Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002895 (sickle cell disease)
 11,747 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The injury-vasospasm hypothesis of IHD was discussed in relation to coronary artery autoregulation and the anoxic-feedback mechanism. Observations in the recent literature, not usually attributed to spasm, were examined in light of this phenomenon. This includes reperfusion models of experimental AMI, the association of AMI with myocarditis, and findings in AMI and SCD as necrotic microlesions, prodromata, and epicardial arterial plaque rupture and hemorrhage. The disparity between the severity of coronary disease and the occurrence of the various types of IHD suggest that atherosclerosis itself does not precipitate attacks of chest pain. It was emphasized that plaque rupture due to spasm might help induce CAT. With exercise, the possible importance of the autoregulatory system was explored in the prevention and induction of AMI and SCD, and the improvement of AP. The role of spasm in IHD should be defined.
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PMID:The injury-vasospasm hypothesis of ischemic heart disease, revisited. 33 91

The possibility that myocardial ischemia may be associated with chest pain during painful crises was evaluated prospectively in 20 patients (11 women and nine men) with sickle cell disease (19 SS, 1 S beta + thalassemia). Sixteen of 20 (80%) had abnormal ECGs, 7 (35%) had transient ST-T wave changes, and 3 (15%) had persistent ST-T wave changes, both consistent with ischemia; 6 (30%) had nonspecific ST-T changes, and 4 (20%) had normal tracings. Serum enzymes (CK, SGOT, LDH) were abnormal in 16 of 19 (84%); 1 had CK-MB detected, (5%) and 1 had LDH1 to LDH2 reversal. All 10 Tc-99m pyrophosphate scans performed were negative; 4 of 6 (66%) thallium-201 scans had focal defects, and 5 of 8 (63%) radionuclide angiograms (MUGAs) had focal wall motion abnormalities. Three of 8 (38%) MUGAs showed cardiac dilation, diffuse hypokinesis, and reduced ejection fractions. Thus, myocardial damage may be a potentially serious complication of patients with sickle cell anemia who present with chest pain during painful crises. Studies are indicated to define the significance and pathophysiology of these observations.
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PMID:Sickle cell anemia: does myocardial ischemia occur during crisis? 203 80

A 17 year old boy with sickle cell anaemia presented with acute myocardial infarction associated with severe hypoxia and reticulocytopenia. Ischaemic heart disease is rare in sickle cell anemia and in this case it is possible that the acute episode of hypoxia led to myocardial infarction.
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PMID:Acute myocardial infarction in sickle cell anaemia associated with severe hypoxia. 208 57

Ticlopidine inhibits platelet aggregation induced by adenosine diphosphate (ADP) and most other platelet agonists in ex vivo studies of human platelets. The drug also improves other abnormalities of platelet function seen in patients with cerebrovascular disease, peripheral arterial disease, ischaemic heart disease or other conditions involving platelet hyperaggregation. Abnormal platelet activity has been implicated in a variety of clinical conditions in which patients are at high risk of thromboembolic events, and thus the effectiveness of ticlopidine has been investigated in such patients. Since the initial review of the drug appeared in the Journal, data from several large multicentre studies have shown that ticlopidine has a substantial benefit to offer patients who have experienced transient ischaemic attacks or stroke, and in those with peripheral arterial disease or ischaemic heart disease. Ticlopidine reduces the incidence of further stroke, myocardial infarction or vascular death, and is superior to placebo and aspirin in this regard in studies of patients with recent stroke or transient ischaemic attacks, or intermittent claudication. Ticlopidine is equally effective in both men and women and also improves symptoms of claudication in patients with peripheral arterial disease, and appears to reduce anginal pain. Patients with subarachnoid haemorrhage and sickle cell disease have shown some improvement with ticlopidine administration. The drug reduces thromboembolic events and re-stenosis in patients undergoing haemodialysis and cardiac surgery, and appears to prevent the progression of nonproliferative diabetic retinopathy. Ticlopidine in large clinical trials is associated with a higher incidence of adverse effects than placebo and an overall incidence similar to aspirin. Most adverse effects do not require withdrawal of treatment. Gastrointestinal symptoms (particularly diarrhoea) are most common, occurring almost twice as frequently with ticlopidine as with aspirin. Other adverse effects associated with ticlopidine include skin rash, haemorrhagic disorders, and haematological effects; these latter effects require careful monitoring of patients during the initial weeks of therapy. In conclusion, ticlopidine is a valuable addition to the prophylactic treatments available for the management of patients with cerebrovascular disease, peripheral arterial disease or ischaemic heart disease, who present a high risk of thromboembolic events. Although tolerability may be a problem for some patients, the overall benefit conferred by the drug would appear to outweigh this potential disadvantage. Because of its antiplatelet activity, ticlopidine has a promising role in other disorders mediated by platelet dysfunction. However, the precise role of the drug in these additional therapeutic indications awaits clarification with wider clinical experience.
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PMID:Ticlopidine. An updated review of its pharmacology and therapeutic use in platelet-dependent disorders. 222 15

The purpose of this study is to investigate the long-term prognosis of ventricular tachycardia (VT) mainly with respect to sudden death (SCD) in patients with ischemic heart disease (IHD), idiopathic cardiomyopathy (ICM), miscellaneous heart disease (MHD) and idiopathic ventricular tachycardia (IVT). The study included 117 patients with VT (80 male, 37 female). The number of patients with IHD, ICM, MHD and IVT were 40, 18, 26 and 33, respectively. Follow-up was conducted by means of a mailed standardized questionnaire. The mean follow-up period was 46.8 +/- 32.0 months (range from 6 to 125 months). In 24 out of the 117 patients the cause of death was SCD, in 9 there was no sudden cardiac death and in 5 no cardiac death. The other 76 were surviving. The number of SCD in IHD, ICM, MHD and IVT was 14/40 (35%), 4/17 (24%), 6/25 (24%) and zero (0%), respectively. The number of having had syncope in IHD, ICM, MHD and IVT was 19/40 (48%), 7/18 (39%), 6/26 (23%) and 6/33 (18%), respectively. Out of the 19 IHD patients with syncope, 15 had had ventricular fibrillation (VF). As for IVT with syncope, only one of the 6 had VF, which was induced by a disopyramide injection. In IVT, the patients with syncope had a significantly higher VT rate than those without syncope (p less than 0.01). There were no significant differences in the electrocardiographical high risk parameters for SCD, the age, follow-up periods, the presence or absence of VF and ejection fraction between the SCD and the surviving groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Long-term prognostic assessment of ventricular tachycardia with respect to sudden death in patients with and without overt heart disease. 263 26

Ischemic heart disease as a basic disease with accompanying findings and exogenous factors comes to a typical triad of SCD. There is a critical midlife situation due to O2-shortage. Dispositional and situational conditions come to be important, especially in cases in which morphological substrates are absent. The complex incident takes place on three levels (organism, heart, and myocardium). Several dying types may occur. Clinical accuracy and morphological diagnosis are of limited value for the relatively fatal importance of each of the single findings.
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PMID:[Acute cardiac death in chronic-ischemic heart disease (CIHD)]. 268 3

The circadian variation of major cardiovascular disorders, that is, TMI, AMI, SCD, and stroke, reflects an increased vulnerability to myocardial and cerebral ischemia and myocardial dysfunction in the early hours of the morning after awakening and rising. A comprehensive approach to treatment in patients with ischemic heart disease must take into consideration the chronobiology of the cardiovascular system and its relevance to the underlying disease process that affects the cardiovascular system.
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PMID:Circadian influence on coronary events. 341 71

To determine whether exercise responses are different from normal in children with sickle cell anemia (SCA), we performed dynamic cycle ergometer exercise testing in 47 patients with SCA, aged 5 to 18 years, and 170 healthy, black age-matched control subjects. Seven (15%) of the patients with SCA had definitely ischemic, 16 (34%) had equivocally ischemic, and 24 (51%) had nonischemic ECG responses. Resting heart rate in the three groups of patients with SCA was higher than control values. Maximum exercise heart rate attained was lowest in the definitely ischemic group. All patients with SCA had decreased blood pressure responses and maximum working capacity when compared with control subjects. Hemoglobin concentration was lowest in the definitely ischemic group and correlated with maximum workload. Long-term myocardial ischemia may lead to fibrosis and the decreased myocardial contractility seen in adult patients with SCA.
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PMID:Hemodynamic and ECG responses to exercise in children with sickle cell anemia. 721 98

Gross and microscopic findings consistent with acute (three patients) and healed (four patients) myocardial infarction were found in seven (9.7%) of 72 consecutive hearts from patients with sickle cell disease studied after autopsy between 1950 and 1982. Gross obstructive and atherosclerotic lesions were absent in all seven patients, while microthrombi were present in the arterioles of infarcted tissue in two patients. Pathophysiological mechanisms responsible for the infarction are unclear, but anemia, platelet thrombi, coronary vasospasm, and abnormal rheology related to sickle cells may all be important. Chest pain occurred clinically in six of the seven patients and ECG findings typical of infarction were found in two patients. One patient died suddenly. These findings suggest that ischemic heart disease may be present in a significant number of patients with sickle cell disease and should be considered in all patients who complain of chest pain, whether or not the patient is in crisis.
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PMID:Myocardial infarction in sickle cell disease. 876 24

For unclear reasons, myocardial infarction is rare in childhood sickle cell disease, whereas lung, bone, and brain infarcts are more common. During vasoocclusive crisis and infection, acute myocardial ischemia and chronic volume overload from anemia may result in myocardial dysfunction. We report a child who had reversible cardiac dysfunction that mimicked myocardial infarction.
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PMID:Transient left ventricular dysfunction in childhood sickle cell disease. 1008 51


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