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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Heparin has been labeled with [99mTc] pertechnetate and its ability to image damaged coronary vessels and myocardium during and following myocardial ischemia has been studied in experimental animals. The data obtained indicate that Tc-99m heparin localizes in damaged myocardium and coronary vessels in canine models of temporary myocardial ischemia and reperfusion and in damaged myocardium during fixed coronary occlusion. Scintigraphic detection of damaged myocardium was possible in both models, but the highest levels of Tc-99m heparin in damaged myocardial tissue were found in those dogs with temporary coronary occlusion and reflow. The data suggest that Tc-99m heparin may be of value as a positive imaging agent when coronary arteries or myocardium are injured and either reperfusion is allowed and/or significant blood flow persists in the damaged area.
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PMID:Technetium-labeled heparin: preliminary report of a new radiopharmaceutical with potential for imaging damaged coronary arteries and myocardium. 66 Feb 85

Arterial emboli were extracted from 79 patients between 1955 and 1963 with polyethylene catheter suction systems and/or retrograde flushing and from 149 patients between 1963 and 1973 with Fogarty catheters. The Fogarty-era patients were older, had a greater incidence of ischemic heart disease, and presented with a greater degree of preoperative peripheral ischemia. The limb salvage rate of 87 percent after Fogarty catheter embolectomy was not statistically different from the salvage rate of 79 percent after suction catheter embolectomy, but the number of limbs with distal pulses postoperatively was significantly greater after Fogarty treatment, 64 vs. 42 percent. Delay in treatment and the presence of prior occlusive vascular disease adversely affected results in both eras. The in-hospital embolic recurrences occurred in 9 percent of the patients anticoagulated postoperatively and in 31 percent of those not anticoagulated. Heparin and warfarin were equally effective in preventing recurrences, but wound complications were seen in 33 percent of the heparinized patients, compared with 7 percent of those receiving warfarin and 4 percent of those not anticoagulated.
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PMID:Arterial embolectomy before and after the Fogarty catheter. 110 16

The functional significance of coronary collaterals in humans has been debated for many years. Correlations have now been made between the anatomic appearance of coronary collateral vessels visualized at the time of intracoronary thrombolytic therapy during the acute phase of myocardial infarction and the creatine kinase time--activity curve, infarct size, and aneurysm formation. These studies demonstrate a protective role of collaterals in hearts with coronary obstructive disease, showing smaller infarcts, less aneurysm formation, and improved ventricular function compared with patients in whom collaterals were not visualized. There is ample evidence that collaterals respond to myocardial ischemia by opening preexistent channels. When the cardiac myocyte is rendered ischemic, collaterals develop actively by growth with DNA replication and mitosis of endothelial and smooth muscle cells. Heparin-binding growth factors are present in the heart, but their biological activity is quiescent under normal physiological conditions. Once ischemia develops, these factors are activated and become available for receptor occupation, which may initiate angiogenesis after exposure to exogenous heparin. This characteristic of heparin to potentiate the mitogenic activity of acidic fibroblast growth factor has recently been used in the clinical setting as a possible therapeutic modality in patients with coronary artery disease. Patients performing 20 rounds of exercise serially after receiving intravenous injection of heparin showed significantly greater increases in exercise capacity and improvement of clinical symptoms compared with the control group who performed the same exercise without heparin. Further study of neovascularization may lead to a new therapeutic strategy for ischemic heart disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Recent insights into coronary collateral circulation. 137 32

To clarify the pathogenesis of an impending infarction and to investigate the difference between the pathogenesis of an acute myocardial infarction and an impending infarction, we have performed percutaneous transluminal coronary angioscopy in 13 patients with an impending infarction and in 13 patients with an acute myocardial infarction. As a result, coronary thrombi were observed in 12 of the 13 patients with an impending infarction, and a similar frequency of thrombi was observed in the patients with an acute myocardial infarction. Further, grayish white thrombi were observed in 9 of 12 patients with an impending infarction, but no such thrombi were noted in those with an acute myocardial infarction. Reddish thrombi, however, were observed in all patients with acute myocardial infarction, whereas such thrombi were observed in only 3 of 12 patients with an impending infarction. Informatively, occlusive thrombi occurred more frequently in patients with an acute myocardial infarction than in those with an impending infarction. As a thrombus plays an important role in an impending infarction, we also evaluated the effect of anticoagulant and thrombolytic therapy for an impending infarction in 79 patients. The incidence of recurrent angina and a subsequent acute myocardial infarction were significantly higher in non-heparin-treated patients and in thrombolytic-treated patients than in heparin-treated patients. In conclusion, a thrombus plays an important role in the pathogenesis of an impending infarction and in an acute myocardial infarction, though the characteristics of the thrombus differ in each instance. This difference may account for the differing results of thrombolytic therapy. Heparin was found an effective treatment for myocardial ischemia in an impending infarction.
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PMID:The pathogenesis of an impending infarction and its treatment--an angioscopic analysis. 145 40

The state of the lymphatic heart perfusion has been studied experimentally on dogs with intact myocardium (control 1), with acute myocardial ischemia (AMI) model (control 2) and during injection of heparin, rheogluman and obsidan in AMI. It has been stated that AMI induces acute distress of the lymphatic heart perfusion system occurring at the first minutes after the onset of the focal myocardial ischemia. Heparin, rheogluman and obsidan demonstrated selective stimulating effect on the function of the lymphatic myocardial system.
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PMID:[Stimulation of cardiac lymphatic drainage by obzidan, heparin and rheogluman in acute myocardial ischemia]. 170 17

We studied the effects of heparin, given as 12,500 units intravenously, on cardiac metabolism during catheterization of the coronary sinus at rest and during repeated rapid atrial pacing in 8 patients with stable angina pectoris, positive stress tests and coronary arterial disease and in 8 patients with normal coronary arteries without objective signs of ischemic heart disease. Heparin did not influence angina, ST-segment depression or myocardial lactate production induced by pacing in the group with diseased coronary arteries. In both groups, heparin increased the arterial levels (70%) and the myocardial uptake (40-50%) of free fatty acids, the latter only during non-ischemic conditions. Myocardial net uptakes of glucose, lactate and glutamate and the release of alanine were reduced by heparin in the subjects with normal coronary arteries but not in those with ischemic heart disease. Myocardial oxygen consumption was unchanged. In the patients with normal coronary arteries, the levels of free fatty acid in the arteries were positively related to myocardial uptake of fatty acids and the release of citrate but inversely related to cardiac uptake of lactate and glucose. These relations were lacking in the patients with diseased coronary arteries. The metabolic effects of heparin on the heart, therefore, were diminished in patients with ischemic heart disease when compared to controls. This is probably due to an altered regulation of substrate preference in ischemic hearts.
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PMID:Cardiac metabolic effects of heparin differentiate between patients with normal and stenotic coronary arteries. 197 Aug 7

Thromboembolic disease is a common medical condition which, if untreated, carries a significant risk of morbidity and mortality. Treatment with anticoagulant therapy, while clearly beneficial, may expose patients to potentially serious side effects. A thoughtful risk-benefit assessment is therefore crucial before initiating therapy. Thromboembolic disease involves syndromes of both the venous and arterial circulation, and its pathogenesis is best understood by considering the elements of Virchow's Triad. This model defines the risk factors for venous thromboembolism and allows us to classify surgical and medical patients into low, moderate and high risk groups. Similar analysis allows risk assessment for patients prone to cardiogenic embolism resulting from nonvalvular atrial fibrillation, ischaemic heart disease, rheumatic heart disease and valvular prostheses. All anticoagulant therapy is prophylactic. Primary prophylaxis involves instituting anticoagulant therapy in patients at risk, before thromboembolism occurs, while secondary prophylaxis involves treating patients with established disease. The 2 major anticoagulants, heparin and warfarin, differ in their mechanism of action, mode of administration and methods of monitoring. Either may be used as primary or secondary prophylaxis. Heparin, because it acts immediately, is the drug of choice for the short term treatment of thromboembolic disease. Warfarin is the drug of choice for long term oral maintenance therapy. The principal complication of heparin therapy is haemorrhage, although thrombocytopenia and osteoporosis may also occur; the complications of warfarin include haemorrhage and skin necrosis. The risks of complications vary with the underlying thromboembolic disease. After the benefits of treatment are weighed against the risks of complications, recommendations for therapy can be established. The use of anticoagulants in pregnancy is especially complex. Here heparin is probably the preferred agent since, unlike warfarin, it does not cross the placenta and is nonteratogenic.
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PMID:Risk-benefit assessment of anticoagulant therapy. 202 54

Heparin and antiaggregating therapy represent an effective treatment of unstable angina. Aspirin is able to prevent myocardial infarction and death in patients with unstable angina, but is not able to control myocardial ischemia. On the contrary, heparin administered by continuous intravenous infusion (about 1,000 U/h) controls myocardial ischemia by very early lowering anginal attacks and silent ischemic episodes. Heparin intermittently administered (6,000 U i.v. four times daily) did not significantly affect anginal attacks and myocardial ischemia. Thrombolytic therapy alone (Alteplase 1.75 mg/kg) reduced, but not significantly, the number of anginal attacks. The reduction of myocardial ischemia induced by continuous infusion of heparin is associated with a decrease of fibrinopeptide A plasma levels, whereas the thromboxane B2 production by platelets seems to be irrelevant in order to obtain a reduction of myocardial ischemia. Thus thrombin formation seems to be a primary factor in the occurrence of refractory unstable angina and in the activation of platelets.
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PMID:Heparin and antiaggregating therapy in unstable angina. 208 63

The Abiomed BVS System 5000 (Abiomed Cardiovascular, Inc., Danvers, Mass.) is a gravity-filled, pneumatically driven external prosthetic ventricle that has been implanted as a circulatory support device in six patients 9 to 58 years of age, presenting with a refractory heart failure nonamenable to any type of corrective operation. Three (including a 9-year-old girl) had an end-stage nonobstructive myocardiopathy, and two (including one patient who had had a massive recent myocardial infarction) had an ischemic heart disease. When first seen, the 58-year-old patient had an acute rejection and graft failure occurring 2 months after a first transplantation. All patients showed evidence of a low-output state (cardiac index less than 1.5 L/min/m2), with renal failure (mean urinary output, less than 27 ml/min) and hypoxia (mean arterial oxygen pressure = 56 torr under 80% forced inspiratory oxygen), despite maximum pharmacologic support (dobutamine, 16 to 18 gamma/kg/min; dopamine, 3 to 18 gamma/kg/min; adrenaline, 0.2 to 0.7 gamma/kg/min; furosemide, 7 to 17 gamma/kg/min). The device was implanted through a midline sternotomy and under peripheral normothermic bypass. Five patients received a biventricular support, and one a single left prosthetic ventricle. The cannulation included a right-angled cannula in both the left and right atrium and a suture of the arterial Dacron tubes onto the ascending aorta and main pulmonary artery. After careful deairing of the tubing and ventricles, the console was activated and the bypass progressively discontinued. Heparin infusion was begun 3 hours after chest closure and was continued for the duration of assist pumping, which was 2 to 11 days (mean duration, 7.43 days). The system could provide a complete support of the circulation with both right and left ventricular index remaining stable at 2.4 to 3 L/min/m2. After a dramatic improvement at the time of the system activation, the urinary output remained adequate, thus allowing for a decreasing need for diuretic therapy. In two cases, including one of isolated left ventricular assist pumping, the circulation could be totally supported during 11 hours and 23 hours, respectively, of refractory ventricular tachycardia. Four of six patients were shortly weaned from inotropic agents. Hematologic studies showed a moderate decrease of the coagulation factors level during the first 6 hours of circulatory support, and this remained stable and within normal limits thereafter. There have been three cases of bleeding complications necessitating surgical revision on the sixth hour, the twelfth hour, and the sixth day, respectively.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Use of the Abiomed BVS System 5000 as a bridge to cardiac transplantation. 236 50

Platelet function and thromboxane A2 release were measured in 71 patients admitted to a coronary care unit with a provisional diagnosis of acute myocardial infarction (AMI). All measurements were carried out within twenty-four hours of admission. Of these, 35 patients had the diagnosis of AMI confirmed. The remainder (n = 36), who did not have AMI (NMI), were divided into two groups: those (n = 18) with an unequivocal history of previous vascular disease and those without vascular disease (n = 18). Platelet aggregation and thromboxane A2 (TXA2) release were significantly increased in the AMI group when compared with those in the NMI without vascular disease group or a healthy control group with similar age and sex distribution. Aggregation and TXA2 release in the NMI patients with vascular disease were greater than those in controls and did not differ significantly from those in the AMI group. Patients in the AMI or NMI with vascular disease groups who were taking beta-blockers or calcium channel antagonists at the time of admission showed significantly less platelet aggregation than those who were not taking these drugs. Heparin, added in vitro at therapeutic concentrations, induced significantly more aggregation in patients in the AMI and NMI with vascular disease groups than in the NMI without vascular disease group. We conclude that: platelets obtained from patients with AMI are hyperaggregable and release more TXA2; platelets from patients with significant vascular disease are hyperaggregable, even in the absence of AMI, although they are not as hyperaggregable as those from AMI; treatment with nifedipine and beta-blockers protects these patients from platelet hyperaggregability; heparin induces significant aggregation of platelets from patients with AMI and NMI with vascular disease. These observations are of importance in considering the pathogenesis and treatment of AMI and ischemic heart disease.
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PMID:Platelet function in patients admitted with a diagnosis of myocardial infarction. 288 May 35


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