UMLS:C0022116 - FACTA Search

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Query: UMLS:C0022116 (ischemia)
91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A prospective single center study was performed to determine the minimal preoperative incidence of unrecognized cardiac injury in patients suffering aneurysmal and presumed aneurysmal subarachnoid hemorrhage (SAH). When caring for such patients in the pre- and post operative period clinicians must be aware of the possibility of cardiac injury even when a history of previous cardiac symptomatology is not present. Forty-seven consecutive patients suffering from SAH over a five-month period underwent serum measurements of the cardiac muscle marker troponin I (cTnI) immediately upon admission. Repeat studies, if possible, were done 24 hours later. EKG was performed in all patients and was available for review in 44 of the 47 cases. Echocardiography was performed in four of eight patients with elevated cTnI levels. Signs and symptoms relating to cardiac ischemia were recorded by the patients' physicians and nurses. Eight individuals (17%) had elevations in cardiac troponin I levels. Because surgical treatment is generally carried out as soon as possible following the hemorrhage, many patients with normal troponin I levels within twenty-four hours of their hemorrhage were operated upon before a repeat enzyme could be obtained or possibly before elevations could be recorded. In addition, a number of patients were referred to our center several days post-hemorrhage at a time when marker levels may have normalized. Therefore, the 17% incidence of elevated cTnI may be an underestimate. Only two of the eight patients had clinical abnormalities in cardiac function. Four patients with elevated levels had echocardiograms, three of which were abnormal. One additional patient died of a myocardial infarction before an echocardiogram could be obtained. EKG was abnormal in six of the seven patients with elevated troponin who had tracings available for review. Recordings consistent with recent myocardial ischemia were present in four of these. Of the 39 patients with negative troponin I levels, 37 had EKG available for review. None had recordings clearly consistent with recent myocardial ischemia although 13 were suggestive of ischemic changes. None of these 39 patients had pre- or post-operative clinical changes in cardiac function. Elevations in troponin I appeared to be unrelated to the patient's Hunt and Hess grade or Fisher score although our numbers were too small to draw any meaningful conclusions.
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PMID:The use of cardiac troponin-I (cTnI) to determine the incidence of myocardial ischemia and injury in patients with aneurysmal and presumed aneurysmal subarachnoid hemorrhage. 952 14

Coronary artery disease (CAD), arterial hypertension, chronic bronchitis and diabetes mellitus are the most frequently encountered diseases complicating the clinical course of the vascular patient. Clinical signs of cardiac or pulmonary disease are often absent in patients with decreased functional capacity due to claudication. For instance, clinical evidence of coronary artery disease was found in 36% of patients scheduled for different vascular surgical procedures, whereas coronary angiography revealed significant stenoses in as many as 53-68%. Patients with chronic hypertensive disease, coronary artery disease and increased impedance to left ventricular ejection due to atherosclerosis frequently develop impairment of left ventricular (LV) function. Even without clinical or radiological evidence, approximately 20-35% of vascular patients have a LV ejection fraction below 50% indicating impaired systolic LV function. The incidence of diabetes mellitus in vascular surgical patients is around 18%. When requiring insulin treatment, diabetes is an independent risk factor for postoperative ischemic events and congestive heart failure. Those with autonomic neuropathy are often asymptomatic as regards coronary artery disease. Coronary artery disease is responsible for over 50% of the immediate, medium- and long-term mortality and morbidity. Unstable myocardial ischemia, acute myocardial infarction which is detected by troponin I and ischemic pulmonary edema are the most common immediate postoperative cardiac complications. A large number of recent studies, using long-term ECG recording techniques, have allowed more accurate estimation of the incidence and time course of perioperative myocardial ischemia in vascular surgical patients. The highest incidence of ischemia when compared to daily life activities has been noted during the first two days after surgery but has been reported to remain elevated even 3-5 days after surgery. Interestingly, the incidence of intraoperative ischemia is lower than that observed during daily life. Knowledge of the etiology of perioperative myocardial infarction is essential if one is to improve cardiac outcome after vascular surgery. Many studies have addressed this important field in patients undergoing vascular surgery. They have documented a relationship between perioperative myocardial ischemia and postoperative myocardial infarction. Although postoperative myocardial infarctions are in most cases limited to endocardium (non Q wave infarction) they significantly reduce life expectancy of the vascular surgical patients. The reduction of cardiac risk following general surgery should focus on methods by which the incidence of myocardial ischemia, particularly during the postoperative period, could be reduced. These methods include intensive intraoperative analgesia or preventive administration of cardiovascular treatment which limit postoperative stress: alpha-2 agonists or betablocking agents. There are, at present, no studies which convincingly confirm an overall decreased mortality if coronary bypass surgery is performed prior to peripheral vascular surgery. Although it has been demonstrated that the mortality of the peripheral procedure is reduced to approximately one half, the mortality of a coronary bypass procedure in vascular surgical patients is five to eight times that recorded in a coronary artery bypass population without peripheral vascular disease. It remains to be shown if the use of coronary angioplasty prior to peripheral vascular surgery can provide a more satisfactory overall outcome. Several non-invasive techniques have been suggested to improve the identification of high-risk patients undergoing vascular surgery. These tests include exercise ECG, ambulatory ECG, dipyridamolethallium scintigraphy and determination of left ventricular ejection fraction by gated radionuclide imaging. (ABSTRACT TRUNCATED)
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PMID:[Physiopathologic introduction to anesthesia and resuscitation of the vascular patient]. 955 51

Reactive oxygen species have been suggested to play an important role in damage to cardiac tissue following ischemia and reperfusion. Oxygen radicals may also contribute to the cardiotoxicity of the anthracycline antibiotics, such as doxorubicin. We tested whether a selective inhibition of muscle gene expression, previously observed in cardiocytes treated with doxorubicin, might be reflective of a more generalized response evoked by oxidative stress in cardiac tissue. Cardiocytes in culture were exposed to hydrogen peroxide or glucose oxidase, and the effects on muscle gene expression were measured. Exposure to these agents led to a reduction in the levels of mRNA for the muscle-specific genes cardiac alpha-actin, troponin I, myosin light chain 2 (slow), and M isoform of creatine kinase, without affecting levels of the non-muscle genes pyruvate kinase and beta-actin. The magnitude of this effect was similar to that observed with doxorubicin. Although the hydrogen peroxide scavenging enzyme catalase and the intracellular radical scavengers N-acetylcysteine and 1,3-dimethyl-2-thiourea were without effect on doxorubicin-dependent reduction in gene expression, they inhibited the reduction in muscle gene expression mediated by hydrogen peroxide. These observations suggest that oxygen free radicals modulate muscle gene expression in cardiocytes by a pathway distinct from that utilized by doxorubicin.
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PMID:Selective inhibition of muscle gene expression by oxidative stress in cardiac cells. 968 91

Selective troponin I (TnI) modification has been demonstrated to be in part responsible for the contractile dysfunction observed with myocardial ischemia/reperfusion injury. We have isolated and characterized modified TnI products in isolated rat hearts after 0, 15, or 60 minutes of ischemia followed by 45 minutes of reperfusion using affinity chromatography with cardiac troponin C (TnC) and an anti-TnI antibody, immunological mapping, reversed-phase high-performance liquid chromatography, and mass spectrometry. Rat cardiac TnI becomes progressively degraded from 210 amino acid residues to residues 1-193, 63-193, and 73-193 with increased severity of injury. Degradation is accompanied by formation of covalent complexes between TnI 1-193 and, respectively, TnC residues 1-94 and troponin T (TnT) residues 191-298. The covalent complexes are likely a result of isopeptide bond formation between lysine 193 of TnI and glutamine 191 of TnT by the cross-linking enzyme transglutaminase. With severe ischemia, cellular necrosis results in specific release of TnI 1-193 into the reperfusion effluent and TnT degradation in the myocardium (25-, 27-, and 33-kDa products). Two-dimensional electrophoresis demonstrated that phosphorylation of TnI prevents ischemia-induced degradation. This study characterized the modified TnI products in isolated rat hearts reperfused after a brief or severe period of ischemia, revealing the progressive nature of TnI degradation, changes in phosphorylation, and covalent complexes with ischemia/reperfusion injury. Finally, we propose a model for ischemia/reperfusion injury in which the extent of proteolytic and transglutaminase activities ultimately determines whether apoptosis or necrosis is achieved.
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PMID:Troponin I degradation and covalent complex formation accompanies myocardial ischemia/reperfusion injury. 991 81

In recent years, cardiac troponins have attracted great interest as a marker for myocardial injury. However, there are limited data on strategies for use of creatine kinase (CK)-MB and troponin I (cTnI) in clinical practice. We sought to develop a testing strategy using prospectively collected clinical data including serial CK-MB and cTnI levels from 1,051 patients aged > or = 30 years admitted to a teaching hospital for acute chest pain. Diagnostic performance was evaluated for peak values of CK-MB and cTnI obtained during the first 24 hours for the combined end point of acute myocardial infarction and/or major cardiac events within 72 hours. The overall diagnostic accuracy was similar for both cardiac markers alone, and for the combination of cTnI and CK-MB (receiver-operating characteristic curve 0.84, 0.86, and 0.87, respectively). In the multivariate analysis, models including cardiac markers showed that both CK-MB and cTnI added information to clinical data to predict the combined end point, but cTnI added significantly less. Using recursive partitioning analysis, we developed a strategy that would restrict routine cTnI use to patients with normal CK-MB results and findings on the electrocardiogram consistent with ischemia. This strategy would divide patients with suspected myocardial ischemia into 4 groups with risks for the combined end point of 4%, 13%, 26%, and 85%. Thus, cTnI adds information to CK-MB mass and clinical data for predicting major cardiac events, but this contribution is mainly in patients with evidence of myocardial ischemia on their electrocardiograms.
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PMID:A proposed strategy for utilization of creatine kinase-MB and troponin I in the evaluation of acute chest pain. 1021 79

The findings of troponin I (TnI) proteolysis (in isolated rat hearts) and induction of selected sarcoplasmic reticulum (SR) calcium-regulatory genes (after repetitive total coronary occlusions in swine) have given rise to the hypothesis that the time course of functional recovery of stunned myocardium reflects the resynthesis of reversibly damaged proteins. Although stunning occurs after brief total occlusions and prolonged partial occlusions (ie, short-term hibernation), the time course of functional recovery varies from a few hours to several days, suggesting that the severity of protein damage or mechanisms responsible for the dysfunction may differ. To study this, we examined SR gene expression and TnI degradation in stunned myocardium produced by 10-minute total left anterior descending coronary artery (LAD) occlusions (n=4) or 1-hour partial LAD occlusions, in which flow was reduced to approximately 50% of control values for 60 minutes (n=6) in swine. One hour after reperfusion, LAD wall thickening was severely depressed in both models despite normal perfusion and no triphenyltetrazolium chloride evidence of necrosis. Normal myocardium exhibited TnI immunoreactivity at 31 kDa and a weak secondary band at 27 kDa. Irreversible injury or calpain activation in vitro produced a marked increase in the intensity of the 27-kDa band, consistent with TnI degradation. Stunned myocardium demonstrated no change in the 31- or the 27-kDa band, and the percentage of the 27- to 31-kDa band remained constant after 10-minute total occlusions (LAD, 5.9+/-0.9%; normal, 4.9+/-1.6%) and 1-hour partial occlusions (LAD, 8.5+/-1.9%; normal, 7.3+/-1.4%) and in sham controls (LAD, 10.9+/-1.5%; normal, 9.8+/-1.4%). Northern analysis showed no alterations in TnI or SR gene expression, but the stress protein HSP-70 was variably induced. Thus, stunned myocardium occurs without TnI degradation or altered SR gene expression, indicating that additional mechanisms are responsible for the reversible dysfunction after single episodes of regional ischemia in swine.
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PMID:Absence of troponin I degradation or altered sarcoplasmic reticulum uptake protein expression after reversible ischemia in swine. 1047 76

Coronary artery disease is highly prevalent in patients with end-stage renal disease, and accounts for much of their observed morbidity and mortality. Despite this, diagnosing myocardial disease in this population remains problematic, because many patients present with abnormal baseline electrocardiograms, frequently compounded by silent or atypical symptoms. Conventionally used enzymatic markers of cardiac injury have not resolved this dilemma because of their poor specificity in end-stage renal disease. In particular, nonspecific elevations in creatinine kinase-muscle brain enzyme, a widely accepted marker of cardiac injury, have been consistently observed in the absence of other demonstrable evidence for cardiac injury. Recently, the cardiac troponins (troponin I and troponin T) have emerged as more sensitive markers for cardiac ischemia, facilitating rapid bedside diagnosis and early risk stratification. Unfortunately, cardiac troponin T shows poor specificity in end-stage renal disease, possibly because of variable expression in extracardiac tissues. On the other hand, troponin I consistently maintains a high sensitivity and specificity, and is the most sensitive marker for ischemic heart disease in this patient population.
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PMID:Current markers of myocardial ischemia and their validity in end-stage renal disease. 1063 Aug 19

Opioid and alpha-adrenergic receptor activation protect the heart from ischemic damage. One possible intracellular mechanism to explain this is that an improvement in ATP availability contributes to cardioprotection. We tested this hypothesis by correlating postischemic left ventricular developed pressure (LVDP) and myofibrillar Ca(2+)-dependent actomyosin Mg(2+)-ATPase from isolated rat hearts treated with the kappa-opioid receptor agonist U-50488H (1 microM) or the alpha-adrenergic receptor agonist phenylephrine (10 microM) + propranolol (3 microM). Preischemic treatment with U-50488H or phenylephrine + propranolol improved postischemic LVDP recovery by 25-30% over control hearts. Ca(2+)-dependent actomyosin Mg(2+)-ATPase was found to be 20% lower in both U-50488H- and phenylephrine + propranolol-treated hearts compared with control hearts. The kappa-opioid receptor antagonist nor-binaltorphimine (1 microM) abolished the effects of U-50488H on postischemic LVDP and actomyosin Mg(2+)-ATPase activity. Reduced actomyosin ATP utilization was also suggested in single ventricular myocytes treated with either U-50488H or the protein kinase C activator, phorbol 12-myristate 13-acetate (PMA), because U-50488H and PMA lowered maximum velocity of unloaded shortening by 15-25% in myocytes. U-50488H and phenylephrine + propranolol treatment both resulted in increased phosphorylation of troponin I and C protein. These findings are consistent with the hypothesis that kappa-opioid and alpha-adrenergic receptors decrease actin-myosin cycling rate, leading to a conservation of ATP and cardioprotection during ischemia.
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PMID:Cardioprotection with kappa-opioid receptor stimulation is associated with a slowing of cross-bridge cycling. 1100 83

To determine the in vivo functional significance of troponin I (TnI) protein kinase C (PKC) phosphorylation sites, we created a transgenic mouse expressing mutant TnI, in which PKC phosphorylation sites at serines-43 and -45 were replaced by alanine. When we used high-perfusate calcium as a PKC activator, developed pressures in transgenic (TG) perfused hearts were similar to wild-type (WT) hearts (P = not significant, NS), though there was a 35% and 32% decrease in peak-systolic intracellular calcium (P < 0.01) and diastolic calcium (P < 0.005), respectively. The calcium transient duration was prolonged in the TG mice also (12-27%, ANOVA, P < 0.01). During global ischemia, TG hearts developed ischemic contracture to a greater extent than WT hearts (41 +/- 18 vs. 69 +/- 10 mmHg, perfusate calcium 3.5 mM, P < 0.01). In conclusion, expression of mutant TnI lacking PKC phosphorylation sites results in a marked alteration in the calcium-pressure relationship, and thus susceptibility to ischemic contracture. The reduced intracellular calcium and prolonged calcium transients suggests that a potent feedback mechanism exists between the myofilament and the processes controlling calcium homeostasis.
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PMID:Ischemic dysfunction in transgenic mice expressing troponin I lacking protein kinase C phosphorylation sites. 1115 84

An 11-year-old patient with diagnosis of hypertrophic cardiomyopathy (HCM) developed marked elevation of troponin I in the absence of electrocardiographic signs of ischemia after two episodes of supraventricular tachycardia. At follow-up the level of troponin I returned to normal. The role of troponin I in patients with HCM as a risk marker deserves further evaluation.
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PMID:Troponin I elevation after supraventricular tachycardia in a child with hypertrophic cardiomyopathy. 1117 73

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