W. Merx

Percutaneous transluminal coronary angioplasty immediately after intracoronary streptolysis of transmural myocardial infarction.

Percutaneous transluminal coronary angioplasty (PTCA) was performed in 21 patients with acute myocardial infarction (AMI) treated by intracoronary infusion of streptokinase within 8 hours after the onset of symptoms. Streptolysis therapy began a mean of 3.6 1.2 hours (±± SD) after the onset of symptoms. The vessel was occluded in 14 patients and highly stenosed in seven. After the infusion of 67,300 ± 63,200 IU of streptokinase over 26.1 21.5 minutes, patency of the occluded vessels was reached. PTCA as performed 20-60 minutes after the end of streptokinase treatment in 19 patients and 24 and 31 hours after treatment in two patients. The dilation was successful in 17 patients (81%). The degree of vessel obstruction was reduced from 90.2 ± 7.3% to 58.6 19.5% (area method) and from 71.4 ± 12.4% to 39.2± 19.7% (diameter method). The improvement was 31.5 18.4% and 32.2 ± 19.3%, respectively. No reocclusion was induced by PTCA. Twenty patients were discharged. One died during hospitalization; at autopsy, the treated vessel was still patent. During the follow-up period, two reinfarctions and one asymptomatic reocclusion occurred. The clinical findings during the hospital course and the follow-up period were compared with those of a control group of 18 patients with AMI and comparable coronary stenoses who were treated only with streptokinase infusion. Four of these patients had a reinfarction during the hospital course, and three died during the follow-up period. PTCA can be performed safely and successfully immediately after intracoronary infusion of streptokinase in patients with AMI. By reducing the subtotal stenosis, this treatment contributes to the reperfusion of the ischemic myocardium, diminishes the risk of a reocclusion and seems to improve the prognosis.

Improved thrombolysis in acute myocardial infarction with front-loaded administration of alteplase: Results of the rt-PA-APSAC patency study (TAPS)

Thrombolysis with recombinant tissue-type plasminogen activator (rt-PA) and anisoylated plasminogen streptokinase activator (APSAC) in myocardial infarction has been proved to reduce mortality. A new front-loaded infusion regimen of 100 mg of rt-PA with an initial bolus dose of 15 mg followed by an infusion of 50 mg over 30 min and 35 mg over 60 min has been reported to yield higher patency rates than those achieved with standard regimens of thrombolytic treatment. The effects of this front-loaded administration of rt-PA versus those obtained with APSAC on early patency and reocclusion of infarct-related coronary arteries were investigated in a randomized multicenter trial in 421 patients with acute myocardial infarction. Coronary angiography 90 min after the start of treatment revealed a patent infarct-related artery (Thrombolysis in Myocardial Infarction [TIMI] grade 2 or 3) in 84.4% of 199 patients given rt-PA versus 70.3% of 202 patients given APSAC (p = 0.0007). Early reocclusion within 24 to 48 h was documented in 10.3% of 174 patients given rt-PA versus 2.5% of 163 patients given APSAC. Late reocclusion within 21 days was observed in 2.6% of 152 patients given rt-PA versus 6.3% of 159 patients given APSAC. There were 5 in-hospital deaths (2.4%) in the rt-PA group and 17 deaths (8.1%) in the APSAC group (p = 0.0095). The reinfarction rate was 3.8% and 4.8%, respectively. Peak serum creatine kinase and left ventricular ejection fraction at follow-up angiography were essentially identical in both treatment groups. There were more bleeding complications after APSAC (45% vs. 31%, p = 0.0019).(ABSTRACT TRUNCATED AT 250 WORDS)

Detection of left atrial thrombi by echocardiography.

A group of 111 patients with mitral valve disease was studied by M-mode and two-dimensional echocardiography. Five left atrial thrombi were demonstrated, two of which had probably been the source of previous embolic events. Two-dimensional echocardiography was superior to M-mode in providing spatial orientation. Using multiple cross-sections the exact localisation and the size of the thrombus formation could be estimated. Thrombus localisations at the upper, lateral, and septal atrial walls, normally inaccessible to the single-beam technique, were successfully imaged. Even two-dimensional echocardiography, however, constitutes an imperfect method. By comparison with the findings at surgery only one-third of confirmed thrombi could be detected non-invasively. According to their localisation seven clots in the appendage were missed by the ultrasound method. One further thrombus fixed to the upper left atrial wall near the entrance of the upper pulmonary veins was also undetected by echocardiography. Despite these limitations, the information provided by echocardiography can be most helpful in patient management. M-mode, in combination with two-dimensional echocardiography, is therefore recommended in all patients with mitral stenosis before diagnostic or therapeutic procedures are undertaken.

QRS mapping in the evaluation of acute anterior myocardial infarction.

In 42 patients with acute anterior myocardial infarction (AMI), we studied the course of Qwave development and R-wave reduction during the first 48 hours after the onset of chest pain. We used precordial mapping in relation to clinical features, hemodynamic measurements and enzyme release. Q waves developed within 6–14 hours (mean 9 hours) after onset of symptoms. R-wave amplitudes demonstrated nearly a reflected image: They reduced abruptly 5–11 hours (mean 9 hours) after onset of chest pain, coinciding with ST-segment elevation. In 14 patients (group A, 33%) after initial QRS alterations, there were no furtherchanges. Twenty patients (group B, 48%) had a distinct new increase of Q waves (δ= 3.0 ± 2.0 mV/hours) and further R-wave reduction (- δR = 1.0 ± 0.6 mV/hour) simultaneous with new severe chest pain and a delayed second increase of enzyme release corresponding with extension of infarction. There were no significant differences between the groups in age, hemodynamics and infarct size calculated from creatine kinase release. Eight patients (group C, 19%) had contradictory findings.Our findings are consistent with previous results indicating that the critical period for intervention is very small except in patients with extension of necrosis.

Controlled trial of prophylatic treatment with lidocaine in acute myocardial infarction.

SummaryThe prophylactic value of lidocaine in the treatment of cardiac arrhythmias in acute myocardial infarction has been assessed quantitatively in 89 patients by continuous monitoring of the ECG. Patients with ventricular fibrillation, flutter or tachycardia on admission, with severe left heart failure or cardiogenic shock were excluded from the study. 41 of the 89 were treated with lidocaine (28:20–30 mg/kg; 13:31–60 mg/kg) and 48 controls received no antiarrhythmic treatment. Ventricular ectopic beats and runs of ventricular extrasystoles were equally common in groups receiving low and high doses of lidocaine. 7.3% of the patients treated prophylactically had ventricular tachycardias and they occurred in 10.4% of the untreated controls. Primary ventricular fibrillation caused the death of one control patient. No other difference in mortality was observed between the groups. 1st and 2nd degree AV-block was observed increasingly often in both groups during the monitoring period. The incidence of AV-block increased two-fold from the first to the third day in the lidocaine group compared with the untreated patients. It is concluded that lidocaine cannot be recommended as a general prophylatic treatment in acute myocardial infarction.

Relation between admission time, haemodynamic measurements, and prognosis in acute myocardial infarction.

dballoon catheter andmonitored for51±51hours in226patients admitted withanacute myocardial infarction (184 survivors and42non-survivors). Mortality was related totimeofadmission after onset ofsymptoms ofinfarction. Of69patients ingroup A 13died inhospital (188%)onetofour hours after onset; ingroupB(five toeight hours after onset) eight of 71patients (11%) died five toeight hours after onset; four of26patients ingroup C(15%) diednine to12hours after onset; 15of42patients (36%) ingroupDdied13to24hours after onset; andtwoof 18patients ingroupEdied(11%) morethan24hours after onset. Irrespective ofadmission time, haemodynamic findings insurvivors weresignificantly better thaninnon-survivors. During thefirst eight to12hours after onset ofinfarction cardiac index andstroke workindex werenormal orabove normal, withraised left ventricular filling pressures. Inpatients admitted later, this compensatory mechanism hadoften collapsed. Wherepumpfailure withsubnormal cardiac index andstroke work index werepresent mortality wasincreased. Allfour patients dying fromacute myocardial rupture hadsignificantly higher values ofcardiac indexandstroke workindexandlowervalues of pulmonary artery end-diastolic pressure compared withthose dying fromother causes. Although theinitial haemodynamic values givesomeprognostic information, longitudinal analysis provides insight into theevolving myocardial disturbance andcompensatory mechanisms. Iftheinitial values ofpulmonary artery end-diastolic pressure andcardiac andstroke workindices remain normal orbecome stable after atransient disturbance intheacute phase, prognosis isgood. If, however, these values deteriorate orremain abnormal, prognosis ispoor. Typically suchpatients havesuffered large infarctions withatendency toexpansion. Ifthehaemodynamic situation during thefirst 24hoursafter onset ofinfarction remains stable for12to15hours, haemodynamic monitoring maybestopped; thechance ofrelapse insuchpatients wasfound tobebelow 10%.Late deterioration, usually manifest byfurther painorbyelectrocardiographic orenzymechanges, should beanindication torestart haemodynamic monitoring sothat treatment canbechosen and adjusted optimally. Thesehaemodynamic measurements inpatients treated traditionally with vasodilators, positive inotropic agents, andfluid will formthebasis forcomparison ofmeasurements inpatients whoarenowtreated within thefirst eight hours with selective intracoronary thrombolysis and,ifpossible, withadjacent intracoronary balloon dilatation oftheunderlying coronary artery stenosis.

Relationship between heart rate and ventricular ectopic rhythm in acute myocardial infarction.

SummaryThe study of 1313 time intervals from 146 patients with acute myocardial infarction showed that a linear relationship exists between the occurrence of ventricular ectopic beats or runs of ventricular ectopic beats and the heart rate. With faster heart rates, the percentage of these arrhythmias is decreased. Ventricular tachycardias and ventricular fibrillation or flutter were also seen most commonly in bradycardia, but there was a second maximum in frequencies exceeding 110/min. It is supposed that in cases with such tachycardial heart action severe heart failure and myocardial hypoxia are often present and that under these circumstances, only relatively few ventricular ectopic beats are necessary to trigger ventricular tachycardias or ventricular flutter/fibrillation.These results underscore in clinical practice that acceleration of heart frequency is a reliable measure to suppress ventricular ectopic rhythm. Electrostimulation of the right atrium is recommended for this purpose, although a stable position for the electrode catheter within the atrium may be difficult to achieve.ZusammenfassungBei 146 Patienten mit akutem Myokardinfarkt konnte anhand der Auswertung von insgesamt 1313 Zeit-Intervallen ein linearer Zusammenhang zwischen dem Auftreten von ventriculären Extrasystolen und ventriculären Salven und der jeweiligen Herzfrequenz nachgewiesen werden: mit zunehmender Herzfrequenz nahm die Häufigkeit dieser Rhythmusstörungen ab. Auch ventriculäre Tachykardien und Kammerflimmern/flattern wurden bei langsamem Grundrhythmus häufiger beobachtet. Überschritt die Herzfrequenz jedoch 110/min, so kam es hier zu einem zweiten Häufigkeitsgipfel. Zur Erklärung wird angenommen, daß in derartigen Fällen überdurchschnittlich häufig eine schwere Herzinsuffizienz und Myokardhypoxie vorliegt und daß unter diesen Umständen bereits relativ wenige ventriculäre Extrasystolen genügen, um bedrohliche ventriculäre Tachyarrhythmien auszulösen.Die Ergebnisse unterstreichen die klinische Erfahrung, daß oft durch die Erhöhung der Herzfrequenz ventriculäre ektope Rhythmusstörungen zuverlässig unterdrückt werden können. Am besten erreicht man eine derartige Frequenzerhöhung durch eine Elektrostimulation des rechten Vorhofes. Es kann allerdings manchmal schwierig sein, eine effektive und stabile Elektrodenlage im rechten Vorhof zu erreichen.

Short and long term results with intracoronary SK with regard to further treatment and age of patients — experiences in Aachen —

Twenty-five years ago Boucek and co-workers (4) described treatment with thrombolysin of eight patients who had suffered acute myocardial infarction. Using a catheter they introduced the drug directly into the sinus of Valsalva and could observe a return to normal within 6 h in the electrocardiograms of two patients. This was then followed in more extensive investigations (29) by systemic application of streptokinase in acute myocardial infarction. The results of eight randomised studies were published between 1969 and 1979 (1–3, 5, 7, 12–14). A significant drop in mortality could only be demonstrated in three of these studies with intravenous injection of streptokinase (5, 12, 13) and for this reason systemic streptokinase treatment was discontinued in most cardiology centres.

Bypass surgery adjacent to streptolysis theraphy

Immediate surgical revascularization for myocardial infarct has been the dream of every progressive cardiac surgeon ever since aorto-coronary bypass surgery became realistic in 1967. As early as 1971 Favaloro [1] reported 11 patients treated surgically for acute myocardial infarct with only one death. Bolooki [2] demonstrated in 1975 that time was the most important factor influencing the early result of such operations. The excellent results achieved by Berg [3] and Philips [4] prove that acute myocardial infarct may be treated surgically.

Postthrombotic Therapy and Patient Follow-Up—The Role of Coronary Balloon Dilatation

After successful thrombolysis, a coronary stenosis of more than 50% of luminal diameter can be found in about 90% of all cases. These stenoses may impede the coronary flow, be the crystallisation point of another thrombus and be responsible for angina pectoris in the future. In 100 patients with successful thrombolysis angioplasty was performed immediately after clot lysis. The success rate was 74%, with no differences in concentric (60 cases) or eccentric stenoses (40 cases). The average diameter of the stenosis was reduced from 77·1 ± 11·0% to 34·4 ± 14·5% (improvement 42·7 ± 14·4±). After 6 mo in a group of 43 patients the mean stenosis rate had risen to 47·7 ± 23·2%. In 3 cases (3%) reocclusion of the vessel was induced by angioplasty. Although the combined method seems to be logical and without major complication rates, its merit has to be proven by randomised studies.