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Biomedical subjects

B Eber

Publications and source records attributed to B Eber.

At least 181 records · Page 10Linked to original sources
PubMed1992

[Abnormal origin of the ramus circumflexus sinister from the left atrium in a 30-year-old patient with aortic isthmus stenosis and atrial septal defect].

In this case report a 30-year-old woman suffering from progressive angina pectoris and dyspnea, having been operated on previously for atrial septum defect at the age of 19 and later aged 24 for coarctation of the aorta, is described. Upon observation, patient showed cardiac symptoms already under mild stress and remained resistant to nitroglycerin. Rest-ECG and serum cardiac enzymes were repeatedly without findings, while stress-ECG at a level of 100 W showed a ST-segment depression of 0.15 mV, at the same time complaining of angina pectoris symptoms. Coronary angiography revealed a left circumflex coronary artery arising from the left atrium being fully supplied by the left anterior descendent artery and the right coronary artery via pronounced collaterals, both originating from the ascending aorta. Despite such severe symptoms patient refused surgery suturing the abnormally arising artery. One year following coronary angiography patient is suffering from stabile angina pectoris without occurrence of myocardial infarction or another cardiovascular event.

Adult↗
PubMed1992

[Differential diagnostic considerations in eosinophilia with reference to a 19-year-old patients with Löffler endocarditis].

In this case report a 19-year-old girl suffering from hypereosinophilia with 3500 cells/mm3 and involvement of the right lung, lymph nodes, skin, serosa and heart is described. Within 10 days of admission an infiltration of the right upper lung lobe disappeared spontaneously and was diagnosed as transient eosinophilic lung infiltration according to Löffler. Both lymph node needle biopsy and several skin biopsies revealed merely general reactive changes whereas a bronchial lavage produced a significant number of eosinophilic granulocytes. Autoimmunologic or infectious-toxic disorders were ruled out as etiologic causes. Within 4 weeks after admission severe mitral and tricuspidal insufficiency as well as AV-block second grade and protodiastolic galloping rhythm developed in addition to progressing polyserositis. The echocardiographic pattern was in accordance with restrictive endocarditis. Due to the greatly reduced left ventricular ejection fraction cortisone (125 mg prednison equivalent) was tentatively administered as therapy. Within 2 weeks heart-, serosa- and lymph-node-findings became normal as well as the eosinophilic count, the scaling skin rash being only partly improved. After 10 months of continuous cortisone therapy (10 mg prednison equivalent) the patient was without evidence of disease. However in conclusion, it may be said that such pattern of findings suggests a hypereosinophilic syndrome with Löffler endocarditis with an unknown future course of disease although generally survival prognosis may not be too high.

Adult↗
PubMed1992

IgG-anticardiolipin-antibodies are markers for cerebral and peripheral artery disease.

Anticardiolipin-antibodies are antibodies to phospholipids which were first detected in patients with arterial thrombosis and lupus erythematosus. In this prospective study, IgG- and IgM-anticardiolipin-antibodies were determined in patients with cerebral and/or peripheral artery disease but without autoimmune disorders. 123 randomly selected patients (88 males, 35 females; mean: 65 +/- 10, range: 41-85 years) were included and divided into four groups: 18 patients with isolated cerebrovascular disease (group A), 35 patients with peripheral artery disease only (group B), 35 patients suffering from cerebral and peripheral artery disease (group C) and 35 patients as controls (group D). In family history, cholesterol, blood sugar and prothrombin time the four patient groups did not differ significantly, whereas patients of group B and C were more often smokers than those in groups A and D. However, IgG-anticardiolipin-antibody-levels were significantly elevated in patients with cerebral and peripheral artery disease compared to controls (p less than 0.01). The highest values were seen in group C where patients suffered from cerebral and peripheral artery disease (n.s.). On the other hand, IgM-anticardiolipin-antibody-levels did not show any differences in the four groups. Furthermore, there was no correlation between vascular risk factors and/or laboratory findings with IgG- and IgM-antibody-levels. Thus, elevated IgG-anticardiolipin-antibodies appear to be independent markers for severe cerebral and peripheral artery disease and should be determined in patients at increased risk.

Adult↗
PubMed1991

Perforated ventricular aneurysm in a male suffering from pneumonia.

In a 49-year-old male with fever, dyspnea, and chest pain, thoracic x-ray revealed pneumonia with enlarged heart silhouette. Antibiotics were successful, pneumonia healed and complaints disappeared. Yet, during the following 3 months, echocardiography showed mild persistent pericardial effusion while in ECG both sinus tachycardia and ST-T changes were found suggesting chronic pericarditis. Magnetic resonance imaging, however, revealed an extensive posterobasal aneurysm with pericardial effusion substantiated by ventriculography. Coronary angiography showed diffuse three-vessel disease. Surgery revealed aneurysm with distinct perforation of the left ventricle and pericardial thrombi, thus aneurysmectomy as well as bypass grafts were performed. One year postoperatively, magnetic resonance imaging confirmed the absence of aneurysm with only a small irreversible posterobasal perfusion defect remaining as shown by thallium scintigraphy.

Adult↗
PubMed1991

Circadian blood pressure pattern in patients with treated hypertension and left ventricular hypertrophy.

Left ventricular hypertrophy in hypertensives is an important determinant of prognosis. In the present study 45 patients with treated essential hypertension were divided into two groups: 23 patients had normal left ventricular dimension and 22 patients had echocardiographic signs of left ventricular hypertrophy (LVH). All patients were adequately treated during daytime, but ambulatory blood pressure monitoring showed a distinct abnormal pattern in the LVH group characterized by a lack of blood pressure reduction during the night; 16 of 22 patients with LVH had no blood pressure decline during the night, whereas 17 of 23 patients without hypertrophy showed this reduction (P less than 0.01). In conclusion, patients with hypertension and LVH often reveal a lack of blood pressure decline during the night, which may be the reason for the development of left ventricular hypertrophy (and thus should be managed by a different circadian blood pressure therapy) or which may be the consequence of progressive structural changes in the resistance vessels, along with the development of left ventricular hypertrophy. It is suggested that patients with hypertension and left ventricular hypertrophy should have ambulatory twenty-four hour blood pressure monitoring.

Antihypertensive Agents↗
PubMed1991

Non-Q-wave myocardial infarction associated with bleomycin and etoposide chemotherapy.

During chemotherapy with bleomycin and etoposide a 28-year-old male, suffering from germ-cell cancer, developed acute myocardial infarction. Under treatment with heparin and aspirin the patient revealed no Q-waves in ECG and recovery was without complications. Four weeks after onset of infarction, thallium-201 scintigraphy showed only a small irreversible, posteroseptal perfusion defect; coronary angiography was not performed. The chemotherapy regimen was continued and modified to etoposide as well as cisplatin and ifosfamide without recurrence of cardiac symptoms or ECG changes.

Adult↗
PubMed1991

New concepts in ischemia prevention.

Transient myocardial ischemia may result from obstruction to flow in the large epicardial coronary arteries or diminished flow reserve due to small vessel disease or left ventricular hypertrophy. In patients with coronary heart disease, calcium blockers have proven to reduce stress induced ischemia in patients with normal left ventricular function and in those with ischemic cardiomyopathy. However, recent studies indicate a need for caution when giving calcium antagonists to patients with postinfarction left ventricular systolic dysfunction. Moreover, calcium antagonists that reduce heart rate (diltiazem) are able as a monotherapy to reduce total ischemic burden. Calcium antagonists that may increase rate (dihydropiridines) have to be combined with beta-blockers to achieve this goal. For 24-h control of ischemia the ischemic threshold should be determined for a differentiated therapy in the individual patient. Is the ischemic threshold of the majority of episodes lower than the exercise threshold, a calcium blocker should work. Angiotensin-converting enzyme (ACE) inhibitors are not effective in stress-induced ischemia, but may reduce total ischemic burden, although this effect is not significant. In patients with left ventricular hypertrophy and/or small vessel disease, calcium blockers and ACE inhibitors are probably effective in regression of left ventricular hypertrophy and vascular hypertrophy. However, it remains to be shown that ischemia is reduced by these drugs.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1991

[Silent myocardial ischemia. Current concepts of pathophysiology and diagnosis].

Silent myocardial ischemia (SMI) is divided into 3 groups: type I: completely asymptomatic patients, type II: patients after acute myocardial infarction with SMI, type III: patients with angina pectoris (AP) and SMI. Pathophysiology on the lack of pain-perception and the cause for high tolerance against pain in SMI-patients has not yet been cleared up. It is most likely that more than one mechanism is involved in every patient, e.g. generally lower pain-perception in SMI-patients, physically counter-regulation in pain, duration and strength of myocardial ischemia. Diagnosis of SMI can be made by exercise- and long-term-ECG, thalliumszintigraphy and coronary angiography, in doing so the pros and cons of the 4 established methods have to be noted. The summary of the findings together with the lack of pain leads to the diagnosis of SMI.

Angina Pectoris↗
PubMed1991

[Silent myocardial ischemia. Current concepts of prognosis and therapy].

Type-I-patients with silent myocardial ischemia (SMI) have a 2-4fold higher longterm-risk for coronary-events than healthy people. With increasing gravity and duration of ischemia type-II-patients have an increased event-risk. Reliable statements about prognosis of type-III-patients are very difficult. Therapy of SMI is equivalent to therapy of "loud" ischemia and comprises: 1) treatment of cardiovascular risk-factors (nicotine, arterial hypertension, hyperlipidemia, adiposis), 2) nitrates as effective straight at the coronary stenosis, 3) beta-blockers, which influence the circadian ischemic rhythm, 4) calcium-channel-blockers with especially for nifedipine little effect, 5) thrombocyte-aggregation inhibitors and 6) invasive therapeutical methods (percutaneous transluminal coronary angioplasty [PTCA] and aorto-coronary bypass grafting [ACBG]).

Angina Pectoris↗
PubMed1991

[Coronary artery anomalies in adulthood].

In a series of 3000 consecutive coronary angiographies carried out in adults (period October 1988 through February 1991) the incidence of coronary artery anomalies was investigated. Among these there were 7.2% of patients with left-, 3.8% with right-sided and 89% with bilateral coronary artery supply. 10 cases revealed a double left anterior descendent artery (LAD), whereas in 2 patients the left circumflex artery (CX) was missing. In approximately 1% of patients origin anomalies of coronary arteries were observed, above all of the right coronary artery (RCA). A pronounced kinking of the coronaries was seen in 22 cases (11 LAD, 11 RCA) and a bridging in 2.5% of patients (74 LAD, 1 CX, 1 RCA). Of the latter, there were 21 hemodynamic active stenoses (more than 75% diameter stenosis) of which in 12 cases this narrowing was the sole cause for the heart complaints. During the same period there were 8 patients with coronary anomalies leading to shunt development out of which a 30-year-old female revealed clinically a coronary steal phenomenon. Aneurysms of the coronary arteries were observed in 54 cases (2%) whether congenital or acquired could not be ascertained. In total, there were 194 coronary anomalies in the total series (6.5%) being clinical significant in 22 cases (0.7%).

Adult↗
PubMed1991

Endothelium-derived relaxing and contracting factors.

Since the description of the essential role of the endothelium in mediating relaxations due to acetylcholine in mammalian arteries, it has become obvious that endothelial cells release several relaxing and contracting substances. The release is activated by a variety of agents including circulating hormones, autacoids, and products liberated by aggregating platelets, but also by changes in shear stress exerted by the blood. There is strong evidence that the major endothelium-derived relaxing factor (EDRF) is the free radical nitric oxide (NO) formed enzymatically from L-arginine. Endothelium-dependent relaxations caused by EDRF are induced through increases in the activity of soluble guanylate cyclase in the smooth muscle. Other relaxing factors, such as prostacyclin and endothelium-derived hyperpolarizing factor (EDHF) contribute to endothelium-dependent relaxations. Beside the recently described and chemically identified peptide endothelin, at least two other endothelium-derived contracting factors appear to exist. The mechanisms by which endothelium-derived contracting factors activate vascular smooth muscle are not yet clear. In certain clinical situations an impairment of the production of EDRF in face of a maintained or augmented release of contracting factors may contribute to the occurrence of localized vasospasm or generalized increases in peripheral resistance.

Arteriosclerosis↗
PubMed1991

[Current state of interventional measures in cardiology].

Interventional cardiology comprises all therapeutic heart procedures which are percutaneously performed via catheterization. Selected patients with severe mitral or aortic stenoses may be efficiently treated by percutaneous transluminal balloon valvuloplasty (PTBV). Percutaneous transluminal coronary angioplasty (PTCA) as a treatment of coronary artery disease has now been applied for more than 10 years, and the main problem appears to be the development of restenosis after 3 to 4 months. The efficacy of newer interventional techniques (the percutaneous transluminal laser ablation [PTCLA], the endatherectomy, rotational catheters, or the application of stents) is studied at present all over the world. The question is whether these procedures may reduce restenosis and increase success rate in patients at risk.

Angioplasty, Balloon, Coronary↗