S. Effert

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.

Early recovery of left ventricular function after thrombolytic therapy for acute myocardial infarction: an important determinant of survival

Thrombolytic therapy for acute myocardial infarction reduces early mortality, but full recovery of left ventricular function after reperfusion is delayed. Therefore, the relations among reperfusion, survival and the time course of left ventricular functional recovery were examined in 226 patients treated with intracoronary streptokinase; 77% (134 patients) had sustained reperfusion and 31 patients had no reperfusion or had reocclusion by day 3. Wall motion was measured from contrast ventriculograms performed in the acute period and 3 days later in the central and peripheral infarct regions and the noninfarct region by the centerline method in 165 patients. Patients with reperfusion had better survival (p less than 0.05, mean follow-up 4.5 years) and a higher ejection fraction at 3 days (52 +/- 12 versus 46 +/- 10%, p less than 0.02) attributable to a significantly different change in peripheral infarct region function between the acute and 3 day studies (0.1 +/- 1.0 versus -0.3 +/- 0.9 SD, p less than 0.05). These early functional changes were significant in patients with anterior myocardial infarction and showed similar trends in those with inferior myocardial infarction. On Cox regression analysis, function measured at 3 days was more predictive of survival than was function measured acutely (chi square for acute ejection fraction = 11.48 versus 24.59 at 3 days). Although, as previously reported, greater than 45% of total recovery of left ventricular function occurs later, the ejection fraction achieved by day 3 is already predictive of survival. Thus, the mechanism by which successful thrombolytic therapy enhances survival is improvement of regional and global left ventricular function early after acute myocardial infarction.

Percutaneous transluminal coronary angioplasty in patients with stable and unstable angina pectoris: Analysis of early and late results

Percutaneous transluminal coronary angioplasty (PTCA) was performed in 50 patients with stable and in 50 patients with unstable angina pectoris, each patient showing an isolated stenosis of more than 80% of the cross-sectional area of a single coronary artery. The technical success rate was 66% in the stable groups (26 of 37 patients [70%] with left anterior descending artery [LAD], 7 of 12 patients [58%] with right coronary artery [RCA]) and 74% in the unstable group (27 of 34 patients [79%] with LAD, 10 of 15 patients [67%] with (RCA). The increase in stenotic area in the unstable group exceeding that in the stable group for LAD stenoses (41.5 +/- 15.1% vs 32.3 +/- 14.5%, p less than 0.03), while in RCA stenoses the results in the stable group were better (45.1 +/- 17.6% vs 32.7 +/- 12.3%, n.s.). One acute vessel occlusion necessitating an emergency bypass operation occurred in each group (2%). The patient in the stable group died (total mortality rate 1%). Sixty-three of the successfully treated patients were routinely restudied 6 months later. According to clinical symptoms, 23% of the stable and 36% of the unstable group were in functional classes III and IV. From the anatomical viewpoint, a restenosis (greater than 85%) was found in 17% of the stable and in 24% of the unstable group. A further spontaneous decrease (greater than 10%) of the vessel obstruction was found in 47% of the stable group and in 12% of the unstable group.(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.

Myocardial infarction and thrombolysis. Electrocardiographic short term and long term results using precordial mapping.

In a consecutive series of 56 patients with acute myocardial infarction, ST segment depression and elevation in the electrocardiographic limb leads I, II, and III were summated for each patient before and immediately after intracoronary streptokinase infusion and the results compared with the angiographic findings. Forty three patients had angiographically confirmed reperfusion of an initially occluded vessel and showed a significant decrease in summated ST shift. The ST segment changes in the limb leads virtually returned to normal in all 43 patients, and in most, inverted T waves developed. Thrombolysis was unsuccessful in 10 patients, and the infarct related coronary artery was already patent in three. When these two groups are combined, all 13 patients without reperfusion showed no significant change in summated ST segment shift. During percutaneous transluminal angioplasty inflation of the balloon in the vessel that was previously occluded simulated reocclusion and was followed by new ST elevation if the artery supplied viable myocardium. In a further consecutive study of 54 patients with anterior myocardial infarction, the precordial R waves and Q waves were studied over the four to six months following infarction using a standardised 48 electrode mapping system. All patients underwent a repeat angiogram after four to six months. In 36 patients the infarct related vessel was patent. They showed a significant mean increase in summated precordial R wave amplitude and a reduction in the mean number of precordial leads without R waves. In 18 patients with unsuccessful thrombolysis or reocclusion there was a further reduction in mean summated R wave amplitude and an increased number of precordial leads not showing R waves. Precordial R wave mapping seems to be a valuable non-invasive method of assessing the salvage of myocardium after reperfusion and the damage caused by reocclusion. Loss of R waves in the acute phase of myocardial infarction does not necessarily mean an irreversibly damaged myocardium.

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.

Hemodynamic effects of prenalterol in patients with ischemic heart disease and congestive cardiomyopathy.

SUMMARY The hemodynamic effects of a new,β agonist, prenalterol, were studied in 13 patients with severe left ventricular failure (New York Heart Association functional class III or IV). Seven patients had ischemic heart disease and six congestive cardiomyopathy. Left ventricular function was studied by catheter‐ tip manometer measurements of left ventricular pressure and simultaneous pressure‐volume analysis. To minimize rate‐related changes in left ventricular function, studies were performed during constant atrial pacing at 100 beats/min unless the intrinsic heart rate was higher. A 12‐mg i.v. dose of prenalterol was infused. The maximum rate of pressure development (peak positive dP/dt) increased from 1084 + 95 mm Hg/sec (mean + SEM) to 1493 ± 176 mm Hg/sec (p < 0.005). Stroke volume and ejection fraction also increased. Left ventricular relaxation, measured as the maximum rate of pressure fall (peak negative dP/dt) improved from −1011 ± 91 to −1202 ± 119 mm Hg/sec. Alteration in the time constant of pressure fall (T) also suggested improved relaxation, as it decreased from 71.8 ± 7.7 to 48.5 ± 6.3 msec. Prenalterol also decreased left ventricular stiffness, particularly in patients with very stiff ventricles. As a positive inotropic agent, prenalterol increased left ventricular mean power from 5.2 ± 0.4 to 6.8 ± 0.7 Wand left ventricular stroke work from 8.3 + 0.7 to 10.2 ± 1.0 W‐sec (p < 0.005). Left ventricular stress did not change significantly. The ratio of the diastolic pressure‐time index to the systolic pressure‐time index increased significantly (0.53 ± 0.04 and 0.63 ± 0.04, respectively, p < 0.005). Despite different absolute values, the percent changes of left ventricular function were similar in both groups. We conclude that even in patients with severe left ventricular failure, ventricular systolic and diastolic function can be improved by prenalterol. As a result of improved contractility, relaxation and stiffness, left ventricular filling pressure decreased. The data indicate a favorable effect on the balance between myocardial oxygen supply and demand. Intravenous prenalterol is a promising new drug for patients with severe heart failure.

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.

Morphometric investigations in mitral stenosis using two dimensional echocardiography.

A method is proposed for comparing the orifice size and the morphology of stenotic mitral valves, removed intact at the time of replacement, with the preoperative two dimensional echocardiographic cross-sections. The excised mitral valve apparatus is suspended on a specially constructed mounting. To avoid shrinkage the orifice is stabilised with an airfilled balloon. A radiography is taken directing the x-ray beam perpendicular to the valve orifice. In 40 of 51 patients this method provided the means of relating the echocardiographic cross-sections to the morphology of the valve. Planimetry of the valve area compared favourably with the postoperatively determined orifice size. Agreement was found in 34 of 40 patients in orifice shape between preoperative echocardiograms and x-rays of th excised valve. The relation between intraoperative estimation of size of the valve, using dilators with known diameters, and the postoperative results was less favourable. Areas of calcification were identified on echocardiography as dense conglomerate echoes. In 30 patients (75%) the localisation of calcium deposits and in 67% the degree of calcification was in agreement with the x-rays of the valve taken after operation. In addition to determination of the area, two dimensional echocardiography allows detailed studies of the stenotic valves, and is of particular importance for planning operative treatment.

Left ventricular ejection power in coronary artery disease during atrial pacing.

Peak and mean left ventricular ejection power were measured during atrial pacing in 6 normal subjects (group I), 6 patients with coronary artery disease without myocardial infarction (group IIa), and 10 patients with coronary artery disease after myocardial infarction (group IIb). Pacing rates were 80 and 120/min. Power was determined by computer analysis of pressure, volume, and time. Data were normalised by end-diastolic volume and left ventricular muscle mass. Peak left ventricular ejection power normalised by end-diastolic volume values at a pacing rate of 120 min were significantly lower in group IIa and IIb than in normal subjects. Mean muscle mass in normal subjects was 179 g and in group IIa 216 g (P smaller than 0.05). Peak power normalised by muscle mass in normal subjects tended to increase at 120/min whereas in group IIa it declined by 26 per cent (P less than 0.001). These data indicate that the energy output of the left ventricle at rest may be the same in patients with significant coronary artery disease as in normal subjects. Increasing the heart rate from 80 to 120/min in a normal myocardium augments power but in coronary artery disease it remains static or falls.