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      Hyperbaric Oxygen and Thrombolysis in Myocardial Infarction: The ‘HOT MI’ Randomized Multicenter Study


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          In a previous pilot study, we demonstrated that adjunctive treatment with hyperbaric oxygen (HBO) appears to be feasible and safe in patients with acute myocardial infarction (AMI) and may result in an attenuated rise in creatine phosphokinase (CPK), more rapid resolution of pain and ST changes. This randomized multicenter trial was organized to further assess the safety and feasibility of this treatment in human subjects. Patients with an AMI treated with recombinant tissue plasminogen activator (rTPA) or streptokinase (STK), were randomized to treatment with HBO combined with either rTPA or STK, or rTPA or STK alone. An analysis included 112 patients, 66 of whom had inferior AMIs (p = NS). The remainder of the patients had anterior AMIs. The mean CPK at 12 and 24 h was reduced in the HBO patients by approximately 7.5% (p = NS). Time to pain relief was shorter in the HBO group. There were 2 deaths in the control and 1 in those treated with HBO. The left ventricle ejection fraction (LVEF) on discharge was 51.7% in the HBO group as compared to 48.4% in the controls (p = NS). The LVEF of the controls was 43.4 as compared to 47.6 for those treated, approximately 10% better (no significant difference). Treatment with HBO in combination with thrombolysis appears to be feasible and safe for patients with AMI and may result in an attenuated CPK rise, more rapid resolution of pain and improved ejection fractions. More studies are needed to assess the benefits of this treatment.

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          The effects of tissue plasminogen activator, streptokinase, or both on coronary-artery patency, ventricular function, and survival after acute myocardial infarction. The GUSTO Angiographic Investigators.

          Although it is known that thrombolytic therapy improves survival after acute myocardial infarction, it has been debated whether the speed with which coronary-artery patency is restored after the initiation of therapy further affects outcome. To study this question, we randomly assigned 2431 patients to one of four treatment strategies for reperfusion: streptokinase with subcutaneous heparin; streptokinase with intravenous heparin; accelerated-dose tissue plasminogen activator (t-PA) with intravenous heparin; or a combination of both activators plus intravenous heparin. Patients were also randomly assigned to cardiac angiography at one of four times after the initiation of thrombolytic therapy: 90 minutes, 180 minutes, 24 hours, or 5 to 7 days. The group that underwent angiography at 90 minutes underwent it again after 5 to 7 days. The rate of patency of the infarct-related artery at 90 minutes was highest in the group given accelerated-dose t-PA and heparin (81 percent), as compared with the group given streptokinase and subcutaneous heparin (54 percent, P < 0.001), the group given streptokinase and intravenous heparin (60 percent, P < 0.001), and the group given combination therapy (73 percent, P = 0.032). Flow through the infarct-related artery at 90 minutes was normal in 54 percent of the group given t-PA and heparin but in less than 40 percent in the three other groups (P < 0.001). By 180 minutes, the patency rates were the same in the four treatment groups. Reocclusion was infrequent and was similar in all four groups (range, 4.9 to 6.4 percent). Measures of left ventricular function paralleled the rate of patency at 90 minutes; ventricular function was best in the group given t-PA with heparin and in patients with normal flow through the infarct-related artery irrespective of treatment group. Mortality at 30 days was lowest (4.4 percent) among patients with normal coronary flow at 90 minutes and highest (8.9 percent) among patients with no flow (P = 0.009). This study supports the hypothesis that more rapid and complete restoration of coronary flow through the infarct-related artery results in improved ventricular performance and lower mortality among patients with myocardial infarction. This would appear to be the mechanism by which accelerated t-PA therapy produced the most favorable outcome in the GUSTO trial.
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            Oxygen tensions in normal and ischemic tissues during hyperbaric therapy. Studies in rabbits


              Author and article information

              S. Karger AG
              October 1998
              28 October 1998
              : 90
              : 2
              : 131-136
              Departments of a Cardiology and b Baromedicine, Long Beach Memorial Medical Center, Long Beach, Calif., USA; c Zemun Clinical Hospital Center, University of Belgrade, Yugoslavia; d Northridge Heart Institute, Northridge Hospital Medical Center, Northridge, Calif., e Indian River Memorial Hospital, Vero Beach, Fla., f Richland Memorial Hospital, Columbia, S.C., USA
              6832 Cardiology 1998;90:131–136
              © 1998 S. Karger AG, Basel

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              Page count
              Figures: 1, Tables: 3, References: 31, Pages: 6
              Coronary Care


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