The clinical impact of circulating caspase-3 p17 level: a potential new biomarker for myocardial injury and cardiovascular disease

2011 ◽  
Vol 7 (4) ◽  
pp. 443-445 ◽  
Author(s):  
Kanwar P Singh ◽  
Allan S Jaffe ◽  
Bruce T Liang
Keyword(s):  
Cardiovascular Disease ◽  
Myocardial Injury ◽  
Caspase 3 ◽  
Clinical Impact

scholarly journals Imaging Evaluation of Pulmonary and Non-Ischaemic Cardiovascular Manifestations of COVID-19

Diagnostics ◽  
2021 ◽  
Vol 11 (7) ◽  
pp. 1271
Author(s):  
Sebastiano Cicco ◽  
Antonio Vacca ◽  
Christel Cariddi ◽  
Rossella Carella ◽  
Gianluca Altamura ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Myocardial Injury ◽  
Nuclear Imaging ◽  
Emergency Setting ◽  
Imaging Evaluation ◽  
Coagulation Abnormalities ◽  
Cardiovascular Involvement ◽  
Highly Sensitive ◽  
Inflammatory Syndrome ◽  
Inflammatory Burden

Coronavirus Disease 2019 (COVID-19) has been a pandemic challenge for the last year. Cardiovascular disease is the most described comorbidity in COVID-19 patients, and it is related to the disease severity and progression. COVID-19 induces direct damage on cardiovascular system, leading to arrhythmias and myocarditis, and indirect damage due to endothelial dysfunction and systemic inflammation with a high inflammatory burden. Indirect damage leads to myocarditis, coagulation abnormalities and venous thromboembolism, Takotsubo cardiomyopathy, Kawasaki-like disease and multisystem inflammatory syndrome in children. Imaging can support the management, assessment and prognostic evaluation of these patients. Ultrasound is the most reliable and easy to use in emergency setting and in the ICU as a first approach. The focused approach is useful in management of these patients due its ability to obtain quick and focused results. This tool is useful to evaluate cardiovascular disease and its interplay with lungs. However, a detailed echocardiography evaluation is necessary in a complete assessment of cardiovascular involvement. Computerized tomography is highly sensitive, but it might not always be available. Cardiovascular magnetic resonance and nuclear imaging may be helpful to evaluate COVID-19-related myocardial injury, but further studies are needed. This review deals with different modalities of imaging evaluation in the management of cardiovascular non-ischaemic manifestations of COVID-19, comparing their use in emergency and in intensive care.

Abstract 16185: Biomarker-based Heart Failure Risk Stratification in Patients With Atherosclerotic Cardiovascular Disease: Observations From HPS-3/TIMI-55-REVEAL

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
David Berg ◽  
Stephen D Wiviott ◽  
Eugene Braunwald ◽  
David A Morrow ◽  
Keyword(s):  
Heart Failure ◽  
Cardiovascular Disease ◽  
Myocardial Injury ◽  
Cox Regression ◽  
Troponin T ◽  
Risk Indicators ◽  
Atherosclerotic Cardiovascular Disease ◽  
Circulating Biomarkers ◽  
Clinical Risk ◽  
Hemodynamic Stress

Background: Circulating biomarkers reflecting pathways implicated in heart failure (HF) may improve HF risk assessment in patients with stable atherosclerotic cardiovascular disease (ASCVD). Hypothesis: We aimed to evaluate the performance of circulating biomarkers of hemodynamic stress, myocardial injury, and inflammation for the prediction of hospitalization for HF (HHF) in a large well-characterized cohort with stable ASCVD followed for a median of 4.1 years. Methods: HPS3/TIMI 55-REVEAL was a randomized, double-blind, placebo-controlled trial of the CETP inhibitor anacetrapib in patients with stable ASCVD. We performed a nested prospective biomarker study, measuring high-sensitivity troponin T (hsTnT), N-terminal pro-B-type natriuretic peptide (NT-proBNP), and growth differentiation factor-15 (GDF-15) (all Roche Diagnostics) at randomization (n=29,673). Hazard ratios were adjusted for covariates of a priori clinical relevance to HHF risk: age, prior HF, hypertension, diabetes mellitus, eGFR <60, body-mass index, and polyvascular disease. Discrimination was assessed using Harrell’s c-index. Results: A significant graded risk of HHF was observed with increasing deciles of hsTnT, NT-proBNP, and GDF-15 (p-trend <0.001 for each) ( Figure ). These associations remained significant after multivariable adjustment for clinical risk factors (p<0.001 for each). When added to a multivariable Cox regression model of clinical risk indicators (c-index 0.74), these 3 biomarkers significantly improved the prognostic performance of the model (c-index 0.85; p<0.001). There was no treatment interaction with anacetrapib. Conclusions: In patients with stable ASCVD, biomarkers of myocardial injury, hemodynamic stress, and inflammation provide incremental information for prediction of HHF. Future studies should address whether these patients are more likely to benefit from emerging HF preventive therapies.

scholarly journals The Blockade of Transmembrane Cl- Flux Mitigates I/R-Induced Heart Injury via the Inhibition of Calpain Activity

2015 ◽  
Vol 35 (6) ◽  
pp. 2121-2134 ◽  
Author(s):  
Jian-Ying Zhang ◽  
Feng Wu ◽  
Xiao-Ming Gu ◽  
Zhen-Xiao Jin ◽  
Ling-Heng Kong ◽  
...  
Keyword(s):  
Myocardial Injury ◽  
Caspase 3 ◽  
Ischemia Reperfusion ◽  
Cardiac Injury ◽  
Calpain Activity ◽  
Rat Hearts ◽  
Marked Decline ◽  
Heart Injury ◽  
Myocardial Ischemia Reperfusion ◽  
Injury Area

Aims: The aim of this study was to determine whether calpain is involved in Cl- -induced myocardial ischemia/reperfusion (I/R) injury. Methods: Isolated rat hearts were subjected to either 45 min of global no-flow ischemia followed by reperfusion or successive perfusion with Ca2+ -free KH solution for 3 min and normal KH solution for 30 min, also known as Ca2+ paradox. Results: The hearts in the I/R group exhibited increases in myocardial injury area, LDH release, caspase 3 activity and apoptotic indices and a marked decline in cardiac performance. As was the case regarding the effects of MDL 28170, an inhibitor of calpain, treatment with 5 µM NPPB, 5 µM DIDS and low Cl- significantly attenuated cardiac injury. Moreover, each of the treatments significantly protected against Ca2+ overload-induced injury in the setting of Ca2+ paradox. The Western blot and immunofluorescence data revealed that there was an increase in the percentages of calpain membrane-positive cells and the numbers of fragments resulting from the calpain-mediated proteolysis of α-fodrin in both the I/R and the Ca2+ paradox, indicating that the activation of calpain occurred. More importantly, these effects were mitigated by the blockade of transmembrane Cl- flux, as was accomplished via MDL 28170. Conclusion: Our results provide evidence that the blockade of transmembrane Cl- flux mitigates I/R-induced cardiac injury via the inhibition of calpain activity. They also indicate that intracellular Ca2+ overload regulates calpain activation in the setting of Cl- -induced injury.

scholarly journals Pattern of serum cardiac troponin-I in symptomatic acute myocardial infarction patients in national institute of cardiovascular disease in Bangladesh

2014 ◽  
Vol 42 (1) ◽  
pp. 3-6
Author(s):  
SS Shahina ◽  
JU Ahmed ◽  
S Ahmed ◽  
E Shahriar ◽  
MN Uddin ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cardiovascular Disease ◽  
Acute Myocardial Infarction ◽  
Myocardial Injury ◽  
Troponin I ◽  
Clinical Symptoms ◽  
Cardiac Injury ◽  
Circadian Variation ◽  
Assay Method ◽  
Ctni Level

Troponin I (cTnI) isoform is cardiac muscle specific protein and shown to have several features as a preferred marker of myocardial injury. It rises early in acute myocardial infarction (AMI) and attains levels that are clearly separated from baseline values. It remains elevated for several days providing a long window for detection of cardiac injury. The objective of the study was to evaluate for the profile of cTnI level among symptomatic AMI patients. The study was conducted at National Institute of Cardiovascular Disease, Dhaka, Bangladesh from July 2007 to June 2008 and total 9552 patients with type 1 or type 2 MI were included. Blood Sample was taken within 3 days of symptoms and cTnI was measured by chemiluminescent immunometric assay method. cTnI was considered positive when the value was >1ng/ml and study population was divided as per age, sex and cTnI level. The mean (+ SD) age of all patients was 55(+ 12.8) years and majority was males (82.20%). Seasonal variation showed highest positive cases in winter. In case of circadian variation positive cTnI results were suggestive of morning peak of AMI. Positive results were obtained in 32.3% of Cases. cTnI is now considered as a better indicator of myocardial injury. Further study in depth is necessary to correlate with clinical symptoms and other diagnostic tests to make a complete profile of AMI according to the latest subtypes. DOI: http://dx.doi.org/10.3329/bmj.v42i1.18969 Bangladesh Med J. 2013 Jan; 42 (1): 3-6

Abstract 232: Role of Transient Receptor Potential Melastatin 2 in Cardiomyocyte Apoptosis Induced by TNF-α

2012 ◽  
Vol 111 (suppl_1) ◽  
Author(s):  
Shuzhuang Li ◽  
Xuan Liu ◽  
Deqin Yu ◽  
Chong Chen ◽  
Xiaolong Chen
Keyword(s):  
Myocardial Injury ◽  
Caspase 3 ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Cardiomyocyte Apoptosis ◽  
Mechanical Trauma ◽  
Causative Role ◽  
Transient Receptor Potential Melastatin ◽  
Tnf Α ◽  
Transient Receptor

Mechanical trauma, such as that induced by motor vehicle crashes, represents a major medical and economic problem in the world. Identifying the mechanisms responsible for post-traumatic secondary myocardial injury is critical in order to reduce overall mortality and improve quality of life after trauma. We have previously demonstrated that mechanical trauma-induced overproduction of TNF-α plays a causative role in cardiomyocyte apoptosis via oxidative/nitrative stress. Transient receptor potential melastatin 2 (TRPM2) is a Ca 2+ permeable non-selective cation channel activated by oxidative stress, expressed in the cardiomyocytes. The present study attempted to identify whether TRPM2 is involved in TNF-α-induced cardiomyocyte apoptosis. Cardiomyocytes were isolated from adult male Sprague Dawley rats and cultured with TNF-α (10 ng/ml) for 12h. RT-PCR and semi-quantitative immunohistochemistry were used to quantify TRPM2 mRNA and protein levels respectively. Significant increases in TRPM2 mRNA and protein expression were observed in TNF-α-treated cardiomyocytes, suggesting that TRPM2 may contribute to TNF-α-induced cardiomyocyte apoptosis. To identify the effect of TRPM2 on TNF-α-induced cardiomyocyte apoptosis, cardiomyocytes were cultured with TNF-α or TNF-α + TRPM2 inhibitor (flufenamic acid (FFA) 100uM or clotrimazole 30uM), respectively. Exposure of cardiomyocytes to TNF-α for 12h induced significant apoptosis as determined by caspase-3 activation (1.7-fold increase vs. control, P < 0.01). In contrast, TNF-α-induced caspase-3 activity increases were significantly depressed by FFA and clotrimazole, respectively (P < 0.05). To further confirm the effect of TRPM2 on TNF-α-induced cardiomyocyte apoptosis, we tested the effects of TRPM2-specific small interfering RNA (siRNA). As a result, impressively, TNF-α-induced increases of caspase-3 activity and lysate nucleosomes were significantly reduced in TRPM2-specific siRNA-treated cardiomyocytes (P < 0.01). These results indicate that TRPM2 plays an important role in TNF-α-induced cardiomyocyte apoptosis. We propose functional inhibition of TRPM2 channels as a new therapeutic strategy for treating mechanical trauma-induced secondary myocardial injury.

scholarly journals Markers of Myocardial Stress, Myocardial Injury, and Subclinical Inflammation and the Risk of Sudden Death

Circulation ◽  
2020 ◽  
Vol 142 (12) ◽  
pp. 1148-1158
Author(s):  
Brendan M. Everett ◽  
M.V. Moorthy ◽  
Jani T. Tikkanen ◽  
Nancy R. Cook ◽  
Christine M. Albert
Keyword(s):  
Cardiovascular Disease ◽  
High Density Lipoprotein ◽  
Cardiac Troponin ◽  
Myocardial Injury ◽  
Troponin I ◽  
Density Lipoprotein ◽  
High Sensitivity ◽  
C Reactive Protein ◽  
Cholesterol Ratio ◽  
Reactive Protein

Background: The majority of sudden cardiac deaths (SCDs) occur in low-risk populations often as the first manifestation of cardiovascular disease (CVD). Biomarkers are screening tools that may identify subclinical cardiovascular disease and those at elevated risk for SCD. We aimed to determine whether the total to high-density lipoprotein cholesterol ratio, high-sensitivity cardiac troponin I, NT-proBNP (N-terminal pro-B-type natriuretic peptide), or high-sensitivity C-reactive protein individually or in combination could identify individuals at higher SCD risk in large, free-living populations with and without cardiovascular disease. Methods: We performed a nested case-control study within 6 prospective cohort studies using 565 SCD cases matched to 1090 controls (1:2) by age, sex, ethnicity, smoking status, and presence of cardiovascular disease. Results: The median study follow-up time until SCD was 11.3 years. When examined as quartiles or continuous variables in conditional logistic regression models, each of the biomarkers was significantly and independently associated with SCD risk after mutually controlling for cardiac risk factors and other biomarkers. The mutually adjusted odds ratios for the top compared with the bottom quartile were 1.90 (95% CI, 1.30–2.76) for total to high-density lipoprotein cholesterol ratio, 2.59 (95% CI, 1.76–3.83) for high-sensitivity cardiac troponin I, 1.65 (95% CI, 1.12–2.44) for NT-proBNP, and 1.65 (95% CI, 1.13–2.41) for high-sensitivity C-reactive protein. A biomarker score that awarded 1 point when the concentration of any of those 4 biomarkers was in the top quartile (score range, 0–4) was strongly associated with SCD, with an adjusted odds ratio of 1.56 (95% CI, 1.37–1.77) per 1-unit increase in the score. Conclusions: Widely available measures of lipids, subclinical myocardial injury, myocardial strain, and vascular inflammation show significant independent associations with SCD risk in apparently low-risk populations. In combination, these measures may have utility to identify individuals at risk for SCD.

scholarly journals Myocardial injury and COVID-19: Serum hs-cTnI level in risk stratification and the prediction of 30-day fatality in COVID-19 patients with no prior cardiovascular disease

Theranostics ◽  
2020 ◽  
Vol 10 (21) ◽  
pp. 9663-9673
Author(s):  
Jiatian Cao ◽  
Yan Zheng ◽  
Zhe Luo ◽  
Zhendong Mei ◽  
Yumeng Yao ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Risk Stratification ◽  
Myocardial Injury ◽  
Ctni Level

scholarly journals Clinical impact of COVID-19 in a single-center cohort of a prospective study in cancer patients receiving immunotherapy

Immunotherapy ◽  
2020 ◽  
Vol 12 (15) ◽  
pp. 1139-1148 ◽  
Author(s):  
Melissa Bersanelli ◽  
Teresa Zielli ◽  
Fabiana Perrone ◽  
Chiara Casartelli ◽  
Fabiana Pratticò ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Respiratory Failure ◽  
Cancer Patients ◽  
Influenza Season ◽  
Clinical Impact ◽  
Single Center ◽  
Pharyngeal Swab ◽  
Influenza Like Illness ◽  
Radiological Features ◽  
A Prospective Study

Aim: Evaluating the incidence and course of COVID-19 in cancer patients treated with immunotherapy. Patients & methods: We reported the influenza-like illness events with diagnosis of COVID-19 within the patient cohort enrolled in the prospective observational multicenter INVIDIa-2 study in the single center of Parma. Results: Among 53 patients, eight experienced influenza-like illness during the influenza season 2019/2020, and three of them had diagnosis of COVID-19. They were males, elderly, with cardiovascular disease. Radiological features of COVID-19 pneumonitis were found in all of three cases, although the pharyngeal swab resulted positive in only two. Two of these three patients died due to respiratory failure. Conclusion: Cancer patients are at high risk of severe events from severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection.

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