Mediastinal chloroma affecting the right heart with superior vena cava syndrome.
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Biomedical subjects
Publications and source records attributed to H Völler.
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BACKGROUND AND PURPOSE: On the assumption that the majority of lacunes are caused by small-vessel diseases and that pial artery infarcts arise from cardio-embolic or large-vessel diseases, 194 patients from the Berlin Cerebral Ischemia Data Bank with either lacunar or pial artery infarcts were analyzed for the frequency of cardiac sources of embolism. The primary hypothesis was that the frequency of cardiac sources of embolism is higher among pial artery infarct subjects. METHODS: The presence of cardiac sources of embolism was estimated by electrocardiographic and transthoracic and transesophageal echocardiographic studies. Cranial computed tomography scans were evaluated by two masked observers. RESULTS: The overall rate of cardiac sources of embolism did not differ significantly between the lacunar and the pial artery infarct group (66% versus 71%; odds ratio, 0.80; confidence interval, 0.43 to 1.50). Echocardiographic evidence of cardiac thrombi was positively associated with pial artery infarcts (odds ratio, 0.18; confidence interval, 0.04 to 0.80); atrial fibrillation and all other cardiac sources were not. CONCLUSIONS: Left cardiac thrombi are significantly associated with pial artery infarcts. Other presumed cardiac sources of embolism, including atrial fibrillation, may often represent coincidental findings or have a less strong tendency to result in pial artery infarcts.
AIM: To investigate the frequency and prognostic impact of early recurrent ST-segment elevation after initial ST-segment resolution in patients with acute myocardial infarction who had been treated with intravenous thrombolysis. METHODS: Eighty-one patients with acute myocardial infarction underwent 24 h Holter monitoring of the infarct-related ST-segment elevation, at the initiation of thrombolytic therapy. Angiography was performed in 88% of the patients 9 +/- 4 days after infarction. RESULTS: Resolution of the ST-segment elevation during the first 4 h, suggestive of early reperfusion, occurred in 67 (83%) patients (group 1). Of these, 31 (46%) had subsequent re-elevations (group 1a), 26 during the first 4 h, and 20 later. Thirty-six (54%) patients had no recurrence of the ST-segment elevation (group 1b). During follow-up, patients in group 1a experienced more in-hospital reinfarctions (26 versus 6%, P = 0.04) and had a higher rate of occluded infarct-related vessels at angiography than patients in group 1b (40 versus 17%, P = 0.01). CONCLUSION: During the first 24 h after initiation of thrombolytic therapy, recurrences of ST-segment elevation are frequent in myocardial infarction patients with ECG signs of an initially reperfused infarct-related artery. Recurrence of ST-segment elevation indicates a higher risk of reinfarction during hospitalization and of long-term occlusion of the infarct artery.
The way Doppler-derived transmitral filling patterns are changed because of myocardial ischemia is controversial. Furthermore, the influence of the filling pressure has not been investigated sufficiently. To evaluate the relationship between transmitral flow profile and pulmonary capillary wedge pressure (PC), 35 patients with exercise-induced myocardial ischemia were examined. Both Doppler-derived transmitral filling patterns and PC were determined simultaneously at rest and during three stages of supine bicycle exercise. Patients were subdivided into two groups according to the hemodynamic response (group 1 = PC < 20 mm Hg; n = 10, and group 2 = PC > or = 20 mm Hg; n = 25). The correlation between PC and transmitral filling patterns was low at rest for all patients, but improved at maximal workload, particularly for the atrial contribution (r = -0.79), as well as the ratio of maximal and integrated early to late diastolic flow velocities (rE/A = 0.74; rEi/Ai = 0.72). Both groups revealed different flow profiles in regard to the hemodynamic response. While group 1 showed an E/A-ratio < 1, an E/A-ratio > 1 was registered in group 2 (0.9 m/s versus 1.61 m/s; p < 0.001). Exercise-induced myocardial ischemia lead to different Doppler-derived transmitral flow patterns with regard to the filling pressure. The relationship to the pulmonary capillary wedge pressure is so close that an E/A-ratio > 1 is a reliable parameter to predict a filling pressure > 20 mm Hg.
Early fluctuations of the ST-segment elevation indicating intermittent opening and reocclusion of the infarct artery has been well documented by angiographic monitoring in individual acute myocardial infarction patients undergoing thrombolytic therapy. However, the frequency of such episodes has not been studied in a consecutive patient group. Furthermore, it is not known what impact this finding has on the reinfarction risk during hospitalization and on left ventricular healing. The present investigation included 79 patients with acute myocardial infarction (pain < or = 6 h). Continuous Holter monitoring of the infarct-related ST elevation was initiated before or directly after starting thrombolytic therapy. During the 24-h observation period, 34 patients (43%) showed episodes of recurrent ST elevation after an initial resolution (group 1). Among those without episodes, ST elevation resolved within 4 h in 34 (43%, group 2) and persisted > or = 4 h in 11 (14%, group 3). Episodes of re-elevation were more frequent during the first 4 h (0.25 episodes per hour) than in the late part of the observation period (0.04 episodes per hour). Most episodes were transient and short lasting; only nine patients showed persistent re-elevations longer than 60 min. During hospitalization, group 1 patients had a higher incidence of reinfarctions and severe ischemic events than those without episodes (group 1 12/34 (35%) vs. group 2 4/34 (12%) vs. group 3 1/11 (9%), p = 0.03).(ABSTRACT TRUNCATED AT 250 WORDS)
Possible intracardiac sources of emboli were looked for by transoesophageal echocardiography (TOE) in 271 patients (149 men, 122 women; mean age 60 +/- 11 years) a mean of 12 +/- 8 days after suffering an episode of cerebral ischaemia. Left atrial thrombi were revealed in 9 patients: they were more frequent in those with atrial fibrillation (odds ratio [OD] 25.2; P < 0.0001) or known cardiac disease (OD 3.5; P = 0.06). Using the two factors together, the 9 left atrial thrombi could be predicted in 96 patients, while in the remaining 175 patients without cardiac abnormalities no left atrial thrombi were found. Overall, TOE is not an essential investigation additional to transthoracic echocardiography to exclude left atrial thrombi in patients without heart disease who are in sinus rhythm. But in those with atrial fibrillation and/or organic heart disease, TOE can in many instances facilitate the indication for anticoagulation.
Exercise testing is generally accepted for prognostic assessment of patients after infarction, but the prognostic value of transient myocardial ischemia during ambulatory electrocardiographic monitoring remains controversial. Of 281 consecutive postinfarction patients, 173 patients (132 men, 41 women) were prospectively studied with 24-hour Holter monitoring 14 +/- 5 days after acute myocardial infarction, and with submaximal exercise testing after 15 +/- 7 days. Patients with either conduction disturbances or pacemaker rhythm and 71 patients with digitalis medication were excluded. Myocardial ischemia was defined as horizontal or descending ST depressions or transient ST elevations > or = 0.1 mV with or without angina pectoris. The follow-up period was 1 year. Myocardial ischemia was observed in 40 patients (23%) during Holter monitoring, and 96% of the episodes were asymptomatic. Ischemia occurred during exercise testing in 46 patients (27%), two thirds of whom had no symptoms. Ischemia was detected by both methods (group A) in 19 patients (11%), with exercise testing only (group B) in 27 patients (16%), and with Holter monitoring only (group C) in 21 patients (12%). In 106 patients (61%), ischemia could not be ascertained at all. The 4 groups were comparable with regard to sex and age distribution, coronary risk factors, and medication. During follow-up, 50 patients (29%) experienced clinical cardiac events: 6 patients died, 7 had recurrent myocardial infarction, 14 developed unstable angina pectoris and required immediate revascularization, and 23 patients had recurrent but stable angina.(ABSTRACT TRUNCATED AT 250 WORDS)
For four months a 28-year-old man had been suffering from a sensation of pressure in his head when lying down, swelling of the face, exertional dyspnoea and weight gain of 9 kg. Biochemical tests and chest radiograph were unremarkable. Echocardiography revealed a 3 x 5 cm mass in the right atrium, extending into the superior vena cava whose lumen was narrowed to a few millimetres. Computed tomography and magnetic resonance imaging were suggestive of a malignant tumour. Bone marrow biopsy as well as transvascular and mediastinoscopically obtained biopsies failed to provide a pathological diagnosis. Exploratory thoracotomy uncovered a nonresectable chloroma surrounding both venae cavae. It had penetrated into the right and left atria, as well as the pulmonary veins. A Gore-tex bypass was placed between the innominate vein and right atrial appendage. The tumour was identified as a local manifestation of acute myeloid leukaemia. Treatment with idarubicin (12 mg/m2 daily for 3 days) and adriamycin (1.5 mg/m2 daily for 4 days) followed by radiotherapy with 35 Gy achieved partial remission and 15 months after onset of treatment the patient is in a good general condition.
49 patients (22 women, 27 men, mean age 43.7 [21-65] years) with Hodgkin's disease were examined by Doppler echocardiography a median of 5.37 (2-10) years after the end of chemotherapy (given according to the COPP/ABVD scheme, with or without mediastinal irradiation) for possible chronic changes in myocardium, pericardium or cardiac valves, as well as for any haemodynamic sequelae. Maximal and integrated early (E, Ei) and late (A, Ai) diastolic flow velocities and their ratio (E/A, Ei/Ai) were measured by pulsed Doppler over the mitral and tricuspid valves. Although on two-dimensional echo 21 patients (42.9%) were found to have valvar thickening, 19 (38.8%) pericardial thickening and 9 (18.4%) a reduced fibre shortening fraction, the Doppler indices were statistically not significantly different from those in 25 controls with normal hearts. These echocardiographic data of functional and morphological parameters indicate that there was no effect on various measurements of diastolic function after chemotherapy with or without mediastinal radiation. In successfully treated patients with Hodgkin's disease the described changes are of minor significance.
The net effects of acute changes in pre- and afterload on left ventricular filling, were examined by altering loading conditions in normal subjects. The specific purpose of this study was to investigate whether Doppler-derived transmitral flow patterns are able to differentiate the type of loading conditions. In 24 normal subjects (13 females, 11 males, mean age 44.1 +/- 11.5 years), the following Doppler variables were determined at baseline, after rapid volume infusion (preload increase), after nitroglycerin administration (preload decrease), during isometric exercise (afterload increase), and after application of a converting enzyme inhibitor (afterload decrease): the peak and integrated early (E, Ei) and late (A, Ai) diastolic flow velocities, their ratios (E/A, Ei/Ai), the percentage of atrial contribution (ACON), and the acceleration and deceleration times (Ac, Dc) of early filling. Reduced preload and increased afterload led to similar filling patterns characterized by a significant E and Ei decrease (p < 0.05, compared to baseline) accompanied by an A and Ai increase with a resultant reduction of E/A and Ei/Ai. Both changes increased the atrial contribution to filling and reduced Ac and Dc. Increased preload only significantly increased E and Ei, while reduced afterload did not induce any significant changes. Different loading conditions alter Doppler-derived diastolic filling patterns. However, the transmitral flow profile is not specific enough to distinguish the manner in which loading conditions have been altered.
The impact of valvular, myocardial and pericardial abnormalities on cardiac haemodynamics in patients treated for Hodgkin's disease with COPP/ABVD with and without mediastinal irradiation was determined in 49 patients 2-10 years after induction therapy. Diagnostic procedures to evaluate cardiac function consisted of history, physical examination, exercise bicycle stress test, M-mode two-dimensional and pulsed Doppler echocardiography. No patient reported symptoms related to cardiomyopathy, and only one of the 49 had evidence of coronary heart disease. Pericardial thickening was seen on echocardiograms in 19/49 patients (38.8%), valvular thickening in 21/49 (42.9%), and reduced fractional shortening in 9/49 (18.4%). The Doppler-derived mean E and A (+/- SD) of transmitral flow were 0.75 +/- 0.14 m/s and 0.56 +/- 0.09 m/s, respectively, in patients receiving chemotherapy and 0.81 +/- 0.19 m/s and 0.63 +/- 0.20 m/s in those with additional mediastinal irradiation. There was no statistically significant difference between mean E and A in transmitral flow in patients treated for Hodgkin's disease and control subjects. Furthermore, the transtricuspid and hepatic vein flow velocities did not differ significantly. Although the present study demonstrates high frequencies of pericardial and valvular thickening in patients treated for Hodgkin's disease with the COPP/ABVD regimen with or without mediastinal irradiation, it showed no impact on cardiac flow velocities. The abnormalities might thus be of minor clinical relevance in these patients.
Dependence of left heart opacification on ventricular function was evaluated for the new transpulmonary echo enhancing agent (SH U 508-A). The contrast agent was injected intravenously in 5 patients with normal cardiac function (ejection fraction [EF] greater than 60% and echocardiographic left ventricular end-diastolic diameter [LVED] less than 56 mm) and in five patients with pathological ventricular function (EF less than 40%, LVED greater than 65 mm). A concentration of 400 mg/mL with dosages of 5, 9, and 16 mL was used in all patients. The visually assessed signal enhancement as well as the videodensitometrically determined peak intensity and duration of signal enhancement did not differ significantly between the two patient groups, while the transit times were markedly prolonged in patients with impaired ventricular function. No significant alteration was found for systemic blood pressure and heart rate. Side effects were transitory and dose related. The noninvasive nature of the procedure and the absence of hemodynamic effects make repeated studies of left ventricular performance with SH U 508-A in patients with varied hemodynamic status possible.
A 22-year-old female patient with an 8-year history of mixed connective tissue disease (systemic sclerosis overlapping with systemic lupus erythematosus) presented with marked respiratory distress, sinus tachycardia (135 bpm), and pulsus paradoxus. The chest x-ray showed an enlargement of the cardiac silhouette, which was due to a 3-cm-wide, circular pericardial effusion, as demonstrated by two-dimensional echocardiography. Pericardiocentesis performed to decompress cardiac tamponade did not lead to clinical improvement. The increase in dyspnea was caused by a rise in pulmonary wedge pressure from 21 to 40 mm Hg following an acute increase of mitral valve regurgitation. In the presence of global hypokinesia of the left ventricle, cardiac output decreased from 3.25 to 2.63 l/min. Intensive care including hemodialysis and plasmapheresis as well as high-dose application of cyclophosphamide and steroids led to a stabilization of the hemodynamic situation over a period of days. The case report presented here supports the general recommendation to perform pericardiocentesis in a stepwise manner under hemodynamic monitoring. This holds true primarily for patients with mitral valve regurgitation and/or cardiac involvement in connection with an underlying disease.
The value of stress echocardiography in the routine diagnosis of coronary heart disease was assessed in 100 consecutive patients (22 women, 78 men; mean age 57 [32-83] years) scheduled for coronary angiography because of suspected angina. Exercise consisted of bicycle ergometry (n = 50), on the one hand, simulated exercise with transoesophageal atrial stimulation (n = 16), dipyridamole (n = 33) and dobutamine (n = 33) infusions, on the other. 91 patients were successfully tested by at least one of these procedures, while exercise electrocardiography was successfully employed in only 78 (P < 0.05). Stress echocardiography had a greater sensitivity than exercise electrocardiography (90% vs 78%) and specificity (90% vs 73%). Semiquantitative measurement of wall movement distinguished patients without functionally effective stenosis from those with single or multiple vessel disease (P < 0.001). Stress echocardiography thus makes it possible in most cases to demonstrate or exclude functionally significant coronary artery stenoses.
To increase the specificity of 24-hour Holter monitoring in detecting transient myocardial ischemia, we separated genuine ST deviations from those dependent on artifacts by adding a detailed shape analysis of real-time printouts to the usual criteria of significant ST segment depression. We screened 116 apparently healthy subjects; 31 had to be excluded, because of pathologic findings in preliminary examinations. The remaining 85 (49 women and 36 men; mean age, 43.1 years) underwent Holter monitoring for assessment of the extent, frequency, and duration of episodes of horizontal and descending ST segment depression of at least 0.1 mV that persisted for at least 60 msec after the J point and that were at least 1 minute apart. On the basis of these criteria, six subjects (7.1%) showed 24 episodes of horizontal or descending ST segment depression with a mean of 0.2 mV (range, 0.15 to 0.25 mV), a frequency of four episodes per 24 hours (one to nine), and a duration of 12.2 minutes (range 3-range 41 minutes). Supplementary criteria--e.g., sudden onset of ST segment depression, identical orientation of PQ and ST segments, or simultaneous increase in R and P wave amplitude--made it possible to identify ST changes caused by artifacts in four volunteers. In only two subjects (2.4%) could true silent ischemia not be differentiated from false positive results. Thus consideration of only the extent, frequency, and duration of episodes does not permit a differentiation between true silent ischemia and false positive results. A supplementary shape analysis increases the specificity of ST segment analysis in detecting transient myocardial ischemia during 24-hour Holter monitoring.
For a more precise understanding of the net effects of acute alterations of pre- and afterload on left-ventricular filling, loading conditions were altered in normal subjects. The specific purpose of this study was to investigate if Dopplerechocardiographically derived transmitral flow patterns are able to differentiate the manner of loading condition. In 24 normal subjects (13 female, 11 male, mean age 44.1 +/- 11.5 years) the following Doppler variables were analyzed at baseline, after rapid infusion of volume (preload increase), nitroglycerine (preload decrease), isometric exercise (afterload increase) and converting enzyme inhibitor (afterload decrease): peak and integrated early (E, Ei) and late (A, Ai) diastolic flow velocities, their ratios (E/A, Ei/Ai), the percentage of atrial contribution (ACON) and the times of acceleration (Az) and deceleration (Dz) of early filling. Preload reduction as well as afterload increase led to a similar filling pattern with a significant decrease (p < 0.05 from baseline) of E and Ei, increase of A and Ai, and, consequently, a reduction of E/A and Ei/Ai. The atrial contribution to filling increased during both alterations; Az and Dz were reduced. Following the increase of preload, only the increase of E and Ei was statistically significant, while afterload reduction showed no significant differences. Different loading conditions alter Doppler-derived diastolic filling patterns. But the transmitral flow profile is not specific enough to differentiate in which manner loading conditions have been altered.
UNLABELLED: In 4920 consecutive missions of the mobile intensive care unit Klinikum Steglitz, 1226 patients (25%) had chest pain of presumed cardiac origin. In 272 patients (22%) an acute myocardial infarction (AMI) was diagnosed in the field. In four patients the diagnosis was wrong; 11 patients with proven coronary artery disease had significant ST-segment elevation, but did not develop AMI. In hospital, a total of 406 patients had evidence of AMI; 173 of these (41%) were seen by an emergency physician in the field already within the first hour after onset of symptoms. In 6%, diagnostic ST-elevation was not recognized by the emergency physician; 27% had non-diagnostic ECG changes (11% bundle-branch block). Prehospital thrombolysis within 4 h after symptom onset was performed in 126 of 205 patients (61%); 74 of these patients were seen by the emergency physician within the first hour. The main reason for exclusion was advanced age. Inclusion of older patients and also those with bundle-branch block could further increase the prehospital thrombolysis rate. CONCLUSION: With an effective emergency medical system a large proportion of all patients with AMI can correctly be identified and properly treated with a thrombolytic drug in the field. The time gain is considerable.
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