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)

We report a case of a 55-year-old male undergoing major orofacial cancer surgery. A stent to the left anterior descending artery had been implanted for ischaemic heart disease 3 years previously. Twenty-four hours after uneventful anaesthesia and surgery, the patient developed myocardial infarction and cardiogenic shock. Immediate percutaneous transluminal coronary angioplasty, intra aortic balloon counterpulsation, and catecholamine therapy failed to stabilise haemodynamics. In light of successful reperfusion therapy and an only moderate elevation of troponin I, myocardial stunning rather than myonecrosis was considered to be the major contributor to life-threatening left ventricular failure. Therefore, the calcium-sensitising drug levosimendan, which exerts positive inotropic activity without increasing myocardial oxygen demand, was administered as a rescue medication. Within 24 h, levosimendan resulted in decreased filling pressures, reduced left ventricular end-diastolic volume, and augmented systemic pressures. Seven days following surgery, the patient was discharged from the intensive care unit in good clinical condition.
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PMID:Levosimendan: a promising treatment for myocardial stunning? 1640 45

Elevations in serum cardiac troponins are used to diagnose myocardial infarction caused by ischemic heart disease. Several other conditions result in elevated cardiac makers in the absence of significant coronary artery disease. While not commonly recognized elevations of troponin I (TNI) may be seen in patients with protracted arrhythmias. We describe three patients with prolonged tachycardia, heart rates of 200-260 beats per minute, who had elevated TNI (0.81-4.6 ng/ml) but no significant coronary artery disease. Two patients presented with ventricular tachycardia and one had an atrioventricular re-entrant tachycardia. None of the patients presented with symptomatic hypotension. Coronary angiography in all three patients did not demonstrate significant coronary artery disease. The finding of an elevated TNI level may be the result of tachycardia and not myocardial infarction related to ischemic heart disease.
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PMID:Tachycardia-induced elevations in cardiac troponin in the absence of coronary artery disease. 1672 50

Sildenafil is widely used as a primary pharmacological treatment of erectile dysfunction in men with and without underlying cardiovascular disease. Although initial reports of adverse cardiac events were reported soon after Food and Drug Administration approval of this agent, a large body of data suggests that sildenafil does not significantly increase the risk of nonfatal myocardial infarction, stroke, or cardiovascular deaths in patients with preexisting ischemic heart disease. We report the case of a 66-year-old man who developed thrombotic occlusion of the left anterior descending artery and presented with acute myocardial infarction after the use of sildenafil. The patient had presented with chest pain syndrome and borderline elevation of serum troponin I levels 1 week before sildenafil use, and a coronary angiogram had demonstrated normal coronary arteries. This case emphasizes the potential of precipitating coronary thrombosis in patients with unstable plaque after sildenafil use, even in patients with angiographically normal coronary arteries.
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PMID:Sildenafil-associated coronary thrombosis in a patient with angiographically normal coronary arteries: a case report with review of literature. 1685 76

We describe a case of a 76-year-old woman who presented with chest pain after a violent argument. On admission the electrocardiogram showed 1-mm ST segment elevation in II, III, aVF, V3-V6 leads; the subsequent electrocardiogram showed T-wave inversion in the same leads. Peak troponin I level was 7.3 ng/dl (normal <0.4 ng/dl). Emergency angiography demonstrated the so-called "apical ballooning", in the absence of any obstructive coronary artery disease. A myocardial contrast echocardiogram performed 5 days later showed a large perfusion defect in the akinetic apical region of the left ventricle; at 1-month follow-up myocardial perfusion and left ventricular wall motion became completely normal. In patients with apical ballooning syndrome a catecholamine-mediated endothelial injury might be responsible of a microvascular coronary dysfunction which causes myocardial ischemia and subsequent myocardial stunning.
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PMID:Transient impairment of myocardial perfusion in a patient with apical ballooning syndrome. 1739 93

The cardiac myofilaments are composed of highly ordered arrays of proteins that coordinate cardiac contraction and relaxation in response to the rhythmic waves of [Ca(2+)] during the cardiac cycle. Several cardiac disease states are associated with altered myofilament protein interactions that contribute to cardiac dysfunction. During acute myocardial ischemia, the sensitivity of the myofilaments to activating Ca(2+) is drastically reduced, largely due to the effects of intracellular acidosis on the contractile machinery. Myofilament Ca(2+) sensitivity remains compromised in post-ischemic or "stunned" myocardium even after complete restoration of blood flow and intracellular pH, likely because of covalent modifications of or proteolytic injury to contractile proteins. In contrast, myofilament Ca(2+) sensitivity can be increased in chronic heart failure, owing in part to decreased phosphorylation of troponin I, the inhibitory subunit of the troponin regulatory complex. We highlight, in this paper, the central role of the myofilaments in the pathophysiology of each of these distinct disease entities, with a particular focus on the molecular switch protein troponin I. We also discuss the beneficial effects of a genetically engineered cardiac troponin I, with a histidine button substitution at C-terminal residue 164, for a variety of pathophysiologic conditions, including hypoxia, ischemia, ischemia-reperfusion and chronic heart failure.
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PMID:Tuning cardiac performance in ischemic heart disease and failure by modulating myofilament function. 1739 43

The present study evaluated the prognosis at different troponin concentrations regardless of the underlying diagnosis in an unselected group of patients admitted to the coronary care unit (CCU) and whether the prognosis is dependent on the cause of the troponin increase. Troponin I was measured with the Stratus CS analyzer (Dade Behring) in 468 consecutively and unselected patients admitted to the CCU at Karolinska University Hospital with possible myocardial ischemia lasting <12 hours before arrival. A troponin I concentration below (0.02 to 0.10 microg/L) the diagnostic cut-off level for myocardial infarction predicted mortality after 40 months. In patients with a troponin I level above the diagnostic cut-off level for acute myocardial infarction, the underlying cause of the troponin increase did not affect the prognosis. In conclusion, we report that a troponin I increase below the new cut-off level for myocardial necrosis was associated with increased mortality in unselected patients with possible myocardial ischemia admitted to the CCU at a university hospital. We also observed that the underlying cause of the troponin increase appears to be less important for outcome.
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PMID:Usefulness of troponin levels below the diagnostic cut-off level for acute myocardial infarction in predicting prognosis in unselected patients admitted to the coronary care unit. 1749 59

Previous studies indicate that adenosine supplementation or nitric oxide synthase (NOS) inhibition during reperfusion exert protective effects against myocardial ischemia-reperfusion (I/R) injury. We wanted to test the hypothesis that NOS inhibition before I/R also protects the myocardium against further injury and aimed to determine the involvement of adenosine receptors in a perfused rat heart model. Rats were injected with 10 mg/kg of L-NAME (N(omega)-nitro-L-arginine methyl ester) or L-NAME + SPT (8-(p-sulfophenyl)-theophylline)--an adenosine antagonist - at 2 x 25 mg/kg or with a saline buffer, 24 hrs prior to heart excision. The hearts, perfused retrogradely were subjected to 60 min of global ischemia followed by 120 min reperfusion. L-NAME decreased NOx (nitrite and nitrate) production (16.2 +/- 3.2 vs. 7.0 +/- 1.8 micromol/L; P<0.05) in vivo and increased the release of troponin I (0.04 +/- 0.01 vs. 0.02 +/- 0.01 microg/L; P<0.05) in the plasma, compared to controls. After 120 min of reperfusion, there was a higher release of adenosine (26.1 +/- 2.2 vs. 2.4 +/- 1.2 nmol/min; P<0.01) and a decrease in troponin I levels (0.19 +/-0.07 vs. 0.59 +/- 0.16 ng/min; P<0.05) in the L-NAME group compared to controls. These results were accompanied by a higher proportion of recovery of left ventricular developed pressure (72.0 +/- 4.0 vs. 60.0 +/- 4.0%; P<0.05) and coronary flow (72.0 +/- 5.0 vs. 51.0 +/- 4.0%; P<0.05) in the L-NAME group. These beneficial effects were not blocked by the adenosine receptor antagonist. The present study reveals that L-NAME protects against I/R injury when the inhibitor is administered 24 hrs before ischemia. The beneficial effects observed in this model appear to be independent of adenosine receptor stimulation.
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PMID:Delayed 24 hours Nomega-nitro-L-arginine methyl ester injection induces pharmacological cardioprotection against reperfusion injury. 1754 24

Unrecognized or silent perioperative myocardial ischemia is common in patients who undergo high-risk surgery, including cystectomy, and could predict cardiac morbidity and mortality in postoperative patients. This disorder is not merely a marker of extensive coronary disease but has a close association with perioperative myocardial infarction (PMI). In a review of published data, including meta-analyses, in the context of high-risk urological surgery, up to 50% of PMIs were found to go unrecognized if only clinical signs and symptoms are considered. Prevention and treatment of these previously unrecognized cardiac events might significantly reduce long-term morbidity and mortality. The emergence of reliable markers of PMI, such as increased levels of troponin I, could help in the detection of events that would have otherwise remained unnoticed. In this Review we examine the effect of these developments in the context of high-risk urological surgery. Changes to preoperative assessment, perioperative management, and prophylaxis of PMI are critically assessed. We performed a prospective audit using postoperative troponin I levels to assess the rate of silent perioperative myocardial ischemia and infarction. An increasingly proactive attitude towards perioperative monitoring for myocardial ischemia and infarction has evolved, and postoperative serial screening with troponin I might be beneficial in high-risk patients undergoing major urological surgery.
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PMID:Therapy insight: prophylaxis, monitoring and treatment of perioperative myocardial ischemia with emphasis on urological surgery. 1755 37

Cardiovascular disease is the leading cause of perioperative morbidity and mortality after vascular surgery. The purpose of this study was to identify risk factors for myocardial ischemia after vascular surgery and to investigate a potential association of ischemia with mortality in a community hospital setting. A retrospective review was conducted after 190 major vascular procedures. Electrocardiogram (ECG) results and troponin I levels were obtained serially during the first 24 postoperative hours. Outcomes analyzed were ischemic ECG changes, troponin I level more than 2 ng/mL, 6-month mortality, and overall survival. The authors investigated any association of these outcomes with each other and the type of operation, history of coronary artery disease, diabetes, recent coronary intervention, age older than 70 years, or postoperative symptoms. Twenty-seven (14%) patients experienced ischemic ECG changes. Twenty-one (11%) patients experienced troponin I elevation. Univariate analysis revealed a history of coronary artery disease, diabetes, concerning symptoms, and troponin elevation to be predictive of ECG change (P < 0.05). ECG change and symptoms were predictive of troponin elevation (P < 0.01). Cox multivariate analysis revealed only infrainguinal bypass to predict 6-month mortality (odds ratio = 2.92, P = 0.02). Diabetes was the sole predictor of overall mortality (odds ratio = 1.94, P = 0.001). Nonsustained ischemic postoperative ECG changes during the first 24 postoperative hours do not independently influence 6-month or overall mortality after major vascular surgery. Postoperative troponin elevation likely conveys a mortality risk in the subsequent 6 months. In the community hospital setting, midterm survival rates after vascular surgery equivalent to those in higher volume centers can be achieved. Patients undergoing infrainguinal bypass and diabetics continue to be the most moribund vasculopaths.
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PMID:Predictors of electrocardiographic change, cardiac troponin elevation, and survival after major vascular surgery: a community hospital experience. 1767 44

Matrix metalloproteinase (MMP)-2 mediates myocardial ischemia-reperfusion injury which is characterized by enhanced peroxynitrite biosynthesis during early reperfusion. Direct infusion of peroxynitrite into isolated hearts activates MMP-2 prior to the loss in mechanical function. The mechanical dysfunction is prevented by MMPs inhibitors. MMP-2 is also found in the sarcomere of cardiomyocytes where it cleaves troponin I and myosin light chain I. Cytoskeletal proteins such as alpha-actinin, desmin and spectrin are found in close association with the sarcomere and are known to be degraded in ischemia-reperfusion injury. It remains unknown whether these proteins are degraded in peroxynitrite-induced myocardial injury and if cytoskeletal proteins are also targets for MMP-2. Peroxynitrite (80 microM) was infused into isolated rat hearts which led to a delayed onset but rapidly developing decline in mechanical function. The MMPs inhibitor PD-166793 or the peroxynitrite scavenger glutathione prevented the decline in cardiac function. At the end of perfusion, alpha-actinin levels were decreased by 45+/-3% in peroxynitrite-infused hearts as compared to control hearts; however, this was normalized to that of control hearts with either PD-166793 or glutathione. Cardiac desmin and alphaII spectrin levels were unaltered following peroxynitrite infusion. alpha-Actinin and to a lesser extent desmin are susceptible to in vitro proteolysis by MMP-2 whereas spectrin is resistant. Cardiac dysfunction induced by peroxynitrite involves degradation of alpha-actinin that may be mediated by the proteolytic action of MMP-2.
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PMID:Matrix metalloproteinase-2 degrades the cytoskeletal protein alpha-actinin in peroxynitrite mediated myocardial injury. 1785 26


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