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Volume manipulations in 27 patients (volume loading n = 22; phlebotomy n = 5) with acute myocardial infarction (AMI) and 7 normal subjects has been performed in order to evaluate left ventricular performance in terms of cardiac index (CI) and pulmonary artery enddiastolic pressure (EDPAP). An EDPAP in the range of 18-22 mm Hg was in general associated with maximal cardiac output. In patients with AMI maximal cardiac performance was significantly lower compared to normal subjects (p less than 0.01). Volume loading that increased the EDPAP beyond the level of 18-22 mm Hg usually deteriorated cardiac performance in AMI. A phlebotomy in 5 subjects with severe pulmonary congestion decreased EDPAP significantly from 32 to 24 mm Hg (p less than 0.1) without a change of cardiac index (2.2 - 2.5 1/min/m2;NS). In 11 patients left ventricular performance was assessed during the acute and convalescent period. 4-6 weeks after AMI resting EDPAP decreased from initially 16 to 11 mm Hg (p less than 0.02), whereas cardiac index did not change significantly (3.1-3.3. 1/min/m2;NS) and even did not rise markedly after volume loading (3.3-3.4 1/min/m2;NS). By plotting the relative change of cardiac index after volume loading against the individual infarct size (n = 16), left ventricular hemodynamic reserve was assessed and revealed a significant depression compared to normal subjects (n = 7). A rough reverse relationship (r = -0.69) between left ventricular hemodynamic reserve and infarct size was observed.

The results of biphasic 201thallium (201Tl) scanning were compared with those of coronary arteriography, left ventricular angiogarphy and stress ECG in 56 patients with coronary artery disease and six with no evidence of heart disease. There were 104 201Tl defects, 50 of them reversible. The defects were always located in the area supplied by a critically stenotic coronary artery. Correlation of regional wall motion with 201Tl activity demonstrated that in all forms of abnormal wall motion there was either ischaemia or fibrosis. The resting LV angiogram thus does not make it possible to distinguish between myocardial ischaemia and fibrosis. Taking the LV angiogram as a standard, the rate of false-positive 201Tl scintigrams was 5%, that of false-negative ones 23%. The biphasic 201Tl scintigram was more sensitive than the stress ECG in detecting myocardial ischaemia. It furthermore made it possible to localize the ischaemic (or fibrotic) region within the LV and to estimate its size.

Idiopathic Mitral Valve Prolapse has been regarded by some authors as a primary cardiomyopathy. To determine, if left ventricular hemodynamics at rest and during exercise are impaired, 20 young symptomatic patients with idiopathic mitral valve prolapse, proven by echo- and phonocardiography, without coronary artery disease or severe mitral regurgitation, underwent supine bicycle exercise stress testing. Pulmonary artery pressure, central venous oxygen saturation and cardiac index as well as heart rate were measured with a Swan-Ganz thermodilution catheter and the results compared with those of 10 voluntary normal subjects. Variance analysis showed no significant differences in global left ventricular hemodynamics between patients with idiopathic mitral valve prolapse and normal subjects at rest as well as during exercise. In addition no significant differences were found between patients with echocardiographical holosystolic or mesosystolic mitral valve prolapse. In patients with idiopathic mitral valve prolapse, global left ventricular hemodynamics are not impaired neither at rest nor during exercise.

The reocclusion rate of infarct vessels following lysis amounted to 61/80 (24%) with a peak during the first week following the acute event. According to Harrison there is a strong correlation between the probability of reocclusion and the diameter of the residual stenosis, while the reocclusion rate is independent from the anti-coagulative regimen. In the presence of preserved myocardial function and significant residual stenoses as well as in patients with multi vessel disease additional PTCA or early bypass surgery seems to be indicated, in order to prevent re-infarction. 55 out of 180 patients following intracoronary lysis, 6 out of 30 following systemic lysis and 2 out of 10 following lysis with TPA were operated upon within one week following the acute event. Hospital mortality was 3.1% (2/63) and late mortality was 1.6% (1/61). Out of 123 bypass grafts 105 (86%) were found to be patent at reangiography. The risk of bleeding was studied in 24 patients who were operated upon within 24 hours following the acute event. Although the clotting factors, especially the serum fibrinogen, had decreased below normal values, there was no increased postoperative blood loss. The coagulation factors had risen to normal values within 24 hours.

In 48 patients with acute myocardial infarction (AMI) the acutely thrombus-occluded coronary artery was successfully recanalized nonsurgically via catheter with intracoronary streptokinase (SK) infusion after a mean occlusion time of 3.1 +/- 1.6 hours. In all cases residual high-grade fixed atherosclerotic stenosis remained after percutaneous transluminal coronary recanalization (PTCR). Subsequent aortocoronary bypass surgery (ACBS) circumventing the stenotic coronary artery was performed during the acute stage of myocardial infarction (within 10 days of AMI onset) in 34 patients and electively (longer than 10 days after AMI onset) in 14 patients. No patient died from early PTCR or from ACBS intervention. There were two late post-ACBS arrhythmogenic deaths, two patients suffered nonfatal reinfarction post ACBS several months after hospital discharge, only two had occasional post-ACBS angina pectoris, and one patient had post-ACBS mild heart failure. The remaining 41 post-ACBS patients were completely asymptomatic throughout long-term follow-up evaluation. In the left ventricular (LV) segment supplied by the initially occluded coronary artery, which was recanalized early by means of SK therapy and subsequently grafted, wall motion improved significantly from the acute to the postoperative stage in patients who underwent early surgery (from 13.6% +/- 1.9% to 40.3% +/- 2.7%, p less than 0.001) and in the electively operated group (from 18.0% +/- 7.1% to 48.2% +/- 6.3%, p less than 0.001). Ischemic wall motion was improved irrespective of whether or not the bypass graft circumventing the residual stenosis of the infarct vessel remained patent. Wall motion of nonischemic segments remained essentially unchanged. In the patients who underwent surgery in the early stage, the closure rate of the bypass graft to the infarct-related vessel was 17%, and in the electively operated group no graft was found to be occluded. In conclusion, coronary artery recanalization, achieved by means of early SK-PTCR therapy with subsequent ACBS, can be performed safely in patients with AMI, and the result will be marked improvement in LV segmental wall motion and global function, diminished reinfarction rate, and reduced incidence of angina pectoris, all benefits that are consistently maintained during long-term evaluation.

The duration of intracoronary lysis is of importance for the success as well as for the side effects of the treatment. The shorter the duration of lysis needed the quicker re-perfusion occurs, thereby increasing the survival changes of the myocardium and minimizing the effect on the blood coagulation due to the accompanying systemic lysis, i.e., the risk of bleeding is reduced. We found the mean duration of lysis to be 29 ± 15 min (mean ± SD).

Since February of 1980, 157 patients who had had symptoms of acute myocardial infarction for less than 3 hours underwent intracoronary lysis. Forty-six patients required early aorta-coronary revascularization. However, operation was believed to be indicated only when intracoronary lysis was successful and myocardium was salvaged. Since left ventricular angiography proved unreliable in assessing the viability of the myocardium in the acute stage, starting in March of 1981 we obtained intracoronary thallium 201 scintiscans in 23 patients before and after intracoronary lysis. Patients in whom there was a significant reduction (greater than 50%) in the initial 201Th defect (n = 12) were considered ideal candidates for operation (Group 3). Patients with poor or unimproved 201Th uptake after successful intracoronary lysis (n = 6) were treated medically (Group 2), as were patients in whom intracoronary lysis was unsuccessful (n = 5, Group 1). In order to validate this new approach, we compared the change in the regional wall motion of the "infarcted area," as shown in the early and follow-up left ventricular angiograms in all three groups. In the acute stage, the mean regional ejection fraction was 19.9% in Group 1, 19.1% in Group 2, and 20.1% in Group 3. Only in Group 3 was there a significant increase in regional ejection fraction to a mean of 51%. The mean ejection fraction obtained at follow-up in Groups 1 and 2 was 16.5% and 17.3%, respectively. From our findings, we conclude that 201Th scintigraphy is a valuable predictor of the salvageability of myocardium immediately following intracoronary lysis. To date, it has been the most valuable tool in assessing those patients suitable for early coronary revascularization.

Der gunstige Effekt einer Beta-Rezeptorenblockade bei der Behandlung der Angina pectoris ist wiederholt dokumentiert [2, 4, 5], auch die Anwendung nach akutem Myokardinfarkt soll nach einer kontrollierten britischen Langzeitstudie positiven Einflus auf Morbiditat und Mortalitat besitzen [11].

Bei 48 Patienten (Pat.) mit akutem Herzinfarkt wurde die verschlossene Koronararterie rekanalisiert und die arteriosklerotische Reststenose bei 34 Pat. akut, bei 14 Pat. elektiv mit einem aorten-koronaren Venenbypass uberbruckt. Kein Pat. verstarb akut, 2 nach Entlassung, 2 erlitten einen Reinfarkt, 2 hatten leichte Angina pectoris. Die ubrigen 42 Pat. waren symptomfrei. Die regionale Wandbewegung im Versorgungsgebiet des uberbruckten „Infarktgefases“ besserte sich von 14 ± 2 auf 40 ± 3 % (p < 0.001) postoperativ bei akut operierten Pat. und von 18 ± 7 % auf 48 ± 6 % (p < 0.001) nach elektiver Bypass-Operation (ACB). Die Zunahme der Wandbewegung war unabhangig davon, ob der Bypass auf das „Infarktgefas“ offen war oder nicht. Die Verschlusrate der Bypass-Venen auf das „Infarktgefas“ betrug bei akut operierten Patienten 17%, nach elektiver ACB war keine Bypass-Vene verschlossen.

A significant arteriosclerotic stenosis remains after successful coronary artery recanalization, implying the risk of reinfarction [2]. Aortocoronary bypass surgery (ACBS) following recanalization is meant to prevent reinfarction and to provide adequate myocardial perfusion. To evaluate the feasibility of such an approach and to determine its efficacy in terms of mortality, morbidity, and ventricular function, we have reviewed our experience with early and elective bypass surgery following successful recanalization.

Zur Beurteilung des funktionellen Verhaltens des LV nach Kunstklappenersatz wurden die Echokardiogramme von Patienten mit Ao.-Insuff. (n = 12) und Mitralstenose (n = 23) vor u. nach einer Kunstklappenimplantation registriert und einer computerisierten Auswertung unterzogen. Post operativ wurde bei den Patienten mit Ao.-Insuff. eine Abnahme des enddiastol. LV-Querdurchmessers von 70 ± 6 auf 53 ±10 mm (p < 0,001) registriert. Die max. Faserverkurzungsgeschwindigkeit sank (VcFmax.) von 1,85 ± 0,6 auf 1,3 ± 0,6 circ/s. (p < 0,01). Die Geschwindigkeit der maximalen fruhdiastol. Durchmesserzunahme nahm von 4,2 ± 0,6 auf 3,1 ± 0,5 sec-1 (p < 0,05) als Ausdruck einer fehlenden Aortenregurgitation ab. Nach Mitralkunstklappenersatz war sowohl eine Zunahme von VpFm als auch der fruhdiast. Durchmesserzunahme (2,8 ± 3 → 3,6 ± 0,2 circ/s; (p

In 20 patients with idiopathic hypertrophic obstructive and nonobstructive cardiomyopathy (IHSS), biphasic Thallium-201 myocardial scintigraphy was performed. Regional myocardial Thallium-201 kinetics of these patients were analysed by a semiquantitative computerized method and compared with those of 6 normal subjects. In 12 of 18 with IHSS and no coronary artery disease 26 regions of interest with irreversible and 6 regions of interest with reversible Thallium-201 defects could be detected. Most of the Thallium-201 defects were localized in the interventricular septum. The defects were not related to the age of the patients and there was no relationship between the occurrence of reversible Thallium-201 defects and pathological myocardial lactate extraction rate during maximal atrial pacing measured in 14 patients. The percentage (6.8%) of irreversible defect regions in patients with LV outflow obstruction at rest (n = 13) was more than twice higher compared to those (n = 5, 3.2%) without LV outflow obstruction or no provocative pressure gradient, resp. These data suggest that IHSS is often associated with regional ischemic myocardial fibrosis despite normal coronary arteries. Therefore in these patients Thallium scintigraphy cannot be used as a noninvasive screening method to exclude or prove coronary artery disease.

Lidocain hat sich als Antiarrhythmikum in der Behandlung von ventrikularen Arrhythmien beim frischen Myokardinfarkt bewahrt [4]. Da es jedoch nur in parenteraler Form wirksam ist [18], ist es der Akutbehandlung von Herzrhythmusstorungen vorbehalten. In den letzten 10 Jahren sind mehrere orale Derivate des Lidocain synthetisiert worden, von denen die meisten jedoch keine ausreichende Wirkung zeigten.

Though it is proven that in the majority of patients with acute myocardial infarction due to complete thrombotic occlusion recanalization can be achieved by selective intracoronary infusion of streptokinase [1, 2], little is known with respect to reduction of mortality and possible late complications. With this goal in mind data on 204 patients pooled by four cardiological centers in West Germany have been evaluated.

Patients who have had acute myocardial infarction or are suffering from unstable angina are candidates for emergency coronary artery surgery. These patients run a high risk of postoperative myocardial insufficiency due to an extremely reduced ischemic tolerance of the myocardium, which is critically impaired even before the revascularization. The perioperative management and especially the intraoperative myocardial preservation of these patients should therefore prevent any additional loss of myocardial function or structure. Our method of myocardial preservation combines hypothermic cardioplegic arrest with maintenance of an oxidative myocardial metabolism. This is done by either intermittent or — if technically feasible — continous cardioplegic coronary perfusions and allows all distal and central vein anastomoses to be performed during a single period of cardiac arrest [1, 2].

Recent echocardiography and angiographic studies have shown that hypertrophic obstructive cardiomyopathy (HOCM) is often associated with abnormal left ventricular (LV) relaxation and an abnormal diastolic filling pattern [1–3]. It was the purpose of this study to examine whether these abnormalities are only typical for this special type of LV hypertrophy or whether they can be found in other forms of LV hypertrophy as well [4].

In a 45-year-old female patient with Prinzmetal angina pectoris coronary angiograms and a 201thallium scintigram were performed during an ergotamine-induced episode of angina. The spontaneous and the ergotamine-induced attacks were characterized by transient ST elevation in the posterior wall ECG leads. The coronary angiogram during the attack showed spasm of the circumflex branch of the left coronary artery. In the 201thallium scintigram a large defect in myocardial thallium uptake was noticed in the posterior wall of the left ventricle. Angina and ECG abnormalities disappeared within 4 minutes. However, the scintigraphic defect disappeared only after 6 hours. The slow recovery of myocardial thallium uptake is thought to represent an alteration of the myocardium after a brief 4 minute interruption of regional coronary arterial blood flow. The diagnostic approach in patients with Prinzmetal angina is discussed.

In einer retrospektiven Studie uber 340 Patienten wurden fur den Zeitraum 1976–1986 die Ergebnisse von systemischen und lokalen Lysen analysiert. Dabei kamen 136 Patienten mit Langzeitlysen bei gesicherter tiefer Beinvenenthrombose zur Auswertung, die zwischen 2 und 32 Tage mit 60000–80000 IE Urokinase (UK)/h behandelt wurden. Auserdem wurden bei einem kardiologischen Krankengut von 204 Patienten aus den Jahren 1981–1986 die Ergebnisse von Kurzzeitlysen mittels lokaler intrakoronarer (ic.) verglichen mit systemischer Applikation. Hierbei wurde unterschieden zwischen 89 Patienten, die einen ic. Streptokina- sebolus von 250000 IE (SK) erhielten; 88 Patienten, die einen Urokinasebolus von 2 Mio.IE (UK) erhielten; und 27 Patienten, die i.v. rtp-A 60 mg in 90 min erhielten. In allen anderen Vergleichsparametern waren diese drei Gruppen statistisch nicht signifikant verschieden.

Obwohl der idiopathische Mitralsegel-Prolaps (MSP) sich als die haufigste Klappenanomalie erwiesen hat, existieren bis heute in der Literatur keine Mitteilungen zur Hamodynamik unter Belastungsbedingungen.

In one of his editorials, Perloff suggested that the history of mitral valve prolapse could be divided into three phases: the “pericardial” phase, the “leaflet-chordial” phase and the “myocardial” phase [1]. The “pericardial” phase began in 1913, when Gallavardin described the variable effects of posture on the timing of the mid-systolic click and late-systolic murmur [2]. He related these auscultatory findings to pericardial adhesions. In 1961 Reid introduced the “leaflet-chordal” phase, when he proposed that the mid-systolic click was caused by the mitral valve [3]. In 1963, Barlow and Pocock demonstrated that mitral valve prolapse was the origin of the acoustic phenomena [4]. The “myocardial” phase began in the late sixties, when contraction abnormalities of the inferior left ventricular wall were observed in patients with mitral valve prolapse. Currently, a variety of exaggerated or depressed segmental contraction patterns are described [5, 6]. In this paper, some aspects that are related to, both, the “leaflet-chordal” and the “myocardial” phase are presented [7, 8].

Acute infarct size was estimated from serial determinations of creatine-kinase (CK) activity. In 15 patients the infarct size was obtained post-mortem, using nitro-blue-tetrazolium stain. There was good correlation between the two measurements (r = 0.98). The relationship between the calculated infarct size and haemodynamic values was obtained in 50 patients (end-diastolic pulmonary arterial pressure [PAEDP], cardiac output, stroke volume, stroke volume/filling pressure of left ventricle [SVI/PAEDP]). On average there was a tendency towards impaired left ventricular haemodynamics with increasing infarct size. Among the survivors the infarct size (51 g) was significantly less (P less than 0.05) than that of those who had died (83 g). PAEDP at 24 mm Hg was significantly higher in those who died than in the survivors (17 mm Hg), cardiac index was 2.95 l/min-m2 in the survivors compared with 2.14 l/min-m2, while SVI/PAEDP was 2.4 ml/m2-mm Hg in the former and 0.9 ml/m2-mm Hg in the latter. However, in individual cases the infarct size sometimes did not correlate with haemodynamic values. Taking into account infarct size and haemodynamics, four classes could be distinguished: (a) infarct size less than 65 g with good haemodynamics (PAEDP less than 18 mm Hg, normal cardiac index); (b) infarct size greater than 65 g with PAEDP greater than 18 mm Hg and markedly reduced cardiac index). Only 10% of those a to c had previously had infarcts, compared with 60% of those in class d (infarct less than 65 g, PAEDP above 18 mm Hg). Small infarcts with markedly impaired haemodynamics thus indicate that there has been previous damage to remaining myocardium.

In addition to digitalis and diuretics, 10 patients with chronic cardiac failure were treated with prazosin (15 mg/d) over a period of 6 months. It was shown that the mean pulmonary artery pressure decreased significantly, on average by 30%, during both rest and exercise. Despite significant decrease of arterio-central venous oxygen difference no improvement of cardiac output was measured after 6 months on prazosin. Cardiac output increased clearly in only 4 patients, particularly during exercise. Heart rate and arterial blood pressure remained statistically unchanged. Eight patients reported subjective improvement of dyspnoea after 6 months. Prazosin plasma levels were between 9.4 and 58.6 ng/ml. Side effects such as orthostatic hypotension, urinary incontinence and disturbances of potency occurred in 4 patients. Antinuclear factors could not be demonstrated after 6 months. These data show that after 6 months of prazosin therapy haemodynamically significant improvement of pulmonary congestion can be demonstrated without concurrent increase of cardiac output. Prazosin is indicated in treatment of chronic cardiac insufficiency with predominant pulmonary congestion an an adjunct to digitalis and diuretic baseline treatment.

In order to test the hypothesis that delayed mitral valve opening (MO) with regard to endsystolic dimension (t DS-MO) is specific for hypertrophic obstructive cardiomyopathy (HOCM), LV echograms of patients with different forms of LV hypertrophy due to chronic pressure overload (CPO; aortic stenosis + arterial hypertension, n = 24) and hypertrophic obstructive cardiomyopathy (n = 24) were recorded, digitized and compared with those of normals (N :n = 28(. In patients with HOCM (93 +/- 37 ms; p less than 0.0001) and CPO (66 +/- 31 ms; p less than 0.0001) the time t DS-MO was significantly delayed compared with N (13 +/- 15 MS), due to abnormal relaxation. This prolonged relaxation time resulted in an abnormal diameter increase (delta D) during the isovolumic relaxation phase (HOCM: 4.0 +/- 2.2 MM/CPO: 3.0 +/- 1.8 mm; p less than 0.0001/N:0.6 +/- 0.5 mm) and the rapid filling phase (HOCM 7.6 +/- 2.7 mm; p less than 0.0001/CPO 9.2 +/- 2.9 mm; p less than 0.05 / N: 10.7 +/- 2.2 mm). The echocardiographical signs of an abnormal relaxation are not specific for HOCM, they can be seen in different forms of secondary LV hypertrophy and are accompanied by changes in the diastolic filling pattern.

Eine pathologische Fullung des linken Ventrikels wird haufig durch eine Hypertrophie, Infiltration, Fibrose oder Ischamie des linksventrikularen Myokards verursacht. Diese Zustande setzen die Dehnbarkeit des linken Ventrikels herab. Die verminderte Dehnbarkeit behindert das diastolische Einstromen des Blutes und kann infolgedessen zu einer Herzinsuffizienz fuhren.

Reperfusion by intracoronary streptokinase infusion resulted in early and late improvement of ejection fraction and local wall motion in the majority of infarct patients treated by this method [15]. Improvement of function and preservation of R waves were more frequent and more marked than in conventionally treated patients [16]. The relationships between the functional changes and both duration of symptoms prior to hospital admission and the presence or absence of angiographically demonstrable collaterals prior to reperfusion will be analyzed in the present collaborative study.

Die Schwere eines Myokardinfarktes ist im wesentlichen abhangig von der Infarktgrose und der Funktion des verbleibenden Myokards. Die Infarktgrose kann durch CPK-Serienuntersuchungen bestimmt werden [1], die hamodynamische Reserve des nicht infarzierten Myokards last sich unter anderem mittels Volumenbelastung erfassen.