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 29,987 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We investigated the level of sympathetic hyperactivity in response to stress exposure in an acute myocardial infarction (AMI) model and the contribution of oxidative and nitrosative damage to this phenomenon. Stress was induced by 20-day administration of different emotional stress factors: daylight/darkness exposure, overcrowding, isolation, new hierarchy, tilting the cage and restriction of water or food. AMI was induced surgically. Heart rate (HR) and heart rate variability (HRV) measurements were done before and after AMI. Oxidant parameters were measured in heart tissue and cortisol levels were measured in plasma specimens. Compared with the nonstressed group, stress-exposed rats showed sympathetic hyperactivity characterized by increased HR together with decreased HRV. In the stressed group serum corticosterone levels were high both before and after AMI. Mean infarct size in the stressed group was significantly larger (44.6+/-3.23% and 53.1+/-4.52%, respectively; P<0.05). Increased tissue malondialdehyde (MDA) levels (0.63+/-0.59 and 1.60+/-0.31 nmol/mg protein, respectively; P<0.05) and decreased superoxide dismutase (SOD) activity and glutathione (GSH) content were seen in stress-exposed rats. Likewise, heart peroxynitrite levels were also high in stress-exposed rats (141.8+/-18 nmol/g tissue vs. 164.2+/-21 nmol/g tissue). Chronic emotional stress is a deteriorating factor for the induction and prognosis of MI. Exaggerated sympathetic activity may be the major contributing factor. Oxidative and nitrosative damage in response to this sympathetic hyperactivity is the key mechanism.
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PMID:Chronic emotional stress exposure increases infarct size in rats: the role of oxidative and nitrosative damage in response to sympathetic hyperactivity. 1927 Oct 23

Stress-induced cardiomyopathy (SIC) is a form of acute heart disease triggered by extreme psychological stress. In patients who develop SIC, the outward symptoms are almost indistinguishable from acute myocardial infarction (AMI). However, some important criteria differentiate patients with SIC from those with AMI. Patients with SIC: (1) experience some form of extreme psychological stress from minutes to hours before developing heart disease, (2) do not suffer from atherosclerosis or coronary artery obstruction, and 3) exhibit abnormal ballooning of the left ventricle. In the present study, the resident-intruder (RI) social defeat test was investigated as a potential rat model for stressed-induced cardiomyopathy. Adult Long-Evans rats were implanted with a biotelemetry transmitter for ECG recordings and habituated for two weeks. An intruder rat was placed in the cage of a resident rat behind a wire-mesh partition for 5 min. The partition was then removed for 5 min to allow direct contact between the intruder and resident rats. After this interval, the wire-mesh partition was replaced and the intruder rat remained behind the partition for an additional 50 min. Behavioral responses were noted and ECG recordings were collected during the entire 60-min testing period. Upon completion of the test, the intruder rat was removed from the cage of the resident rat and sacrificed. The heart was examined and blood was collected. Heart weight/body weight ratio, left ventricle/body weight ratio, heart length, plasma corticosterone levels, and plasma troponin I levels of intruder rats were significantly higher as compared to control rats. Intruder rats significantly increased their heart rate during the first 5 min of the RI test. It is concluded that the RI test to induce social defeat is a novel rodent paradigm for modeling stress-induced cardiomyopathy in the human.
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PMID:An animal model of stress-induced cardiomyopathy utilizing the social defeat paradigm. 2396 81

Progress in cancer therapy over the past decades improved long-term survival but increased cancer therapy-related cardiotoxicity. Many novel treatment options have been implemented with yet incompletely characterized cardiovascular side effects including heart failure, coronary artery disease, arrhythmias, valvular disease, venous thromboembolism and myocarditis. Diagnosis of potential cardiotoxic side effects is essential for an optimal treatment but remains challenging. Cardiac biomarkers troponin and brain natriuretic peptide/N-terminal proBNP (BNP/NT-proBNP) have been extensively studied in heart failure and acute coronary syndromes. Emerging evidence implicates a significant role in the detection of cardiotoxicity and guidance of therapy in cancer patients. Elevated troponin or BNP/NT-proBNP levels were associated with increased all-cause mortality in cancer patients and have been shown to predict manifest heart failure. BNP/NT-proBNP may be useful for the prediction of cancer therapy-related heart failure and response to heart failure therapy in adult and pediatric cancer patients while troponin can indicate acute myocardial infarction in patients with cancer therapy-related risk for coronary artery disease. Furthermore, troponin may be used for the identification of immune checkpoint inhibitor-related myocarditis with very high sensitivity. Finally, even D-dimer levels have been shown to improve risk stratification and diagnosis in cancer-associated venous thromboembolism. This review aims to summarize the current knowledge about biomarkers in cancer therapy-related cardiotoxicity. We also outline possible clinical recommendations for the detection and treatment of subclinical and clinically apparent cardiotoxic effects using biomarkers.
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PMID:Biomarkers for the detection of apparent and subclinical cancer therapy-related cardiotoxicity. 3070 Oct 97