Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of this study was to determine the effect of blood coagulation and platelet aggregation on the perfusability of arterioles (19-50 micron) and capillaries in subepicardial and subendocardial ischemic and nonischemic myocardium of anesthetized open-chest rabbits. Fluorescein isothiocynate-dextran (MW 150,000) was injected intravenously to label perfusable myocardial microvessels of rabbits that were subjected to 60 min of coronary artery occlusion. Fluorescent microscopy was used to identify the perfusable vessels and an alkaline phosphatase stain was employed to locate the total microvasculature of the heart. Stereological principles were utilized to determine various morphometric parameters. About 25% of the capillaries were incapable of being perfused but virtually all arterioles were perfusable in occluded myocardium of the control group. Essentially all capillaries and arterioles were perfusable in nonoccluded myocardium. Collagen infusion produced a perfusion defect in 14% of the capillaries and arterioles in nonoccluded myocardium and in 33% of the capillaries and arterioles in occluded myocardium. Heparin, prostaglandin E1 (PGE1), or PGE1 + heparin did not prevent the perfusion defect in capillaries of occluded myocardium. It is concluded that while promotion of blood coagulation and platelet aggregation was able to produce microvessel obstruction, these hemostatic mechanisms were not primarily responsible for the capillary obstruction observed during myocardial ischemia in the rabbit heart.
 ...
PMID:Effect of blood coagulation and platelet aggregation on perfusable capillaries and arterioles in ischemic and nonischemic myocardium. 365 5

The optimal approach to management of patients after thrombolytic therapy for acute myocardial infarction (AMI) is unclear. The role of anticoagulation with heparin was evaluated in 75 consecutive patients who received intravenous streptokinase for AMI. Heparin therapy was titrated to keep the partial thromboplastin time (PTT) between 90 and 120 seconds. Seventeen episodes of definite myocardial ischemia (associated with reversible electrocardiographic changes) were observed in 13 patients. When episodes of probable myocardial ischemia are included (typical chest pain relieved by nitroglycerin or associated with more than a 15-mm Hg change in blood pressure but without electrocardiographic changes), 52 episodes occurred in 28 patients. Four episodes of definite and 4 of probable myocardial ischemia occurred within 24 hours of discontinuation of heparin. Analysis of the level of anticoagulation as assessed by PTT at the time of the ischemic events shows that ischemia occurred more often at lower PTTs. Nine hemorrhagic complications occurred, all within 24 hours of streptokinase infusion. In 4 patients bleeding was believed to be major and heparin administration was discontinued; 2 patients with gastrointestinal bleeding required blood transfusions. Our data suggest that after thrombolytic therapy for AMI, the level of anticoagulation is inversely related to the frequency of recurrent ischemic events; that discontinuation of heparin is frequently associated with ischemia; and that administration of heparin is associated with a low incidence of hemorrhagic complications.
 ...
PMID:Role of heparin after intravenous thrombolytic therapy for acute myocardial infarction. 381 72

In spite of all the scientific and technical advances in recent years, shock that is not rapidly correctable with fluid can have a morbidity rate exceeding 80%. Consequently awareness of such precipitating factors as sepsis and early diagnosis and treatment are essential. Treatment should be rapid and should follow a previously outlined protocol. Such protocols should include correction of the precipitating problem and aggressive resuscitation to assure adequate ventilation and oxygenation of the blood and optimal oxygen delivery to the tissues. Fluid and blood should be given as needed until filling pressures begin to rise rapidly with further fluid infusion. With hemorrhagic shock in previously healthy individuals, a hemoglobin level of 10.0 g/dL is usually adequate. In older, septic, or cardiogenic shock patients, a hemoglobin level of 12.5 to 14.0 may be preferable. If an optimal preload does not increase cardiac output to normal or higher levels, inotropic agents should be used. If shock still persists, one must be sure that the arterial pH is not excessively high or low. Glucocorticoids may then be given in low dose (200 mg hydrocortisone) in case some degree of adrenal insufficiency is present. They can also be given in high doses (equivalent to 150 mg/kg hydrocortisone) early in septic shock primarily to prevent excess complement activation and to preserve membrane integrity. Vasopressors may occasionally be required if there is excessive vasodilation, especially if there is persistent hypotension in the presence of high-grade coronary or cerebral artery stenosis. Vasodilators may be used to try to correct myocardial ischemia (nitroglycerin), excessive preload (nitroglycerin), or excessive afterload (nitroprusside or hydralazine). Combinations of vasodilators and inotropic agents may be required in some patients with high systemic vascular resistance and persistently low cardiac outputs. Mechanical assist with IABP can be of great value in persistent cardiogenic shock. Diuretics may occasionally help prevent renal failure in patients who are persistently oliguric after blood flow and pressure are restored. Heparin is occasionally of value if DIC develops with no concomitant fibrinolysis. Antibiotics are important in septic shock and may also be important if persistent shock has reduced gastrointestinal mucosal integrity so that bacteria and bacterial products can enter the portal system.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Science and shock: a clinical perspective. 389 56

Interventional angiographic techniques are of increasing importance in the management of arteriosclerosis and its complications. Two areas of particular interest are the treatment of focal arterial stenoses by percutaneous transluminal angioplasty and the treatment of arterial thromboemboli with selective infusion of thrombolytic agents. The administration of multiple drugs, in various combinations, is a critical factor in the success of these interventions. To effectively use this new pharmacoangiography, it is important to understand both the pathophysiology of the atherosclerotic or thrombotic process being treated and the actions of the drugs used. Preserving the effect of angioplasty relies on preventing thrombus formation and preventing recurrence of the atherosclerotic obstruction. Heparin during the procedure is clearly useful for the former, and aspirin in small doses and other antiplatelet medications are indicated for the latter. The precise utility of long-term anticoagulation, of low molecular weight dextran, and of various antiplatelet regimens remains to be proven. The theoretical importance of these medications in improving long-term patency rests on the effects they have on platelet and vessel wall prostaglandins, on intimal smooth muscle cell proliferation, and on the thrombogenicity of injured arterial intima. Fibrinolytic therapy, with streptokinase and urokinase, has been used for many years. Selective intraarterial use, however, is a new and promising application. Intracoronary streptokinase infusion during acute myocardial ischemia appears to prevent or limit infarction in certain patients. Peripheral use for acute arterial occlusion, either in native vessels or in grafts, is an area of great promise. Key considerations are thrombus age, size, and location, and the status of the arterial flow proximal and distal to the obstruction.
 ...
PMID:Pharmacology of angioplasty and intravascular thrombolysis. 618 69

Bovine testicular hyaluronidase (BTH) reduces experimental myocardial infarct size and ameliorates electrocardiographic signs of ischemia. This study was done to determine if heparin, an in vitro inhibitor of hyaluronidase activity, blocks the action of BTH in the myocardium of dogs after coronary artery occlusion. BTH was administered intravenously as 5,000 NF units/kg at 0.5 and 2.5 hours after coronary occlusion. Heparin was administered intravenously as a 150-unit/kg loading dose, followed by 10 units/kg per hour i.v., beginning 15 minutes before coronary occlusion. The area of myocardial ischemia at risk was assessed by a radiolabeled microsphere technique; the area that developed necrosis was assessed by a histochemical technique. In vivo activity of BTH was assessed by a colorimetric analysis of the BTH substrate, i.e., hyaluronic acid (HA), extracted from myocardial tissue. For biochemical analysis of HA, the heart was divided into anterior myocardium, which included ischemic tissue and posterior nonischemic myocardium. The myocardial HA content of dogs treated with BTH plus heparin (anterior, 3.44 +/- 0.40 micrograms HA/mg protein; posterior, 3.69 +/- 0.33 micrograms HA/mg protein) was not significantly different from control (anterior, 3.61 +/- 0.29 micrograms HA/mg protein; posterior, 3.55 +/- 0.23 micrograms HA/mg protein). In contrast, BTH lowered myocardial HA content (anterior, 2.16 +/- 0.21 micrograms HA/mg protein; posterior, 2.08 +/- 0.14 micrograms HA/mg protein) compared with either BTH plus heparin or control groups in both anterior myocardium (p = 0.006) and posterior myocardium (p = 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Heparin inhibits bovine testicular hyaluronidase activity in myocardium of dogs with coronary artery occlusion. 670 49

During ergometric examination of 92 patients with ischemic heart disease and 35 healthy individuals blood coagulation was studied by recording thromboelastograms and electrocoagulograms and determining blood platelet aggregation, fibrinolytic activity and levels of fibrinogen and free heparin in blood. In 65 patients these values in ergometry were determined after treatment with obsidan. It was shown that during physical load there is an intensification of hypercoagulation processes embracing all phases of blood coagulation with simultaneous activation of anticoagulation mechanisms; in contrast to healthy individuals patients with ischemic heart disease are marked by prevalent hypercoagulation. Shifts in the system of blood coagulation depend on the volume of physical load. Heparin and fibrinolytic activity increases up to a certain load level, but when this is surpassed hypercoagulation processes prevail. This may be used as an additional criterion in determining the level of the training regimen in physical rehabilitation of patients.
 ...
PMID:[Change in the blood coagulating properties during ergometry in ischemic heart disease]. 737 93

Although a functional role of coronary collaterals has been continuously debated, we observed the following facts in our studies during intracoronary thrombolytic therapy: (a) Myocardial ischemia is important for the development of collateral circulation, (b) collaterals can perfuse the infarcted myocardium, and (c) the presence of collaterals prevents the left ventricular aneurysm formation in acute myocardial infarction, even when the amount of the salvaged tissue is small. Thus, coronary collaterals are not merely markers of severe ischemia but help to preserve the functional integrity of the myocardium in the presence of coronary obstruction. We then attempted to promote collateralization to treat patients with angina pectoris. Patients with chronic stable effort angina were treated with heparin followed by treadmill exercise twice a day for 10 days. Treadmill capacity was found to improve in association with an increase in coronary collateral circulation. Heparin treatment of ischemic patients was found to be a noninvasive alternative to percutaneous transluminal coronary angioplasty and coronary bypass surgery for patients who are not candidates for invasive procedures.
 ...
PMID:Effect of coronary collateral circulation on myocardial ischemia and ventricular dysfunction. 794 75

UAP is a frequent manifestation of ischaemic heart disease; it is intermediary between stable angina and myocardial infarction and sudden death resp. The hospitalization mortality is 5%, approximately 15% of the patients with UAP develop myocardial infarction. The aim of UAP treatment is: 1. prevention of ischaemic episodes, 2. prevention of infarction and 3. control or elimination of risk factors, to improve the long-term prognosis in these patients. As antianginal drugs in UAP as a routine calcium antagonists, beta-blockers and nitrates are used. A very important part in the treatment of UAP is played by antithrombotic and thrombolytic treatment as in this disease rupture or fissure of plaques and subsequent thrombus formation is important. Non-occlusive thrombi are present in 80% in UAP, while in infarctions they are present in 21%. Rupture of an atherosclerotic plaque leads to thrombocyte activation, release of tissue thromboplastin and activation of the coagulation system aspirin inhibits platelet function and thus reduces thromboxane A2 formation. Heparin affects the coagulation process in UAP, reduces the number of anginal attacks and protects from the development of infarction. Treatment of UAP with streptokinase and rt-PA has no great advantages, when compared with heparin. Surgical treatment of UAP has somewhat better results than conservative treatment. Coronary angioplasty is an ideal solution in UAP when one or two arteries are damaged.
 ...
PMID:[The present status of treatment of unstable angina pectoris]. 807 49

In the primary prevention of arterial disease, there may be a role for anti-oxidant vitamins and for oestrogen replacement therapy in postmenopausal women. For the secondary prevention of thrombotic complications of atherosclerosis, aspirin has proven efficacious in reducing both mortality and morbidity. Patients with ischaemic heart disease and moderately elevated serum cholesterol benefit from simvastatin administration. Heparin and oral anticoagulants are the mainstay in the primary and secondary prevention of venous thrombosis. More potent antithrombotic compounds, the direct thrombin inhibitors and the glycoprotein IIb-IIIa antagonists, are mainly being evaluated in emergency coronary medicine. Preliminary results are encouraging but haemorrhagic problems need to be solved. The trend toward a decrease in late restenosis following coronary angioplasty using a IIb-IIIa antagonizing Fab fragment may prove to be a major therapeutic breakthrough.
 ...
PMID:Clinical trials of primary and secondary prevention of thrombosis and restenosis. 857 89

The purpose of this study was to evaluate whether combined treatment with a cardiovascular exercise rehabilitation program and low doses of heparin can induce changes in ergometric parameters of ischemia in patients with coronary artery disease (CAD). Heparin may potentiate the development of new vessels promoted by ischemia and therefore may produce important clinical improvement. Thirty-six patients with stable CAD and evidence of myocardial ischemia on exercise testing were randomized into three groups: a control group (n = 11) received the usual medical treatment; another group (n = 11) underwent three exercise sessions per week during 12 weeks; and a third group (n = 14) undertook this exercise program and also received calcium heparin 12,500 IU subcutaneously 20 to 30 minutes before each exercise session. Pretreatment and posttreatment exercise tests were compared. Patients who underwent the rehabilitation program had an increase in exercise duration and workload at the onset of 1 mm ST-segment depression, but only patients who received calcium heparin showed a significant increase in rate-pressure product at the ST-segment ischemic threshold (p = 0.035). This result suggests that higher levels of myocardial oxygen consumption were now tolerated, a change that may be related to an improvement in myocardial perfusion.
 ...
PMID:Exercise training and heparin pretreatment in patients with coronary artery disease. 889 65


<< Previous 1 2 3 4 Next >>