Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034065 (pulmonary embolism)
 14,979 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The measurement of cardiac troponins (cTn) is of considerable usefulness in the diagnosis of acute coronary syndrome. Abnormal levels of serum cTn are occasionally found in patients who are not suffering a myocardial infarction. This may be observed in several well-known situations including pulmonary embolism, pericarditis, myocarditis, coronary vasospasm, sepsis, congestive heart failure, supraventricular tachycardia with hemodynamic compromise, re-nal insufficiency, and prolonged strenuous endurance exercise. Endogenous antibodies such as heterophile antibodies, rheumatoid factor, and other autoantibodies are known to interfere with the immunoassay measurements of many different analytes, including the widely used Abbot AxSYM cTnI analyzer. Other sources of circulating antibodies include immunotherapies, vaccinations, or blood transfusions that may interfere with these immunoassays as well. We examine the case of a 48-year-old man with a history of hypercholesterolemia and obesity who presented with chest pain and was found to have elevated Tn I levels on two separate occasions. Further work-up revealed that the Tn I levels were spuriously elevated because the patient's blood revealed a normal cTnI level when mixed with polyethylene glycol to inactivate any antibodies interfering with the cTnI assay.
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PMID:Falsely elevated cardiac troponin I levels. 1732 64

To determine whether troponin I (cTnI) and right ventricular (RV) dysfunction predict adverse in-hospital outcomes in patients admitted to the Emergency Department (ED) with definite nonmassive pulmonary embolism (PE) independent of and in addition to a recently validated clinical prognostic risk score. From a pool of 168 patients with suspected PE, 89 had nonmassive PE confirmed by spiral lung angio-computed tomography. By the clinical prognostic score, in our study sample, 14% had very low risk; 17% had low risk, 20% had intermediate risk, whereas high risk and very high risk were identified in 29 and 20%, respectively. Prevalence of elevated cTnI (>0.1 microg/L, 57%) at admission was comparable among patients grouped by clinical prognostic score (P = NS); echocardiographic RV dysfunction (54%) was more prevalent with intermediate or high clinical risk score (P < 0.02). Increased cTnI predicted primary end-point (development of hemodynamic instability, overall 33 cases, 37%) independent of and in addition to the clinical risk class and RV dysfunction (P < 0.01 for interaction). Fatal events (12 cases, 14%, 5 definite, 7 possible PE-related) were predicted by higher clinical risk score (P < 0.05). In patients with nonmassive central PE admitted to the ED, increased cTnI contributed to identifying those with increased risk of development of hemodynamic instability independent of and in addition to a validated clinically based risk score.
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PMID:Troponin I and right ventricular dysfunction for risk assessment in patients with nonmassive pulmonary embolism in the Emergency Department in combination with clinically based risk score. 1827 Jul 91

High-sensitivity troponin (hs-cTn) assays enable the troponin cutoff value to be lowered, resulting in an increase of sensitivity at the cost of specificity. In the present study, the risk of a short-term adverse outcome was assessed in patients with acute pulmonary embolism (PE) using high-sensitivity troponin I (hs-cTnI). We used a cutoff value of 0.1 ng/ml in accordance with current guidelines for unstable angina (UA)/non-ST-segment elevation myocardial infarction (NSTEMI), although the detection limit of the troponin assay is lower. In addition, the risk of an adverse outcome in patients with acute PE was investigated with respect to initial D-dimer serum concentrations. In 65 patients with confirmed acute PE, hs-cTnI and D-dimer values were measured. Adverse clinical outcome was defined as cardiogenic shock, cardiopulmonary resuscitation, mechanical ventilation, vasopressor therapy, thrombolysis, catheter intervention or mortality within 60 days of PE. Patients with acute PE and serum hs-cTnI values >0.1 ng/ml showed significantly higher D-dimer concentrations (P= 0.0467) and a 5-fold increased risk of an adverse clinical outcome [odds ratio (OR), 4.9; 95% confidence interval (CI), 1.28-18.66; P=0.0235] compared with patients with acute PE and hs-cTnI values <0.1 ng/ml. In patients with acute PE suffering from adverse clinical outcome, D-dimer concentrations were significantly elevated compared with those in patients with acute PE without adverse clinical outcome (P=0.02). In patients with acute PE, a hs-cTnI cutoff value of 0.1 ng/ml, which is identical to the recommended cutoff value of NSTEMI, may identify patients with a 5-fold increased risk of a short-term adverse outcome. D-dimer values are significantly higher in PE patients with elevated hs-cTnI values as well as in patients with an adverse outcome.
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PMID:Predictive value of high-sensitivity troponin I and D-dimer assays for adverse outcome in patients with acute pulmonary embolism. 2340 84

Acute myocardial infarction (AMI) remains a major cause of death in the US. An early and reliable diagnosis may warrant immediate initiation of reperfusion therapy to potentially improve the survival rate among the AMI patients. Currently, cardiac troponins (i.e. cTnT and cTnI) and creatine kinase MB (CK-MB) are widely used for AMI diagnosis. However, elevation of these biomarkers is also observed in human patients with myocarditis, aortic dissection, pulmonary embolism, congestive heart failure and renal failure. Furthermore, measurable amounts of troponin proteins are usually not released from damaged myocardium before 4 to 8 h after onset of symptoms, making an early biomarker-based diagnosis of AMI rather difficult. Therefore, new biomarkers with high sensitivity and specificity in early diagnosis of AMI are greatly needed.
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PMID:Whether Circulating miRNAs or miRNA-Carriers Serve as Biomarkers for Acute Myocardial Infarction. 2519 85

Previous studies suggested possible application of postmortem biochemistry of myocardial biomarkers to the investigation of sudden cardiac death; however, differences from clinical findings should be considered in autopsy materials. The present study involved a comprehensive investigation of cardiac troponin T and I (cTnT and cTnI), and creatine kinase MB (CK-MB) in cardiac and peripheral external iliac venous blood, pericardial fluid (PCF) and cerebrospinal fluid (CSF) for reassessment, with special regard to the estimated postmortem interval in relation to the cause of death, reviewing a large number of forensic autopsy cases (n=1923). These cardiac biomarkers showed cause-of-death- and postmortem-time-dependent differences: blood and PCF levels of each marker were higher in hyperthermia (heatstroke), bathwater drowning and chronic congestive heart disease in cases of postmortem interval (PMI) <12h. After 12h postmortem, these markers were also higher in fatal drug abuse, spontaneous cerebral/subarachnoid bleeding, electrocution and pulmonary embolism. In addition, most other causes of death, including ischemic heart disease, showed substantial elevations, while these markers remained low in acute hemorrhagic death from sharp instrument injury, hypothermia (cold exposure) and sea-/freshwater drowning during PMI of <48h. CSF cTnI and CK-MB showed similar findings. There was no difference between myocardial infarction and other causes of death to be discriminated, including asphyxiation, drowning and fire fatality. These findings are similar to clinical observations in critical ill patients, suggesting that elevated cardiac biomarkers cannot be a specific finding for death from acute ischemic heart disease, but indicate the severity of myocardial injury in postmortem investigation.
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PMID:Cardiac biomarkers in blood, and pericardial and cerebrospinal fluids of forensic autopsy cases: A reassessment with special regard to postmortem interval. 2605 7

This study aims to investigate the long-term prognosis and the affecting factors towards the patients with acute pulmonary thromboembolism (APTE). The clinical data of 903 PTE patients, diagnosed by the spiral CT pulmonary angiography (CTPA) or lung ventilation perfusion scanning when hospitalized in the Second Hospital of Hebei Medical University from January 1998 to December 2013, were collected, among who 548 patients were performed the long-term follow-up, and the factors that would affect the prognosis were statistically analyzed. The univariate analysis showed that many factors would affect the prognosis of PTE. The multivariate non-conditional logistic regression analysis showed that: the relevant factors of re-embolization included the idiopathic pulmonary embolism, RVD, D-dimer positive, anticoagulation treatment < 3 months, post-treatment PASP > 40 mmHg, the relevant factors of death included the D-dimer positive, anticoagulation treatment < 3 months, cTnI positive, post-treatment PASP > 40 mmHg. RVD and post-treatment PASP > 40 mmHg would increase the risk of chronic thromboembolic pulmonary hypertension (CTEPH). The idiopathic pulmonary embolism, RVD, D-dimer positive, anticoagulation treatment < 3 months, cTnI positive and post-treatment PASP > 40 mmHg were the important factors that would affect the long-term prognosis of PTE patients.
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PMID:Long-term prognosis and related factors towards patients with acute pulmonary thromboembolism. 2622 47

The novel coronavirus disease (COVID-19) outbreak, caused by SARS-CoV-2, represents the greatest medical challenge in decades. We provide a comprehensive review of the clinical course of COVID-19, its comorbidities, and mechanistic considerations for future therapies. While COVID-19 primarily affects the lungs, causing interstitial pneumonitis and severe acute respiratory distress syndrome (ARDS), it also affects multiple organs, particularly the cardiovascular system. Risk of severe infection and mortality increase with advancing age and male sex. Mortality is increased by comorbidities: cardiovascular disease, hypertension, diabetes, chronic pulmonary disease, and cancer. The most common complications include arrhythmia (atrial fibrillation, ventricular tachyarrhythmia, and ventricular fibrillation), cardiac injury [elevated highly sensitive troponin I (hs-cTnI) and creatine kinase (CK) levels], fulminant myocarditis, heart failure, pulmonary embolism, and disseminated intravascular coagulation (DIC). Mechanistically, SARS-CoV-2, following proteolytic cleavage of its S protein by a serine protease, binds to the transmembrane angiotensin-converting enzyme 2 (ACE2) -a homologue of ACE-to enter type 2 pneumocytes, macrophages, perivascular pericytes, and cardiomyocytes. This may lead to myocardial dysfunction and damage, endothelial dysfunction, microvascular dysfunction, plaque instability, and myocardial infarction (MI). While ACE2 is essential for viral invasion, there is no evidence that ACE inhibitors or angiotensin receptor blockers (ARBs) worsen prognosis. Hence, patients should not discontinue their use. Moreover, renin-angiotensin-aldosterone system (RAAS) inhibitors might be beneficial in COVID-19. Initial immune and inflammatory responses induce a severe cytokine storm [interleukin (IL)-6, IL-7, IL-22, IL-17, etc.] during the rapid progression phase of COVID-19. Early evaluation and continued monitoring of cardiac damage (cTnI and NT-proBNP) and coagulation (D-dimer) after hospitalization may identify patients with cardiac injury and predict COVID-19 complications. Preventive measures (social distancing and social isolation) also increase cardiovascular risk. Cardiovascular considerations of therapies currently used, including remdesivir, chloroquine, hydroxychloroquine, tocilizumab, ribavirin, interferons, and lopinavir/ritonavir, as well as experimental therapies, such as human recombinant ACE2 (rhACE2), are discussed.
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PMID:COVID-19 and the cardiovascular system: implications for risk assessment, diagnosis, and treatment options. 3235 35