Sarcoidosis and tuberculosis: a connection to the human leukocyte antigen system.

Infectious, genetic factors, and autoimmunity have been considered as potential causes of sarcoidosis (SA). Pathological similarities between SA and tuberculosis (TB) suggest M. tuberculosis antigen(s) as causative agent(s). Our published comparative analysis of the human leukocyte antigens (HLA) system in patients with SA or TB in the same ethnic group revealed that some antigens were connected with high risk of developing of SA or TB, but other were comparable in both patient populations. Is it possible that the predominating occurrence of HLA antigens characteristic for TB may cause tuberculosis in patients with SA? To answer this question we evaluated the HLA class I and II alleles frequency by PCR amplification with sequence-specific primers in three women with histopathologically proven pulmonary SA, who developed bacteriologically confirmed TB on a corticosteroids (CS) therapy. Analysis of HLA in every case separately revealed a trend for higher occurrence of both alleles predisposing and protecting from TB than SA, in comparison with healthy individuals in our previously mentioned HLA genotyping study. Overall, the number of alleles predisposing to TB was statistically greater than the number of alleles connected with a high risk of developing SA. Also, the frequency of protecting alleles was statistically higher for TB than for SA. Therefore, SA in these patients developed at first, and the presence of additional environmental factors, e.g., age, CS might decrease an immune response and provoked TB. There is a possibility that the occurrence of HLA antigen more associated with high risk of developing TB than SA causes the development of tuberculosis in our patients with sarcoidosis.

[The short- and long-term motivational effects of a patient education programme for patients with coronary artery bypass grafting]. / Die kurz- und langfristigen motivationalen Effekte eines Patientenschulungsprogramms für Herzbypasspatienten.

PURPOSE: An important rehabilitation aim following coronary artery bypass graft (CABG) surgery is to modify cardiovascular risk factors positively. Among the most potent possibilities for improvement of these factors is a lifestyle change in terms of increasing sports exercise, changing diet patterns, stress reduction, etc. An indispensable condition for these changes is the motivation to implement the necessary changes. In our working group a patient education programme was developed aimed at enhancing the motivation for lifestyle change, which was already applied in a cardiac surgery hospital. In evaluating the programme, we could observe that various cognitive factors of motivation for lifestyle change had dropped in untreated patients and risen in patients participating in the programme. Based on these preliminary findings we examined the motivation for lifestyle change one year after CABG surgery. METHOD: Each patient was evaluated for his/her value in motivation for lifestyle change using a 30-item questionnaire which measures the six factors Vulnerability, Intention, Social Expectations, Outcome Expectation, Self-Efficacy Expectation, and Perceived Severity two days before CABG surgery as well as ten days and one year after CABG surgery. Between January and May 2002 patients in usual care were investigated as control group (n=70). From January to May 2003, n=70 patients had the opportunity to take part in a comprehensive patient education programme that was provided by a specifically trained psychologist. Data from 108 patients could be evaluated one year after CABG surgery (response rate=77.1%). The programme had comprised individualized units, as well as a group lecture. If partners were available they were included in the process. RESULTS: One year after CABG surgery no significant differences between the control group and the intervention group could be found. CONCLUSION: The positive effects of the patient education programme measured ten days after surgery were found to have vanished one year after the operation. A possible reason is the short duration of the programme. Long-term, structured aftercare programmes should help stabilize the positive effects obtained in the short term.

[Nisoldipine in the treatment of essential hypertension. Efficacy and tolerance]. / Nisoldipin in der Therapie der essentiellen Hypertonie. Wirkung und Verträglichkeit.

The antihypertensive effect after a single dose of one tablet of Nisoldilpine (Bay k 5552) containing 5 mg, 10 mg or 20 mg respectively, was tested in a double-blind cross-over trial with intra-individual comparison on 60 patients with stable essential hypertension. Mean age was 51.6 +/- 7.1 years, mean body-weight 78.0 +/- 11.8 kg, mean height 169.8 +/- 8.2 cm and mean duration of illness 6.1 +/- 4.3 years. 34 patients were in WHO stage I, 24 in stage II. After 5 mg nisoldipine the blood pressure fell from 150/96 to 135/92 mm Hg, after 10 mg from 153/98 to 130/88 mm Hg and after 20 mg from 149/97 to 127/84 mm Hg. Compared with placebo pre-test levels there was also a significant reduction in blood-pressure at an exercise level of 100 W. Side effects were rare and dose-dependent.

Four years of experience in endomyocardial biopsy--an immunohistologic approach.

Left ventricular biopsies from 376 patients (including 78 patients undergoing bypass surgery) were analyzed by light microscopy (necrosis, infiltration with or without fibrosis) and by immunohistology (bound antibodies). Circulating antisarcolemmal antibodies (ASA) were determined at the time of biopsy using a double-sandwich technique. Circulating antimyolemmal antibodies were assessed in intact rat and human cardiocytes. Histologic findings, heart catheterization, and echocardiography together with the patient's history established the diagnosis of perimyocarditis, myocarditis, postmyocarditic dilated cardiomyopathy, healed myocarditis, and healed perimyocarditis. Both bound and circulating ASA were found in up to 100% of cases in acute inflammatory heart disease and postmyocarditic cardiomyopathy, indicating a secondary immunopathogenesis of the myocardial disease. Analysis of immunoglobulin subclasses revealed: IgG-binding does not discriminate between acute/healing/healed carditis and postmyocarditic dilated heart disease (61.1%-91.7% positive); IgM binding is diagnostic for acute or healing perimyocarditis but has a relatively low incidence (33.3%); IgA binding occurs in acute or healing myocarditis (45.5%), perimyocarditis (33.3%), and in postmyocarditic heart disease (39.4%), but not in controls; complement fixation was never seen in controls, but was seen in acute myocarditis (45.4%), perimyocarditis (25%), and postmyocarditic heart disease (46%). Pretreatment of cryostat sections with collagenase to avoid "nonspecific" binding of antibodies to collagen considerably reduced the sensitivity but increased the specificity. Thus, endomyocardial biopsy proved a safe and valuable method for the further analysis of patients with carditis and myocardial disease of unknown origin.

Diagnostic relevance of humoral and cytotoxic immune reactions in primary and secondary dilated cardiomyopathy.

Circulating muscle-specific antimyolemmal antibodies (AMLAs) were found in 18 of 61 patients with secondary dilated cardiomyopathy (DC). All 18 patients had clinical or histologic evidence of previous perimyocarditis. AMLAs were found both in patients' serum samples and bound to the sarcolemmal sheath of the autologous myocardial biopsy specimen. Only AMLAs in postmyocardiac DC induced cytolysis of vital cardiocytes in the presence of complement, whereas hepatocytes remained unaffected. Titers of AMLAs correlated with the degree of cardiocytolysis. In contrast, antiinterfibrillary antibodies were found in 49% patients with primary DC (n = 79) and in 61% of patients (n = 30) with alcoholic DC. The incidence of antifibrillary antibodies of the antimyosin type was 23 and 24%, respectively. Incidence of both antibodies increased according to the severity assessed by New York Heart Association functional classes. Circulating immune complexes assayed by a new Clq-solid phase fluorometric assay were present in 30% of patients with postmyocarditic DC only. Lymphocyte-mediated cytotoxicity against heterologous cardiac target cells (K-cell activity) was measured in 33% of patients each with primary and secondary alcoholic DC but not postmyocarditic DC. There were no blocking factors in primary but were some in alcoholic heart disease.

Effect of intravenous and intracoronary nifedipine on coronary blood flow and myocardial oxygen consumption.

The effect of intravenous and intracoronary nifedipine on coronary sinus blood flow, coronary vascular resistance, and myocardial oxygen consumption was studied in 20 patients with coronary artery disease. An intravenous infusion of 1.0 mg nifedipine resulted in a decrease in mean aortic pressure, an increase in heart rate and coronary blood flow, and no significant change in myocardial, oxygen consumption. In contrast, the intracoronary injection of 0.1 mg nifedipine led to a moderate reduction in mean aortic pressure, no change in heart rate, an increase in coronary blood flow, and a significant reduction in myocardial oxygen consumption. During rapid atrial pacing before and approximately 6 minutes after the intracoronary nifedipine injection, coronary blood flow and myocardial oxygen consumption reached identical levels. Thus, only intracoronary injection of nifedipine increases coronary flow in the presence of reduced myocardial oxygen consumption. After intravenous administration, reflex tachycardia counteracts the direct myocardial effect of nifedipine and the potential oxygen-saving effect of afterload reduction. There is no evidence of a prolonged oxygen-sparing effect after cessation of the immediate effects.

[Effect of nitroglycerin on the heart]. / Zur Nitroglyzerin-Wirkung am Herzen.

Nitroglycerin injection into the left coronary artery triggers an increase of ionized Ca concentration in coronary sinus blood. This coincides with a significant dilatation of the coronary artery and a decrease in left ventricular contractility. According to the results of the investigation it seems to be possible that nitroglycerin stimulates the Ca-ion efflux from the smooth muscle cells and the myocytes.

[Effect of intracoronary nifedipine on coronary sinus blood flow and myocardial oxygen consumption in patients with coronary artery disease]. / Koronarsinusfluss und myokardialer Sauerstoffverbrauch nach intrakoronarer Nifedipininjektion bei Patienten mit koronarer Herzerkrankung.

UNLABELLED: Reflex sympathetic nerve activation obscures the direct myocardial effect of Nifedipine after intravenous administration. Consequently, in 10 patients with coronary artery disease 0.1 mg of Nifedipine were injected into the left coronary artery to evaluate its specific effect on coronary sinus blood flow (CSF), coronary vascular resistance (CVR), and myocardial oxygen consumption (MVO2). One minute after Nifedipine, CSF increased from 115 +/- 15 to 193 +/- 47 ml/min (p less than 0.001), and CVR decreased from 0.92 +/- 0.16 to 0,54 +/- 0.12 mm Hg X min X ml-1 (p less than 0.001). Mean aortic pressure dropped from 107 +/- 5 to 99 +/- 3 mm Hg (p less than 0.01). MVO2 was reduced from 14.6 +/- 2.6 to 11.7 +/- 2.8 ml O2 X min-1 (p less than 0.05). After five minutes CSF (113 +/- 18) and MVO2 (14.9 +/- 3.1) had returned to their preinjection level. Additionally, CSF and MVO2 were measured during rapid atrial pacing (mean rate 118 +/- 6 min-1). Average CSF and MVO2 values were 172 +/- 63 and 19.8 +/- 5.0 before and 177 +/- 69 and 20.6 +/- 7.3 approximately 6 minutes after Nifedipine injection. CONCLUSIONS: Intracoronary Nifedipine results in coronary vasodilation and subsequently in an increase in coronary flow. The concomitant reduction in MVO2 provides evidence for an oxygen sparing, negative inotropic effect of Nifedipine, which, however, is of very limited duration. A sustained oxygen-saving effect during periods with increased oxygen demand could not be shown.

[Thrombolytic therapy in a case of mitral valve thrombosis (author's transl)]. / Streptokinasebehandlung einer Thrombose an einer Mitralklappenprothese.

In this paper we present a case in which thrombolytic treatment with Streptokinase was successful in a 53-year-old patient, who developed valve thrombosis one year after aortic and mitral-valve replacement by Björk-Shiley tilding-disk-valve prosthesis. The patient suffered from pulmonary congestion and cardiogenic shock. In spite of Arterenol infusion the blood pressure fell down to 90/50 mm Hg. The systolic pulmonary artery-pressure rose up to 120 mm Hg, the cardiac output was 1.8 l/min. The patient became anuric. A transport to the next department of cardiovascular surgery was impossible. In this extraordinary critical situation for the patient we introduced a thrombolytic therapy with Streptokinase. Within a few hours, the systolic pulmonary artery-pressure fell down by 33%, the cardiac output increased by 100%. One and half days later the patient did not need Arterenol infusion and the blood pressure was 120/80 mm Hg. Referring to this observation, we conclude that Streptokinase therapy can be a successful emergency-treatment of a life-threatening artificial heart-valve thrombosis, if surgical treatment is impossible.

[Transfemoral embolus aspiration from both renal arteries]. / Transfemorale Embolusaspiration aus beiden Nierenarterien.

In a 50-year-old female patient who had suffered from coronary heart disease for about 3 years, a cerebral embolus resulted in left-sided hemiparesis. Four days later she became anuric. Acute thromboembolis occlusion of the renal arteries was assumed and renal angiography was performed. The angiography showed complete obstruction of the left renal artery and partial obstruction of the right renal artery. Due to the poor general condition of the patient it was not possible to carry out renovascular surgery or streptokinasetherapy. An attempt was therefore made to remove the emboli from the renal arteries by a new technique (transfemoral embolus aspiration). The subsequent angiography showed normal circulation in the right kidney and improved circulation in the left kidney. Ten days of dialysis treatment were required until urine production started again. Death then occurred from other causes. The autopsy confirmed free permeable renal vessels and absence of permanent sequelae in the parenchyma.

[Heart tumour in the right atrium: clinical recognition and therapeutical management (author's transl)]. / Herztumor im rechten Vorhof: Diagnostik und Therapie.

A 62 year old lady came to the hospital in cause of right heart failure. Right and left heart catheterization and cineangiocardiography revealed a tumour in the right atrium. Further angiographic investigations demonstrated a hypernephroma in the left kidney. The operation of both tumours was successful. Pathohistological examination confirmed the diagnosis of hypernephroma in the left kidney with metastasis into the right atrium.

[Mitral valve replacement in large hearts (author's transl)]. / Der Miralklappenersatz bei grossen Herzen.

Of 61 patients with mitral valve defects operated on, 9 had a heart with an external volume of more than 1700 ml. Five of these patients died, four are still alive today. Three patients from the group with an external heart volume between 1247 ml and 1700 ml died, and in the group of patients with an external heart volume of less than 1247 ml no patient has died as yet. Under certain circumstances, the preoperative size of the heart can be a measure with which the limits of surgical mitral valve replacement can be defined.

Arteriosclerotic coronary arterial aneurysms in a 49-year-old man with crescendo angina: family history, natural course and prevalence.

In a 49-year-old man with crescendo angina, elevated serum cholesterol level and an old posterior myocardial infarction, selective coronary arteriography showed multiple arteriosclerotic aneurysms of the right coronary artery associated with extensive and severe arteriosclerotic disease of the left coronary artery. The patient's mother and brother have both died of a myocardial infarction. Another brother suffers from angina and has documented arteriosclerotic coronary artery disease. Two sisters suffer from angina as well. The possibility of embolization of distal vessels from a friable clot of the aneurysms as a cause of the patient's infarction is discussed. To the best of our knowledge, this is the tenth patient with nonfistulous arteriosclerotic coronary artery aneurysm diagnosed and documented angiographically ante mortem. Including the present case and reviewing the literature, the prevalence of this condition among nonfistulous coronary aneurysms diagnosed ante mortem is 35 per cent and henceforth cannot be regarded as an incidental autopsy finding in cardiac asymptomatic patients.