Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although heart-type fatty acid-binding protein (H-FABP) can be a marker of sarcolemmal injury due to acute myocardial ischemia, the diagnostic or prognostic value is not established in patients with acute chest pain. This multicenter prospective study aimed to determine the diagnostic and prognostic values of H-FABP in 133 patients presenting to an emergency room with suspected acute coronary syndrome (ACS) by comparing with those of conventional biomarkers. H-FABP and myoglobin had greater positive results than did creatine kinase-MB or troponin T. Receiver operating characteristics analysis revealed that H-FABP was the most reliable for detection of ACS and that H-FABP had the greatest sensitivities for identification of patients requiring emergency hospitalization, coronary angiography, and interventional therapy within 7 days among the biomarkers. Thus, H-FABP can be an early diagnostic and prognostic biochemical marker, particularly within the first 6 h from the onset of chest symptoms, in patients with chest pain at an emergency department.
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PMID:Human heart-type fatty acid-binding protein as an early diagnostic and prognostic marker in acute coronary syndrome. 1271 85

To clarify the incidence and pathophysiological mechanism of cardiovascular adverse effects of tacrolimus, the present prospective study performed scheduled cardiovascular examinations at 1, 2, 4, 8, 16, 20, and 24 weeks after starting the tacrolimus therapy in 68 consecutive kidney transplantation recipients enrolled from 26 institutes in Japan. Patients with previous coronary artery disease or congestive heart failure were excluded. The examinations included any subjective symptoms, changes in resting ECG, ambulatory Holter's dynamic ECG, two-dimensional echocardiography, and monitoring of serum drug concentrations and cardiac troponin T levels. Cardiac nuclear imaging and/or coronary angiography were performed in the case of suspicious coronary events. During the investigation, chest pain in 9 (13.2%) and palpitation in 6 patients (8.8%) were reported, both closely related to elevated blood drug concentrations (37.2 +/- 18.7 ng/mL, mean +/- SD). Cardiovascular examinations detected development of resting ECG abnormalities in 12 patients (17.6%), asymptomatic ST depression following increased heart rate in 11 (16.2%) and ventricular arrhythmias in 7 patients (10.3%) on Holter's dynamic ECG. Elevation of troponin T was detected in 3 patients (4.4%), which was also closely related to elevated drug concentrations and interpreted as myocardial damage associated with the therapy. Assessments by thallium(Tl)-201 myocardial scintigraphy and/or coronary angiography in patients with suspicious coronary events revealed only two patients (2.9%) were considered to be myocardial ischemia associated with coronary vasospasm or microcirculatory disturbance. Sequential evaluations on echocardiography revealed significant (p<0.05) decrease in LV end-diastolic dimension (4, 8, 18 and 24 weeks) and LV end-systolic dimension (from 1 to 24 weeks), and significant (p<0.05) increase in LV ejection fraction 1 to 4 weeks after the kidney transplantation. Thickening of LV wall (>2 mm compared with baseline) was detected in only one patient. The present prospective study detected totally 30.9% incidence of cardiovascular adverse events. Symptomatic events and troponin T elevation were closely related to elevated blood drug concentrations (>20 ng/ml). Coronary vasomotor dysfunction seemed to be related to these adverse events especially when the blood drug concentration was exceeding 20 ng/ml.
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PMID:Multicenter prospective investigation on cardiovascular adverse effects of tacrolimus in kidney transplantations. 1297 96

Myocardial stunning is a form of reversible myocardial ischemia/reperfusion injury associated with systolic and diastolic contractile dysfunction. In the isolated rat heart model, myocardial stunning is characterized by specific C-terminal proteolysis of the myofilament protein, troponin I (cTnI) that yields cTnI1-193. To determine the effect of this particular C-terminal truncation of cTnI, without the confounding factor of other stunning-induced protein modifications, a series of solution biochemical assays has been undertaken using the human homologue of mouse/rat cTnI1-193, cTnI1-192. Affinity chromatography and actin sedimentation experiments detected little, or no, difference between the binding of cTnI (cTnI1-209) and cTnI1-192 to actin-tropomyosin, troponin T, or troponin C. Both cTnI and cTnI1-192 inhibit the actin-tropomyosin-activated ATPase activity of myosin subfragment 1 (S1), and this inhibition is released by troponin C in the presence of Ca2+. However, cTnI1-192, when reconstituted as part of the troponin complex (cTn1-192), caused a 54+/-11% increase in the maximum Ca2+-activated actin-tropomyosin-S1 ATPase activity, compared with troponin reconstituted with cTnI (cTn). Furthermore, cTn1-192 increased Ca2+ sensitivity of both the actin-tropomyosin-activated S1 ATPase activity and the Ca2+-dependent sliding velocity of reconstituted thin filaments, in an in vitro motility assay, compared with cTn. In an in vitro force assay, the actin-tropomyosin filaments bearing cTn1-192 developed only 76+/-4% (P<0.001) of the force obtained with filaments composed of reconstituted cTn. We suggest that cTnI proteolysis may contribute to the pathophysiology of myocardial stunning by altering the Ca2+-sensing and chemomechanical properties of the myofilaments.
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PMID:C-terminal truncation of cardiac troponin I causes divergent effects on ATPase and force: implications for the pathophysiology of myocardial stunning. 1455 Dec 40

Impaired heart rate variability (HRV) has been described postoperatively. Diminished HRV may be related to myocardial ischemia and potentially causes circulatory instability. Cardiac ischemic events and a compromised cardiovascular function are not uncommon after aortic surgery. Circadian variation of HRV seems to be a prognostically more important parameter than HRV itself with respect to the development of cardiac dysfunction. We therefore investigated whether the diurnal rhythm of HRV is simultaneously altered postoperatively and the potential contribution of myocardial ischemia. After approval by the hospital ethics committee and having obtained informed consent, we studied 11 consecutive male patients undergoing elective aortic surgery. Patients were monitored with a Holter-ECG perioperatively. Spectral HRV measures (total, low, and high frequency power) were determined and night/day ratios calculated. Ischemic ECG changes were recorded and serum was sampled for troponin T analysis. A remarkable decline in circadian variation accompanied the decrease in all HRV parameters postoperatively. Five patients showed ECG changes suggestive of myocardial ischemia and two had increased levels of troponin T. These two patients showed greatly diminished HRV postoperatively with a similarly reduced circadian rhythm. We have demonstrated that the circadian rhythm of HRV is not preserved after aortic surgery. Diminished diurnal variability seems to be a general manifestation and myocardial ischemia may just be one contributing factor. An altered biorhythm in combination with stress related changes in the neuroendocrine system after surgery most likely have a more significant influence on the circadian rhythm of HRV.
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PMID:Diminished circadian rhythm of heart rate variability after aortic surgery appears to be independent of myocardial ischemia. 1458 46

A 71-year-old man presented with left upper quadrant abdominal pain. Serial electrocardiograms (ECGs) demonstrated an evolving left bundle branch block, a sign of acute myocardial infarction (AMI). However, a coronary angiogram demonstrated minimal coronary artery disease, and serum troponin T was undetectable in serial serum measurements. Later, serum pancreatic enzyme levels were elevated and a computed tomography scan of the abdomen was consistent with pancreatitis. In patients presenting with acute pancreatitis and ECG changes suggesting AMI, measurement of serum troponin T concentrations can aid in differentiating ECG changes driven by acute pancreatitis from those of true myocardial ischemia or infarction.
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PMID:A case of acute pancreatitis presenting with electrocardiographic signs of acute myocardial infarction. 1473 Jan 76

Marginal elevations of troponin T among patients with chest pain are often considered to be insignificant. We sought to define the prognostic value of marginal troponin T elevations in patients presenting to the emergency department with suspected myocardial ischemia. Four hundred twenty-eight consecutive patients presenting to the emergency department with ongoing chest pain were evaluated, followed through their hospital course, and contacted for follow-up 4 months after discharge. Two hundred ninety-nine patients had undetectable troponin T levels (<0.01 microg/L), 76 had marginal troponin T elevations (0.01 to 0.09 microg/L), and 53 had frank troponin T elevations (> or =0.1 microg/L). Patients with either marginally or frank elevated troponin levels were older and more likely to be men, but did not differ from patients with undetectable troponin levels with regard to the prevalence of coronary artery disease risk factors, history of coronary disease, or race. While in the hospital, the undetectable and marginal troponin groups were referred for cardiac testing in equal proportions (58% and 59%, respectively), whereas 87% of the elevated group underwent further testing. After adjustment for possible confounders, a significantly increased rate of death/myocardial infarction/revascularization was observed in the marginal troponin group compared with the undetectable troponin group (p = 0.004). Marginal elevations of troponin T identified a currently underevaluated high-risk subgroup of patients with suspected myocardial ischemia who are more likely to have adverse clinical outcomes than those with undetectable troponin levels.
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PMID:Prognostic usefulness of marginal troponin T elevation. 1475 74

We have previously shown that atherosclerotic apolipoprotein E-deficient (apoE(-/-)) x LDL receptor-deficient (LDLR(-/-)) mice develop myocardial infarction when exposed to hypoxic stress. This study was performed to assess the role of thrombin and thrombosis in this process. ApoE(-/-) x LDLR(-/-) mice were fed a cholesterol-rich diet for 8 mo and were then subjected to hypoxic stress while receiving isoflurane anesthesia. One group received a bolus dose (5.6 micromol/kg) of the thrombin inhibitor melagatran, and control animals received PBS 10 min before the hypoxic stress. The mice were exposed to 10 min of hypoxia followed by normoxia. Ten minutes after the stress, Alzet pumps delivering melagatran (20 nmol x kg x (-1)min(-1)) or PBS were implanted, and the mice were allowed to recover for 48 h. The cardiac response was analyzed by histology, immunohistochemistry, and serum troponin T assay. All animals showed reversible ECG changes as a sign of ischemia during hypoxic stress, and 50% developed infarctions afterward as judged by troponin T levels. The group that received thrombin inhibitor had significantly lower troponin T and smaller myocardial infarctions than the PBS-treated group. These data show that thrombin generation is an important pathogenetic factor and suggest that coronary thrombosis is involved in myocardial infarction in atherosclerotic mice. Exposure of atherosclerotic mice to hypoxia leads to myocardial infarction through a two-phase pathway in which acute transient ischemia is followed by thrombin-dependent, irreversible, myocardial ischemia and myocardial cell death.
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PMID:Thrombin inhibitor reduces myocardial infarction in apoE-/- x LDLR-/- mice. 1503 Nov 24

We assessed the influence of the prophylactic use of a combination of the IV beta-adrenergic blocker, esmolol, and the phosphodiesterase III inhibitor, enoximone, on postbypass hemodynamic status, inflammation, and endothelial and organ function in a prospective, randomized, placebo-controlled study in 42 patients aged >65 yr undergoing aortocoronary bypass grafting. In 21 patients, esmolol (aim: heart rate <70 bpm) plus enoximone (initial bolus of 0.5 mg/kg followed by a continuous infusion of 2.5 microg x kg(-1) x min(-1)) was started after induction of anesthesia and continued until the morning of the first postoperative day; another 21 patients received saline solution as placebo. Hemodynamics, splanchnic perfusion (gastric-arterial CO(2) gap), liver function (glutathione transferase-alpha plasma levels), renal function (creatinine clearance, urine concentrations of N-acetyl-beta-D-glucosaminidase), myocardial ischemia (creatine-kinase MB and troponin T plasma levels), inflammation (elastase, interleukin-6 and -8 plasma levels), and endothelial integrity (adhesion molecules plasma levels) were assessed at baseline, before and after cardiopulmonary bypass (CPB), and in the intensive care unit until the first postoperative day. Catecholamine requirements were significantly less in the treated than in the nontreated patients. Heart rate was significantly slower, cardiac index was higher, and gastric-arterial CO(2) gap was significantly lower in the treatment group. Troponin T, beta-N-acetyl-beta-D-glucosaminidase, glutathione transferase-alpha, and soluble adhesion molecules increased significantly in the untreated control, but remained almost normal in the esmolol+enoximone patients. Inflammatory responses (elastase/interleukins) were attenuated by esmolol+enoximone. We conclude that, in comparison to an untreated control, the prophylactic use of a combination of esmolol and enoximone in elderly patients undergoing cardiac surgery with cardiopulmonary bypass resulted in overall beneficial effects on postbypass hemodynamic status, organ function, inflammatory response, and endothelial integrity.
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PMID:The prophylactic use of the beta-blocker esmolol in combination with phosphodiesterase III inhibitor enoximone in elderly cardiac surgery patients. 2145 Oct 80

All novel markers of myocardial ischemia (ischemia-modified albumin, choline, unbound free fatty acids) lack cardiac specificity. Therefore, for the specific detection of myocardial ischemia selective blood sampling from an inserted coronary sinus catheter is needed, which limits the applicability of these markers in most clinical routine settings. In addition, the superiority of these novel markers over the calculation of myocardial lactate production, the current criterion standard for the laboratory diagnosis of myocardial ischemia, has not been demonstrated so far, and even comparative data is frequently lacking. Further the superiority of these new candidate markers over lactate determination for the diagnosis of myocardial ischemia in peripherally drawn blood samples has not been demonstrated either, and these novel parameters appear not to be a breakthrough for laboratory diagnosis of myocardial ischemia during or after percutaneous coronary interventions or coronary artery bypass grafting. The determination of cardiac troponin I or troponin T is the current criterion standard for the laboratory diagnosis of myocardial damage due to their higher sensitivities and specificities compared to creatine kinase isoenzyme MB. According to current knowledge, troponin increases in peripherally drawn blood samples must be regarded as an indicator of myocardial necrosis which, however, may be limited, only detectable by troponin and may be missed by creatine kinase isoenzyme MB determination. After on-pump coronary artery bypass grafting the generally applied troponin discriminator limits are not valid as there is limited, inevitable cardiac tissue damage occurring during the surgical procedure. Therefore, troponins are significantly increased after reperfusion of the arrested heart over values seen before bypass and also in patients without complications. Perioperative myocardial infarctions can be reliably identified by their characteristic troponin time courses, and both peak concentrations and time of peak values are diagnostic criteria. Troponin release is lower in off-pump compared to on-pump bypass surgery. Despite the controversy over the significance of troponin elevations after clinically uncomplicated and successful procedures, it is tempting to postulate that less myocardial damage as detected by troponin release is beneficial for the patient. After elective percutaneous coronary interventions, only troponin increases >8-fold the upper reference limit were associated with increased mortality in long-term follow-up.
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PMID:Markers for perioperative myocardial ischemia: what both interventional cardiologists and cardiac surgeons need to know. 1609 33

We report of two patients with severe ketoacidosis, minute elevations of myocardial biomarkers (troponin T and CK-MB) and initial ECG changes compatible with myocardial infarction (MI). All successive investigations, including coronary arteriography, were normal, and the patients recovered fully without further evidence of ischemic heart disease. We suggest that acidosis and very high levels of free fatty acids could cause membrane instability and biomarker leakage. Regardless of the pathogenesis, these two case stories suggest that nonspecific myocardial injury may occur in severe diabetic ketoacidosis and that the presence of minute biomarker elevation and ECG changes does not necessarily signify MI.
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PMID:Myocardial injury with biomarker elevation in diabetic ketoacidosis. 1626 Mar 54


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