Clinical cardiology
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Clinical cardiology · Mar 1990
Randomized Controlled Trial Comparative Study Clinical TrialVariability of thrombolytic coronary reperfusion: an angiographic study of streptokinase and anistreplase.
A total of 1,615 angiographic readings in 240 patients with acute myocardial infarction were analyzed from a randomized trial of intravenous anistreplase (Eminase), also known as anisoylated plasminogen streptokinase activator complex (APSAC), versus intracoronary streptokinase. Coronary arteriography was performed at baseline and at 15, 30, 45, 60, 75, and 90 minutes after drug infusion. Coronary flow in the infarct-related artery was defined using the TIMI criteria. ⋯ All of these changes in flow were statistically more common for the circumflex coronary artery and early treatment (less than 4 h), but did not differ for anistreplase or streptokinase. We conclude that frequent alterations in coronary blood flow occur early during reperfusion therapy and that these findings may explain reports with varying results of thrombolytic therapy. Any angiographic assessment of thrombolytic drug efficacy should take these variations as well as interobserver variability into account.
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Clinical cardiology · Mar 1990
Multicenter Study Clinical Trial Controlled Clinical TrialAngiographic assessment of patency and reocclusion: preliminary results of the Dutch APSAC Reocclusion Multicenter Study (ARMS).
The main objective of the ARMS (APSAC Reocclusion Multicenter Study) trial was to obtain patency and reocclusion data. In an open multicenter study, a total of 156 patients were treated with 30 U of anistreplase or anisoylated plasminogen streptokinase activator complex (APSAC) within 4 h after onset of pain. Patency of the infarct-related vessel was assessed by coronary angiography performed 90 minutes after anistreplase administration. ⋯ The preliminary data of the first 148 patients indicate that the patency rate at 90 min was 73-75% and the reocclusion rate at 24 h was 4%. This patency rate corresponds with previous studies. The low reocclusion rate is noteworthy and probably reflects the prolonged action of anistreplase.
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Clinical cardiology · Mar 1990
ReviewRole of the emergency department in decreasing the time to thrombolytic therapy in acute myocardial infarction.
Delay from the onset of acute myocardial infarction (AMI) symptoms to initiation of thrombolytic therapy can be reduced by improving patient recognition of AMI symptoms and encouraging speedier action in seeking medical assistance and improving the time it takes for medical personnel to evaluate the patient's symptoms and initiate appropriate therapy. Attempts to improve patient response to AMI symptoms have met with limited success. Prehospital administration of thrombolytic drugs may be of value, but many AMI patients are not transported by the emergency medical services system. ⋯ Unfortunately, much of what is known about the time sequence of ED thrombolytic therapy in the United States comes from organized trials in a small number of centers. Little is known about how often non-ED physicians participate in the decision-making process (either in person or by phone consultation), or how many delays are potentially avoidable. Current evidence suggests that preestablished ED treatment plans and protocols can reduce the time delay for many patients who present with AMI, especially if paramedics can transmit diagnostic quality ECGs to the hospital.
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Clinical cardiology · Nov 1989
Case ReportsTraumatic thrombosis of the left main coronary artery and myocardial infarction caused by blunt chest trauma.
We report the case of a 38-year-old man who, after a blunt chest trauma, developed an acute transmural myocardial infarction. Coronary arteriography revealed a thrombus in the left main artery, occlusion of the distal left anterior descending artery, and a diagonal branch caused by emboli.
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Clinical cardiology · Sep 1989
Effect of isosorbide dinitrate on cardiac output in severe cardiac failure: relation to initial hemodynamics, ventricular volume, and the preload reserve mechanism.
Isosorbide dinitrate (ISDN) improves the clinical and hemodynamic state of patients with heart failure, but may cause dizziness and syncope. To characterize patients in whom cardiac output falls with high-dose nitrate therapy and to examine further the pathophysiology of the fall in cardiac output in these patients, we studies the effect of sublingual ISDN on forward cardiac output in 14 patients with severe cardiac failure (New York Heart Association grades 3-4). ⋯ Initial systemic arterial pressure, LV ejection fraction, wedge and LV transmural filling pressures were similar in both groups, but Group 2 patients had a lower systemic vascular resistance (p = 0.07) and tended to have a larger initial LV end-diastolic volume and increased end-diastolic compliance; following ISDN the decrease in LV filling pressure and end-diastolic volume was larger and the product of the changes greater (p less than 0.02). Thus ISDN decreases filling pressure and improves forward cardiac output in some patients with congestive heart failure, but large doses may decrease cardiac output in a subset of patients who have a lower systemic vascular resistance and a larger more compliant ventricle, maintaining forward blood flow predominantly by a preload reserve mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)