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)

This review summarizes previously unpublished and recently published autopsy findings of prehospital sudden coronary death (SCD) in four different counties (Olmsted, Minnesota; Albany, New York; Dade, Florida; and San Francisco Bay Area, California), totaling 868 patients. The prevalence of cardiomegaly and significant coronary atherosclerosis, and the relative infrequency of acute coronary thrombosis in prehospital SCD, well documented in the past, have been reaffirmed in current studies. Differences in the patient populations and laboratory techniques notwithstanding, these independent autopsy studies showed that 62% to 74% of cases of SCD had either acute or old myocardial infarction (MI); the incidence of acute MI ranged from 12% to 47%, and that of old MI from 22% to 53%. The prospective autopsy study of 120 Olmsted County SCD cases showed that among those with established acute MI, subendocardial lesions outnumbered transmural lesions by the ratio of 2:1, and the infarcts ranged in histological age from less than 24 hours to 4 weeks. Evidence of acute myocardial ischemia, as determined by the histological criteria of myofibrillar degeneration, sinuous fibers, and positive HBFP staining, was present in 52% to 81% of patients. Such high incidence of myocardial ischemia is compatible with the proposed mechanism of the terminal event in SCD, namely ventricular fibrillation or asystole, and underscores the importance of presymptomatic diagnosis of coronary heart disease. The lack of specific or acute anatomical lesions in the conduction system in SCD, however, does not preclude the possibility of bradyarrhythmias occurring shortly before death.
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PMID:Pathology of the myocardium and the conduction system in sudden coronary death. 118 81

Acadesine (5-amino-4-imidazole carboxamide riboside) is a purine nucleoside analog that has been shown in animals to reduce myocardial ischemic injury by selectively increasing the availability of adenosine in ischemic tissues. Because patients undergoing coronary artery bypass graft (CABG) surgery are especially vulnerable to developing myocardial ischemia, we investigated whether perioperative use of this adenosine-regulating drug with potential anti-ischemic properties could modify the incidence and severity of perioperative myocardial ischemia. The goals of this study were to evaluate safety and the effects of acadesine on myocardial ischemia, left ventricular function, and, secondarily, on adverse clinical outcomes (myocardial infarction, heart failure, life-threatening dysrhythmias, and death) in patients undergoing CABG surgery. One hundred sixteen patients were randomized to receive one of three continuous intravenous dosing regimens (placebo [control] or one of two doses of acadesine [high- and low-dose infusion]) in double-blind fashion intraoperatively and in the early postoperative period (total infusion time was 7 h). Multidose cold crystalloid cardioplegia (each containing either acadesine or placebo) was used for myocardial protection. All were monitored for potentially drug-related adverse events and the presence of myocardial ischemia was assessed by continuous Holter electrocardiography (ECG) and transesophageal echocardiography (TEE). All patients received standardized anesthetic, surgical, and hemodynamic management during the intraoperative period. All research data (ECG, TEE, outcome data) were evaluated at the coordinating center (San Francisco) in blinded fashion to ensure that uniform data analysis criteria were employed. The administration of acadesine was safe: mild increases in plasma uric acid (a metabolite of acadesine) occurred only in patients receiving high doses (mean increase 1.6 +/- 0.2 mg/dL) and were without clinical sequelae. Before drug administration in the preoperative period (baseline), the incidence and severity of ECG ischemia did not differ among the three groups (placebo = 18%; low-dose = 14%; high-dose = 14%). During prebypass, the incidence of ECG ischemia was similar in all three groups (0%, 3%, 3%, respectively). The incidence of TEE ischemia was numerically lower in the two acadesine groups (high-dose = 6%, low-dose = 15%) than in the control group (19%), but this was not statistically significant (P = 0.22). During postbypass, the incidence of ECG ischemia was 11% in the high-dose group, 22% in the low-dose group, and 18% in the control group (P = 0.42), and TEE ischemia was similar in incidence in all groups (placebo = 29%; low dose = 27%; high-dose = 24%) (P = 0.86).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:An initial multicenter, randomized controlled trial on the safety and efficacy of acadesine in patients undergoing coronary artery bypass graft surgery. SPI Research Group. 797 87

The relationship of dyslipidemia, particularly hypercholesterolemia to coronary heart disease is now well established. Although ischemic heart disease and stroke share many of the same risk factors, the relationship of cholesterol to stroke remains controversial. The 6-year and 12-year follow-up of the MRFIT study showed that elevated cholesterol significantly increased the risk for fatal nonhemorrhagic stroke. Atkins found no evidence that lowering plasma cholesterol influenced the incidence of fatal or nonfatal stroke and regression analysis showed no statistical association between the magnitude of cholesterol reduction and the risk for fatal stroke. We cannot preclude the possibility that more effective cholesterol lowering over a longer period of time might be effective. Hypertension is the most powerful risk factor for stroke. The San Antonio Heart Study reported a clustering of cardiovascular risk factors in individuals who developed hypertension during an eight-year follow-up period (higher levels of BP, fasting TC and LDLC, TG, glucose and insulin, and BMI, less favourable fat deposition, and lower HDL). Insulin resistance may be the unifying factor that results in those phenomena, the so-called syndrome X. The important factor underlying syndrome X may be central or visceral obesity, suggesting that maintenance or attainment of ideal weight would be a powerful preventive factor against both CHD and nonhemorrhagic stroke. There is evidence from the Treatment of Mild Hypertension Study that nutritional/hygienic measures can reduce the syndrome X risk factors and hence the risk of coronary heart disease and stroke.
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PMID:Dyslipidemia and metabolic factors in the genesis of heart attack and stroke. 791 92

Recent data indicate that low-birthweight adults are at a higher risk than their high-birthweight peers of developing ischemic heart disease or a cluster of conditions known as the IRS, which includes dyslipidaemias, hypertension, unfavorable body fat distribution and NIDDM. Thus far these observations have been limited to Caucasians from the United Kingdom. we extended these observations to a broader segment of the general population by studying the association of birthweight and adult health outcomes in a biethnic population of the United States. We divided a group of 564 young adult Mexican-American and non-Hispanic white men and women participants of the San Antonio Heart Study into tertiles of birthweight and compared metabolic, anthropometric, haemodynamic, and demographic characteristics across these tertile categories. Additionally, we studied birthweight as a predictor of the clustering of diseases associated with the IRS, defined as any two or more of the following conditions: hypertension, NIDDM or impaired glucose tolerance, dyslipidaemia. Normotensive, non-diabetic individuals whose birthweight was in the lowest tertile had significantly higher levels of fasting serum insulin and a more truncal fat deposition pattern than individuals whose birthweight was in the highest tertile, independently of sex, ethnicity, and current socioeconomic status. Also, the odds of expressing the IRS increased 1.72 times (95% confidence interval: 1.16-2.55) for each tertile decrease in birthweight. These findings were independent of sex, ethnicity, and current levels of socioeconomic status or obesity. In conclusion, low birthweight could be a major independent risk factor for the development of adult chronic conditions commonly associated with insulin resistance in the general population.
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PMID:Birthweight and adult health outcomes in a biethnic population in the USA. 792 49

The causes of perioperative ischemia and myocardial infarction (MI) in coronary artery bypass graft (CABG) patients are almost certainly multifactorial, although not well understood. Ultimately, outcome after CABG is dependent on myocardial preservation and prevention of further myocardial ischemia. The largest number of ST-T-wave events come immediately after protamine is given, suggesting that re-establishment of coagulation function after cardiopulmonary bypass (CPB) may be an important event. CPB induces an inflammatory state that involves platelet-endothelial-cell interactions and vasospastic responses that result in low flow states in the coronary vasculature. The fibrinolytic system is activated during CPB, with raised tissue plasminogen activator (tPA) levels and related falls in plasminogen activator inhibitor (PAI-1). PAI-1 levels rise during the postoperative period. There is a huge variability in human response. However, the patients with the highest tPA surge are not the same patients who have the highest PAI surge. It could be postulated that patients with high PAI-1 levels are at highest risk for early ischemia. New data just being evaluated from the Multicenter Study of Perioperative Ischemia (McSPI) Research Groups' database in San Francisco may support the hypothesis that coagulation influences perioperative ischemia. The study of approximately 2,400 patients undergoing CABG surgery at 24 major institutions in the United States revealed that intensive care unit (ICU) entry hematocrit was significantly related to the risk for postoperative MI. Patients entering the ICU with hematocrits below 24% had the lowest MI rate (3.7%), whereas those with hematocrits greater than 34% had the highest rate (8.1%). Patients with ICU entry hematocrits below 18% had a zero incidence of perioperative MI. One possible explanation for these findings is that platelets are involved. As red cells stream down vessels, they marginate the smaller formed elements of the blood. As hematocrit is increased, the number of platelets moved to the outer sides of the vessels increases. Therefore, the number of endothelial-platelet interactions would increase over time with higher hematocrits.
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PMID:Ischemia--a coagulation problem? 893 82

We previously developed a technique (R. Kumar, R. Wilders, R. W. Joyner, H. J. Jongsma, E. E. Verheijck, D. A. Golod, A. C. G. van Ginneken, and W. N. Goolsby. Circulation 94: 833-841, 1996) for study of a mathematical model cell with spontaneous activity, viz. a "real-time" simulation of a rabbit sinoatrial node cell (SAN model cell; R. Wilders, H. J. Jongsma, and A. C. van Ginneken. Biophys. J. 60: 1202-1216, 1991) simultaneously being electrically coupled via our "coupling clamp" [H. Sugiura and R. W. Joyner. Am. J. Physiol. 263 (Heart Circ. Physiol. 32): H1591-H1604, 1992] circuit to a real, isolated ventricular myocyte. We now apply this technique to investigate effects of coupling conductance (Gc), cell size, and the modulation of membrane potential by elevated extracellular potassium concentration on the ability of an ectopic focus, represented by the SAN model cell, to successfully drive a ventricular cell. Values of Gc and the relative sizes of the two cells define three possible outcomes: 1) spontaneous pacing of the SAN model cell but not driving of the ventricular cell, 2) cessation of spontaneous pacing, or 3) pacing of the SAN model cell and driving of the ventricular cell. Below a critical size of the SAN model cell only the first two of these outcomes is possible. Above this critical size there is a range of Gc that allows successful operation of the system as an ectopic focus. Elevation of extracellular potassium concentration from 4 to 8 mM increases both the lower bound and upper bound of Gc for this range. Elevation of extracellular potassium concentration, as commonly observed in myocardial ischemia, may have effects on either inhibiting or releasing from inhibition an ectopic focus.
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PMID:Modulation of propagation from an ectopic focus by electrical load and by extracellular potassium. 913 60

Platelet-mediated coronary thrombosis is the primary pathophysiologic mechanism of acute coronary syndromes (ACS) and acute ischemic complications of percutaneous coronary intervention (PCI). The final common pathway of platelet aggregation that leads to thrombotic occlusion of coronary arteries involves cross-linking of receptor glycoprotein (GP) IIb-IIIa on adjacent platelets by adhesive plasma proteins, primarily fibrinogen. Clinical trials of several GP IIb-IIIa inhibitors have demonstrated an unequivocal clinical benefit of this potent antithrombotic therapy in patients with ACS as well as in those undergoing PCI. Nevertheless, a significant number of patients with ischemic heart disease may still be expected to require elective or emergency coronary artery bypass graft (CABG) after treatment with GP IIb-IIIa inhibitors. In the emergency CABG setting, complications and platelet blockade with GP IIb-IIIa inhibitors may further enhance the already heightened risk of bleeding as compared with elective procedures. This issue became apparent in the first large clinical trial of the GP IIb-IIIa inhibitor abciximab (c7E3 Fab, ReoPro((R)); Centocor, Malvern, Pa, and Eli Lilly and Co, Indianapolis, Ind) in patients undergoing high-risk PCI. In this study, mortality rates and bleeding complications were increased among patients undergoing emergency CABG after treatment with a bolus plus infusion of abciximab. Subsequent clinical experience also suggests that the potential for bleeding complications related to emergency CABG may be increased in patients treated with abciximab, particularly if the drug is discontinued within 6 hours of the operation. Higher bleeding risk with abciximab is a result of its prolonged antiplatelet effect, which is in contrast to the readily reversible platelet blockade provided by more recently developed small-molecule GP IIb-IIIa inhibitors such as the peptide eptifibatide (Integrilin((R)); COR Therapeutics, South San Francisco, Calif, and Key Pharmaceuticals, Kenilworth, NJ) and the nonpeptide tirofiban HCl (MK-383, Aggrastat((R)); Merck & Co, Whitehouse Station, NJ). Therefore, among patients requiring CABG after treatment with GP IIb-IIIa inhibitors, eptifibatide and tirofiban may be associated with fewer bleeding episodes than is abciximab. With recent approval of eptifibatide for patients with ACS and those scheduled for PCI and of tirofiban for patients with ACS, the number of patients receiving GP IIb-IIIa inhibitor therapy who subsequently undergo CABG is expected to increase significantly. Strategies for improved management of bleeding complications in these patients, including the choice of a GP IIb-IIIa inhibitor, are clearly needed and are discussed in detail.
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PMID:Safety of glycoprotein IIb-IIIa inhibitors: A heart surgeon's perspective. 1050 36

Optison (human albumin microspheres; Mallinckrodt Inc., San Diego, CA) is an injectable suspension contrast agent indicated for use in left-ventricular chamber opacification and endocardial-border delineation. Substantial proportions of patients undergoing echocardiography have inadequate endocardial delineation and, therefore, wall motion (including stress echocardiography) without contrast. The extent of use of Optison for its current indications is likely to vary, and its use will depend upon the patient population and image quality obtained from noncontrast examinations. Early reports exist of its use in as many as 60% of patients undergoing studies in a given echocardiography laboratory. The rate of acceptance for endocardial delineation in stress echocardiography appears to be particularly high, because of the higher proportion of technically challenging studies whether with fundamental or second harmonic imaging. The ability to aid in differentiation of potential artifacts from pathology in the cavity has also been reported. Clinical studies have been conducted or are currently underway to evaluate Optison in the assessment of acute and chronic ischemic coronary artery disease. Studies in patients with unexplained acute chest pain and during exercise and pharmacologic stress have evaluated the ability of Optison to detect perfusion abnormalities as well as wall-motion abnormalities. The rapid evolution of ultrasound imaging modalities such as harmonic Doppler and broad-bond imaging will further enhance Optison's ability to characterize ischemic heart disease patients.
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PMID:Cardiac imaging using Optison. 1099 46

The electrocardiogram continues to be the gold standard for the diagnosis of cardiac arrhythmias and acute myocardial ischemia. The treatment of arrhythmias in critical care units has become less aggressive during the past decade because research indicates that antiarrhythmic agents can be proarrhythmic, causing malignant ventricular arrhythmias such as torsade de pointes. However, during the same period, the treatment of acute myocardial ischemia has become more aggressive, with the goal of preventing or interrupting myocardial infarction by using new antithrombotic and antiplatelet agents and percutaneous coronary interventions. For this reason, critical care nurses should learn how to use ST-segment monitoring to detect acute ischemia, which is often asymptomatic, in patients with acute coronary syndromes. Because the electrocardiographic lead must be facing the localized ischemic zone of the heart to depict the telltale signs of ST-segment deviation, the challenge is to find ways to monitor patients continuously for ischemia without using an excessive number of electrodes and lead wires. The current trend is to use reduced lead set configurations in which 5 or 6 electrodes, placed at convenient places on the chest, are used to construct a full 12-lead electrocardiogram. Nurse scientists at the University of California, San Francisco, School of Nursing are at the forefront in developing and assessing the diagnostic accuracy of these reduced lead set electrocardiograms.
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PMID:Celebrating the 100th birthday of the electrocardiogram: lessons learned from research in cardiac monitoring. 1210 39

In our studies an attempt was undertaken to establish whether there is a relationship between total cholesterol and LDL fraction concentrations and LDL receptors expression on monocytes in various clinical types of atherosclerosis and in subjects without clinical manifestations of this disease before and after 40 years of age. The study included 77 subjects divided into 4 groups: I--after myocardial infarction, II--after cerebral ischaemic stroke, III--with obliterative atheromatosis of the lower limbs, and control group IV without clinical symptoms of atheromatosis: a) subjects below 40 years of age b) over 40 years of age. Receptor expression on monocytes was tested with LDL Receptor Test (Orpegen Pharma, Heidelberg, Germany) using flow fluorometry method (FAC Scan, Backton Dickinson, San Jose, USA). The value of LDL receptors expression was calculated based on the difference of mean fluorescence intensity of monocytes incubated in low-lipid (LPDS) and autologous sera. It has been demonstrated that particular types of atheromatosis vary in the value of total cholesterol and LDL fraction concentrations. The highest concentrations of these lipid fractions were observes in ischaemic heart disease and only in this group they correlated with the value of LDL receptors expression on monocytes. This observation suggests that various clinical types of atheromathosis may differ pathogenically and lesions in the vessels may be the consequence of cholesterol transport defect or of lipid molecule modification; they not necessarily depend on the value of absolute lipid concentration in blood.
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PMID:[LDL-receptors expression on peripheral blood monocytes in various clinical types of atherosclerosis, depending on LDL concentration in serum]. 1293 20


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