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Wir berichten uber einen 31jahrigen turkischen Patienten mit einer rechtskardialen Raumforderung, Leistungsminderung, Gewichtsabnahme und intermittierenden Fieberschuben. Im peripheren Blut bestand keine Eosinophilie, die kardiale Funktion war primar unauffallig. Neben einer Endokarditis fibroplastica Loffler bestand differentialdiagnostisch der Verdacht auf ein entzundliches Geschehen sowie einen malignen Herztumor. Bei echokardiographisch untypischer Morphologie der rechtsventrikularen Raumforderung konnte durch Myokardbiopsie die Diagnose nicht gesichert werden. Bei raschem Wachstum der Raumforderung, fulminanter Embolie und Infiltration in die Trikuspidalklappe konnte erst durch die operative Tumorexstirpation die histologisch-pathologische Diagnose einer Endokarditis fibroplastica Loffler im thrombotischen Stadium gestellt werden. Die Behandlung bestand in einer antiphlogistischen Therapie mit Kortikosteroiden. Im Auslasversuch kam es nach 6 Monaten zu einem Tumorrezidiv. Eine Steroid-Dauermedikation in Kombination mit Azathioprin fuhrte anschliesend zu einer erneuten Tumorregression und Stabilisierung seit 8 Monaten nach Beginn der Medikation.

We report on a male, 31 year old, Turkish patient with an intracardiac mass in the right ventricle, reduction of performance and weight, as well as intermittent fever. No eosinophilia was documented in the peripheral blood; cardiac function was primarily normal. Besides the differential diagnosis of Löffer's endocarditis (endomyocardial fibrosis) an inflammatory disease and a malignant cardiac tumor were suggested. The diagnosis of Löffler's endocarditis could not be confirmed morphologically by echocardiography nor histologically by right ventricular biopsy. Operative removal of the mass lesion was necessary because of fast tumor progression, fulminant pulmonary embolism, and infiltration of the tricuspid valve. Only then, histologically Löffler's eosinophilic endocarditis of thrombotic stage was diagnosed. Antiphlogistic therapy with cortisone was initially performed. With a dose reduction after 6 months, a relapse of the thrombotic mass occurred. Therefore, continuous treatment with cortisone and azathioprine was induced followed by further tumor regression and further clinical stabilization since 8 months of treatment.

It is still a matter of dispute to what extent a direct loss of nitrate mediated vasodilatation (true tolerance) contributes to the development of nitrate tolerance. Aim of this study was to assess to what extent the dilatation of non-obstructed segments of epicardial arteries is attenuated during a continuous 24- and 48-h-infusion of nitroglycerin. In a prospective, randomized and blinded study we investigated 32 patients who underwent diagnostic coronary angiography. All cardiac medication was withdrawn at least for 24 h; patients were randomized to either a 24 h NTG-infusion (group A; 0-24 h saline infusion followed by a 24 h NTG-infusion; n = 16) or a 48 h NTG-infusion (group B; 0-48 h of NTG-infusion; n = 16) in a dosage of 1.5 micrograms/ kg/min. The patients were included if 5 proximal segments of the left coronary artery showed no visible atherosclerosis. A coronary angiography was performed after 24 and 48 h respectively. The lumen diameters were measured by quantitative coronary analysis at baseline and 1 and 3 min after application of 0.2 mg of NTG intracoronarially (i.c.). Blood samples were drawn before and after 24 and 48 h of infusions to measure hematocrit and neurohormones. In group A after 24 h of saline infusion there was a significant increase in lumen diameter from 3.14 +/- 0.17 mm at baseline to 3.51 +/- 0.11 mm (p0.001) and 3.60 +/- 0.21 mm (p0.001) after 1 and 3 min of NTG i.e. respectively. After 24 h of NTG-infusion there were no significant changes in baseline and values after further NTG i.e. In group B after 24 h of NTG-infusion no significant change in lumen diameter was detectable after NTG i.e. (3.57 +/- 0.23 mm to 3.63 +/- 0.13 mm) and the mean diameter remained unchanged after prolongation of NTG to 48 h (3.58 +/- 0.33 mm). There were no significant differences between the baseline values and the responses to i.e. NTG after 24 and 48 h of NTG infusion. Hematocrit and aldosterone levels decreased significantly after NTG-infusion but not following saline. Renin and norepinephrine remained unchanged throughout the NTG-infusion-periods.The vasodilatation of non-obstructed segments of epicardial arteries persists during a prolonged infusion period and there is no induction of vascular tolerance between the 24 and 48 h infusion period. These findings further support that there is a different susceptibility of arteries and veins to nitrate tolerance.

Obstructive sleep apnea (OSA) and coronary heart disease (CHD) are both frequent in the middle ages. Both disease share a similar spectrum or risk factors and attendant diseases. The aim of the study was to determine the prevalence of obstructive sleep apnea in patients with coronary heart disease diagnosed by coronary angiography. Furthermore, influence of sleep apnea and attendant diseases and risk factors for coronary heart disease, especially the risk for myocardial infarction and reduced left ventricular ejection fraction, was investigated. We included in this study 143 patients (121 men, 22 women mean age 60 +/- 8 years (35-81) who underwent coronary angiography because of angina pectoris or were suspicious for CHD due to noninvasive investigations. These patients has symptoms of OSA based on a standardized questionnaire. They underwent a four-channel screening with a non-laboratory-monitoring-system (NLMS) for detection of sleep-related breathing disorders. In addition, spectrum of risk factors and concomitant diseases were considered. Sleep apnea was more frequent in patients with CHD (30.6%) in comparison to patients without CHD (21.8%), but did not reach statistical significance. Patients with CHD and OSA had a significantly higher frequency of a history of myocardial infarction and had a significantly lower left ventricular ejection fraction than patients without OSA.Patients with the combination of OSA and CHD are at higher risk for myocardial infarction and reduced left ventricular ejection fraction. Patients with CHD should be screened for OSA in case of secondary prevention.

A pacemaker syndrome manifested as transient sensoric aphasia in a 68-year-old woman with a VVI-pace-maker implanted after SA-block. The attack occurred during long-term blood pressure recording and Holter monitoring. Borderline hypotension was documented during ventricular pacing which induced a retrograde excitation of the atrium. Clinical investigations excluded any intracranial abnormality, any source of embolism or stenosis of extra- and intracranial cerebral arteries. Cerebral blood flow measurements revealed a significant increase during pacing at elevated heart rate. Therefore, a device for AV-sequential pacing was implanted and basic pacing rate was elevated. The present case report indicates that focal and not only global cerebral ischemia can be produced by an impairment of systemic hemodynamics due to hypotension and a pacemaker syndrome. Improvement of cerebral blood flow during pacing is an unexpected finding contrasting with the concept of autoregulation. In addition, pacemaker implantation should be discussed in patients with transient cerebral perfusion deficits if an improvement of cerebral blood flow is documented along with rising heart rate.

The present study was performed in order to investigate the effect of dilated cardiomyopathy and severe aortic valve disease on cerebral blood flow. Cerebral perfusion was determined in 39 healthy volunteers representing two control groups of different age (77.7 +/- 8.7; 79.7 +/- 8.1 ml/100 g/min), in 7 patients with dilated cardiomyopathy (64.0 +/- 4.7 ml/100 g/min), in 11 patients with severe aortic stenosis (71.1 +/- 14.8 ml/100 g/min), and in 6 patients with severe aortic regurgitation (54.6 +/- 5.8 ml/100 g/min). Regional cerebral blood flow was measured with the 133Xenon inhalation method. Cerebral blood flow in severe aortic regurgitation patients (p = 0.006) was markedly and significantly reduced versus controls, whereas in dilated cardiomyopathy patients (p = 0.197) and in patients with severe aortic stenosis (p = 0.111) cerebral blood flow was not significantly reduced. A chronic adaptation of cerebral blood flow to the profound reduction of cardiac output is assumed in dilated cardiomyopathy patients. The collapsing pulse and the maximal reduction of mean arterial blood pressure in severe aortic regurgitation patients cause the reduction of autoregulatory capacity of cerebral blood flow with subsequent decrease of brain perfusion. Measurement of cerebral blood flow appears to be suitable for evaluation of perfusion deficits due to cardiac abnormalities. It provides an additional parameter for estimating the indication of valve replacement in patients with aortic valve disease.

Calcium channel blockers have a negative inotropic effect and protract the relaxation of the normal myocardium. These effects may vary in patients with coronary artery disease (CAD) and with the different kinds of calcium antagonists. In the present study we therefore compared the hemodynamic effects of intravenously given equihypotensive dosages of diltiazem (D) and nisoldipine (N) in patients with CAD.Each group contained 10 patients. After administration of a bolus of 300 micrograms/kg (D) and 5 micrograms/kg (N) respectively and following continuous infusion of 5.4 micrograms/kg/min (D) and 0.2 micrograms/kg/min (N) respectively, the mean arterial pressure was reduced by 15.5 +/- 6.0 (D) and 16.6 +/- 4.1 (N) mm Hg. Atrial pacing was performed in all patients to avoid reflectory heart rate effects. The pulmonary artery pressure decreased slightly with both drugs, whereas the cardiac index increased only with the use of N from 3.44 l/min x m2 to 3.93 l/min x m2. A significant change in the maximal rate of rise of left ventricular pressure (dP/dt max) as an index for inotropy was not detected for N or for D. The parameters of the diastolic function (the time constant of ventricular relaxation (tau) and the maximum rate of left ventricular isovolumic pressure decline (dP/dt min)) also did not indicate unequivocal drug effects. Doppler echocardiography of the mitral valve flow was performed simultaneously with invasive pressure measurements. The flow propagation derived from the color-M-mode correlated significantly with tau and was slightly improved by D.(ABSTRACT TRUNCATED AT 250 WORDS)

Transluminal coronary extraction-endarterectomy is an alternative interventional approach for treatment of coronary artery disease. The atherectomy system consists of a catheter assembly including a cutter and torque tube which is rotated at a relatively low rate of 750 rotations per minute, when introduced to the coronary artery over a guide-wire via a guiding catheter. Excised tissue is withdrawn from the coronary artery by suction applied through the catheter by means of an attached vacuum bottle. We report acute results in 18 patients and the clinical outcome of 14 patients who up to now underwent angiographic follow-up catheterization after 6 months. Initial angiographic success (residual stenosis less than 50%) using TEC-atherectomy alone was obtained in 6/18 patients (33%), 11/18 patients (60%) required additional PTCA in order to achieve primary success (9/18) or to treat total occlusion (2/18) after TEC-atherectomy. Major complications consisted in 1-vessel perforation with non-Q-wave-infarction but no need of surgical intervention and 2 occlusions due to dissection (treated with PTCA). 14 patients underwent angiographic follow-up (6 months) and restenosis (greater than 50%) was confirmed in 7 patients (50%). Considering the low primary success rate of TEC-atherectomy alone and the tendency to high restenosis rate, we cannot recommend it as an alternative to conventional PTCA in general clinical practice. Further studies should be designed to directly compare TEC-atherectomy to PTCA in specific patient subgroups (e.g. bypass grafts, intraluminal thrombus, diffuse disease) in order to define the role of this interventional device.

We report on a male, 31 year old, Turkish patient with an intracardiac mass in the right ventricle, reduction of performance and weight, as well as intermittent fever. No eosinophilia was documented in the peripheral blood; cardiac function was primarily normal. Besides the differential diagnosis of Loffer's endocarditis (endomyocardial fibrosis) an inflammatory disease and a malignant cardiac tumor were suggested. The diagnosis of Loffler's endocarditis could not be confirmed morphologically by echocardiography nor histologically by right ventricular biopsy. Operative removal of the mass lesion was necessary because of fast tumor progression, fulminant pulmonary embolism, and infiltration of the tricuspid valve. Only then, histologically Loffler's eosinophilic endocarditis of thrombotic stage was diagnosed. Antiphlogistic therapy with cortisone was initially performed. With a dose reduction after 6 months, a relapse of the thrombotic mass occurred. Therefore, continuous treatment with cortisone and azathioprine was induced followed by further tumor regression and further clinical stabilization since 8 months of treatment.