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In view of today's efforts to preserve myocardial function in acute myocardial infarction, the prevalence and extent of persistent right ventricular dysfunction was analysed in a prospective study of 127 patients admitted with a first myocardial infarction without thrombolysis. Right ventricular ejection fraction measured at hospital discharge by radionuclide angiocardiography was related to the location of infarction as judged electrocardiographically, its size as estimated enzymatically, and by the simultaneously measured left ventricular ejection fraction. Two opposite patterns of right and left ventricular function were observed in relation to the location of infarction: the right ventricular ejection fraction was significantly depressed in inferior, but not in anterior, infarction and the reverse was true for left ventricular ejection fraction (P less than 0.001 between infarct locations for both right ventricular ejection fraction and left ventricular ejection fraction). There were significant correlations between peak levels of creatine kinase and left ventricular ejection fraction for anterior (r = 0.76, P less than 0.001) and inferior (r = 0.57, P less than 0.001) infarction, while peak levels of creatine kinase and right ventricular ejection fraction correlated only in inferior infarction (r = 0.45, P less than 0.01). There was no overall correlation for left ventricular ejection fraction and right ventricular ejection fraction (r = 0.28, P NS), despite the fact that right ventricular ejection fraction was lower in patients with severely reduced left ventricular ejection fraction than in those with normal left ventricular function (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

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MDL 19205 4-ethyl-1-,3-dihydro-5-(4-pyridinylcarbonyl)-2H-imidazol-2-one, a new cardioactive agent, has been shown to increase myocardial contractile force in animals. It is effective by both oral and intravenous routes. We studied 11 patients with congestive heart failure--in 10 cases owing to coronary artery disease, and in one to cardiomyopathy. All patients had symptoms of NYHA class II or III, left ventricular ejection fractions (LVEF) less than 55%, and left ventricular end-diastolic pressures (LVEDP) greater than 15 mm Hg. Following routine coronary angiography and ventriculography, 0.5 mg/kg MDL 19205 was administered intravenously over 5 min to six patients. Thirty minutes after injection, hemodynamic measurements and ventriculography were repeated. Mean LVEF increased from 42 to 49% (p less than 0.05 for baseline vs. 30 min). In five patients ventriculography was repeated 60 min after placebo administration: LVEF decreased from 45 to 40%. LVEDP decreased from 29 +/- 8 to 16 +/- 8 mm Hg after MDL 19205 administration (p less than 0.05) and remained constant at 24 mm Hg in the placebo group. The small although nonsignificant increase of LVdP/dt after MDL 19205 administration (10 +/- 33%), together with a considerable decrease in LVEDP, was consistent with a positive inotropic effect. LVdP/dt/total pressure developed (VPM), a measure of contractility relatively independent of changes in pre- and afterload, increased from 1.0 +/- 0.3 to 1.3 +/- 0.3 s-1 (p less than 0.05). Neither parameter of contractility (LVdP/dt and VPM) changed significantly in the placebo group.(ABSTRACT TRUNCATED AT 250 WORDS)

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To assess the prognostic significance of right ventricular dysfunction after a first myocardial infarction for complex ventricular arrhythmias and or sudden cardiac death in relation to infarct location, size and left ventricular function, a series of 127 consecutive patients was prospectively studied and followed up for one year. Prior to hospital discharge, a 24-hour electrocardiographic recording and radionuclide angiocardiography were performed. Right ventricular ejection fraction was related to inferior infarct location and size (r = 0.45, P less than 0.01): similarly left ventricular ejection fraction was related to anterior infarct location and size (r = 0.76, P less than 0.001). The incidence of severe ventricular arrhythmias was significantly higher in patients with isolated right or left ventricular dysfunction compared to patients with normal function; it was highest in patients with severe depression of both ventricles. Patients with complex ventricular arrhythmia and/or sudden cardiac death had significantly reduced left and right ventricular ejection fractions. Detailed analysis in patients with left ventricular ejection fraction greater than 0.40 vs. less than or equal to 0.40 showed that presence of complex ventricular ectopic activity and/or sudden cardiac death after myocardial infarction was related not only to left, but also independently to right ventricular dysfunction. These results imply a significant prognostic contribution of right ventricular dysfunction to the occurrence of severe ventricular arrhythmias and/or sudden cardiac death after myocardial infarction independent of and additive to left ventricular dysfunction.

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In a prospective series of 190 patients under the age of 70 with a first myocardial infarction, the risk profile for ischemia, heart function and arrhythmias was investigated at the time of hospital discharge. Fifteen of these 190 patients had had ventricular fibrillation within 24 hours after admission which could be converted into sinus rhythm. In comparison, patients with ventricular fibrillation had a significantly larger infarct as estimated with the thallium-defect score (11.0 +/- 5.8 vs. 7.3 +/- 5.4; p less than 0.02)). In addition, left ventricular ejection fraction at rest was lower, at 42.7 +/- 17.4% compared to 50.0 +/- 14.0, but the p-value reached only 0.07. Persistent arrhythmias and ischemia were not significantly different in the two groups. In the first year after infarction none of these 15 patients died, compared to 8/175 patients.

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In a prospective study, the relationship between extent and location of myocardial infarction and the resulting left ventricular dysfunction was assessed and the question asked, how well these parameters may be assessed non-invasively a few weeks after the acute event. One hundred and fifty survivors of a first myocardial infarction were studied in the acute stage by serial ECG and CPK recordings and 5 weeks later by thallium201-(Tl)-scintigraphy and radionuclide angiocardiography. Myocardial damage was assessed enzymatically (maximal CPK; CPKmax) in the acute phase and scintigraphically in the subacute phase using a Tl-score considering extent (in percent of total myocardium in each projection) and severity (decrease in thallium-uptake) of scintigraphic infarct defects. There were significant correlations between Tl-score and max. CPK (r = .69) as well as between Tl-score and left ventricular ejection fraction (LVEF) (r = .65; p less than .001 each), but this correlation was better for subgroups with anterior vs. inferior infarctions (r = -.68 vs. r = -.59; p less than or equal to .001 for each). Furthermore, LVEF could be predicted based on the Tl-score: 88% of patients with values less than 7 had an LVEF of greater than 45%, whereas 77% of patients with a thallium-score of more than 12 had an LVEF less than 45%. Reproducibility of the Tl-score assessed in 30 patients over 3 months was excellent (r = .96) with low variability between the two analyses (+/- 1.5). Thus, after a first myocardial infarction, a direct relationship between enzymatically and scintigraphically, assessed infarct size and LVEF could be demonstrated.(ABSTRACT TRUNCATED AT 250 WORDS)

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Incidence and course of complex ventricular ectopic activity (VEA) after myocardial infarction was prospectively evaluated in 217 patients in relation to infarct size, location, ventricular function and signs of persistent ischemia. Complex VEA (Lown greater than III) was found acutely in 138 patients (63.6%) and at hospital discharge in 42 (19.3%). Of 79 patients with VEA Lown less than or equal to III in the first 24 hours, 93.7% remained VEA-free at follow-up. Patients with persistent complex VEA differed from those who became VEA-free only in left and right ventricular ejection fraction, whereas all the other infarct related factors had no influence on the course of VEA.

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A series of 63 patients were studied by gated radionuclide angiocardiography 51/2 weeks after their first acute myocardial infarction. Left (LVEF) and right (RVEF) ventricular ejection fraction were assessed in three groups of patients: 12 patients with transmural anterior infarctions, 35 patients with transmural inferior infarctions and 16 patients with non-transmural infarctions. LVEF was depressed only in the group of patients with anterior infarctions (34.4 +/- 16.3%) but remained within normal limits in the other two groups. RVEF was reduced in 64% of patients with inferior infarctions; the mean value in this group was 36.3 +/- 10.2% (normal range 48 +/- 8%, p less than 0.02). In the other two groups RVEF was only rarely reduced and the mean values were within normal limits. Regional wall motion abnormalities ( WMA ) were found in 47% of all patients, those localised in the left ventricle matching ECG localisation of necrosis in 86% of cases. Only patients with infarctions of the inferior left ventricular wall were found to have WMA in the right ventricle. Functional signs of ischemia (decrease of RVEF or LVEF during physical exercise) were found in 34% of patients with transmural infarctions and 57% of patients with non-transmural infarctions. Radionuclide angiocardiography showed itself a valuable method for assessing persistent dysfunction after acute myocardial infarction not only of the left but also of the right ventricle, a phenomenon not easily detected clinically.

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Reliability of a computer-assisted system for determination of left ventricular volumes was judged by multiple measurements of rotation ellipsoids, cadaver hearts, and cineangiograms from patients. The volume measurements in cadaver hearts provided a volume correction factor necessary for reproducible results. Variation coefficient for intraobserver and interobserver variability did not exceed 2.3% when calculated using rotation ellipsoids and was highest at 12.0% for the end-systolic volumes derived from patient films. When appropriate calibration methods are employed, different observers can make reliable left ventricular volume measurements aided by such systems.

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To assess the incidence of silent ischemia after myocardial infarction, a prospective series of 100 consecutive patients was studied 5 weeks after the acute event. Objective evaluation of myocardial ischemia included a 9-lead ECG, thallium-201 scintigraphy and radionuclide ventriculography, each at rest and during symptom-limited bicycle ergometry. Diagnostic criteria were ECG: greater than or equal to 1 mm horizontal or downsloping ST depression or greater than or equal to 1 mm ST elevation; thallium scintigraphy: a clearly reversible perfusion defect at rest, detectable only after exercise; radionuclide ventriculography: an exercise-induced decrease in global LVEF greater than or equal to 5% and/or in anyone regional EF greater than or equal to 14%. Presence of ischemia was assumed if at least 2 of 3 objective ischemic signs were found. This was the case in 28 of 100 patients. During exercise, 15 of 100 patients complained of chest pain, but only 8 (54%) had objective evidence of ischemia. Thus, silent ischemia was demonstrated in 20 of 100 patients. The sensitivity of both nuclear cardiology procedures was markedly superior to that of the ECG in diagnosing post-myocardial ischemia.

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To assess the accuracy of serial myocardial perfusion scintigraphy with thallium-201 (201Tl) to predict graft patency early and late coronary artery bypass surgery, rest and exercise 201Tl and coronary arteriography were performed preoperatively and 2 weeks and 1 year after operation. The scintigraphic results were compared with graft patency, symptoms, left ventricular function and physical work capacity in a consecutive series of 55 patients with a total of 154 grafts. Serial 201Tl had an 80% sensitivity, 88% specificity and 86% overall accuracy in detecting or excluding graft occlusion, which was predicted by reversible ischemia as well as persistent "new scar" segments. Occluded grafts were correctly localized by 201Tl scintigraphy in 61%. Postoperative apical 201Tl defects were frequent (two-thirds of cases), and were the result of intraoperative transapical venting of the left ventricle. After coronary bypass graft surgery, ejection fraction at rest was unchanged. Left ventricular end-diastolic pressure and physical work capacity improved significantly. In the presence of new perfusion defects detected postoperatively, physical work capacity was reduced significantly. New 201Tl defects in addition to typical or atypical angina provided a high probability of graft occlusion, while in the absence of new 201Tl defects all grafts were patent in more than 90% of patients, all of whom had no or only atypical chest pain. We conclude that serial 201Tl imaging after coronary artery bypass surgery is an accurate noninvasive method that can be used routinely to assess graft function, to localize spatially occluded grafts and to identify patients with a high likelihood of graft occlusion who may need invasive studies.

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The influence of aging and pre- and post-mortem conditions on the activities of glycolytic enzymes and of the ATPases was determined in samples of autoptic human cerebral cortex and putamen. These results were compared with results obtained from an aging collective of rats (four groups ranging from 20 to 120 weeks of age). The results revealed an interlinked significant age-related increase in soluble hexokinase (HK) and a significant decrease in phosphofructokinase (PFK) activity in human autoptic tissue, whereas no significant age-dependent differences could be observed in rat brain. Subdivision of the cases according to duration of agony and other pre-mortem conditions revealed reduced variance and therefore statistically more significant PFK age-dependence in cases with a short agony. All other cases are not dependent on age. In addition to the pre- and post-mortem effects, the age-dependence of PFK and soluble HK can be clearly demonstrated in human autoptic brain tissue.

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The results of the present experiments show that capillary blood flow in the cerebral cortex fluctuates, whether the cat's head is supplied by the animal's intact circulation or by an artificial circulation system. These variations in blood flow last about 5 to 15 min and range from about 10% below to 10% above the mean. When the perfusion pressure is gradually reduced from 140 mmHg to 60 mmHg, the cortical microflow and the electrical activity of the brain remain almost constant. However, a reduction in perfusion pressure of this magnitude causes a 75% fall in total blood flow through the isolated head.

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A model consisting of a cat head perfused in isolation with the animal's own blood is described. The use of endogenous blood allows the organ to function under physiological conditions for several hours. The blood is taken from the abdominal aorta of the anaesthetized animal and passed to the carotid arteries via an extracorporeal circulation system. The perfusion pressure can be varied at will and is regulated electronically. The volume of blood in the extracorporeal circulation system is only 6 ml. The tests performed on this model were designed to study the behaviour of the cortical EEG and the cortical micro flow. Neither of these parameters underwent any change after institution of the artificial perfusion, and the blood gases also remained fairly stable. The model is suitable for studying both physiological and pharmacological problems.

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Cardiac glycosides which inhibit Na/K-ATPase (ouabain, scilliroside, scillirosidin) as well as heparin and histamine were infused into a cannulated branch of the middle cerebral artery or by isolated head perfusion in cats and dogs. Ouabain permeating the blood-brain barrier (BBB) caused the same selective swelling of astrocytes and of certain presynaptic elements as after direct application to the brain tissue. The other cellular elements of brain tissue and the vascular endothelium did not react, although the latter was exposed to the highest drug concentrations (about 10-3 M ouabain). By the swelling about one third of the capillaries became more or less constricted accompanied by an increase in endothelial vesiculation and in the number of osmiophilic inclusions in all cells of the vascular wall and of the pericapillary tissue. Osmiophilic material resembling plasma proteins occured in widened intercellular clefts indicating an increased BBB permeability after survival times (40 min). In contrast to the capillaries some terminal vessels are dilated which may correspond to shunt vessels causing an inhomogeneous, even increased cerebral blood flow after ouabain. Scilliroside and scillirosidin cause essentially the same changes as ouabain, but of smaller intensity and extent. In the present study, neither histamine nor heparin caused any structural change of the vessels or brain tissue.

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