Right ventricular apical activation times in patients with conduction disturbances occurring during acute transmural myocardial infarction.

His bundle and right ventricular apical electrograms were recorded in 18 patients with acute transmural myocardial infarction in whom catheter insertion was considered necessary for clinical reasons. The V-RVA and H-V intervals were of normal duration (5 to 30 and 35 to 55 msec, respectively) in five patients (Group 1) with persistently narrow (less than 100 msec) QRS complexes. In contrast, 13 patients (Group 2) who manifested a "complete" right bundle branch block pattern within 96 hours after admission had prolonged V-RVA intervals (range 50 to 80 msec, mean 59.2 msec) and H-V intervals that were at the upper limits of normal or prolonged (range 55 to 90 msec, mean 63 msec). In 6 of these 13 patients, the duration of the V-RVA interval became normal when the "complete" right bundle branch block pattern disappeared and was replaced by a "complete" left bundle branch block pattern in three patients and by narrow QRS complexes in the three other patients. This study showed that transmural myocardial infarction in itself did not increase the duration of the V-RVA interval even when "complete" left bundle branch block was present. Moreover, a prolonged V-RVA interval coexsting with a "complete" right bundle branch block pattern was not due to distal right bundle branch block but resulted from a conduction disturbance located in the proximal portions of the right bundle, or perhaps, even within the His bundle itself.     

Epicardial and endocardial mapping of ventricular tachycardia in patients with myocardial infarction. Is the origin of the tachycardia always subendocardially localized?

BACKGROUND. Left ventricular endocardial reentry is the conventional concept underlying surgery for ventricular tachycardia (VT). We assessed the incidences of patterns showing complete reentry circuits at either the subendocardial or subepicardial level and of patterns in which left ventricular endocardial mapping could only in part account for a reentrant mechanism. METHODS AND RESULTS. We retrospectively analyzed epicardial and left ventricular endocardial isochronal maps of 47 VTs induced in 28 patients with chronic myocardial infarction (inferior, 14 patients; anteroseptal, 14 patients). Electrograms were recorded intraoperatively from 128 sites with epicardial sock and transatrial left ventricular endocardial balloon electrode arrays. Given the methodology used in this study, the mapping characteristics of the tachycardias suggested five types of activation patterns: 1) complete (90% or more of VT cycle length) subendocardial reentry circuits in seven VTs (15%) and seven patients (25%), 2) complete subepicardial reentry circuits in four VTs (9%) and four patients (14%), 3) incompletely mapped circuits with a left ventricular endocardial breakthrough preceding the epicardial breakthrough in 25 VTs (53%) and 21 patients (75%), 4) incompletely mapped circuits with a left ventricular epicardial breakthrough preceding the endocardial breakthrough in three VTs (6%) and three patients (11%), and 5) a right ventricular epicardial breakthrough preceding the left ventricular endocardial breakthrough in eight VTs (17%) and seven patients (25%). After surgery, one type 3 VT and three type 5 VTs were reinducible. Thus, left ventricular endocardial reentry substrates (types 1 and 3) accounted for 68% of VTs, but substrates involving subepicardial (types 2 and 4) and deep septal layers (type 5) accounted for 32% of VTs. CONCLUSIONS: In a substantial number of VTs, a substrate localization that is at variance with the conventional concept can be detected by simultaneous epicardial and endocardial mapping and may require modification of the surgical approach conventionally aimed at endocardial layers.     

Precordial ST-segment mapping 4. Experience with mapping of ST-segment depression in anterior transmural myocardial infarction

In order to assess the relative significance of precordial ST-segment elevations and depressions, 32 patients with anterior transmural myocardial infarction were studied utilizing serial 49-lead precordial maps. Theoretically, zones of ST-segment depression adjacent to major zones of ST-segment elevation might represent border areas of mild ischemia, and hence could be more readily amenable to intervention therapy. As expected, an extensive zone of ST-segment elevation was observed precordially in each of these patients. However, zones of ST-segment depression in adjacent areas were noted to occur inconsistently, were limited in distribution and magnitude, and bore no fixed relationship to zones of ST-segment elevation. Thus, mapping of precordial ST-segment depression in anterior transmural infarction probably has a limited role in assessing evolution of ischemic injury or therapy in these patients. This finding does not, however, vitiate the significance of ST-segment depressions in angina, intermediate coronary syndrome, or non-transmural infarction, conditions which may deserve further study using mapping techniques.     

The comparative hemodynamic effects of antiarrhythmic drugs in acute myocardial infarction (comparison of propafenone and lidocaine) (author's transl)

Hemodynamic changes after single intravenous injection of antiarrhythmic doses of propafenone (70 mg) and lidocaine (100 mg) were measured comparatively in 11 patients with acute myocardial infarction, stable cardiac rhythm and without evidence of manifest left heart failure. The effects of propafenone were characterized by a significant decrease of cardiac index by 6% and an increase in left and right ventricular filling pressures by 15% and 23%. Mean arterial pressure was significantly lowered (8%) and left ventricular stroke work index decreased by an average of 11%. Mean pulmonary artery pressure significantly increased by 7%. A fall in systemic vascular resistance by 7% was not statistically significant. Intravenous administration of propafenone at a dose of 70 mg thus caused a transitory decrease in ventricular function and acute vasodilation with a fall in systemic blood pressure. The intravenous administration of lidocaine did not result in significant changes of cardiac index or left and right ventricular filling pressures. Mean pulmonary artery pressure, systemic blood pressure and vascular resistance increased significantly.     

Abnormalities of endocardial activation pattern in patients with previous healed myocardial infarction and ventricular tachycardia

Endocardial catheter mapping was performed in 27 patients with anterior wall acute myocardial infarction (AMI) and in 10 patients with inferior wall AMI. All patients had a history of ventricular tachycardia. Left ventricular breakthrough occurred at 10 +/- 4 ms after the QRS complex in inferior AMI and 11 +/- 7 ms after the QRS complex in anterior AMI. Total electrical activity recorded during sinus rhythm was 164 +/- 46 ms in inferior and 144 +/- 28 ms in anterior AMI (p = 0.05). Nine of the 10 patients with inferior AMI had complete activation of the anterior wall within the initial one-half of the QRS complex, compared with only 15 of the 27 patients with anterior AMI (p = 0.05). All 10 patients with inferior AMI had activation of the ventricular septum within the initial half of the QRS complex compared with only 13 of 27 with anterior AMI (p less than 0.005). None of the patients with inferior AMI had activation of the inferoposterior base within the initial one-half of the QRS complex, compared with 21 of 27 patients with anterior AMI (p less than 0.001). Complete activation of the anterior wall occurred at 33 +/- 15 ms in inferior and 58 +/- 30 ms in anterior AMI (p less than 0.005). Complete activation of the septum occurred at 38 +/- 12 ms in inferior and 63 +/- 28 ms in anterior AMI (p less than 0.005). Complete activation of the inferoposterior base occurred at 100 +/- 38 ms in inferior and 50 +/- 21 ms in anterior AMI (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Differential effects of procainamide, lidocaine and acetylstrophanthidin on body surface potentials and epicardial conduction in dogs with chronic myocardial infarction

Twenty-eight anesthetized mongrel dogs were studied 2 to 74 months after experimental myocardial infarction in order to examine the effects of procainamide, lidocaine and acetylstrophanthidin on conduction within the infarcted region and the way such effects relate to changes in body surface potentials and antiarrhythmic efficacy. In each animal, 100 to 200 QRS complexes in the X, Y, Z leads were signal averaged, vector summed and high pass filtered at 50 Hz. Susceptibility to ventricular arrhythmia was evaluated using routine programmed ventricular extrastimulation in the anesthetized open chest animal. Epicardial electrograms were sequentially recorded at 45 standard sites within the infarcted region and referenced to the beginning of the QRS complex. Of the three agents, only procainamide exhibited antiarrhythmic action whereas lidocaine and acetylstrophanthidin produced inconsistent effects. Procainamide prolonged the time at which activity in the epicardial electrographic recordings ended relative to the beginning of the body surface QRS complex. This effect was significantly greater in electrograms that ended late in the QRS complex in the control state than for those that ended earlier. Such preferential effect on more abnormal sites was reflected on the body surface as a greater effect of procainamide in prolonging the lower energy terminal portion of the signal-averaged QRS complex than the earlier high energy portion. In contrast, lidocaine significantly prolonged the time at which electrograms ended only for those relatively normal electrograms that ended early in the QRS complex in the control state. In the signal-averaged body surface QRS complex, lidocaine produced a small but significant prolongation of the early high energy portion of the QRS complex but no change in the late portion. Acetylstrophanthidin produced a significant prolongation in early-ending electrograms and, surprisingly, significantly shortened the end time of electrograms that ended late in the QRS complex in the control state. Such effects were not reflected, however, on the body surface because acetylstrophanthidin had no significant effect on either the early or the late portion of the QRS complex. It is concluded that procainamide's differential effect between early- and late-ending electrograms is detected on the body surface by a greater prolongation in the terminal portion of the QRS complex. The signal-averaged body surface QRS complex is less sensitive in detecting the more subtle effects on conduction caused by lidocaine and acetylstrophanthidin.(ABSTRACT TRUNCATED AT 400 WORDS)     

Hemodynamic effects of procainamide in patients with acute myocardial infarction and comparison with lidocaine

Comparative hemodynamic and electrocardiographic investigation of antiarrhythmic doses of procainamide and lidocaine was carried out in 19 patients with acute myocardial infarction or with severe left ventricular failure of other etiologies. In 12 patients in whom the standard recommended dosage of these agents was equally effective in abating ventricular tachyarrhythmias, there were no significant adverse hemodynamic and electrical effects or differences (p > 0.05) between relatively small salutary doses of lidocaine and procainamide after their intravenous administration in similar quantity and manner (100 mg in 3 min followed by 2 mg/min for 20 min). Furthermore, larger doses of procainamide (500 mg given 20 mg/min intravenously), which were also therapeutically beneficial in seven additional patients with acute myocardial infarction, caused no significant alteration (p > 0.05) in hemodynamic function. With the 500 mg dose, there was a small difference (p < 0.05) in the directional change of cardiac index which was dependent on the control values: the variable rose slightly in patients with normal indexes whereas it declined slightly in those with low values. Significant Q-T prolongation (p < 0.05) occurred with 500 mg of the agent; otherwise, there were no adverse electrocardiographic or untoward extracardiac effects. Thus, intravenous procainamide is equally effective in acute myocardial infarction and is a relatively safe alternative to lidocaine.     

Precordial mapping of ST-segment elevation and Q waves following anterior myocardial infarction. The effects of established beta-blocking drugs.

The electrocardiographic (ECG) signs of ST-segment elevation and the development of Q was using 72-lead precordial surface mapping, and the release of creatine kinase (CK) activity has been studied in 47 patients with uncomplicated anterior myocardial infarction. These findings were compared with a further nine patients who had acute myocardial infarction but were receiving long-term beta-blocking drugs. It was found that ST-segment elevation and Q waves had rapidly changing and different natural histories and that beta-blocking drugs altered the natural history of ST-segment changes but had no effect on the pattern and time course for the loss of electrically active myocardium. There was a close relationship between the precordial area of ST-segment elevation at 2--3 h and the final development of Q waves in the patients with uncomplicated anterior myocardial infarction. No similar relationship could be found in those on beta-blocking drugs. The pattern of changes in plasma CK and its MB isoenzymes activity were similar for both groups. The relationship between early ST-segment elevation and the final area of Q waves may prove useful in clinical practice. This may not apply where beta-blocking drugs are commenced before the initial recording of ST-segment elevation.     

Epicardial mapping of the onset of ventricular tachycardia initiated by programmed stimulation in the canine heart with chronic infarction.

The initial beats of ventricular tachycardia (VT) induced by programmed stimulation (PS) of the heart have frequently been observed to differ in QRS configuration from the subsequent uniform QRS complexes of tachycardia. The transient nature of these initial beats has made their study difficult during epicardial mapping with conventional, hand-held recording electrodes. Twenty-four dogs were studied with PS 1-10 months after coronary ligation. Twenty-six epicardial electrograms were recorded simultaneously during PS. The data were digitized for computer generation of isochronic maps for any desired beat. Three patterns of initiation were observed in episodes of tachycardia in which the initial beats differed from the subsequent beats of VT (11 of 18 runs of VT). Most frequently, the initial beats of VT originated near the pacing electrode before moving to a stable infarction zone location. Less frequently, the initial beats were due to transient reentry in the bundle branches or a transient shifting of early breakthrough sites in the infarction zone.     

Body surface mapping of ectopic left ventricular activation. QRS spectrum in patients with prior myocardial infarction.

To improve electrocardiographic localization of the site of origin of ectopic left ventricular (LV) impulse formation in the heart with prior myocardial infarction, 62-lead body surface QRS integral maps were studied during LV pacing at a total of 221 endocardial sites in 14 patients with previous anterior (AMI), inferior (IMI), lateral (LMI), or anterior and inferior (AMI/IMI) myocardial infarction. The anatomic location of each pacing site was computed using digitized biplane fluoroscopic images and plotted on standardized LV endocardial polar projections. A data base of characteristic AMI and IMI mean QRS integral maps was developed after visually selecting subgroups with nearly identical QRS integral morphology from the ectopic activation sequences produced at 110 sites in eight patients with AMI and at 66 sites in four patients with IMI. Intrasubgroup pattern uniformity and intersubgroup pattern variability were statistically verified. The endocardial pacing site locations belonging to each AMI and IMI subgroup were depicted as segments on the respective LV polar projections. In patients with AMI, a total of 18 typical mean QRS integral patterns were obtained, whereas 22 different mean total QRS integral patterns showing more substantial intersubgroup variation were acquired in patients with IMI. Posterolateral regions exhibited a relatively low electrocardiographic sensitivity (six AMI and five IMI patterns) as compared with anteroseptal regions (12 AMI and 17 IMI patterns). Total QRS integral patterns obtained at 24 sites in one patient with LMI were largely compatible with the IMI mean total QRS integral patterns, whereas the majority of total QRS integral patterns acquired at 21 sites in one patient with AMI/IMI corresponded with the AMI mean total QRS integral patterns. The results show that total body surface QRS integral maps generated during LV pacing in patients with prior myocardial infarction cluster by pattern and that each QRS integral pattern is related to a circumscribed endocardial segment of ectopic impulse formation. The relation between a given QRS integral pattern and the position and size of the corresponding paced segment is dependent on infarct location. The present infarct-specific data base of characteristic total body surface QRS integral patterns provides a clinical tool to obtain detailed electrocardiographic localization of ventricular arrhythmias in patients with previous myocardial infarction.     

The effect of oral cimetidine on total and unbound serum lidocaine concentrations in patients with suspected myocardial infarction

In this study, we prospectively evaluated the effect of oral cimetidine on serum lidocaine concentrations in 6 patients with suspected myocardial infarction. Compared to baseline lidocaine levels, total lidocaine concentrations increased by 8.2 +/- 7.8% at 6 hours, 16.4 +/- 9.0% at 12 hours and 27.9 +/- 9.4% at 24 hours after two doses of oral cimetidine. Unbound lidocaine concentrations increased by 14.3 +/- 4.1% at 6 hours, and 18.3 +/- 10.3% at 24 hours after cimetidine. In patients with myocardial infarction (3), total lidocaine concentrations increased by 24.2 +/- 10.4%, whereas unbound lidocaine increased by 8.9 +/- 10.2% at 24 hours. Therefore, increases in total lidocaine concentrations after cimetidine administration were considerably less than those previously reported and empiric dosage reductions of lidocaine in patients receiving cimetidine may not be appropriate.     

Raised concentrations of glucose and adrenaline and increased in vivo platelet activation after myocardial infarction.

Plasma concentration of beta thromboglobulin was used as an index of in vivo platelet activation in 36 patients after acute myocardial infarction. Twelve patients had diabetes, seven had pulmonary oedema or cardiogenic shock (pump failure) or both, and 17 had uncomplicated infarcts. On the first day of admission, concentrations of beta thromboglobulin were higher in the patients with diabetes and those with pump failure than in those with uncomplicated infarcts. Concentrations of beta thromboglobulin in the non-diabetic patients were studied by multiple regression analysis and were significantly associated with plasma concentrations of adrenaline, pump failure, and glucose but not with noradrenaline or infarct size. When all subjects were considered together, glucose, adrenaline, and pump failure were associated with the beta thromboglobulin concentration but diabetes was without significant effect. Hyperglycaemia and raised plasma adrenaline concentration after myocardial infarction may activate platelets, and this could contribute to poor outcome in such patients.     

Lidocaine, mexiletine and propafenone in the treatment of arrhythmias complicating myocardial infarction. A case report

We describe a case of acute myocardial infarction complicated by atrial and ventricular arrhythmias in which it was possible to verify the effectiveness of lidocaine, mexiletine and propafenone. Intravenous administration of mexiletine was ineffective both on atrial and ventricular rhythm disturbances. The lidocaine therapy reduced ventricular ectopic frequency, but did not prevent the appearance of several paroxysms of atrial fibrillation. Intravenous infusion of propafenone, 11 micrograms/kg per min, after a 1 mg/kg i.v. bolus, immediately and completely suppressed atrial arrhythmias. The increase in infusion rate up to 22 micrograms/kg per min also suppressed ventricular ectopy. This dosage of propafenone did not provoke serious adverse effects in our patient.     

Increased serum leptin concentrations in patients with chronic stable angina pectoris and ST-elevated myocardial infarction

Leptin is an adipocytokine that is produced mainly by adipose tissue; it is also identified in atherosclerotic lesions in human coronary atherosclerosis. However, the relation of serum leptin concentrations to ischemic heart disease (IHD) is still obscure. The aims of the present study were to investigate serum leptin concentrations in patients with ST-elevated myocardial infarction (STEMI) and with chronic stable angina pectoris (CSAP) and to evaluate the possible correlations of leptin to other atherosclerotic risk factors; including serum high sensitive C-reactive protein (Hs-CRP), serum homocysteine, and fibrinogen concentrations. For this purpose, 35 patients with CSAP, 40 with acute STEMI, and 30 control subjects with normal findings from coronary angiography were taken into the study prospectively. Serum leptin concentrations were significantly higher in patients with CSAP and STEMI compared to the control group (7.74 +/-1.34 vs 6.37 +/-1.85 ng/mL, p=0.021 and 8.22 +/-3.13 vs 6.37 +/-1.85 ng/mL, p=0.023, respectively). In addition, serum homocysteine concentrations were significantly increased in patients with CSAP (15.23 +/-5.96 vs 11.40 +/-2.11 micromol/L, p=0.025) and patients with STEMI (15.90 +/-5.02 vs 11.40 +/-2.11 micromol/L, p=0.012) compared to the control group. Serum fibrinogen concentrations were significantly increased only in the CSAP group as compared to controls (4.15 +/-1.39 vs 3.45 +/-1.19 g/L, p=0.025). No significant correlation was found between leptin levels and selected risk factors. In conclusion, serum leptin concentrations were significantly higher in both the CSAP and STEMI groups. However, owing to the lack of correlation between the leptin levels and selected classical coronary risk factors, it may be considered that leptin can be evaluated as one of the independent risk factors for IHD. Further randomized and controlled studies will be required to determine the pathophysiological meaning of the increased leptin levels and the central role between adipocyte function and atherosclerosis.     

Baroreflex sensitivity and neurohormonal activation in patients with acute myocardial infarction.

OBJECTIVE--To examine the relationship between baroreflex sensitivity and neurohormonal activation in patients with an acute myocardial infarction. METHODS--Baroreflex sensitivity, plasma noradrenaline, atrial natriuretic factor, endothelin-1, and plasma renin activity were measured in 37 male patients about 10 days after their first myocardial infarction, and in 15 healthy controls. Baroreflex sensitivity was assessed from the regression line relating the change in RR interval to the change in systolic blood pressure following an intravenous bolus injection of phenylephrine. The measurements were repeated after a follow up of three months. RESULTS--There was a significant inverse correlation between baroreflex sensitivity and plasma noradrenaline measured before hospital discharge (r = -0.43, P < 0.01). Patients with increased plasma noradrenaline (> or = 2SD above the mean of the age matched control group) had significantly lower baroreflex sensitivity than patients with normal plasma noradrenaline (8.7 (SD 4.6) v 12.1 (6.1) ms/mm Hg, P < 0.05). The change in baroreflex sensitivity during the follow up showed a significant inverse correlation with the change of plasma noradrenaline (r = -0.450, P < 0.01). Furthermore, when patients with increased plasma noradrenaline before hospital discharge were analysed separately, baroreflex sensitivity at three months in patients in whom plasma noradrenaline had decreased to normal values was significantly higher than in patients in whom plasma noradrenaline had remained increased (14.6 (5.7) v 8.1 (8.1) ms/mm Hg, P < 0.05). On the other hand, baroreflex sensitivity was not related to the levels of plasma atrial natriuretic factor, plasma endothelin-1, or plasma renin activity. Neither was any relationship found between change in baroreflex sensitivity and change in plasma atrial natriuretic factor, endothelin-1, or plasma renin activity during the follow up. CONCLUSIONS--The impairment baroreflex sensitivity after myocardial infarction was associated with increased concentration of plasma noradrenaline, that is, sympathetic activation, but not with plasma atrial natriuretic factor, endothelin-1, or plasma renin activity. Baroreflex sensitivity provides information about cardiac vagal control as well as about the balance of cardiac sympathetic-parasympathetic regulation.     

Hemodynamic and metabolic effects of skin and blood-stream cooling in experimental myocardial infarction with shock

The hemodynamic and metabolic effects of moderate hypothermia (28–30 °C.) induced by skin or blood cooling were studied in dogs with acute myocardial infarction and shock produced by plastic sphere coronary embolization. There was no increase in ventricular fibrillation, asystole or congestive heart failure in the hypothermic animals, whether cooled by skin or blood stream, as compared to animals with acute infarction remaining normothermic for similar periods. All cooled animals demonstrated, upon rewarming, more adequate return of cardiac output, aortic pressure and systemic vascular resistance than did animals remaining normothermic, although skin cooling was associated with metabolic acidosis, slower cooling and less decline in left ventricular work during hypothermia than blood-stream cooling. Chlorpromazine, which diminished shivering, resulted in postrewarming depression of cardiac output and aortic pressure.

Skin cooling resulted in apparently favorable hemodynamic alterations in the postrewarming period despite shivering and maintenance of relatively high left ventricular work during hypothermia. It is suggested that benefit may be derived from hypothermia in acute myocardial infarction through physiologic mechanisms in addition to reduction of the oxygen requirement of the left ventricle.     

Thrombolytic treatment in acute myocardial infarction: neutrophil activation, peripheral leucocyte responses, and myocardial injury.

OBJECTIVE--To examine early leucocyte responses and neutrophil activation in acute myocardial infarction treated by streptokinase and to relate the findings to coronary recanalisation and indices of myocardial damage in order to provide further information about the role of neutrophils in the evolution of injury. DESIGN--Group analysis of paired blood samples, obtained before streptokinase treatment and one hour after it, and of three indirect measures of myocardial injury: left ventricular ejection fraction, QRS score, and peak creatine kinase. SETTING--The coronary care unit of a district general hospital. PATIENTS--39 patients with acute myocardial infarction who underwent paired blood sampling (before streptokinase and one hour after streptokinase) and cardiac catheterisation 5 (3-8) days later. END POINTS--Changes in peripheral white cell and neutrophil counts and plasma elastase one hour after streptokinase infusion. Comparison of these variables in patients with and without patency of the infarct related coronary artery. Correlations between these variables and indirect measures of myocardial injury. RESULTS--Neutrophil activation, as reflected by plasma elastase, increased sharply one hour after streptokinase. Total white cell and neutrophil counts also increased. Changes tended to be more pronounced in patients with patency of the infarct related artery, though the trend was not statistically significant. Neutrophil activation before streptokinase was unrelated to indirect indices of myocardial injury but only one hour after streptokinase a weak negative correlation with left ventricular ejection fraction had developed. Peripheral neutrophil responses showed a similar relation to ejection fraction and also correlated with peak creatine kinase and QRS score. CONCLUSIONS--Thrombolytic treatment in acute myocardial infarction is associated with an abrupt reactive neutrophil response which provides an early measure of injury. It is also associated with neutrophil activation, probably in response to coronary recanalisation and myocardial reperfusion. Activated neutrophils are recognised as mediators of reperfusion injury in experimental infarction and the data in the present study provide preliminary evidence of a similar pathogenic role in the clinical setting.     

Thrombolytic treatment in acute myocardial infarction: neutrophil activation, peripheral leucocyte responses, and myocardial injury.

OBJECTIVE--To examine early leucocyte responses and neutrophil activation in acute myocardial infarction treated by streptokinase and to relate the findings to coronary recanalisation and indices of myocardial damage in order to provide further information about the role of neutrophils in the evolution of injury. DESIGN--Group analysis of paired blood samples, obtained before streptokinase treatment and one hour after it, and of three indirect measures of myocardial injury: left ventricular ejection fraction, QRS score, and peak creatine kinase. SETTING--The coronary care unit of a district general hospital. PATIENTS--39 patients with acute myocardial infarction who underwent paired blood sampling (before streptokinase and one hour after streptokinase) and cardiac catheterisation 5 (3-8) days later. END POINTS--Changes in peripheral white cell and neutrophil counts and plasma elastase one hour after streptokinase infusion. Comparison of these variables in patients with and without patency of the infarct related coronary artery. Correlations between these variables and indirect measures of myocardial injury. RESULTS--Neutrophil activation, as reflected by plasma elastase, increased sharply one hour after streptokinase. Total white cell and neutrophil counts also increased. Changes tended to be more pronounced in patients with patency of the infarct related artery, though the trend was not statistically significant. Neutrophil activation before streptokinase was unrelated to indirect indices of myocardial injury but only one hour after streptokinase a weak negative correlation with left ventricular ejection fraction had developed. Peripheral neutrophil responses showed a similar relation to ejection fraction and also correlated with peak creatine kinase and QRS score. CONCLUSIONS--Thrombolytic treatment in acute myocardial infarction is associated with an abrupt reactive neutrophil response which provides an early measure of injury. It is also associated with neutrophil activation, probably in response to coronary recanalisation and myocardial reperfusion. Activated neutrophils are recognised as mediators of reperfusion injury in experimental infarction and the data in the present study provide preliminary evidence of a similar pathogenic role in the clinical setting.