Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

---

Query: UMLS:C0022116 (ischemia)
91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The restoration of anterograde coronary flow long after coronary thrombosis may be of benefit to patients with continuing ischemia. To determine whether "old" intracoronary thrombi are susceptible to lysis with thrombolytic agents, 18 patients with angina at rest during evolving acute myocardial infarction (AMI) and total occlusion of the infarct vessel were treated with intracoronary streptokinase 3 to 13 days after onset of AMI. In 12 of the 18 patients (67%), successful recanalization of the artery was achieved 6.9 +/- 2.7 days after AMI. Thrombolysis was followed by coronary angioplasty in 2 patients. To evaluate the efficacy of this approach in reducing post-AMI ischemia, the number of episodes of angina at rest was compared in patients with successful and unsuccessful attempts at recanalization. Even in patients without angioplasty, the mean number of daily episodes decreased from 1.02 +/- 0.6 to 0.09 +/- 0.2 in patients in whom reperfusion was achieved, and from 1.07 +/- 0.8 to 0.88 +/- 0.8 in those in whom it was not (p = 0.027 for the difference between the groups). Thus, in patients with early post-AMI angina, intracoronary streptokinase can restore flow in the occluded artery, may decrease the frequency of angina, and allows angioplasty to be performed.
...
PMID:Intracoronary thrombolysis 3 to 13 days after acute myocardial infarction for postinfarction angina pectoris. 400 87

The role of beta-adrenergic receptor blockade in preventing ventricular fibrillation in a conscious canine model of sudden coronary death was examined using d,l-nadolol and the non-beta-adrenergic receptor blocking isomer, d-nadolol. On day 4, after a temporary 90-min occlusion of the left anterior descending coronary artery, an anodal current of 150 microA was applied to the intimal surface of the left circumflex coronary artery. Occlusive or nonocclusive thrombosis of the artery was accompanied by ST-segment changes. In saline-treated animals (n = 15), ST-segment changes were followed by sinus tachycardia and QT-segment prolongation, with development of ventricular premature beats. Ventricular fibrillation developed in 14 animals (93%). Pretreatment with 1 (n = 9) or 8 mg/kg d,l-nadolol (n = 13) did not alter the development of left circumflex coronary artery thrombosis and ischemic ST-segment changes, but decreased the incidence of ventricular fibrillation and increased survival at 24 h (56% and 63%, respectively) (p less than 0.01 versus saline). d,l-Nadolol also attenuated the sinus tachycardia and QT-interval prolongation accompanying acute ischemia. d-Nadolol (1 mg/kg), the non-beta-adrenergic receptor blocking isomer, failed to prevent development of ST-segment changes. Sinus tachycardia and QT-interval prolongation were not prevented, and ventricular fibrillation developed in all eight animals (100%). In animals without previously induced anterior myocardial ischemic injury (n = 10), left circumflex coronary artery thrombosis failed to produce sinus tachycardia and QT-interval prolongation and was associated with a lower incidence of ventricular fibrillation (20%, p less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Antifibrillatory actions of d,l-nadolol in a conscious canine model of sudden coronary death. 619 59

Thirty-four patients with acute myocardial infarction (mean age 55 years) who received intracoronary streptokinase for coronary thrombosis were followed for a mean of 9.4 months (longest 25 months) following the procedure of percutaneous transluminal coronary recanalization (PTCR). Twelve patients had undergone coronary artery bypass graft surgery (CABG), one had percutaneous transluminal coronary angioplasty (PTCA), and 21 received medical therapy. Among patients having CABG and PTCA, nearly 70% no longer had chest pain or reinfarction, and 62% were in New York functional class I status; there were no deaths, and there was only one reinfarction, in a patient who had graft closure. In contrast, 43% of medically treated patients had chest pain or reinfarction or had died on follow-up; only 32% of survivors were in class I functional status. Further, 71% of medically treated patients who were receiving warfarin had no chest pain and on reinfarction, whereas the majority (56%) of patients who did not receive either warfarin or antiplatelet agents either had chest pain or reinfarction or died. The importance of CABG/PTCA and anticoagulant therapy is stressed to prevent recurrent ischemia, reinfarction, and reocclusion following successful reperfusion by means of PTCR in acute myocardial infarction.
...
PMID:Importance of follow-up medical and surgical approaches to prevent reinfarction, reocclusion, and recurrent angina following intracoronary thrombolysis with streptokinase in acute myocardial infarction. 621 40

The term coronary artery spasm should not be used interchangeably with the specific clinical syndrome "variant angina" since it does occur in other acute and chronic ischemic heart disease syndromes. The term coronary artery spasm should not be applied to patients with ischemic heart disease unless there is clinical, angiographic, and physiologic evidence of its presence. The diagnosis of coronary artery spasm is confirmed by angiography, i.e. change in caliber of the coronary arteries plus evidence of ischemia. Probable diagnosis is in patients who have the syndrome of variant angina, i.e. rest angina associated with ST segment elevation on the electrocardiogram. One can be highly suspicious that the spasm is at work in patients who have rest angina, especially those with unstable angina. One can be suspicious of patients who have variable effort angina or walk-through angina. Coronary artery spasm is a possibility in patients with an acute myocardial infarction or acute re-infarction and is also possible that sudden death in patients with normal coronary arteries can be related to coronary artery spasm. Coronary artery spasm is the usual cause of myocardial ischemia in patients with rest angina without effort angina. This has also commonly been documented in patients with rest and effort angina. There are isolated reports suggesting that patients with effort angina pectoris also develop coronary artery spasm. Coronary artery spasm has been documented to occur in association with acute myocardial infarction. Whether coronary artery spasm is the cause or the result of myocardial infarction has not been determined at this time. However, the recent combined use of intracoronary nitroglycerin and intracoronary streptokinase in patients with acute myocardial infarction has shown reversal of totally obstructed arteries and suggests the relationship between coronary artery disease, coronary artery spasm, and in situ coronary thrombosis. The incidence of sudden death in patients with documented coronary artery spasm is unknown. But, since complete heart block and/or ventricular tachycardia occur during episodes of coronary artery spasm, it is not unreasonable to assume that some patients have died as a result of these rhythm disturbances. The prognosis of patients with coronary artery spasm seems to depend on the presence or absence of severe coronary atherosclerosis, i.e. those with severe disease have a worse prognosis. Current therapy of patients with coronary artery spasm involves the use of nitrates and calcium antagonists.(ABSTRACT TRUNCATED AT 400 WORDS)
...
PMID:Role of coronary artery spasm in ischemic heart disease. Therapeutic implications. 633 45

The in-vivo effects of the new antithrombotic compound nafazatrom on experimental thrombosis of the left circumflex coronary artery, on hemodynamics and on ultimate infarct size were studied in pentobarbital-anesthetized, open-chest dogs. Coronary artery thrombosis was induced by low amperage stimulation (150 microA, DC for 6 hr) of the circumflex artery intimal lining. The effects of oral pretreatment of 1%-Tylose suspension as drug diluent and 5 mg/kg nafazatrom plus vehicle were determined. Both agents were administered twice a day before onset of current stimulation. In the drug vehicle group, coronary thrombosis caused severe hemodynamic alterations, e.g. blood pressure and left ventricular pressure decrease, as well as reduction in the LV dP/dtmax associated with increases in end-diastolic filling pressure and heart rate. Time to coronary artery occlusion was delayed by nafazatrom (5.2 +/- 1.1 vs 3.1 +/- 0.4 hr, p less than 0.05). Smaller blood pressure and LV dP/dtmax reductions and minor heart rate and filling pressure increases around the time of thrombus formation suggested cardioprotection with the drug. Smaller R wave changes and S-T segment elevation indicated minor ischemia at the time of occlusive coronary artery occlusion in nafazatrom-treated hearts (24 +/- 0.5 vs 72 +/- 7% ST segment elevation, p less than 0.01). Thrombus wet weight was 18.4 +/- 2.6 mg in the nafazatrom group, but 63.7 +/- 3.1 mg in controls (p less than 0.01). Thus, ultimate infarct size was smaller in nafazatrom-treated hearts as related to left ventricular mass (8.4 +/- 1.4 vs 32.3 +/- 3.1%, p less than 0.02) or to the occluded artery perfusion area at risk for infarction (16 +/- 3.4 vs 53 +/- 6.2%, p less than 0.05). No ex-vivo effect of nafazatrom on collagen-induced platelet aggregation was observed. These results may indicate efficacy of the drug in prevention of acute coronary artery disease as one cause of ischemic jeopardy of the myocardium and/or therapeutic value in coronary artery spasm.
...
PMID:The effects of oral nafazatrom (= BAY g 6575) on canine coronary artery thrombosis and myocardial ischemia. 661 99

Three cases (one, newborn infant and two infants--one of them recently published--) who present electrocardiographic and enzymatic alterations comparative with diagnosis of ischemia and myocardial infarction are reported. Rarity of this entity in infants is stressed as most of published cases are secondary to ananomolous coronary artery. Etiology of the cases presented shows a myocardiac fibrosis with Schwachman's syndrome in one case, a coronary thrombosis secondary to a disseminated intravascular coagulation in a second case, and finally a generalized hypoplasia of coronary arteries. Hypoxia appears in these cases a factor acting in favour of myocardial ischemia. Diagnostic criteria of acute myocardial infarction are based on typical electrocardiogram and rise of isoenzymes of LDH and CPK-MB. Although rare, it is a diagnosis to be considered in cases of unknow cardiac insufficiency in newborns and infants.
...
PMID:[Myocardial infarction and myocardial ischemia in newborn children and infants, not secondary to an abnormal coronary]. 666 Jun 44

The thrombolytic and hemodynamic properties of intracoronary streptokinase (SK) application were studied in an in-vivo canine model with left circumflex coronary artery thrombosis, initiated by electrical stimulation (150 microA, DC for 6 h) of the artery's intima via an implanted silver wire. In pentobarbital-anesthetized, open-chest dogs acute myocardial ischemia was determined by a dehydrogenase-dependent staining of the coronary artery perfusion area. Thrombus weight was determined post-mortem. Saline-treated control animals developed coronary thrombosis after 3.1 +/- 0.4 h of stimulation. Thrombus weight was 64 +/- 3.1 mg. Acute infarct volume was 32 +/- 3.1% of total left ventricle, and 53 +/- 6.2% of the coronary artery risk region for infarction. At occlusive thrombosis, blood pressure, ventricular pressure and the LV dP/dtmax fell significantly, whereas heart rate and the end-diastolic filling pressure increased. Severe ST-segment elevation and loss of R wave voltage indicated myocardial ischemia. At 20 min into thrombotic vessel occlusion, 2,000 IU/min SK were infused by way of a Sones-catheter advanced to the thrombus. Coronary thrombosis consistently lysed after 12 +/- 0.7 min of SK infusion, and coronary blood flow as well as hemodynamics were restored. Only minor acute infarction was found indicating viability of ischemic jeopardized myocardium. In another group, the continuous SK-infusion (20 IU/kg/min) concomitant with electrical vessel stimulation prevented coronary thrombosis and acute ischemia, and no significant hemodynamic alterations were noted. These results indicate that intracoronary SK-infusion can lyse acute thrombosis as sequel of electrical stimulation. This prevents development of acute myocardial infarction. Continuous SK-infusion can completely prevent coronary thrombosis in response to intimal injury.
...
PMID:Thrombolytic effects of intracoronary streptokinase on canine coronary artery thrombosis. 673 17

In anesthetized dogs, a silver wire electrode was inserted into the lumen of the circumflex coronary artery (LCX) and myocardial infarction was produced by a temporary 90-minute occlusion of the left anterior descending coronary artery (LAD) followed by reperfusion. Four days later while in the ambulatory state, a 150 microA current was applied to the intimal surface of the LCX of saline (n = 10) and bretylium (n = 10) treated animals. Intimal injury and coronary thrombosis produced ST segment changes at 138 +/- 39 minutes (chi +/- SEM), followed by premature ventricular beats (at 142 +/- 37 minutes), ventricular tachycardia (at 156 +/- 49 minutes), and ventricular fibrillation (at 163 +/- 51 minutes) in 9 of 10 saline-treated animals. In bretylium-treated animals, ST segment changes appeared at 128 +/- 35 minutes, with six animals surviving for 24 hours (p less than 0.03 vs saline). LAD infarction was present in both saline (14.1 +/- 2.3%) and bretylium (15.1 +/- 2.1% of left ventricle) treated animals with only bretylium-treated animals developing LCX infarcts (16.1 +/- 2.1%). Bretylium prevents ventricular fibrillation (VF) resulting from ischemia at a site distant to prior myocardial infarction in the conscious dog and deserves further attention as a potential antifibrillatory agent for prevention of sudden coronary death in man.
...
PMID:Prevention of ventricular fibrillation by bretylium in a conscious canine model of sudden coronary death. 684 13

In the first few hours after acute coronary thrombosis, clinical coronary angiography is associated with enhanced risk of ventricular fibrillation. In these experiments, the ventricular fibrillation threshold (VFT) was measured in anesthetized dogs before and during acute occlusion of the left circumflex coronary artery. Ischemia alone reduced the fibrillation threshold. Angiography with 1- or 2-ml does of Renografin 76 lowered VFT significantly more than did equal doses of iohexol or iopamidol. It is concluded that nonionic agents may be safer for coronary angiography in the presence of acute coronary insufficiency.
...
PMID:Changes in ventricular fibrillation threshold induced by contrast agents during acute coronary artery occlusion. 686 5

The association of coronary thrombosis and transmural myocardial infarction is well documented. We have recently observed apparent intracoronary thrombi in patients with unstable myocardial ischemia without transmural infarction. To assess the frequency and angiographic characteristics of intracoronary defects consistent with thrombi, we reviewed the angiograms of all patients undergoing catheterization within 1 month of the onset of unstable angina or the intermediate coronary syndrome. Of 129 such patients, eight (6.2%) had nonoccluding, hazy, or nonopacified intracoronary filling defects consistent with thrombus in angiographically well-opacified vessels. All defects were just distal to a significant (80% to 99%) coronary stenosis. In each instance the thrombus-involved vessel supplied a myocardial segment referable to the electrocardiographically defined area of ischemia. Support for the theory that the intracoronary defects were thrombi includes three patients with enlargement of the filling defects, who underwent repeat angiography within 7 days, and two patients with embolization of defect fragments. Furthermore these defects were angiographically similar to poststenotic intraluminal defects seen transiently in some patients after partial intracoronary streptokinase recanalization. In conclusion, we have observed, angiographically, intracoronary filling defects consistent with thrombus in some patients with unstable myocardial ischemia.
...
PMID:Intracoronary thrombus in syndromes of unstable myocardial ischemia. 731 24


<< Previous 1 2 3 4 5 6 7 Next >>

---