[Hartnell GG, Wakeley CJ, Tottle A, Papouchado M, Wilde RP Limitations of chest radiography in discriminating between aortic dissection and myocardial infarction: implications for thrombolysis. J Thorac Imaging 1993 Spring;8(2):152-5.] Abstract: It has been stated that chest radiographic features of aortic dissection are a contraindication to intravenous thrombolysis in patients with suspected acute myocardial infarction. Excluding aortic dissection could significantly delay such treatment in patients who would benefit from thrombolysis. Initial chest radiographs of 18 patients with acute aortic dissection and 25 patients with acute myocardial infarction were evaluated. The radiographs were studied by two experienced radiologists for signs of aortic dissection. No radiographic signs or combinations of signs accurately distinguished aortic dissection from myocardial infarction. Patients with chest radiographic signs suggesting aortic dissection but with clinical features suggesting myocardial infarction should not be denied the benefits of immediate intravenous thrombolysis. [Nicolini. FA, et al. Concurrent nitroglycerin therapy impairs tissue-type plasminogen activator-induced thrombolysis in patients with acute myocardial infarction. Am J Cardiol 1994;74(7):662.] BACKGROUND: Previous animal studies have indicated that concomitant administration of nitroglycerin and tissue-type plasminogen activator (t-PA) decreased the thrombolytic potential of t-PA. METHODS: This study, which was conducted in Italy but co-authored by individuals from the University of Florida and the Cleveland Clinic Foundation, examined the effect of nitroglycerin administration in patients with acute myocardial infarctions (AMIs) who were treated with t-PA. In addition to t-PA infusions (100mg given over three hours), 47 patients were treated with either IV nitroglycerin infusions (mean dose, 43mcg/min) or saline beginning with initiation of thrombolytic therapy and continuing for nine hours. RESULTS: When compared with control patients, those treated with nitroglycerin exhibited significantly lower mean plasma t-PA antigen concentrations. EKG and enzymatic evidence of early reperfusion was noted in 10/11 controls (91%) and 26/36 patients receiving nitroglycerin (72%). Ten of these latter 26 (but no control patient) manifested subsequent evidence of intermittent or sustained reocclusion. Thus, ongoing reperfusion was sustained in 91% of controls but in only 44% of patients receiving t-PA plus nitroglycerin. Control patients manifested a greater reduction in ST elevation than patients receiving nitroglycerin, and a shorter time to CK release. CONCLUSIONS: The authors suggest that concomitant administration of IV nitroglycerin with t-PA may impair thrombolysis in patients with AMIs, possibly due to augmentation of hepatic blood flow with resultant facilitation of t-PA degradation. 17 references [Romeo F, et al. Concurrent nitroglycerin administration reduces the efficacy of recombinant tissue-type plasminogen activator in patients with acute anterior wall myocardial infarction. Am Heart J 1995; 130(4):692.] BACKGROUND: Although patients being treated with recombinant tissue-type plasminogen activator (rTPA) for acute myocardial infarction (AMI) often receive concomitant IV nitroglycerin, a previous animal study has suggested that nitroglycerin may adversely affect the thrombolytic potential of rTPA. METHODS: This randomized, nonblinded, Italian study examined the impact of adding IV nitroglycerin to rTPA on a variety of markers of efficacy in 60 patients with a first anterior AMI treated within four hours of the onset of symptoms. All patients got heparin and aspirin, as well as rTPA (100mg given over three hours), while 27 patients also received concurrent IV nitroglycerin (100mcg/min given over eight hours). RESULTS: On the basis of indirect EKG markers (angiograms were not routinely done), patients treated with IV nitroglycerin plus rTPA were felt to be significantly less likely than those treated with rTPA alone to reperfuse (56% vs. 76%, p<0.05), and more likely to reocclude (53% vs. 24%, p<0.05). Mean time to presumed reperfusion was longer in the nitroglycerin group, and patients receiving IV nitroglycerin had larger infarcts based on analysis of cardiac enzymes and more frequent development of nonfatal ventricular fibrillation (3/27 vs. 0/33), sustained ventricular tachycardia (10/27 vs. 5/33), pulmonary edema (4/27 vs. 1/33), or congestive heart failure (3/27 vs. 1/33). Plasma TPA antigen levels in patients receiving concomitant IV nitroglycerin were lower than those noted in patients receiving TPA alone. CONCLUSIONS: Preliminary findings in this small group of patients sugggest a possible adverse effect of IV nitroglycerin on the actions of rTPA, perhaps due to promotion of rTPA catabolism by nitroglycerin. 24 references