Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0008031 (chest pain)
 17,248 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

ADP-induced and whole blood platelet adhesiveness have been studied by repeated measurements during the acute stage of the disease and the following two months in 86 randomly selected patients admitted to a coronary care unit because of acute central chest pain. In the patients who developed ECG and enzyme changes typical of infarction (group 1), platelet adhesiveness was significantly increased on admission compared with the rest of the patients (group 2) and controls (group 3). Patients in groups 1 and 2 showed a secondary increase during the first week, but two months after admission the means had returned to values within the normal range. No correlation was found between platelet adhesiveness and infarction size or fatal outcome of the disease. Platelet adhesiveness did not differ between patients with ECG changes indicating a transmural infarct and those with mainly subendocardial infarction.
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PMID:Platelet adhesiveness in myocardial infarction in relation to clinical course. 93 73

Platelet aggregation studies were performed in five men with coronary artery disease and angina pectoris and five men with nonspecific chest pain before and after receiving 1,000 I.U. of alpha-tocopherol acetate orally per day for 8 days. There was no significant difference in the platelet aggregation response to three concentrations of ADP and two concentrations of epinephrine between the pre- and post-vitamin E periods among the 10 patients. If tocopherol acetate (vitamin E) has any beneficial effect on the prevention of thromboemolism or in the treatment of angina pectoris and peripheral vascular disease, it is not via inhibition of platelet aggregation.
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PMID:The effect of vitamin E on platelet aggregation. 125 49

The effects of the intravenous administration of 100 mg of trapidil on systolic and diastolic left ventricular functions and coronary sinus blood flow, as well as on myocardial lactate metabolism and platelet aggregation, were investigated before and after pacing in 12 patients with coronary artery disease. Pacing without administration of trapidil provoked angina in 6 of these patients. During rest, trapidil decreased the mean blood pressure by an average of 5 mmHg (from 112 +/- 15 to 107 +/- 8 mmHg, p less than 0.05) and the left ventricular end-diastolic pressure by an average of 4 mmHg (from 10 +/- 3 to 6 +/- 2 mmHg, p less than 0.05). Trapidil also caused both the max dp/dt and the coronary sinus blood flow to increase slightly, although it had no significant effect on diastolic function, myocardial lactate metabolism, or platelet aggregation. During the pacing that followed trapidil administration, chest pain was not provoked in the same 6 patients who had previously experienced chest pain on pacing. The extent of ST-segment depression also improved from -1.6 +/- 0.3 to -0.9 +/- 0.7 mm (p less than 0.05) and there was a significant suppression of the production of myocardial lactate. When pacing was terminated, trapidil caused a decrease in left ventricular systolic pressure from 173 to 156 mmHg (p less than 0.05), and also caused a decrease of the left ventricular end-diastolic pressure, from 16 +/- 4 to 8 +/- 2 mmHg (p less than 0.05). Trapidil had no significant effect on platelet aggregation activity with either a 1 microM or a 2 microM dose of ADP (adenosine diphosphate). However, the beta-TG level was suppressed, decreasing from 119 +/- 14 to 99 +/- 19 ng/ml in the arterial blood (p less than 0.1) and from 114 +/- 9 to 103 +/- 17 ng/ml (p less than 0.1) in the coronary sinus blood. Reductions in the preload and afterload by trapidil were of far greater magnitude than either its coronary dilatory or positive chronotropic effects in patients with coronary artery disease. Thus trapidil, a new antianginal agent appears to inhibit the production of platelet derived growth factors and may, therefore, protect the arteries from atherosclerosis as it promotes beneficial systemic hemodynamics in patients with depressed ventricular function.
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PMID:The effects of trapidil on left ventricular function and platelet aggregation in patients with coronary artery disease subjected to pacing. 183 67

To investigate the pathophysiology of intracoronary thrombus formation we measured whole blood aggregation in response to ADP, platelet activating factor (PAF) and collagen, along with thromboxane B2 (TXB2) production during collagen induced aggregation, plasma TXB2 and plasma levels of lyso-PAF, in 38 subjects with and without ischaemic heart disease (12 with acute myocardial infarction, 9 with prolonged ischaemic chest pain without infarction and 17 normals). Lyso-PAF was measured, after in vitro acetylation to active PAF, by bioassay using 14C-serotonin labelled rabbit platelets. TXB2 was measured by radioimmunoassay. Plasma TXB2 was elevated at presentation only in patients with myocardial infarction (p less than 0.01). While impedance aggregation was similar in the three groups, aggregation to collagen resulted in greater release of TXB2 in subjects with myocardial infarction (p less than 0.01), an abnormality persisting 2-4 months later. Plasma lyso-PAF levels were significantly depressed throughout the first week in subjects with infarction (p less than 0.002), but after 2 to 4 months the level was greater than in normal subjects (p less than 0.001), changes presently unexplained. It is possible that the disorder of platelet function preceded and predisposed to coronary thrombosis. The findings strengthen the grounds for aspirin therapy in acute myocardial infarction.
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PMID:Whole blood aggregation, thromboxane release and the lyso derivative of platelet activating factor in myocardial infarction and unstable angina. 259 Sep 11

Forty-one patients with chest pain and angiographically normal coronary arteries were studied for platelet abnormalities. Patients with conditions known or suspected to be associated with chest pain or platelet dysfunction were excluded. After coronary angiography and 2-week withdrawal from all medications, platelet aggregometry was performed using peripheral venous plasma samples and 3 concentrations of adenosine diphosphate, 2.34, 1.17 and 0.58 microM, and epinephrine, 11, 1.1 and 0.55 microM, as stimuli. Platelet morphology in response to surface contact (adhesion) was evaluated by transmission electron microscopy to determine the percentage of platelets in the round/abortive (inactive), dendritic (intermediate) and spread (activated) forms. Plasma specimens obtained from healthy volunteers of similar age and sex were analyzed in parallel and served as control subjects. Compared with control subjects, patients had increased aggregation at all concentrations of both adenosine diphosphate and epinephrine (p less than 0.001). Patients also had fewer platelets in the dendritic form and more in the round/abortive and spread forms. Thus, patients with chest pain and normal coronary arteries have platelet hyperaggregability in vitro, although the clinical relevance of this finding is unclear.
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PMID:Platelet hyperaggregability in patients with chest pain and angiographically normal coronary arteries. 395 53

Ticlopidine is a powerful antiplatelet activator that inhibits adenosine diphosphate (ADP)-induced platelet aggregation. Its most common side-effects are skin rashes, diarrhea and neutropenia. Aplastic anemia is rare. This paper reports a patient with severe aplastic anemia that developed after the use of ticlopidine. The 85-year-old woman developed fever, chills and chest pain 5 weeks after starting ticlopidine 250 mg twice daily. Severe aplastic anemia was proved by blood examination, bone marrow aspiration and biopsy. In spite of the recovery of absolute neutrophil count to more than 1,000/mm3, 16 days after ticlopidine was stopped and administration of strong antibiotics, the patient died from candidal sepsis.
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PMID:Severe aplastic anemia induced by ticlopidine: report of a case. 852 78

Pathophysiologic mechanisms in syndrome X (anginal chest pain, positive exercise stress test, and angiographically normal coronary arteries) have been extensively studied. Recent reports suggest an ischemic origin of the pain to be less probable. Other contributing mechanisms that have been hypothesized are enhanced sympathetic drive or sensitivity or an abnormal muscle metabolism. Our aim in this study was to characterize exercise performance, skeletal muscle characteristics, and sympathetic control of blood flow in patients with syndrome X. Seven female patients aged 50 to 65 years and 5 matched controls were tested. Exercise test was performed according to clinical routine. Plasma catecholamine and blood lactate levels were measured before, during, and after exercise. Autonomic blood flow control was measured plethysmographically in the resting contralateral forearm during isometric handgrip. Muscle biopsy specimens were obtained at rest from the lateral part of Musculus vastus at midthigh. The biopsy samples were investigated for the relative number of different fiber types, phosphagen content, and energy charge, calculated as (adenosine triphosphate +/- 1/2 adenosine diphosphate)/[adenosine triphosphate +/- adenosine diphosphate +/- adenosine monophosphate]). Exercise capacity was markedly decreased in syndrome X compared with controls (85 +/- 14 vs 156 +/- 11 W, p <0.0005) and all patients discontinued exercise because of chest pain (Borg CR-10, 5 +/- 3). Peak heart rate was lower in syndrome X (150 +/- 18 vs 176 +/- 7 beats/min, p <0.01), whereas systolic blood pressure and double product did not differ. Peak norepinephrine plasma levels were lower than in controls (11 +/- 6 vs 24 +/- 13 nmol/L, p <0.04), whereas peak blood lactate levels did not differ. Blood flow increase in the resting forearm during isometric handgrip was similar to that in controls. The proportion of different fiber types, phosphagen content, and energy charge were normal. Thus, patients with syndrome X have a reduced physical exercise capacity but no skeletal muscle abnormalities. Catecholamine hypersensitivity may contribute to their condition.
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PMID:Impaired exercise performance but normal skeletal muscle characteristics in female syndrome X patients. 1042 36

Previous studies have demonstrated shortened bleeding times in patients with acute coronary syndromes, especially in myocardial infarction (MI). In this study we have investigated platelet hyper-function using the PFA-100 with collagen/adenosine diphosphate and collagen/epinephrine cartridges in 78 patients presenting with acute chest pain. Patients were classified into MI, unstable angina (UA) and non-specific chest pain. All patients received 300 mg aspirin (ASA) more than 2 h before blood samples were collected. Twenty healthy normal subjects were also tested before and 2 h after 300 mg ASA (n = 10). The collagen/adenosine diphosphate closure time was significantly shorter in MI patients (median, 71 s; P = 0.0237) but not in UA patients (median, 81 s; P > 0.05) compared with normal subjects (median, 92.5 s). The collagen/epinephrine closure times were significantly longer in UA patients (median, 233 s) than in untreated controls (median, 125 s; P < 0.0001), as expected, but there was no difference in MI patients (median, 149.24 s; P > 0.05), suggesting that the MI patients were not all responding to ASA. Analysis of a subset of the apparent ASA non-responders (n = 5) by platelet aggregation demonstrated that this was not related to failure of ASA to block cyclo-oxygenase activity. Von Willebrand factor levels were significantly elevated in both UA and MI patients compared with normal subjects (mean, 175.5 and 248.9 versus 89.1 s; P < 0.0001 and P < 0.0001, respectively) and were also significantly higher in the MI group compared with the UA group (P < 0.05). There is evidence for platelet hyper-function and elevated von Willebrand factor levels in the MI group that could explain their decreased responsiveness to ASA on the collagen/epinephrine cartridge.
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PMID:Platelet hyper-function in acute coronary syndromes. 1626 28

Several studies indicate that thrombosis plays an important role in the pathogenesis of coronary heart disease (CHD). Fibronectin is a multifunctional protein in plasma, other body fluids, and cell surface and plays an important role in platelet functions, including mediation of cell-cell and cell-surface interactions. Sialic acid is a regular constituent of glycoproteins and gangliozides in the outer cell membrane of mammalian cells. Therefore, the sialic acid content of platelets, which are characterized by their ability to aggregate with each other, can be important in leading to thrombus formation. In this study, platelet fibronectin, sialic acid-, and adenosine diphosphate (ADP)-induced platelet aggregation levels were determined in patients with CHD. Platelet sialic acid concentrations were determined by Warren's method. Platelet aggregation tests with ADP in platelet-rich plasma (PRP) were analyzed by use of an aggregometer. Platelet homogenate fibronectin levels were determined by ELISA. Total protein levels were determined by Lowry method. Our results indicate that, in patients with no vessel disease (patients with no obstructed vessel but suffering from chest pain, like angina pectoris) platelet fibronectin levels were significantly lower than the total of the other patients (patients with 1, 2, or 3 obstructed coronary vessels) (p<0.05). Sialic acid levels in patients with no vessel disease were significantly lower than the total of the patient group (p<0.05). There was significant (+) correlation between platelet aggregation, platelet fibronectin, platelet sialic acid, and severity of disease (p<0.05). Our preliminary findings suggest that, especially platelet fibronectin levels potentially represent a pathogenic factor for CHD.
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PMID:Preliminary study showing the relationship between platelet fibronectin, sialic acid, and ADP-induced aggregation levels in coronary heart disease. 1763 93

A 62-year-old woman presented to the emergency department with sudden collapse, intractable ventricular fibrillation, and an inferior wall myocardial infarction (MI). An emergent cardiac catheterization showed a totally occluded right coronary artery (RCA). A bare-metal stent was placed in the stenosis, resulting in thrombolysis in myocardial infarction (TIMI)-III flow with 0% residual stenosis. Four days after stenting, the patient developed chest pain. A repeat cardiac catheterization showed a totally occluded stent. The patient was subsequently tested using a thrombelastograph (TEG) Platelet Mapping assay to exclude clopidogrel resistance. The assay confirmed the patient to be non-responsive to clopidogrel for the inhibition of platelet ADP receptors. In an attempt to increase ADP inhibition, the ADP antagonist was changed to ticlopidine. Further testing was confounded by the presence of abciximab; however, the patient has remained free of cardiac events.
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PMID:Use of a thrombelastograph platelet mapping assay for diagnosis of clopidogrel resistance: a case report. 1936 Oct 30


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