Identification of dissection or aneurysm of the descending thoracic aorta by conventional and transesophageal two-dimensional echocardiography.
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Biomedical subjects
Publications and source records attributed to W Grosse-Heitmeyer.
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Twelve consecutive patients (five males and seven females, aged 24-61 years) with peri- or paracardial space-occupying lesions were studied by transthoracic and transesophageal 2-D echocardiography (2-DE). The tumor was localized by transthoracic 2-DE in six patients. In four patients the lesion was suspected after transthoracic 2-DE, but only transesophageal 2-DE defined the tumor and separated it from surrounding tissues. In two cases of pericardial tumor transthoracic 2-DE at first misdiagnosed it as pericarditis with pericardial effusion. In eight patients transthoracic and in four transesophageal 2-DE made it possible to assess cardiac function. The findings demonstrate that transthoracic 2-DE may not demonstrate peri- or paracardial tumors; transesophageal 2-DE adds an at times decisive additional diagnostic method.
Surgically-obtained tissue specimens from 41 patients with ventricular aneurysm were studied electron microscopically. The tissue from the resected aneurysms showed substantially varied morphological differences. In some, there were extensive regions of scar containing increased fibrotic material and few cells, in others there were also larger contiguous regions of myocardium with an essentially normal appearance. In the preserved myocardial regions, the cardiac cells showed moderate hypertrophy. There was an increase in contractile substance in parallel with an increase in mitochondria and enlargement of the nucleus with frequent waves and invaginations in the cell membrane. The cells at the marginal regions between fibrous tissue and preserved myocardium were frequently isolated from adjacent cells. In particular, when the isolated cells were completely surrounded by fibrous tissue, clear degeneration was apparent. These cells showed mainly a fibrillolysis with dissolution of the cross-bands and loss of the entire contractile apparatus. In compensation, occasionally there was proliferation of other cell structures, especially the free sarcoplasmatic reticulum. The hypertrophy of the still intact myocardial cells is considered compensatory for the infarct-incurred loss of tissue. The degenerative appearance is mainly attributable to fibrous tissue invasion. The diminished oxygen supply, compromised or abolished impulse conduction, loss of function and passive stretch during systole may be regarded as causes of the degeneration.
Transthoracic (tth) and transesophageal (TEE) 2D-echocardiography (E) were performed in 20 consecutively examined patients (17 males, 3 females, age 18 to 76 years, mean age 48.6 +/- 18.9 years) with dissecting (n = 11) and nondissecting thoracic aortic aneurysms confirmed by angiography or surgery. In 7 out of 9 cases, nondissecting aneurysms were detected by 2-DE, whereas in 2 patients diagnosis was established only by TEE. Three out of 6 type I dissections and 1 type II dissection could be diagnosed by tth 2-DE. But in 3 type I dissections and in all cases with type III aneurysms (n = 4) the intimal flaps and the DeBakey type of classification were identified only by TEE. In 1 patient with an extensive aneurysm of the ascending aorta and severe aortic insufficiency, a dissection was erroneously diagnosed by TEE, but not confirmed by surgery. In 1 case with type I dissection, spontaneous echo contrast within the false lumen was revealed by TEE. Complications due to TEE were not observed. Thus, in the diagnosis of thoracic aortic aneurysms and dissections the combination of tth 2-DE and TEE is superior to only tth 2-DE.
Dissecting aortic aneurysms require immediate diagnosis and accurate knowledge of extension. In two patients with dissecting aortic aneurysms the extension of the dissection could be evaluated by the noninvasive method of 2-D-echography. All aortic regions could be visualized in both cases, The diagnosis of dissection was established by visualization of intimal flaps in short and long exis views.
Investigations in 13 hospitalized patients with pheochromocytomata showed peculiar characteristics of heart rate variation at rest, when compared with normals. All patients were given alpha- and beta-sympatholytic drugs. In one case alpha-methyl-Tyrosine caused I-II degree AV blocks and a stable high frequency sinus rate without physiological variations. Resting heart rate in pheochromocytoma varied interindividually from 55-105/min, in the absence of clinical attacks of the underlying disease. The frequency profile was characterized in 12 patients by sudden and inadequate rises of heart rate (200%) of short duration, which were often recorded within 20 seconds of the onset of muscular activity. A similar but less pronounced heart rate modulation was found 1-2 weeks after operation in 3 cases. Our observations indicate that the heart rate profile described may be a sensitive parameter of dysfunction of the autonomous nervous system in pheochromocytoma. Whether the heart rate characteristics are of diagnostic value has to be assessed by further studies.
The effect of the new antiarrhythmic drug Flecainide was examined in a controlled long-term study (1 to 44 months [x = 17.7 +/- 12.4]) in 36 patients, aged 18 to 76 years (x = 44 +/- 16.3), suffering from ventricular arrhythmias. In 12 cases coronary heart disease, in 11 cases myocarditis, in 2 cases each of dilatative cardiomyopathy and mitral valve prolapse syndrome, and one in case each of combined aortic and mitral valve disease and postoperative condition of Fallot Trilogy was present. In 7 cases the etiology of the dysrhythmias could not be elucidated. 18 patients had been treated before by more than 3 other antiarrhythmic drugs without sufficient result. The daily dose administered was assessed by the degree of the dysrhythmias and the response to the drug. In most cases 300-400 mg Flecainide was given. The therapeutic success was assessed by 24 h Holter-ECG before and during therapy. In most cases two registrations were performed before and three registrations during therapy. In 29 patients (81%) a rate reduction of VES over 70% could be observed. Rate reduction of VT (n = 8) was total in 5 cases, in one case over 90%, in two cases over 70%. Salvos (n = 10) were abolished in 7 cases and reduced over 90% in two and over 70% in one of the cases. R-on-T-phenomena (n = 2) disappeared completely. An increase of rate or degree of the dysrhythmias was never observed. In no case had therapy to be interrupted due to severe side effects. Changes of laboratory values were not observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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In 203 patients with clinical symptoms of coronary artery disease, cardiac and extracardiac side effects of the dipyridamole test were investigated. Following dipyridamole (0.75 mg/kg body wt. i.v.), heart rate increased significantly, whereas arterial blood pressure remained almost constant. Dyspnea was noted in 80 cases (40.5%). In 48 patients (23.6%) rhythm disturbances were recorded; 58.1% suffered from extracardiac side effects such as congestion in the head, vertigo, heaviness of arms and legs, sensations of heat, upper abdominal pain, and nausea. A detailed report is given of 4 cases with extraordinary symptoms during or after the injection of dipyridamole. A life-threatening status anginosus with dyspnea, ST-segment elevation, and cardiac arrhythmia was observed in one of these cases. High-dose dipyridamole cannot be considered to be harmless. The test should not be performed without continuous ECG monitoring and other safety measures.
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10 male patients with angina pectoris and a history of increased severity of angina under cold conditions were investigated. The coronary angiograms of all patients showed severe stenoses of coronary arteries. Observations were made by continuous ECG monitoring (Holter ECG) during rest and exercise under normal (room temperature) and cold conditions (-6 degrees C). In addition to ECG changes only anginal attacks occurring spontaneously were of interest in this study. Therefore, the patients were not informed about the purpose of the investigation. In spite of a history of increasing angina during exposure to cold, no patient spontaneously complained of cardiac symptoms while changing from a normal to a cold environment. In none of the patients did exposure to cold lead to ECG alterations such as arrhythmias or ST-segment depression. There was no significant difference in ST-segment changes during and after exercise under normal or cold conditions. The history of cold intolerance in patients with angina pectoris is a nonreproducable, nonspecific parameter. We conclude that angina pectoris under cold conditions is not due to myocardial ischemia, but is very likely to be induced by psychovegetative factors.
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The management of septicemia associated with an infected endocardial pacemaker lead prerequisites removal of the latter nidus. If the infected electrode cannot be manually withdrawn, continuous traction may be employed. Should this attempted fail or should the severed end of the electrode fragment be inaccessible to a superficial approach, thoracotomy may be necessary. As an alternative procedure, we have successfully removed infected electrode fragments from three patients with septicemia by use of a Dotter retrieval catheter monitored with biplane fluoroscopy. The septicemia was subsequently irradiated in all cases.
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In standardized experiments on both conscious and anaesthetized young (n = 11) and old (n = 7) dogs differences in haemodynamics, contractility and myocardial oxygen consumption correlated to age were evaluated. Under resting conditions no significant differences were observed. Following stimulation with catecholamines young (n = 6), and old (n = 6) dogs displayed an almost parallel increase in (dp/dt) max. After administration of orciprenalin, the maximum increase in heart rate was similar in both groups of animals; however, a significant difference in the maximum heart rate following atropine was observed, which was significantly lower in old than in young animals. The decreased performance of the aged myocardium does not appear to be predominantly due to an age-dependent reduction of the contractility reserve. It could result from a deficient sympathetic stimulation of the heart.