Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: DrugBank:APRD00528 (Monit)
 35,110 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Silent myocardial ischemia (SMI) is a manifestation of coronary artery disease in which persons have episodes of myocardial ischemia that are not accompanied by chest or anginal pain. Episodes of SMI have been described as the predominant form of transient myocardial ischemia in patients with stable angina, those with unstable rest angina and even variant angina. Silent myocardial ischemia is also known to occur in some patients with myocardial infarctions and resuscitated from episodes of sudden cardiac death, thus occur frequently in patients with all of the usual symptomatic phases of coronary artery disease. A number of studies have now clearly demonstrated that patients with silent ischemia have increased risk for coronary events: sudden death or myocardial infarction. SMI is most often recognized during exercise testing or fortuitously with ambulatory electrocardiography. For today it is imperative to investigate every patient in whom multiple risk factors of IHD have been recognised, even in the absence of chest pain. The early detection of SMI may help to prevent later cardiac events. If the ischemia (symptomatic and silent) itself is the cause of the higher mortality rate, then the goal of therapy should be to abolish it either by pharmacological means or by invasive interventions as balloon angioplasty or coronary bypass surgery.
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PMID:[Silent myocardial ischemia]. 1083 3

An analysis was performed of comprehensive (non-invasive and invasive) observations of IHD patients presenting with atherosclerotic lesions of coronary arteries of the heart and atypical clinical picture of the condition. A possibility was shown of a significant obstruction of arteries of the heart in atypical localization of pain and in those patients who had not derived much benefit from nitroglycerin during the development of ischemia and measures instituted against it. Inadequate reaction to nitroglycerin may be explained by specificities of changes in the vegetative nervous system, by the hemodynamics reaction, and, in the first place, by a propensity for developing tachycardia under physical loading, emotional stress, and after ingestion of nitroglycerin.
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PMID:[Sudden cardiac death: the possible role of latent myocardial ischemia in the mechanisms of its formation and development]. 1087 65

Several unfavorable cardiovascular events show a well-defined pattern in their occurrence throughout the day. Myocardial infarction and ischemia, sudden cardiac death and stroke occur with greater frequency in the morning hours after awakening. Multiple biologic functions such as blood pressure, heart rate, sympathetic neurotransmission, vascular tone, platelet aggregability, and coagulation parameters also show a diurnal variation and appear to contribute to adverse cardiac outcomes. Recent studies have emphasized the importance of 24 h control in decreasing cardiovascular risk. The renin-angiotensin system (RAS), through the important effector peptide, angiotensin II (Ang II), has potent effects on blood pressure, salt and water homeostasis, and target-organ damage. Inhibiting the RAS consequently becomes an important therapeutic avenue for treating hypertension and target-organ damage. Ang II receptor antagonists selectively compete with the binding of Ang II to the Ang II type 1 receptor and, by inhibiting the multiple activities mediated by Ang II at this receptor, may confer cardiovascular benefits additional to that of blood pressure control. Ang II receptor antagonists with an intrinsically long duration of action that produce smooth, sustained antihypertensive activity over the dosing period provide a similar 24 h benefit of Ang II inhibition.
Blood Press Monit 2000
PMID:Factors affecting circadian variability. 1090 36

In 30 patients after myocardial infarctum with actual silent ischemia (no pain during last 12 months) mononitrate (Olicard 40) was administered and red blood cell deformability was determined. Clinical improvement and decrease of aforementioned deformability were observed after mononitrate therapy.
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PMID:[Influence of nitrates on red blood cell deformability and clinical parameters in patients with silent ischemia]. 1090 22

The number of granulocytes, their ability to generate superoxide anion (O2-) and the activities of Cu, Zn--superoxide dismutase (SOD-1), glutathione peroxidase (GSH-Px), catalase (CAT) as well as malonyldialdehyde (MDA) concentrations in erythrocytes in the blood extracted from the venous sinus and aorta under coronary artery bypass were examined with the use of St. Thomas Hospital cardioplegic solution. Specimens at the peak of ischemia of the right atrium for ultrastructural examination of the endothelial cells of capillary vessels and sarcomers were taken. The blood was obtained during cardiopulmonary bypass (CPB) before the aorta clamping and immediately after aorta declamping (peak of ischaemia) between 1-3 minute and 10-13 minute of reperfusion. Increase of the number of granulocytes both in the coronary sinus and aortal blood at all examined intervals as well as decrease in the number of ones in sinus compared with aortal blood was noted. The ability to produce superoxide anion radical decreased at the peak of ischemia and during reperfusion. The activity of SOD-1 was lower both after the period of ischemia and reperfusion. The increase in aortal blood activity during reperfusion was characteristic of GSH-Px; the activity was higher in the blood sample from the coronary sinus taken during ischemia and initial reperfusion. With the exception of the initial reperfusion the activity of CAT diminished in all observed cases. MDA concentration did not demonstrate any significant changes with the exception of the initial reperfusion in the aortal blood and later towards the end of reperfusion in the blood from the coronary sinus. Ultrastructural studies indicated overhydration of the cells both in the endothelium and the intercellular space. The obtained data demonstrate that the applied cardioplegic solution protects the myocardium from harmful effects of reactive oxygen species produced as a result of ischemia and reperfusion.
Med Sci Monit
PMID:Moderate systemic hypothermia and cold crystalloid cardioplegia influence on myocardial ischemic and revascularisative injury. 1120 42

The article discusses the role of vascular endothelial growth factor(VEGF) in angiogenesis in embryonic development, particularly the effect of VEGF on capillary formation in response to chronic tissue ischemia and hypoxia. The sources and action of numerous angiogenic and angiostatic factors responsible for morphologic development of endothelial cells and disturbances in VEGF and FGF secretion are also presented. Increased VEGF and VEGF receptor expression enhances vascular permeability and angiogenesis, and is the cause of tissue edema as well as tumor and metastasis formation. VEGF appears to have a beneficial effect only in ischemic diseases of the heart and peripheral vessels. The article highlights the therapeutic implication of VEGF suppression in other areas of ischemia.
Med Sci Monit
PMID:Vascular endothelial growth factor (VEGF) and its effect on angiogenesis. 1120 53

Energetic function impairment is one of the main reasons of liver ischemia-reperfusion injury. The aim of the study was to estimate the influence of temporary rat liver ischemia on energetic functions of the organ in the early and late reperfusion period and to answer the question whether the reduction of destructive factors release in sinusoids in the early phase of reperfusion can prevent liver energetic function impairment. To perform the experiment 55 Wistar rats divided into 5 experimental groups were used. 60 min. partial ischemia of the liver was applied, with 30 min, 72 h and 5 days reperfusion period. Suppression of KC was performed by intravenous administration of GdCl3. In the group of animals subjected to liver ischemia a considerable decrease of reaction to SDH and LDH activity was observed in the reperfusion period. In animals with KC suppression the loss of reaction to SDH intensity in zones I of acini was insignificant and the decrease of reaction to LDH was more orderly and proceeded in a more regular manner. The value of AKBR fell significantly after 30 min. of reperfusion in both groups of animals subjected to ischemia, while the serum level of AspAT and LDH increased rapidly. Temporary ischemia of the rat liver induces a decrease of the organ energetic functions in the early and the reperfusion period. The elimination of Kupffer cell activity in the early reperfusion phase does not prevent liver energetic functions impairment, but reduces the time in which they return to initial values in remote observation.
Med Sci Monit
PMID:Influence of temporary ischemia on energetic functions of rat liver in early and late reperfusion period. 1138 14

Coronary artery disease is the number one cause of adult mortality due to a medical illness in the United States. Exciting new studies are looking at the role transient ischemia may play in preconditioning the myocardium to reduce the degree of infarction following a sustained ischemic insult. In this speculative review, we surmise ischemic preconditioning and the resulting protection afforded by it in response to abnormal insults arises from an already existing physiological process that may be associated with exercise. A brief ischemic episode mimics the cells response to normal dips in ATP levels caused by metabolic demand. In so doing, via constitutive nitric oxide synthase derived nitric oxide, it temporarily down regulates a cells excitatory state, thus protecting it from the next insult. Within this context, opiate and opioid actions can be incorporated into the protection scenario, as can other signal molecules since they may release nitric oxide. Instead of ischemia inducing nitric oxide release via a drop of ATP levels, various signal molecules, such as opiate alkaloids, have their cell surface receptors coupled to constitutive nitric oxide synthase thereby releasing nitric oxide, initiating associated cell activity dampening action. In conclusion, it appears as though endogenous nitric oxide stimulators offer their selective preconditioning protection by joining an already existing process that limits activation following normal physical exertion.
Med Sci Monit
PMID:Ischemic preconditioning - an opiate constitutive nitric oxide molecular hypothesis. 1168 57

Many recent experimental and clinical studies have provided evidence for the presence of inflammation in atherosclerotic lesions. Ongoing inflammatory reactions within coronary atherosclerotic plaques are increasingly thought to be crucial determinants of the clinical course of patients with coronary artery disease (CAD). These facts lead to a search for reliable markers reflecting the inflammatory process in the atherosclerotic plaques. Circulating markers may consist of cytokines directly released from inflammatory cells present in the plaques and tissues exposed to recurrent ischemia as well as other reactants produced in response to these cytokines such as adhesion molecules and acute phase proteins. Recent studies suggest that markers of inflammation may reflect different aspects of the atherothrombotic process at different points in the continuum of acute coronary syndromes, have a potential role for the prediction of risk for developing CAD, and may correlate with severity and future risk for CAD. In spite of these findings, the clinical utility of measuring these markers is limited by the availability of reproducible diagnostic test assays. In addition, it remains to be determined whether markers of inflammation actually have a causal relation with cardiovascular disease, or simply reflect the underlying disease process. Such determination becomes important with the potential use of these markers in targeting preventive therapies. Therefore, further well-designed prospective evaluation of each of these markers is needed before their use in routine practice.
Med Sci Monit 2002 Jan
PMID:Markers of inflammation and coronary artery disease. 1178 89

Multifocal manifestation of atherosclerosis (ATS) is common for this pathology and demands special diagnostic and therapeutic approaches. The need of active screening of basic clinical forms of multifocal ATS--carotid, peripheral arterial disease (PAD), aortic abdominal aneurysms(AAA) and coronary (IHD) is mandatory along with precise indications of therapeutical strategy and operative tactics in cases when surgical treatment is needed. The aim of this study is the evaluation of our results in operative treatment of combined forms of ATS and proper indication for simultaneous or two staged surgical approach. Our experience dictates simultaneous operative strategy only in cases of: 1. Carotid stenosis > 70% even asympthomatic, or > 50% sympthomatic stenosis (group A) combined with coronary artery disease in III-IV stage and 2-3 main vessel disease and unstable angina. 2. AAA > 7 cm. (group B) associated with IHD. 3. PAD with critical limb ischemia associated with unstable IHD. The absence of this specific indications allows not so aggressive surgical approach--two staged procedures (coronary artery bypass surgery first and several months later arterial reconstructive surgery of carotid or abdominal aortic lesions.
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PMID:[Combined surgical treatment of patients with multifocal atherosclerosis]. 1202 51


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