Increased Serum Cardiac Troponin Research Articles

Effects of chronic stress on rat heart function following regional ischemia: a sex-dependent investigation.

Chronic psychological stress is a recognized, yet understudied risk factor for heart disease, with potential sex-specific effects. We investigated whether chronic stress triggers sex-dependent cardiac dysfunction in isolated Wistar rat hearts subjected to ischemia-reperfusion injury. The experimental cohort underwent 1 h of daily restraint stress for 4 wk versus matched controls, followed by euthanasia (sodium pentobarbital) and heart excision for ex vivo perfusion. Blood analysis revealed sex-specific alterations in stress hormones and inflammatory markers. When compared with controls, chronic restraint stress (CRS) males displayed decreased plasma brain-derived neurotrophic factor (BDNF) levels (P < 0.05), whereas CRS females exhibited elevated plasma adrenocorticotropic hormone (ACTH) (P < 0.01) and reduced corticosterone (P < 0.001) alongside lower serum estradiol (P < 0.001) and estradiol/progesterone ratio (P < 0.01). Of note, CRS females showed increased serum cardiac troponin T (P < 0.05) and tumor necrosis factor-α (TNF-α) (P < 0.01) with suppressed interleukin (IL)-1α, IL-1β, IL-6, and IL-10 levels (P < 0.05) when compared with controls. Ex vivo Langendorff perfusions revealed that CRS female hearts displayed impaired postischemic functional recovery for baseline stroke volume (SV, P < 0.01), work performance (P < 0.05), aortic output (AO, P < 0.05), coronary flow (CF, P < 0.01), and overall cardiac output (CO, P < 0.01) when compared with matched controls and CRS males (P < 0.05). Our findings reveal intriguing sex-specific responses at both the systemic and functional levels in stressed hearts. Here, the dysregulation of stress hormones, proinflammatory state, and potential underlying cardiomyopathy in females following the stress protocol renders them more prone to damage following myocardial ischemia. This study emphasizes the importance of incorporating sex as a biological variable in cardiac research focusing on stress-related cardiomyopathy.NEW & NOTEWORTHY Although chronic psychological stress is a risk factor for cardiovascular diseases, the underlying mechanisms remain poorly understood. This study revealed that chronic restraint stress resulted in systemic changes (dysregulated stress hormones, proinflammatory state) and potential cardiomyopathy in females versus controls and their male counterparts. The stressed female hearts also displayed reduced functional recovery following ex vivo ischemia-reperfusion. This highlights the importance of incorporating sex as a biological variable in cardiac research.

Serum cardiac troponin I concentration increases in sheep with uterine torsion

It is currently unclear whether myocardial damage occurs in sheep suffering from uterine torsion. Increased serum cardiac troponin I (cTnI) concentration is considered as the gold standard indicator of myocardial damage. The purpose of this study was to investigate the serum cTnI concentrations in sheep with uterine torsion and the relationship of serum cTnI concentrations in cases of uterine torsion to hematological and biochemical variables, the degree of uterine torsion and the estimated duration of labor. A total of 32 sheep were included in the study and were assigned to uterine torsion (UT, n = 14), other types of dystocia requiring cesarean section or manual assistance (OTD, n = 11), and unassisted vaginal delivery (UVD, n = 7) groups based on inclusion criteria. Advia Centaur TnI-Ultra, a human-specific immunoassay, was used to measure serum cTnI concentrations. The median serum cTnI concentration was significantly higher in the UT group than in the OTD and UVD groups (UT: 0.507 ng/mL (0.040–18.521); OTD: 0.044 ng/mL (0.016–0.135); UVD: 0.036 ng/mL (0.023–0.059); p < 0.001). In uterine torsion cases, serum cTnI concentrations correlated positively with serum CK (r = 0.556, p = 0.042), AST (r = 0.613, p = 0.022) and LDH activities (r = 0.609, p = 0.024), and degree of uterine torsion (r = 0.563, p = 0.036). The results indicated that uterine torsion leads to an increase in serum cTnI concentration. Further investigations can be undertaken to explore possible factors contributing to the release of cTnI from the myocardium into the circulation and whether the myocardial damage in uterine torsion is reversible or irreversible.

Type I Diabetes Mellitus Increases the Cardiovascular Complications of Influenza Virus Infection

People with diabetes mellitus are susceptible to both cardiovascular disease and severe influenza A virus infection. We hypothesized that diabetes also increases risks of influenza-associated cardiac complications. A murine type 1 (streptozotocin-induced) diabetes model was employed to investigate influenza-induced cardiac distress. Lung histopathology and viral titres revealed no difference in respiratory severity between infected control and diabetic mice. However, compared with infected control mice, infected diabetic mice had increased serum cardiac troponin I and creatine-kinase MB, left ventricular structural changes and right ventricular functional alterations, providing the first experimental evidence of type I diabetes increasing risks of influenza-induced cardiovascular complications.

Serum Cardiac Troponin I concentrations in cats with anaemia – a preliminary, single‐centre observational study

A range of cardiovascular abnormalities have been associated with anaemia. However, it remains unclear whether anaemia is associated with cardiac myocyte damage in cats. The aim of this study was to assess if cats with anaemia have an increased prevalence of cardiac myocyte damage, as assessed by serum concentrations of cardiac troponin I, compared to non-anaemic, ill cats. Serum cardiac troponin I concentrations were measured in 18 anaemic cats and in 31 non-anaemic, ill cats with non-primary cardiac, non-renal and non-primary haematological disorders. The serum cardiac troponin I concentrations in the anaemic group (0·43 ng/mL) were significantly higher (P=0·0002) than in the non-anaemic ill group (0·04 ng/mL). Using a cut-off of less than 0·16 ng/mL, 12 of the 18 anaemic cats had an increased serum cardiac troponin I concentration, which was significantly higher (P=0·005) than the non-anaemic ill cats (7 of 31 cats). Serum cardiac troponin I concentrations were higher in cats with anaemia in this study. Further studies are required to establish whether the anaemia or other confounding factors is the cause of the increased serum cardiac troponin I concentrations.

Matrix metalloproteinase inhibition attenuates right ventricular dysfunction and improves responses to dobutamine during acute pulmonary thromboembolism

Activated matrix metalloproteinases (MMPs) cause cardiomyocyte injury during acute pulmonary thromboembolism (APT). However, the functional consequences of this alteration are not known. We examined whether doxycycline (a MMP inhibitor) improves right ventricle function and the cardiac responses to dobutamine during APT. APT was induced with autologous blood clots (350 mg/kg) in anaesthetized male lambs pre-treated with doxycycline (Doxy, 10 mg/kg/day, intravenously) or saline. Non-embolized control lambs received doxycycline pre-treatment or saline. The responses to intravenous dobutamine (Dob, 1, 5, 10 μg/kg/min.) or saline infusions at 30 and 120 min. after APT induction were evaluated by echocardiography. APT increased mean pulmonary artery pressure and pulmonary vascular resistance index by ∼185%. Doxycycline partially prevented APT-induced pulmonary hypertension (P < 0.05). RV diameter increased in the APT group (from 10.7 ± 0.8 to 18.3 ± 1.6 mm, P < 0.05), but not in the Doxy+APT group (from 13.3 ± 0.9 to 14.4 ± 1.0 mm, P > 0.05). RV dysfunction on stress echocardiography was observed in embolized lambs (APT+Dob group) but not in embolized animals pre-treated with doxycycline (Doxy+APT+Dob). APT increased MMP-9 activity, oxidative stress and gelatinolytic activity in the RV. Although doxycycline had no effects on RV MMP-9 activity, it prevented the increases in RV oxidative stress and gelatinolytic activity (P < 0.05). APT increased serum cardiac troponin I concentrations (P < 0.05), doxycycline partially prevented this alteration (P < 0.05). We found evidence to support that doxycycline prevents RV dysfunction and improves the cardiac responses to dobutamine during APT.

Elevated Serum Cardiac Troponin I in Cattle with Theileriosis

Theileria annulata is a blood parasite affecting ruminants. Hemolytic anemia, secondary hypoxia, and vasculitis are the most important features of tropical theileriosis. Evaluation of electrocardiographic findings and changes in cardiovascular biochemical markers including cTnI concentrations in cattle naturally infected with theileriosis in the absence of acute cardiac failure. Ninety adult Holstein cattle (>1 year) with clinical and laboratory evidence of theileriosis and 30 healthy cattle served as controls. Case-control study in which blood samples were collected and randomized after clinical, hematologic, parasitologic examination and laboratory confirmation and electrocardiographic recording on all animals, serum cardiac troponin I (cTnI), aspartate aminotransferase (AST), and creatine kinase-MB (CK-MB) were evaluated. Serum concentration of cTnI was significantly higher in cattle with theileriosis (mean: 0.028 ng/mL; range: 0.005-0.21 ng/mL; control mean: 0.011; range: <0.005-0.09 ng/mL; P = .003). There was significant correlation between serum level of cTnI and PCV (r = -0.257; P < .001) and also between cTnI and parasitemia (r = 0.515; P < .001). Mean serum activities of AST and CK-MB were 107 ± 46 and 301 ± 103 U/L in sick animals, which were significantly higher than healthy cattle (P = .002 and P = .041, respectively). There were no pathologic arrhythmias detected in sick animals. Theileriosis is a risk factor for elevation of cardiac biomarkers in naturally infected Holstein cattle. Severity of anemia and parasitemia might contribute to the pathophysiology of myocardial damage. The prognostic significance of increased serum cardiac troponin I concentrations in cattle with hemolytic anemia merits further investigation.

Doxycycline protects against right ventricular dysfunction and dilatation caused by acute pulmonary thromboembolism

We examined whether pretreatment with doxycycline (a matrix metalloproteinase MMP inhibitor) protects against acute pulmonary thromboembolism (APT)‐induced right ventricular dysfunction and dilatation.APT (350 mg/kg of autologous blood clots) increased mean pulmonary artery pressure (MPAP) and pulmonary vascular resistance index (PVRI) by approximately 186% and 196% respectively. Ecocardiography showed that right ventricle (RV) diameter increased in animals with APT (from 10.7±0.8 to 18.3±1.6 mm, P&lt;0.05), but not in embolized animals pretreated with doxycycline at 10 mg/kg i.v. (from 13.3±0.9 to 14.4±1.0 mm, P&gt;0.05). Dobutamine stimulation induced minor improvements in RV function in embolized animals. However, doxycycline improved the RV contractile reserve. APT increased serum cardiac troponin I concentrations and RV gelatinolytic activity, and doxycycline prevented theses increases (P&lt;0.05).These results suggest that MMPs are involved in APT‐induced cardiomyocyte injury, RV dysfunction and dilatation, and degrade contractile proteins. Doxycycline improves the responses to dobutamine during APT.Funded by FAPESP, CNPq, and CAPES (Brazil).

Myocardial Mononuclear Cell Infiltrates Are Not Associated with Increased Serum Cardiac Troponin I in Cynomolgus Monkeys

Myocardial mononuclear cell infiltrate is a spontaneous cardiac finding commonly identified in laboratory cynomolgus monkeys. The infiltrates are predominantly composed of macrophages with lesser lymphocytes and are not typically associated with histologically detectable cardiomyocyte degeneration. These infiltrates are of concern because they confound interpretation of test article-related histopathology findings in nonclinical safety toxicology studies. The interpretation of safety studies would be simplified by a biomarker that could identify myocardial infiltrates prior to animal placement on study. We hypothesized that monkeys with myocardial mononuclear cell infiltrates could be identified before necropsy using an ultrasensitive immunoassay for cardiac troponin I (cTnI). Serum cTnI concentrations in monkeys with myocardial infiltrates were not higher than those in monkeys without infiltrates at any of the sampling times before and on the day of necropsy. Increased serum cTnI levels are not suitable for screening monkeys with myocardial mononuclear cell infiltrates before placement in the study.

Serum cardiac troponin I in dogs with primary immune-mediated haemolytic anaemia

The assessment of serum cardiac troponin I concentrations in dogs with a range of nonprimary cardiac illnesses has revealed that cardiac myocyte damage is commonplace in many canine diseases. Whilst it is well established that dogs with fatal immune-mediated haemolytic anaemia frequently have cardiac pathology based on post-mortem examinations, there is limited information on the incidence of cardiac myocyte damage in this population of dogs. Serum cardiac troponin I concentrations were measured in 11 healthy dogs, 27 dogs with primary haemolytic anaemia and 49 hospitalised dogs without primary cardiac or haematological disorders. Dogs with primary haemolytic anaemia have higher serum concentrations of cardiac troponin I than hospitalised ill dogs (P<0.005) and healthy dogs (P<0.01). Using a cut-off of less than 0.1 ng/mL, 20 of 27 dogs with primary haemolytic anaemia had increased serum cardiac troponin I concentrations, which was a significantly higher proportion compared to the hospitalised ill dogs (P<0.001, 16 out of 49 dogs) and healthy dogs (P<0.05, 3 out of 11 dogs). Dogs with primary haemolytic anaemia have a higher incidence of subclinical myocyte damage than healthy dogs or dogs with non-haematological or primary cardiac illnesses. The prognostic significance of increased serum cardiac troponin I concentrations in dogs with primary haemolytic anaemia merits further investigation.

Cardiovascular Manifestations in Patients With Thrombotic Thrombocytopenic Purpura: A Single‐center Experience

Cardiovascular manifestation in patients with thrombotic thrombocytopenic purpura. The aim of this study was to investigate the incidence of acute myocardial infarction (AMI), arrhythmias, congestive heart failure, and mortality in patients hospitalized for thrombotic thrombocytopenic purpura (TTP). Thirty-eight patients (27 women and 11 men), mean age 44 years, were hospitalized with the diagnosis of TTP confirmed by a hematologist. We investigated the incidence of AMI which developed during hospitalization for TTP. AMI was diagnosed by new electrocardiographic changes, increased serum cardiac troponin I levels, and clinical symptomatology. The patients with AMI were also monitored for development of arrhythmias during hospitalization. Of the 38 patients, 8 (21%) developed new Q-wave AMI. There was no significant difference in baseline characteristics between patients who developed AMI and those who did not develop AMI. Of the 8 patients with AMI, 2 (25%) developed atrial fibrillation, 1 (13%) developed atrial flutter, 1 (13%) developed supraventricular tachycardia, and 2 (25%) developed congestive heart failure. Death occurred in 3 of 8 patients (38%) with AMI and in 1 of 30 patients (3%) without AMI (P < 0.01). New Q-wave AMI developed in 21% of 38 patients hospitalized with TTP. Supraventricular tachyarrhythmias developed in 50% of 8 patients with TTP who developed AMI. Patients hospitalized for TTP should be monitored for adverse cardiac events due to the high incidence of new AMI, supraventricular tachyarrhythmias, and mortality.

Chronic administration of membrane sealant prevents severe cardiac injury and ventricular dilatation in dystrophic dogs

Duchenne muscular dystrophy (DMD) is a fatal disease of striated muscle deterioration caused by lack of the cytoskeletal protein dystrophin. Dystrophin deficiency causes muscle membrane instability, skeletal muscle wasting, cardiomyopathy, and heart failure. Advances in palliative respiratory care have increased the incidence of heart disease in DMD patients, for which there is no cure or effective therapy. Here we have shown that chronic infusion of membrane-sealing poloxamer to severely affected dystrophic dogs reduced myocardial fibrosis, blocked increased serum cardiac troponin I (cTnI) and brain type natriuretic peptide (BNP), and fully prevented left-ventricular remodeling. Mechanistically, we observed a markedly greater primary defect of reduced cell compliance in dystrophic canine myocytes than in the mildly affected mdx mouse myocytes, and this was associated with a lack of utrophin upregulation in the dystrophic canine cardiac myocytes. Interestingly, after chronic poloxamer treatment, the poor compliance of isolated canine myocytes remained evident, but this could be restored to normal upon direct application of poloxamer. Collectively, these findings indicate that dystrophin and utrophin are critical to membrane stability-dependent cardiac myocyte mechanical compliance and that poloxamer confers a highly effective membrane-stabilizing chemical surrogate in dystrophin/utrophin deficiency. We propose that membrane sealant therapy is a potential treatment modality for DMD heart disease and possibly other disorders with membrane defect etiologies.

Cardiac arrhythmias associated with piroplasmosis in the horse: A case report

Cardiac dysfunction is a rare complication of babesiosis in domestic animals. The horse in this report showed clinical signs of anorexia, depression, fever, icterus and brown urine, and laboratory results (monocytosis, thrombocytopenia, azotemia, hyperbilirubinemia and bilirubinuria) indicated sub-acute piroplasmosis. Furthermore, junctional and polymorphic ventricular premature complexes and tachycardia associated with increased serum cardiac troponin I and myocardial-bound creatine kinase concentration were found. The diagnosis of piroplasmosis was confirmed by serology. Specific and supportive therapy for babesiosis allowed remission of clinical signs and laboratory profile abnormalities, including those of myocardial involvement. Myocardial damage associated with cardiac arrhythmia may be a complication of equine babesiosis as already demonstrated in other species.

Does the serum cardiac troponin I level increase with stress test-induced myocardial ischemia?

To evaluate the sensitivity of the serum cardiac troponin I level in detecting stress test-induced myocardial ischemia, the authors conducted a prospective study including patients admitted for chest pain to the telemetry floor of Our Lady of Mercy Medical Center at Bronx, NY. Consecutive 134 telemetry patients that agreed to participate in this study were included. All of these patients had a nuclear stress test and were divided into various groups based on the prestress test probability of having coronary artery disease. To assess serum cardiac troponin I levels, blood samples were drawn before and after stress testing and compared with the stress test results. Overall, 30 patients (22%) had reversible perfusion defects on stress images, and none (0%) had increased serum cardiac troponin I levels. One patient of 18 patients (6%) in group C with negative stress test results had an elevated serum cardiac troponin I level after the stress test, but none of group A or group B patients had elevated troponin I levels. These data show that serum cardiac troponin I levels do not increase with stress test-induced myocardial ischemia.

Why is Troponin T Increased in the Serum of Patients with End-Stage Renal Disease?

Haller et al. (1) have strengthened the argument that the increased serum cardiac troponin T (cTnT) found in many patients with end-stage renal disease (ESRD) originates in heart muscle and not regenerating skeletal muscle, as suggested by others (2). We recently measured serum cTnT using the Elecsys 2010 immunoassay system (Boehringer Mannheim), a …

Prognostic value of serum cardiac troponin I and T in chronic dialysis patients: A 1-year outcomes analysis

To determine the incidence and prognostic value of increased serum cardiac troponin I and T concentrations over 12 months in chronic hemodialysis patients, we performed a retrospective chart review in 16 patients undergoing chronic renal hemodialysis randomly selected from the Regional Kidney Disease Program without prior knowledge of their cardiac status. Serum markers of myocardial injury (cardiac troponin I [cTnI], cardiac troponin T [cTnT], and creatine kinase MB [CK-MB]) were measured and clinical outcomes were assessed. At the beginning of the study, 12 of 16 (75%) patients had increased serum enzyme-linked immunosorbent assay (ELISA) cTnT concentrations greater than 0.20 μg/L, eight (50%) had increased serum CK-MB greater than 5.0 μg/L, and three (19%) had an increased cTnI greater than 0.8 μg/L. Over the 1-year study period, the cardiac event rate (n = 4 with fatal myocardial infarction) was correlated to the patients who displayed the higher elevations of cTnT, CKMB, and cTnI. In the remaining 12 patients studied at the end of 1 year, seven (58%) had increased ELISA cTnT levels and five (42%) had increased CK-MB levels; no patients had elevated cTnI levels. Reanalysis of ELISA cTnT values with a newly formulated Enzymun cTnT assay showed no significant differences. Our data suggest that whereas substantial increases in cardiac markers tended to have a poor prognostic outcome, there was a high incidence of increased cTnT and CK-MB concentrations without evidence of myocardial injury in chronic hemodialysis patients. The lack of absolute cardiospecificity of cTnT and CK-MB may prove cTnI to be the desired serum marker for the detection of myocardial injury in patients with chronic renal disease.