructural analyses were performed. Calanus oil treatment significantly ameliorated isoproterenol-induced structural and functional alterations in echocardiography. Calanus oil also reduced the relative heart weight, significantly decreased the elevated cardiac enzymes (LDH and CK-MB) and the lipid peroxidation marker (MDA), augmented the myocardial antioxidant status (TAC), and ameliorated the histopathological and ultrastructural changes in cardiac tissues and prevented interstitial collagen deposition. The present study, for the first time, provided morphometric, biochemical, histological and ultrastructural evidences supporting the promising anti-hypertrophic effect of calanus oil against ISO-induced cardiac hypertrophy. This anti-hypertrophic effect of calanus oil is via regulating myocardial remodeling and oxidative stress. Therefore, it could be used as potential pharmacological intervention in the management of cardiac hypertrophy.

Clinical Profile and Outcome of Acute Myocardial Infarction among Young Adults at a Tertiary Care Centre in Manipur, India: A Cohort Study

Introduction: The incidence of Acute Myocardial Infarction (AMI) is rising in young adults. Timely control of cardiovascular risk factors is important to prevent the increasing incidence of AMI in young adults. Aim: To analyse the clinical profile, risk factors, and outcomes of AMI among the young adult population in Manipur, India. Materials and Methods: A hospital-based cohort study was conducted in a tertiary care centre at Department of Medicine, Regional Institute of Medical Sciences, Imphal, Manipur, India from January 1, 2021, to December 31, 2022, among patients aged 45 years or younger attending the medicine Outpatient Department (OPD), admitted to the Intensive Care Unit (ICU) and Intensive Coronary Care Unit (ICCU) with the first attack of AMI. Cases involving pregnancy, known cases of pericarditis, and Congenital Heart Disease (CHD) were excluded. Data were collected using a performa regarding demographic profile, clinical presentation, risk factors, and treatment outcomes. The data were analysed using Statistical Package for Social Sciences (SPSS) 21.0 and expressed as descriptive statistics. Results: A total of 39 cases were reported with a mean age of 40.2±4.6 years, with a male-to-female ratio of 9:1. The majority of cases presented with chest pain (74.3%), followed by shortness of breath (40%), nausea (13%), and collapse (10%). 75% of cases presented with multiple clinical features. The most common risk factors in young adults were smoking (84.6%), alcohol consumption (56.4%), family history of heart disease (25.6%), hypertension (20.5%), substance abuse (20.5%), diabetes (17.9%), and dyslipidemia (25.6%). Cases showed elevated cardiac enzymes - Creatine Kinase-Myocardial Band (CK-MB) (92.3%) and Troponin I (94.9%). Electrocardiogram (ECG) changes revealed ST segment elevation MI (89.7%). Only one case resulted in death during the hospital stay. Conclusion: The incidence of AMI among young adult populations is increasing, emphasising the need to raise awareness regarding cardiovascular risk factors and lifestyle modifications. However, the cases have shown good clinical outcomes among young adults with the disease.

A CASE REPORT OF BEHÇET'S DISEASE WITH CORONARY ARTERY INVOLVEMENT

ABSTRACT
 We present a case of coronary artery thrombosis due to Behçet's disease. A 49-year-old female patient, diagnosed with Behçet's disease and followed up by us, applied to the emergency department with sudden onset of pressure-type chest pain, and was evaluated as acute myocardial infarction due to elevated cardiac enzymes and ST segment elevation in the anterior leads on electrocardiography (ECG). Coronary angiography revealed near-total thrombosis in the lumen of the left anterior descending artery (LAD) and in the circumflex (CX) artery,it was intervened with anticoagulant therapy. The patient's cardiac risk was found to be low and differential diagnosis was made in terms of myocardial infarction. Thereupon, the causes of hypercoagulability were investigated in the patient who was consulted to us, and acute phase reactants were found to be high. This was related to the coronary artery involvement of Behçet's disease and in addition to the treatment containing antiaggregant, statin, angiotensin receptor blocker, intravenous (IV) high-dose methylprednisolone and cyclophosphamide-mesna treatment was given for immunosuppressive purposes. It should not be forgotten that there may be vascular involvement due to Behçet's disease and coronary arteries may also be affected.

Acute myocarditis masquerading as anterior wall myocardial infarction: A case report

Myocarditis is the inflammation of the myocardium. The clinical presentation of myocarditis ranges from asymptomatic state to acute heart failure which may mimic acute coronary events. Because of the similar presentation of chest pain, elevated cardiac enzymes, and electrocardiographic (ECG) changes, acute myocarditis may rarely masquerade as acute myocardial infarction (AMI). High suspicion is often necessary for treating such patients, keeping in mind the different treatment protocols required for managing each pathology. SCARE 2020 Guidelines. We report a case of a young female presenting with sudden onset chest pain with ECG changes suggestive of acute anterior wall myocardial infarction (AWMI). Further investigations ruled out AWMI, and she was diagnosed with acute myocarditis. She was treated for myocarditis and showed a prompt recovery. Acute myocarditis may present clinically similarly to ACS; hence a high level of suspicion is required to differentiate the two entities. The absence of significant cardiovascular risk factors for atherosclerotic coronary artery disease, absence of RWMA, and normal coronary angiogram are further suggestive of myocarditis.

A Rare Case Report of Ruptured Sinus of Valsalva Aneurysm

<p>主動脈竇動脈瘤是一種罕見的心臟結構病變，因具非特異性表徵及困難診斷，容易導致高死亡風險。本案例是一位53歲男性患者，因急性胸痛入院治療，藉由實驗室檢查發現心肌酵素升高、D-二聚體升高，心電圖檢查為aVR導程ST段上升、於第I、II、V4~6導程出現ST-T波段變化，初步診斷為左冠狀動脈主幹心肌梗塞，立即行冠狀動脈攝影檢查發現無異常。個案出現胸痛合併心因性休克之症狀，從中排除主動脈剝離、肺栓塞、心包填塞等診斷，深入檢視病史紀錄及影像報告，發現心臟超音波、胸部電腦斷層及冠狀動脈血管攝影檢查有由左流向右心室的瘻管分流，最終確診為主動脈竇動脈瘤破裂。患者緊急接受右冠狀竇動脈瘤修補及主動脈瓣置換手術治療後，胸痛、休克狀況改善且左心室功能恢復，術後預後良好。在面對急性胸痛合併血液動力學不穩定的患者時，除了須考慮症狀相關的疾病診斷外，當聽診發現S1及S2連續性心雜音時，建議將主動脈竇動脈瘤破裂列入考慮，以掌握治療處置之重要時機。</p> <p> </p><p>Aneurysm of the sinus of Valsalva is a rare cardiac anomaly due to the nonspecific symptoms and dif-ficult confirmation of diagnosis leading to high mortality. This report describes the case of a 53-year-old man who had suffered from acute chest pain. The electrocardiogram showed the ST segment ele-vation in lead aVR and ST-T wave changes in leads I, II and V4-6. Elevated D-dimer levels and cardi-ac enzymes were also observed. Acute myocardial infarction caused by the left main coronary artery obstruction was initial diagnosed. Coronary angiogram was performed immediately and the result indicated non-obstructive coronary artery. However, cardiogenic shock with persistent chest pain was discovered. Aortic dissection, pulmonary thromboembolism and cardiac tamponade were gradually excluded. Through detailed review and analysis of medical history, physical assessment and image ex-aminations with echocardiography, chest computed tomography and coronary angiogram, a ruptured sinus of Valsalva aneurysm was eventually diagnosed based on image examinations which revealed left-to-right shunt communicating with the right-sided heart chambers. The patient received emergen-cy right coronary sinus aneurysm repairment and aortic valve replacement surgery. Symptoms with chest pain and shock gradually disappeared and left ventricular function was restored postoperatively. The patient demonstrated excellent recovery. In facing relevance diagnostics for patients with acute chest pain and hemodynamic instability, a ruptured sinus of Valsalva aneurysm must be considered to endure best treatment timing if heart auscultation reveals S1 and S2 continuous murmurs.</p> <p> </p>

COVID-19 Vaccine-Induced Cardiac Concerns

Myocarditis has been increasingly recognized as a rare complication of COVID-19 mRNA vaccinations, especially in young adolescent males. According to the US Centers for Disease Control and Prevention, the incidence of myocarditis in males 16–29 years of age is approximately 10.7 cases per 100,000. Of those diagnosed with myocarditis, roughly 69% were diagnosed 3–5 days after their second vaccination. Most recent reports have shown clinical presentations consistent with chest pain, elevated cardiac enzymes, ST elevations on ECG, and further echocardiogram or cardiac MRI findings displaying mild to moderate left systolic dysfunction. Although mechanisms in the development of myocarditis are still not clear, a promising hypothesis is that myocarditis is exacerbated by a hyperimmune response to the second dose of the vaccine. Children have a robust immune response to COVID-19, which has been exemplified by increasing cases of multisystem inflammatory syndrome in children. This report will review trends seen in patients with vaccine-induced myocarditis and highlight the benefit to risk assessment of cardiovascular complications associated with COVID-19.

Toxic Cardiac Manifestation in a Young Male with Organophosphate Poisoning with Breakthrough Seizures

Organ phosphorus compounds are used as pesticides and represent a common cause of poisoning in developing countries including Pakistan due to their widespread availability. Toxicity due to these agents can affect many organs including the heart. Here, we report a case of acute organophosphorus poisoning in a patient, followed by acute myocardial infarction; documented by clinical features, electrocardiographic changes, and elevated cardiac enzymes. This case report will help a physician to look for acute myocardial injury in a patient with OP poisoning to reduce fatal complications and improve mortality, as such presentation with OP poisoning is rarely seen especially in a pediatric population.

Agomelatine ameliorates cadmium-induced toxicity through the modification of HMGB-1/TLR-4/NFκB pathway

Cadmium (Cd) has potential hazards on human beings. Consequently, this study was performed to explore the protective effects of agomelatine (AGO), a melatonin receptor agonist, against Cd-induced toxicity in rats. AGO (40 mg/kg/day) was administered orally concomitant with intra peritoneal injection of Cd (0.4 mg/kg/day) for 14 days. Then, blood, biochemical parameters and histological examination of affected organs including, heart and testis, were evaluated. Interestingly, AGO significantly counteracted Cd-induced elevation of serum cardiac enzymes. Similarly, AGO significantly improved the deterioration of serum testosterone level with Cd administration. The oxidative balance was corrected by AGO, as evidenced by decrease malondialdehyde (MDA), and superoxide dismutase activity in cardiac and testicular tissues. Additionally, AGO increased silent information regulator 1 protein (SIRT-1) and decreased High mobility group box 1 (HMGB1), Toll like receptor-4 (TLR-4), and Myd88 levels that subsequently reduced expression of nuclear factor-κB (NF-κB). Moreover, level of apoptotic marker; caspase-3 was inhibited by AGO. In accordance with the biochemical and molecular results, AGO restored structure of cardiac myofibers and seminiferous tubules. Collectively, AGO mitigated cardiac and testicular toxicity of Cd via modulation of SIRT-1/HMGB1 and its downstream pathway.

DELAYED-ONSET CORONARY VASOSPASM FOLLOWING RADIOFREQUENCY CATHETER ABLATION OF ATRIAL FIBRILLATION

DELAYED-ONSET CORONARY VASOSPASM FOLLOWING RADIOFREQUENCY CATHETER ABLATION OF ATRIAL FIBRILLATION

Evaluation of Cardiac Biomarkers and Expression Analysis of IL-1, IL-6, IL-10, IL-17, and IL-25 among COVID-19 Patients from Pakistan.

Coronavirus disease 19 (COVID-19) is caused by viral infection of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Where upregulation of several important biomarkers and multiple organ dysfunction occurs, this study aimed to evaluate the association of cardiac biomarkers and CS induced acute lung damage with disease severity and mortality in survival of COVID-19 patients. A total of 500 COVID-19 patients with elevated cardiac biomarkers were studied for the analysis of myocardial abnormality through cardiac enzymes, inflammatory biomarkers, and the expression analysis of various cytokines, including IL-1, IL-6, IL-10, IL-17, and IL-25 genes. The elevation of various cardiac enzymes including LDH (87%), CK (78.4%), TNI (80.4%), CK-MB (83%), and D-dimer (80.8%) were found correlated (p < 0.001) with COVID-19 infection. Cardiac enzyme elevation was highly associated with an increased level of inflammatory biomarkers such as CRP (14.2%), SAA (11.4%) and erythrocyte sedimentation rate (ESR) (7.8%) (p = 0.001 for all). The quantitative expression analysis of IL-10, 1L-17, and 1L-25 were found to be high, while those of IL-1 and IL-6 were moderately elevated. The death-to-live ratio of COVID-19 patients was 457:43 indicating that the patients having elevated levels of both CKMB, D-dimer, CK and IL-1, IL-6, IL-10 and D-dimer, Troponin, CK and IL-1, IL-10 had high fatality rate (73% and 12% respectively). The current finding concludes that the evaluation of cardiac biomarkers with cytokine storm plays a significant role in COVID-19-associated anatomical organ damage, myocardial injury, and mortality. Physicians should pay special attention to cardiac biomarkers in patients with old age, inflammation, and comorbidities among COVID-19 infections.

Case Report: Treatment for steroid-refractory immune-related myocarditis with tofacitinib

IntroductionImmune therapy has ushered in a new era of tumor treatment, at the expense of immune-related adverse events, including rare but fatal adverse cardiovascular events, such as myocarditis. Steroids remain the cornerstone of therapy for immune-related myocarditis, with no clear consensus on additional immunosuppressive treatment for steroid-refractory cases yet.Case reportHere, we report a patient with stage IV nasopharyngeal carcinoma who developed immune-related myocarditis in the fourth course of therapy with immune checkpoint inhibitors. The patient presented with precordial discomfort with elevation of cardiac enzymes and interleukin-6, atypical electrocardiographic abnormalities, and reduced left ventricular ejection fraction. Coronary computed tomography angiography excluded the possibility of acute coronary syndrome. The therapy with tofacitinib targeting the Janus kinase-signal transducer and activator of transcription signal pathway was successfully conducted, since there was no significant improvement in troponin under high-dose steroid and intravenous immunoglobulin treatment. The patient recovered without major adverse cardiac events during hospitalization.DiscussionThe safety and efficacy of tofacitinib in a patient with steroid-refractory immune-related myocarditis were investigated, hoping to provide a basis for prospective therapeutic strategies. Tofacitinib led to remarkable remissions in primary autoimmune disease by blocking the inflammatory cascade, indicating its potential therapeutic use in immune-related adverse events.

Association of Growth Differentiation Factor 15 with Arterial Stiffness and Endothelial Function in Subpopulations of Patients with Coronary Artery Disease: A Proof-of-Concept Study.

Growth-differentiation factor-15 (GDF-15) is a biomarker belonging to the transforming growth factor-beta cytokine superfamily, which is linked to many pathological conditions, including inflammation and myocardial injury. Pulse wave velocity (cfPWV) and augmentation index (AIx) are indices of arterial stiffness, which are associated with the severity of coronary artery disease (CAD). Flow-mediated dilatation (FMD) is a well-studied surrogate marker of endothelial-dependent dysfunction and systemic inflammation. In this proof-of-concept study, we aimed to investigate the relationship between circulating GDF-15, endothelial dysfunction, and indices of arterial stiffness in different settings of coronary artery disease and myocardial injury. In this cross-sectional single-center study, we enrolled patients (n = 22) after interventional treatment for acute myocardial infarction (AMI), patients (n = 11) admitted with chest pain and elevated cardiac enzymes but without evidence of obstructing CAD (MI-NOCAD) in percutaneous coronary angiography (CAG), and patients (n = 20) who underwent CAG according to indications without evident obstructive CAD in CAG (NOCAD). FMD was assessed at the brachial artery. AIx of the central aortic pressure and cfPWV were estimated by applanation tonometry at the radial and carotid-femoral site, respectively, with a validated acquisition system (Sphygmo- Cor, AtCor Medical, Sydney (NSW), Australia). ELISA was used to determine circulating GDF- 15 serum levels (R&D Systems, Minneapolis, MN). Clinical and demographic data and values of routine biochemical biomarkers were obtained. The highest high-sensitive cardiac Troponin I (hsTpnI) value during hospitalization was also recorded. Left ventricular ejection fraction (LVEF) was assessed with a transthoracic echocardiogram. Patients with AMI were older, had worse LVEF, higher values of hsTpnI and increased circulating GDF-15 levels. Importantly, AMI patients had increased cfPWV values, deteriorated AIx values, blunted FMD and worse serum creatinine levels compared to MI-NOCAD and NOCAD patients, respectively, whereas MI-NOCAD and NOCAD did not differ from each other significantly on these biomarkers. Both AMI and MI-NOCAD patients presented a higher but comparable white blood cell count than NOCAD patients. A strong linear correlation between GDF-15 and cfPWV, hsTpnI, AIx, white blood cell count and creatinine but not with FMD was demonstrated in the general study population. This proof-of-concept study showed that higher circulating levels of GDF-15, an inflammatory biomarker, were associated significantly with increased arterial stiffness only in AMI patients, whereas elevated GDF-15 demonstrated a linear relationship with the severity of the myocardial injury.