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A 28-year-old male patient with sickle cell disease developed a vasoocclusive crisis with an acute chest syndrome and severe lung failure.After partial substitution transfusion the patient was successfully treated extracorporeal membrane oxygenation (ECMO). After 12 days he was weaned from the ECMO, 2 days later the patient's tracheostoma was removed. 19 days after the event the patient had recovered completely and was moved to a hospital in Paris from where he came.Apparently data is sparse regarding the use of ECMO for treatment of a life-threatening acute chest syndrome in sickle cell disease. However, the therapy approach seems to be promising and is worth considering in this particular situation.

Commonly, pulmonary hypertension is clinically suspected because of unexplained exertional dyspnoea or as a chance finding in clinical examination revealing signs of right heart failure. The systematic diagnostic approach and exact classification is based on the Venice classification. Basic investigations include ECG, chest radiograph, lung function studies and echocardiography. Echocardiography is the most important investigation for the diagnosis of pulmonary hypertension. It also serves as non invasive control during treatment and as the main screening test for pulmonary hypertension. Echocardiographic criteria of pulmonary hypertension are a dilated and hypertrophied right ventricle, paradoxic septum movement, a dilated right atrium, and a distended inferior Vena cava. Using Doppler echocardiography, the right ventricular and thus pulmonary arterial systolic pressure can be determined from the tricuspid regurgitant jet velocity. CT of the chest serves to exclude pulmonary embolism and interstitial lung disorders. Cardiac MRI is increasingly being used for analysis of right ventricular morphology, function and haemdynamics. The 6 minute walk test and cardiopulmonary exercise test are used to assess severity and response to treatment and give prognostic information. For the definite diagnosis of pulmonary hypertension, right heart catheterisation is required for the determination of the pulmonary vascular resistance and pharmacological testing of "reversibility".

More than 25 years ago it was demonstrated that an improvement in various parameters of blood flow in patients who have an hyperviscosity syndrome improves coronary blood flow. Hyperfibrinogenemia with resulting increase in plasma viscosity and erythrocyte aggregation has been demonstrated in patients with coronary heart disease. Poiseuille's law, which describes the interaction between vascular resistance, vessel geometry and blood viscosity, indicates--when applied to coronary artery disease--that an increase in the viscosity of blood, especially of plasma, can in the poststenotic microcirculation be a flow-limiting factor and a critical determinant of oxygen supply to myocardium that is at risk of ischaemia. An increased concentration of fibrinogen, which is the substance that causes the increase in plasma viscosity, has been shown to correlate prospectively with the risk of serious cardiovascular events. Patients with multiple-vessel coronary heart disease and treatment-refractory angina pectoris have clearly increased fibrinogen values. Chronic intermittent urokinase administrations--given with the aim of achieving fibrinogenolysis of the elevated fibrinogen concentration at a dose of 500 000 IU urokinase three times weekly -improves the rheological parameters and achieves an impressive decrease in symptoms. It is thus important in clinical practice to take into account that patients with atherosclerosis and a fibrinogen concentration of more than 300 mg may develop perfusion disorders and worsening of their symptoms.

Whereas the right ventricle tolerates volume loads without any substantial increase of the pressure in the pulmonary circulation by recruiting capacitance vessels and capillaries, it possesses only small contractile reserves and reacts unadapted with right ventricular dysfunction. Its size and pressure load are relevant factors for prognosis of all forms of pulmonary hypertension, in particular if linked to left-sided heart failure. Differentiation of pulmonary hypertension according to the Venice classification is highly important. Right-sided ventricular heart failure worsens left ventricular hemodynamics due to reduced ejection fraction and in addition due to direct diastolic ventricular interaction in which left ventricular diastolic dysfunction increases even though the left ventricular systolic function is still intact. Right ventricular ejection fraction40% is an important predictor of prognosis after myocardial infarction or chronic stages of left ventricular heart failure. The most important noninvasive diagnostic method is transthoracic echocardiography with determination of the Tei index and Doppler echocardiographic estimation of pulmonary artery pressure. Chronic obstructive pulmonary disease is the most frequent cause of cor pulmonale. While long-term oxygen therapy in patients with COPD and cor pulmonale and for example the administration of endothelin receptor antagonists in patients with idiopathic pulmonary hypertension is beneficial, the therapeutic use of drugs effective for left-sided heart failure is very limited in patients with right ventricular dysfunction.

Patients with ischaemic heart disease commonly have an impaired glucose tolerance. On the 2004 congress of the ESC, the 75-75-rule was announced, indicating that 75% of all diabetics die of cardiovascular complications, and that 75% of all patients with myocardial infarction have diabetes or an (often undiagnosed) impaired glucose tolerance. Data of our "Esslinger Koronarregister" confirm that diabetics and in particular women with diabetes have a higher mortality both after STEMI and NSTEMI. During acute myocardial infarction, a higher blood glucose level strongly correlates with increased mortality. This increased blood glucose level on the one hand is due to preexisting diabetes mellitus or metabolic syndrome, but on the other hand may be a marker of larger myocardial damage with excess katecholamine release. Recent data indicate that intensive glucose control results in a reduction of cardiovascular risk, e. g. the risk of sudden cardiac death. The data presented show that an early intervention in preclinical diabetics aiming at normalization of blood glucose control is necessary in order to reduce cardiovascular mortality.

A 64-year old woman was admitted because of unstable angina pectoris. The coronary angiogram revealed two-vessel coronary disease with predominantly subtotal stenosis of the right coronary artery, which was treated by primary coronary stenting. The post-interventional clinical course after closure of the right femoral artery was complicated by the development of a complex pseudoaneurysm: its ultrasound-guided compression was unsuccessful.The clinical findings included a marked superficial hematoma in the right groin without any evidence of an abscess, confirmed by color duplex ultrasonography.24 hours later a successful percutaneous ultrasound-guided thrombin injection of the pseudoaneurysm was performed without any problems regarding the injection into the aneurysm. A small area within the aneurysm remained perfused and was treated by additional ultrasound-guided compression. A few minutes after the compression complete thrombosis of the right superficial femoral artery occurred with acute critical ischemia of the right leg, probably due to leakage of thrombin into the femoral artery at the sheath puncture. The immediate therapy, including interventional recanalization of the right femoral superficial artery and subsequent fibrinolysis, produced a complete reperfusion of the right femoral superficial and popliteal artery. The fibrinolytic therapy resolved the thrombosis of the pseudoaneurysm. The remainder of the perfused pseudoaneurysm was treated surgically after one week without problems.This case demonstrates a so far rarely published complication of the displacement of thrombin from an intervention ally treated pseudoaneurysm into the right superficial femoral artery through a broad compound channel after ultrasound-guided compression.

Besides classical, modifiable risk factors (hypercholesterolemia, hypertension, smoking) abnormalities of the glucose metabolism (diabetes mellitus, impaired glucose tolerance) are strong emerging cardiovascular risk factors. Epidemiological data indicate that 8 % of the population and up to 60 % of patients with coronary artery disease have abnormalities of glucose metabolism. The prevalence of these abnormalities will increase as the population ages and the mean body weight increases. An abnormal glucose concentration damages the endothelium in several ways: increased oxidative stress, inflammatory processes and an activation of procoagulant factors all impair endothelial function. A blood glucose normalising therapy is thought to decrease the incidence of cardiovascular events in these patients. In patients with an acute myocardial infarction and diabetes mellitus an early intensive insulin therapy improves the outcome of these patients. In summary, the early detection and treatment of abnormalities of glucose metabolism reduces cardiac events.

Various studies demonstrated an interdependence between rheological parameters and advanced stages not only of ischaemic heart disease and peripheral arterial occlusive disease, but also of chronic obstructive lung disease. In ischaemic heart disease, rheological alterations in the poststenotic circulation can result in impairment of the oxygen supply of the myocardium. Rheological therapies aim for a reduction in plasma viscosity and improved microcirculatory flow by means of a reduction of the elevated levels of fibrinogen. As an example, intermittent therapy with urokinase has been established as a treatment of refractory angina pectoris. Treatment with fibrates also can result in an improvement of microcirculation due to reduced hepatic fibrinogen synthesis. Treatment with statins leads to an improvement of microcirculation due to effects on serum lipids. In patients with chronic obstructive lung disease and cor pulmonale who, secondary to chronic hypoxia, develop polycythaemia and disturbances in pulmonary microcirculation, isovolumic haemodilution may result in a reduction of pulmonary arterial pressure with consecutively increased cardiac output and improved exercise capacity.

During pregnancy, major cardiovascular changes occur. The aim of the following study was to investigate the course of hemodynamic parameters under the increased volume load during pregnancy and delivery in women with insulin-dependent diabetes mellitus.We examined 51 pregnant diabetic and 51 healthy pregnant women. The control group consisted of 51 healthy non-pregnant women. In all women, left ventricular mass and fractional shortening were calculated. To evaluate left ventricular diastolic function, mitral inflow and pulmonary venous flow profiles were analyzed.During pregnancy left ventricular mass increased, fractional shortening decreased and diastolic dysfunction was found. While the healthy pregnant women developed signs of disturbed relaxation during pregnancy, pregnant diabetic women showed signs of a disturbed relaxation already at the beginning of gestation. A total of 29 pregnant diabetic women developed a restrictive filling pattern already at the 24th week of gestation. The remaining 22 diabetics had a comparable restrictive filling pattern only during vaginal delivery. In 10 of the 29 pregnant diabetic women dangerous complications were documented, while there were no complications in the healthy pregnant women and the other 22 diabetic pregnant women.In healthy women pregnancy results in a reversible physiologic left ventricular hypertrophy, a disturbed relaxation pattern and a temporary decrease of left ventricular systolic function. In contrast, pregnant diabetic women demonstrated a delayed relaxation at the beginning of pregnancy and developed a restrictive filling pattern. The early development of a restrictive filling pattern may predispose to complications during delivery in pregnant diabetic women.

This study was designed to determine the effect of successful coronary revascularisation on left ventricular diastolic function.We consecutively studied the time course of diastolic function by Doppler echocardiography in 100 patients with one-vessel disease before and 48 hours after elective coronary angioplasty. Three abrupt vessel closures occurred within 24 hours after intervention. These three patients were excluded from the study. 58 patients were initially successful treated with coronary angioplasty (residual stenosis40%). In 39 patients stents were used to improve an inadequate result after coronary angioplasty. The following parameters of left ventricular diastolic function were evaluated before and 48 hours after coronary intervention: peak early (VE, m/s) and peak late diastolic (VA, m/s) flow velocity, E/A ratio, acceleration time (AT, ms), deceleration time (DT, ms) and isovolumetric relaxation time (IVRT, ms). Ejection fraction (EF; %) was determined and used to characterise systolic left ventricular function.Both patient groups (58 patients with coronary angioplasty and 39 patients with combined coronary angioplasty and stent implantation) showed no relevant differences concerning sex, age, atherosclerotic risk factors, exercise capacity and results of exercise electrocardiography. All patients who underwent stent implantation showed an early improvement of left ventricular diastolic function 48 hours after revascularisation. Surprisingly there was no significant short-term improvement (48 hours) of diastolic function in patients with initially successful angioplasty.We suppose that stent implantation faster normalises coronary blood flow than coronary angioplasty.

During pregnancy eminent cardiovascular changes occur. The aim of the following study was to investigate the course of hemodynamic parameters under increased volume load during pregnancy in women suffering from mild arterial hypertension.Altogether 47 women (age: 25 +/- 4 years) with mild arterial hypertension detected during pregnancy underwent echocardiography at the 9th, 24th and 33rd week of gestation. Furthermore echocardiography was performed postpartum at weeks 1 and 8. The control group comprised 45 healthy pregnant women. In all patients left ventricular muscle mass index and systolic shortening fraction were measured. The following Doppler echocardiographic parameters were ascertained: peak early diastolic and peak late diastolic flow, VE/VA ratio, acceleration time, deceleration time and isovolumetric relaxation time.During pregnancy all patients had an increase of left ventricular muscle mass index and a decrease of fractional shortening. All patients developed a relevant diastolic dysfunction. While the control group developed signs of disturbed relaxation as reduction of peak early diastolic flow (0.89 +/- 0.07 versus 0.82 +/- 0.08 m/s*), VE/VA ratio and an increase of isovolumetric relaxation time (72 +/- 12 versus 123 +/- 7*) at the 33rd week of gestation (* p0.01), all pregnant women with mild arterial hypertension developed a diastolic dysfunction with signs of delayed relaxation already at the beginning of gestation. 26 pregnant women with arterial hypertension developed a restrictive diastolic filling pattern at 24 weeks of gestation. The other 21 pregnant women only showed restriction for a short time at the end of gestation. In healthy pregnant women, volume load results in a reversible physiologic left ventricular hypertrophia, a significant alteration of diastolic left ventricular function in terms of a disturbed relaxation pattern and a temporary decrease of systolic function. In comparison hypertensive pregnant women show a delayed relaxation at the beginning of pregnancy and 50% developed early signs of restrictive cardiomyopathy. These changes may predispose to critical complications during pregnancy.

Patients with dilated cardiomyopathy (DCM) generally have an impaired functional capacity and poor long-term out-comes. A mortality of 5-15% per year has been described actually. Aim of this study was to verify the prognostic relevance of invasive and non-invasive parameters of diastolic function in patients with DCM. In 33 patients with DCM, cardiac catheterization was performed and left ventricular systolic (ejection fraction (EF; %)); left ventricular enddiastolic pressure (LVEDP; mmHg) and diastolic function (time constant of relaxation (T, ms); the constant of myocardial stiffness (b) were derived from biplane laevocardiography and simultaneous micromanometric registration of pressure-volume curves. For evaluation of clinical out-come, the follow-up period was defined as beginning on the day after cardiac catheterization and ending on the most recent date or with a cardiac event (death or cardiac transplantation). All patients were reevaluated for NYHA functional class and completed a standard questionnaire. The following hemodynamic parameters were evaluated: invasive parameters of left ventricular diastolic function (constant of relaxation: tau (ms), constant of myocardial stiffness: b)), as well as parameters of systolic function (ejection fraction (EF; %)), left ventricular pressure (LVEDP; mmHg), left ventricular muscle mass index (LVMMI; g/m2), left ventricular enddiastolic volume index (LVEDVI; ml/m2) and non-invasive parameters of morphological data, left ventricular systolic (fractional shortening (FS, %) and ejection fraction) and diastolic parameters with echocardiography. During the follow-up period of 36 months, 11 of 33 patients experienced a major cardiac event (cardiac death n = 8, heart transplantation n = 3). The major cause of death was progressive pump failure. The remaining 22 patients were further classified with respect to changes in functional status. While clinical symptoms could be improved medically in patients with moderate increase of myocardial stiffness, patients with severe increase of myocardial stiffness (b: 76.1 +/- 12.1 vs 17.9 +/- +8.1, p0.001) could not be improved and suffered more cardiac events. Doppler echocardiographic measurements in these patients showed a restrictive filling pattern (VE 0.91 +/- 0.21 vs 0.64 +/- 0.18 m/s; p0.01; VA 0.52 +/- 0.23 vs 0.57 +/- 0.24 m/s; p0.01, deceleration time 129 +/- 17 vs 211 +/- 14 ms; p0.01). The medical heart failure therapy was comparable in both groups. In patients with cardiac events, the diastolic left ventricular variables did not significantly differ between patients who underwent heart transplantation and those who died. Patients who demonstrated a sole impairment of relaxation (tau:50 ms) suffered no cardiac events. Impaired diastolic function contributes to the clinical picture of congestive heart failure. Parameters of left ventricular diastolic function are powerful and important predictors of major cardiac events in patients with DCM, like heart transplantation and non-sudden death, and may indicate future clinical success of medical treatment. Invasive and non-invasive parameters of diastolic function reveal comparable information for the estimation of prognosis of patients with DCM in order to initiate early therapy.

Patients with hypertensive heart disease and left ventricular hypertrophy demonstrate impaired left ventricular diastolic filling. Aim of this study was to find out if physiological left ventricular hypertrophy induced by endurance training causes abnormal left ventricular systolic and diastolic filling.We examined 42 athletes with left ventricular hypertrophy due to endurance training (aged 25 +/- 7 years), 31 patients with left ventricular hypertrophy due to hypertensive heart disease (aged 28 +/- 6 years) and 20 untrained, healthy subjects (controls, aged 26 +/- 8 years) by conventional echocardiography and calculated left ventricular muscle mass and fractional shortening. In addition the following Doppler-echocardiographic parameters were measured: maximal early and late velocity of diastolic filling, ratio of maximal early and late velocity of diastolic filling, acceleration and deceleration time and isovolumetric relaxation time.All three study groups showed normal fractional shortening. Conventional echocardiography revealed a higher left ventricular muscle mass in the two study groups as compared to the controls (controls: 119 +/- 12 g, athletes: 225 +/- 18 g*; hypertensive patients: 216 +/- 16 g*; * p0.01 versus controls). In the athletes with physiological left ventricular hypertrophy a normal left ventricular diastolic filling pattern was documented (VE: 0.64 +/- 0.1 m/s; VA: 0.51 +/- 0.2 m/s). In hypertensive heart disease a diastolic dysfunction in terms of a delayed relaxation pattern with a decrease of maximal early velocity of diastolic filling (VE: 0.45 +/- 0.09 m/s) and a compensatory increase of the maximal late velocity of diastolic filling (VA: 0.54 +/- 0.1 m/s) was demonstrated.In pathological left ventricular hypertrophy due to hypertensive heart disease a pathological diastolic filling pattern was documented. In athletes with physiological left ventricular hypertrophy a normal left ventricular diastolic filling pattern was revealed. Thus Doppler-echocardiographic parameters of left ventricular diastolic function can be of diagnostic importance for discriminating between pathological and physiological left ventricular hypertrophy.

During pregnancy many substantial changes occur in the cardiovascular system. Aim of this study was to examine how physiological preload alterations influence left ventricular haemodynamic parameters.During the 9th, 24th and 33rd weeks of pregnancy and 8 weeks after childbirth 36 patients underwent echocardiographic studies. 36 young not pregnant women (25 +/- 7 years) served as controls. The following Doppler echocardiographic parameters were measured: peak early diastolic flow velocity (VE, ms); acceleration (AT; ms) and deceleration time (DT; ms) of flow velocity in early diastole; peak late diastolic flow velocity (VA; m/s) and isovolumetric relaxation time (IVRT; ms). In all women the left ventricular muscle mass index (LVMMI), fractional shorting (FS; %) and the ratio between septum and posterior ventricular wall were calculated.During pregnancy all women showed an elevation of the left ventricular muscle mass index (LVMMI: from 66 +/- 6 to 100 +/- 9 g/m2; p0.01) and a decrease of fractional shortening (FS: from 38 +/- 4 to 31 +/- 3%). All patients developed a relevant diastolic dysfunction: reduced early diastolic flow velocity (VE: from 0.89 +/- 0.11 to 0.83 +/- 0.19 m/s; P0.01), reduced E/A ratio (1.7 +/- 0.4 to 1.2 +/- 0.4; P0.01), prolonged IVRT (72 +/- 12 to 114 +/- 12 ms; P0.01) and deceleration time (DT: to 189 +/- 17 to 227 +/- 18 ms; P0.01). Eight weeks after childbirth all parameters of left ventricular systolic and diastolic functions were normal.Preload alterations during normal pregnancy lead to reversible physiological left ventricular hypertrophy. Furthermore, we found a short-time reduction of systolic function just before childbirth and a significant alteration of the left ventricular diastolic filling pattern (abnormal relaxation pattern). While left ventricular systolic function was normal in all patients one week after childbirth, left ventricular hypertrophy and left ventricular diastolic dysfunction persisted for nearly two months.

Systemic capillary leak syndrome is a rare idiopathic disorder characterized by recurrent episodes of hypotension and hemoconcentration due to sudden transient extravasation of up to 70% of plasma. Less than 40 cases have appeared in the literature. Mortality rates 5 years after diagnosis have been reported to be up to 75%. Clinical findings are generalized edema and intravasal fluid deficiency. Laboratory features include hypoalbuminemia and extreme hemoconcentration. A common finding is a monoclonal gammopathy. Rare manifestation of this syndrome is rhabdomyolysis due to increased compartment pressure and ischemic myonecrosis. Early diagnosis and exclusion of other clinical disorders like rheumatic myopathies and myositis are critical concerning prognosis and therapy. We describe a 46-year-old woman with rhabdomyolysis and systemic capillary leak syndrome whose condition is stable for a total of 30 months under a prophylactic regimen with oral terbutaline plus theophylline. A brief survey of the literature is given.

The report presents a transluminal angioplasty (PTCA) of a severe stenosis of the left anterior descending artery (LAD) behind the anastomosis; the internal thoracic artery (ITA) graft was used as a conduit. Before and after the PTCA the changing of velocity flow patterns under rest and stress conditions with a handgrip-maneuver were measured with a noninvasive transthoracic ultrasound Doppler system. The mean diastolic velocity, which represent coronary perfusion through the ITA graft, increased after successful PTCA at rest and under stress conditions. An additional increasing of the mean diastolic velocity at rest and under stress conditions was seen after six months before the catheterization proposing no signs of restenosis. For this reason the vessel could be classified prospectively patient. This could be confirmed during coronary angiography. We also present a review of the published reports concerning PTCA of ITA grafts and PTCA of the native vessel using the ITA as a conduit. In this review 286 cardiac interventions on 273 patients with a primary rate of success of 87% could be counted, the documented rate of restenosis was 30%, and the rate of complication was approximately 1%. The PTCA in ITA grafts or of the native vessel via ITA grafts, respectively, represent an alternative to reoperation. The ultrasound-duplex measurements are gaining an increasing significance for the noninvasive patency rate and post-interventional monitoring of the long-term PTCA result. With the augmentation of the ITA as a coronary bypass and expected increase of post-operative interventions, a noninvasive tool is necessary.

Meningococcal septicemia is still associated with high mortality with most deaths occurring within the first 24 hours.We report on 3 patients with severe meningiococcemia. All patients had an aprupt onset of clinical illness with fever and unspecific prodomi like arthralgias, myalgias and abdominal pain. On admission all patients had severe prostration, hypotension and tachycardia. Two patients presented purpuric rash and petechiae, meningitis was found in only 1 patient. Gram-negative diplococci were demonstrated in spinal fluid primarily in 2 patients, in all patients meningococcae could be cultured in serial blood specimens. Because of severe cardiorespiratory distress all patients required mechanical ventilation and catecholamine support within 24 hours of diagnosis. Complications of meningococcemia demonstrated by these patients were coagulopathy, meningitis, myocarditis with alterations of echocardiographic and ECG records and elevations of CK levels and surgical relevant peripheral gangrene. Antibiotic therapy was initiated with penicillin on the day of admission, which resulted in stabilisation and recuperation in all patients.In patients with aprupt onset of acute illness, which include fever and sudden petechial rash, severe meningococcal septicemia has to be taken in consideration without clinical signs of meningitis. The prompt diagnosis, the use of parenteral antiobiotics in suspected meningococcal disease as well as the management of meningococcemia and its complications in intensive care units is crucial for the prognosis of the individual patient.

The early determination of the myocardial manifestation is of considerable importance, since the prognosis of patients (P) with insulin dependent diabetes mellitus (IDDM) is generally masked by secondary cardiac complications. The aim of this study was to investigate whether young, asymptomatic P with IDDM and persisting normal systolic left ventricular (LV) function already show a diastolic LV dysfunction.An echocardiographical examination of 92 IDDM patients (age: 25 +/- 4 years) without known cardiac disease and of 50 control persons (C) of similar ages was carried out. P with a cardiac disease or long-term diabetic syndrome were excluded. Using M-mode echocardiography, morphological parameters and systolic time-intervals (fractional shortening; ejection fraction) were determined. Doppler indices were then measured: maximal early and late diastolic flow velocity (VE; VA), E/A ratio, acceleration and deceleration time (DT), isovolumetric relaxation time (IVRT).Although the left atrial and left ventricular dimensions, as well as the systolic functional parameters of all P with IDDM were normal, they showed a diastolic dysfunction with a reduction of the early diastolic filling (VE; 0.54 +/- 0.07 m/s vs 0.72 +/- 0.04 m/s; p0.01) and the E/A ratio (0.9 +/- 0.15 vs 1.99 +/- 0.22; p0.01), an increase in the atrial filling (VA; 0.76 +/- 0.05 m/s vs 0.39 +/- 0.04 m/s, p0.01), an extension of the IVRT (129 +/- 23 ms vs 78 +/- 6 ms, p0.01), and an increased DT (248 +/- 27 ms vs 188 +/- 8 ms, p0.01).Even young P with IDDM, with a normal systolic ventricular function, suffer a diastolic dysfunction which serves as a marker of a diabetic cardiomyopathy. Therefore, echocardiography with measurements of systolic and diastolic functional parameters appears to be a sensible method for evaluating the course of diabetic cardiomyopathy.

Right ventricular dysfunction is common in patients with chronic obstructive pulmonary disease. Right ventricular function might be influenced by the afterload, which depends on pulmonary artery pressure (PAP) and pulmonary vascular resistance (PVR). To evaluate the influence of the right ventricular afterload on right ventricular performance, we investigated 30 patients with chronic obstructive pulmonary disease without clinical signs or history of left heart failure or coronary heart disease. The study includes lung function tests, analysis of blood gases and right heart catheterisation. RV function was assessed by a thermodilution technique using a pulmonary artery catheter equipped with a rapid response thermistor (produced by Baxter, USA). There are 9 patients with normal, 12 with latent and 9 with fixed pulmonary hypertension. Median RVEF was measured to be 33.3% (19-44%). There was a significant correlation between RVEF and PAP (r = -0.66; p0.0001) and RVEF and PVR (r = -0.54; p0.0018). RVEF was not directly influenced by lungfunction or pulmonary capillary wedge pressure (PCWP). Under treadmill exercise RVEF and cardiac index increased without a change of PCWP. A low RVEF at rest seems to be a predictive value for a reduced exercise capacity. A reduced RVEF has a predictive value of pulmonary hypertension with a sensitivity of 66% in patients with unstable and 89% in patients with lasting pulmonary hypertension. In a subgroup of 6 cases treadmill exercise led to a RVEF decrease. These patients showed no difference in afterload, blood gases or lung function-tests compared with the total group. In conclusion, right ventricular ejection fraction seems to be influenced by PVR and PAP which determinate the right ventricular afterload. The validity of the method depends on the severity of pulmonary hypertension, and hence measurement of RVEF might not provide a reliable estimation of pulmonary arterial pressure in patients suffering from mild to moderate pulmonary hypertension.

Fibreoptic bronchoscopy is an established diagnostic procedure for HIV-associated pulmonary infections. We retrospectively evaluated the diagnostic effectivity and safety of fibreoptic bronchoscopy with bronchoalveolar lavage (BAL) and transbronchial biopsy (TBB) in 153 patients with late-stage HIV infection and clinical signs of pulmonary infection or abnormal chest radiograph. Bronchoscopy leads to diagnosis in 82.4% and changed therapy in 54%. 45 patients (30%) were found to have pneumocystis carinii pneumonia (PCP), the most common bronchoscopic finding, followed by bacterial lung disease (29.3%). BAL had a sensitivity of 78% for PCP. Diagnostic yield of BAL for PCP was higher in patients without previous treatment (positive results in 82%) with regard to PCP independend of the prior treatment. Serious complication occurred in 22 cases (pneumothorax: 6 (3.9%), bleeding: 12 (7.8%), hypoxaemia: 4 (2.6%)). High serum levels of lactate dehydrogenase (LDH) correlated with pulmonary complications like pneumothorax. Age, sex and kind of pulmonary infection did not influence complication rates. 6 (3.9%) episodes of spontaneous pneumothorax occurred in the further course, 3 of them concurrently with PCP or prior history of PCP. We conclude that fibreoptic bronchoscopy is of great value for diagnosing pulmonary infection in HIV-seropositive patients. TBB provides incremental diagnostic information not available from BAL, especially in patients pretreated with cotrimoxazol or pentamidin. For that reason we believe that TBB should be performed in these patients.

Antithrombotic therapy is a basic part in the treatment of acute as well as chronic coronary syndromes. The rationale is an enhanced platelet activity with predomination of procoagulatory mechanisms in coronary artery disease. The current status of antiplatelet drugs, anticoagulation, and chronic thrombolysis used in the treatment of chronic coronary syndromes is discussed. It is concluded that low-dose aspirin is the current drug of choice for long term oral treatment in patients with stable chronic coronary artery disease. In contrast, oral anticoagulation with coumadin should be considered in patients with higher risk for atrial or ventricular thrombosis. The impact of long-term intermittent urokinase therapy in patients with end-stage coronary artery disease and refractory angina pectoris leads to a marked improvement of clinical symptoms. Oral blockade of platelet membrane glycoprotein IIb/IIIa receptor and clinical trials regarding antiischemic effects of low-molecular weight heparins in chronic coronary syndromes are expected for the future.

During the last 25 years the internal thoracic artery has become a well established conduit for coronary revascularization. Next to angiography, duplex-sonography is increasingly used as a non-invasive imaging procedure for the evaluation of this graft vessel. Preoperative investigation in 117 patients has yielded a high level of agreement between angiography and duplex-sonography. While the preoperative flow-pattern is dominated by systolic flow as it is typical for vessels supplying skeletal muscle, the postoperative findings show an adaptation to the coronary vascular bed as the diastolic flow increases. These non-invasive measurements are well matched with invasive intravascular recordings. Coronary angiography and duplex-sonography of the internal thoracic artery yielded comparable findings in respect to the procedural result. Considering the increasing use of the internal thoracic artery in coronary artery bypass surgery, this non-invasive method should gain increasing relevance.

Patients with refractory angina pectoris and end-stage coronary artery disease represent an increasing clinical problem. Numbers of these patients will increase in the future for improved survival due to effective secondary prevention of coronary artery disease. Next to the evaluation of clinical symptoms non-invasive objective parameters of myocardial ischemia are of major relevance before initiation of alternative treatment modalities and for verification of antiischemic effectiveness. Based on our own experience it can be shown that in these patients testing which is mainly based on the patients physical exercise capacity is only of limited value due to the early occurrence of clinical symptoms. Furthermore diffuse perfusion abnormalities reduce the sensitivity of electrocardiographic and scintigraphic detection of ischemic changes. In contrast indirect measures of ischemia relating to the systolic or diastolic function of the left ventricle like doppler-echocardiography and radionuclide ventriculography seem to be promising approaches. This is confirmed by the results from the application of long-term intermittent urokinase therapy. Long-term intermittent urokinase therapy leads to an absolute enhancement of myocardial perfusion, which makes this approach superior to other medical interventions which are mainly based on a reduction of cardiac work-load.

A 55-year-old female patient reported left-sided chest pain at rest as well as during exercise, which recurred during the last three years before admission. Cardiovascular risk factors included hypercholesterolemia and smoking. The physical examination of the patient was unremarkable.The ECG at rest showed T-wave inversions in leads I, aVL, V3-V6 and ergometric exercise testing resulted in angina pectoris and descending ST-segments in leads V3-V6. Stress thallium 201 scintigraphy demonstrated a reversible perfusion deficit of the the anterior wall at peak exercise. The left ventricular angiogram and echocardiogram revealed normal end-diastolic dimensions and regular systolic contractions without signs of left ventricular hypertrophy. Selective coronary arteriography excluded hemodynamically relevant stenosis of the coronary arteries. A coronary artery fistula originating from a large, ectatic first diagonal branch with drainage into the left ventricle was observed.Because the patient rejected interventional therapy she was treated conservatively and follow-up investigations 3 and 4 years after arteriography revealed unchanged clinical symptomatology.In this case a "coronary steal" phenomenon caused by the coronary fistula induced myocardial ischemia. Therefore if present congenital coronary anomalies have to be considered in patients with chest pain and normal coronary angiogram.

To investigate in patients with arterial hypertension (HT) the extent of left ventricular (LV) hypertrophy and diastolic function in relation to atrial arrhythmias.In 112 hypertensive patients (40 women, 72 men; mean age 50 +/- 6.6 years) with a mean systolic blood pressure for the cohort of 170 +/- 5 mmHg, their first invasive coronary angiography was performed between July 1995 and October 1997 because of angina pectoris and/or an abnormal stress electrocardiogram. After excluding coronary heart disease LV dimensions and diastolic function were measured by echocardiography; in 59 of the 112 patients LV hypertrophy was demonstrated. In addition, long-term blood pressure monitoring, exercise and long-term electrocardiography, late-potential analysis and measurement of heart rate variability were undertaken. The control group consisted of 51 patients without arterial hypertension after exclusion of coronary heart disease.Even in the hypertensive patients without LV hypertrophy diastolic LV function and ergometric exercise capacity were reduced. The risk of LV arrhythmias was significantly higher in patients with LV hypertrophy than those without and in the control group, as measured by the complexity of atrial arrhythmias (P0.001), the incidence of abnormal late potentials (P0.001) and reduction in heart rate variability (29.3 +/- 5.3 ms vs 47.8 +/- 12.1 ms vs 60.7 +/- 6.6 ms; P0.001). There were similar results regarding severe complex atrial arrhythmias (38.5 vs 15.0 vs 0%; P0.001). The incidence of atrial arrhythmias correlated with the LV diameter (r = 0.68, P0.001), LV morphological dimensions and diastolic function (isovolumetric relaxation time r = 0.44, P0.001) and the ratio of early to late diastolic inflow (r = 0.46; P0.001).Hypertensive patients have a higher risk of atrial and ventricular arrhythmias, depending on the degree of LV hypertrophy. But atrial arrhythmias, in contrary to ventricular arrhythmias, are also closely related to abnormalities in LV diastolic function.

Diagnostic and interventional heart catheterization in peripheral vascular disease often requires due to iliacal disease additional methods of arterial approach besides the Judkin's technique. The percutaneous catheterization of the brachial artery finds widespread use. A major complication linked with this method is an increased rate of thrombotic occlusions at the puncture site. Thus, we investigated in a prospective set-up the ability of duplex ultrasound to identify predictive risk factors for vascular complications. Over a period of 20 months, 8000 patients referred to heart catheterization were studied. Routine catheterization via the femoral route was contraindicated in 34 out of 8000 mostly due to severe peripheral vascular disease with multiple vascular risk factors (diabetes, hypertension, and smoking). 53 patients who had a comparable low risk-profile served as the control group. The brachial artery was examined by ultrasound duplex for vessel anatomy and diameter at the puncture site before coronary angiography. Both groups (patient and control group) showed in 15% a variable anatomy with a premature division of the brachial artery in 6% proximal of the elbow and in 9% already distal to the axillary artery. Because of reduced diameters of these variable vessels no procedure was carried out at these arms. In all cases the opposite arm was successfully used instead, because the variants were always located only at one arm. The diameter of the brachial artery measured in average 5.0 +/- 0.8 mm and 4.8 +/- 0.7 mm in patients and controls, respectively. Women had a significantly smaller vessel diameter than men, measuring a difference of 0.4 and 0.6 mm, respectively (p0.05). For coronary angiography 6F and 7F arterial sheats were used equally, and in 32% of all cases a coronary intervention was performed. 31 (91%) procedures were carried out without complications; there was a false aneurysm in 1 patient (3%) and an occlusion of the brachial artery at the puncture site in 2 patients (6%). The occluded vessels of two diabetic women had a reduced diameter at the level of 10% of the standard distribution and an unfavorable ratio of sheat-to-vessel-diameter which lead initially to an obstruction of nearly 50% of the vessel lumen during catheterization. Screening of the brachial artery by ultrasound duplex before a percutaneous catheterization for coronary angiography and intervention showed reproducibly the variable anatomy and differences in vessel diameter, which can be risk factors for thrombotic occlusion. Important details for the location of the puncture site and the possible size of the arterial sheat can be obtained, so that coronary interventions with 7F catheter systems are still practicable. This technique is a simple and efficient method to estimate the relative risk of arterial occlusion prior to percutaneous puncture of the brachial artery, especially in a group of patients with severe atherosclerosis and elevated vascular risk-factors.

Even in the era of coronary stenting, acute coronary artery occlusion continues to represent a significant limitation of percutaneous transluminal coronary angioplasty (PTCA). Despite application of heparin and aspirin, abrupt vessel closure still occurs in 2-8%, depending on the definition applied. Especially patients receiving PTCA for acute coronary syndromes are at high risk for abrupt vessel closure. The formation of an intracoronary thrombus plays a central role in the pathogenesis of abrupt vessel closure. Dipyridamole induces dilatation of coronary arteries and prevents platelet aggregation by a mechanism that differs from that of aspirin. The primary purpose of the study was to evaluate whether adjunctive local intracoronary therapy with dipyridamole could reduce the incidence of coronary artery occlusion following PTCA. Secondary endpoints were defined as myocardial infarction, necessity for bypass grafting, and death. In 939 PTCA procedures performed for stable angina and in 155 angioplasty procedures for acute coronary syndromes (unstable angina, acute myocardial infarction), patients were randomized to receive conventional pretreatment consisting of heparin 15,000 I.E. and aspirin 500 mg i.v. or additional intracoronary infusion of dipyridamole (0.5 mg/kg body weight). Dipyridamole was applied in 550 interventions (455 interventions in men, 95 interventions in women, age = 59.2 +/- 8.4; 74 emergency procedures); conventional pretreatment was performed in 544 interventions (444 interventions in men, 100 interventions in women, age 58.3 +/- 7.9; 81 emergency procedures). Intracoronary application of dipyridamole resulted in a significant reduction in the incidence of abrupt vessel closure following PTCA. This significant reduction was observed in patients presenting with stable ischemia as well as in patients receiving PTCA for acute coronary syndromes. Concerning secondary end points, intracoronary application of dipyridamole did not affect the need for bypass grafting or the incidence of death following PTCA. Intracoronary application of dipyridamole was associated with a reduction in the incidence of myocardial infarction following PTCA which, however, failed to reach significance.

Despite progress in the invasive revascularization procedures and even though conventional antianginal treatment has improved the quality of life in patients with symptomatic coronary artery disease considerably, an increasing number of patients suffers from end-stage coronary artery disease and refractory angina pectoris. For these refractory patients long-term intermittent urokinase therapy was developed as an antithrombotic intervention, which is based on its capacity to enhance thrombolysis and blood rheology, and may possibly lead to plaque regression. The coronary syndrome of refractory angina pectoris is characterized by a mismatch of severe coronary insufficiency and a relatively large amount of viable myocardium as indicated by an only moderately impaired left ventricular function. Prior to initiation of long-term intermittent urokinase therapy all potential measures to improve myocardial perfusion have to be considered in each patient. These supportive measures include rigorous reduction of LDL-cholesterol, which has proven antiischemic properties due to an improved endothelial function of epicardial conductance vessels possibly resulting in an antianginal effect. Apart from the proven antiischemic properties of long-term intermittent urokinase therapy in patients with refractory angina pectoris, objective signs of ischemic myocardial heart failure improve. Follow-up studies demonstrated a significant increase of left ventricular ejection fraction as evaluated with multi-gated blood pool analysis. Furthermore, left ventricular diastolic function normalized after a treatment period of 12 weeks. As the clinical effects last well beyond the actual treatment period and as they are accompanied by a remarkable increase in the quality of life, a complex approach as this one is justified in this highly symptomatic patient group.

Patients with untreated sleep apnea syndrome have a higher cardiovascular mortality. It is not known which mechanisms lead to this increase in mortality and whether it is independent from the often associated coronary heart disease and systemic hypertension. In 48 consecutive patients with coronary heart disease confirmed by angiography, exercise-ECG, Holter-ECG, echocardiography, spirometric tests, analysis of ventricular late potentials, heart rate variability and a test for sleep-disordered breathing with a screening device were performed. Seventeen patients showed disordered breathing during sleep (obstructive sleep apnea) with a desaturation index ofor = 10 (mean desaturation index 17.3 +/- 9.3 vs. 2.6 +/- 3.1 in the patients without sleep-disordered breathing). There are no significant differences in age (58.9 +/- 6.1 vs. 59.7 +/- 7.6 years), body-mass-index (28.6 +/- 3.7 vs. 27.7 +/- 3.3 kg/m2), left ventricular ejection fraction (57.2 +/- 13.6 vs. 64.0 +/- 14.6%), forced expiratory volume in 1 second/vital capacity 95.4 +/- 13.9 vs. 92.9 +/- 11.2% predicted, heart rate variability (standard deviation of the RR-intervals 39.4 +/- 29.4 vs. 37.2 +/- 17.0 ms), the frequency of premature ventricular beats over 24 h and at night, the frequency of multivessel disease (71 vs. 68%), additional hypertension 53 vs. 48%), status postmyocardial infarction (47 vs. 48%) and positive late potential analysis (24 vs. 13%). There were no ST segment depressions during the night. Patients with coronary heart disease and mild sleep-disordered breathing show no significant differences in the investigated parameters compared with patients without obstructive sleep apnea or sleep-disordered breathing.

Patients with end-stage renal disease (ESRD) have a high incidence of coronary artery disease. In 30-60% of these patients coronary artery disease can be demonstrated by coronary angiography often prompting myocardial revascularization. Previous studies on PTCA in patients with ESRD have suggested a high rate of procedural complications and restenosis. We studied the rate of restenosis after PTCA in 23 patients with chronic renal failure (17 males, 6 females, age: 52.5 +/- 18.3 years). After primarily successful PTCA all patients were restudied angiographically within 6-12 months. Using quantitative coronary angiography 13 patients (56%) demonstrated restenosis (stenosis50% luminal diameter). In 11 of these patients further revascularization therapy was indicated (6 x PTCA, 5 x CABG). Before follow-up angiography 12 patients demonstrated recurrence of angina pectoris, the sensitivity of clinical symptoms for angiographic restenosis was 69%. High concentrations of triglycerides (265 +/- 160 mg/dl), total cholesterol (258 +/- 53 mg/dl) with low HDL-levels (34 +/- 14 mg/dl) as well as elevated plasma levels of fibrinogen (481 +/- 114 mg/dl) were measured before PTCA. The mechanisms contributing to the high rate of coronary restenosis in patients with ESRD remain unclear, influence of lipid abnormalities, hemostatic factors and fibrinolytic state as well as primarily uremic factors have to be discussed. Prospective interventional studies are needed to address the relevance of PTCA for myocardial revascularization in this patient group.

We analyzed the incidence and management of major vascular complications at the arterial puncture site following diagnostic or interventional cardiac catheterization. 27387 cardiac catheterization procedures were performed for diagnostic (n = 19581) or interventional (n = 7806) purposes at our institution during a 7-year study period. A total number of 114 major vascular complications (0.42%) were identified. In 36 (0.13%) patients an arterial occlusion at the puncture site was detected, 34 patients (0.12%) had severe hematoma (blood transfusion or surgical repair necessary), 32 patients (0.12%) developed false aneurysms, 9 patients (0.03%) with av-fistulas and 3 patients (0.01%) had other complications. The following factors were predictive for a significant increase in the incidence of major vascular complications: Female gender, interventional catheterization using larger introducer sheaths and necessitating effective perioperative doses of heparine, and peripheral vascular disease. Operative repair was necessary in 62 patients (54%), 34 patients (30%) were treated conservatively. In 18 patients (17%) acute vascular occlusion could be managed by percutaneous transluminal balloon dilatation and intravascular thrombolysis of the obstruction, in 3 patients additional stent-implantation was necessary in the presence of a large occlusive dissection. Overall the rate of clinically significant major vascular complications is low. In the future a greater number of vascular complications at the entry site for cardiac catheterization will be treated with nonoperative methods (e.g. manual compression of pseudoaneurysms or catheter-based techniques for recanalization of acutely occluded vessels.

Apart from the relevance of disorders of lipid metabolism for the clinical and morphological progression of coronary artery disease, coronary thrombosis has received increasing attention in recent years. It is undoubtedly the decisive factor in the pathogenesis of acute coronary syndromes, which is underlined by the therapeutic success of various antithrombotic interventions. Furthermore coronary thrombosis is regarded to be a key factor for morphological disease progression also in stable coronary syndromes, which eventually may lead to critical limitation of myocardial perfusion. This is caused by the formation of subclinical coronary thrombi, which either undergo endogenous lysis or become morphologically fixed as they are incorporated into the plaque. Besides local factors, systemic disturbances of hemostasis and endogenous thrombolysis are of relevance. The concept of thrombotic progression of coronary thrombosis is supported by data on the reduction of morphological disease progression or antiischemic effectiveness of anti-thrombotic interventions like aspirin, low-molecular weight heparin and low-dose intermittent urokinase therapy. Percutaneous transluminal coronary angioplasty results in deep mechanical injury of the vessel wall, which is accompanied by secondary coronary thrombosis in the majority of the cases, not necessarily leading to abrupt vessel closure. Particularly, dilatation of primary thrombus as it has been described as the substrate of the culprit lesion in unstable coronary syndromes, promotes release of thrombin and activation of platelets, which in turn furthers the proliferative processes in the pathogenesis of restenosis. Even though data on the reduction of the rate of restenosis by the use of platelet aggregation inhibitors like aspirin, ticlopidin and dipyridamole have not consistently supported this concept, the EPIC. Study has shown that even in patients with stable angina pectoris clinical restenosis rate may be reduced by a platelet-IIb/IIIa-antagonist.

Long-term intermittent urokinase therapy has been developed for patients with severe coronary artery disease and refractory angina pectoris. This therapeutic approach is predominantly effective at the microcirculatory level based on a combination of rheologic and fibrinolytic effects; furthermore, plaque regression seems to be a possible mechanism. Patients with refractory angina pectoris are characterized by severe coronary artery disease without a therapeutic option for conventional revascularization procedures, only slight impairment of left ventricular systolic function and hyperfibrinogenemia, which results in further enhancement of myocardial ischemia due to microcirculatory impairment of blood flow. In this article data on the anti-ischemic effectiveness as well as first results on the impact of this therapeutic approach on hemodynamics are described. A dose-response study, which compared 3 x 50,000 IU with 3 x 500,000 IU urokinase three times a week over a treatment period of 12 weeks demonstrated subjective as well as objective antiischemic effectiveness. Only patients who were treated with 500,000 IU per injection achieved marked increases in exercise capacity, while some patients in the low-dose group presented even with a deterioration of exercise performance. First hemodynamic studies could not show marked changes of systolic parameters, either at rest or during exercise. But a decrease of pulmonary capillary wedge pressure at rest after treatment with 500,000 IU per injection indicates an improvement of diastolic function as a result of enhanced myocardial perfusion. Echocardiographic measurements of transmitral Doppler flow in 21 patients with end-stage coronary artery disease demonstrated normalization of early and late diastolic filling rates in most cases. These changes were accompanied by a reduction of clinical signs of heart failure. Long-term intermittent urokinase therapy is a valuable approach as it not only improves quality of life during the actual treatment period but by the persistence of therapeutic effects following the cessation of therapy.

Endothelin (ET), the most potent endogenous vasoconstrictor with mitogenic potency, is generated from its precursor big-endothelin (BET) in a proteolytic process and discussed as a pathogenetic factor in coronary artery disease and in the acute coronary syndromes. Several studies documented elevated plasma endothelin concentrations in acute myocardial infarction, but conflicting results were reported in patients with stable and unstable angina. Only few studies determined big endothelin, although it half-life and plasma concentrations are higher in comparison to endothelin. ET and BET levels (Radioimmunoassay, Biomedica GmbH, Vienna) were determined in patients with stable angina (SAP, n = 20), unstable angina (IAP, n = 12), acute myocardial infarction (AMI, n = 12) and healthy subjects (NP, n = 11). The concentrations of ET and BET (median (minimum-maximum) in fmol/ml) of the patients with stable angina (SAP: ET 0.7 (0.3-1.1); BET 1.7 (0.7-2.9)), unstable angina (IAP: ET 1.0(0.5-1.7); BET 2.5 (1.3-4.1)) and acute myocardial infarction (AMI: ET 1.2 (0.6-2.3); BET 3.6 (3.2-5.3)) showed a significant difference compared to controls (NP: ET 0.5 (0.4-0.7); BET 1.4 (1.1-1.7)) (SAP vs. NP: ET p0.01; BET p0.05; IAP and AMI vs. NP: ET and BET p0.001). Also, the concentrations of the peptides differed significantly dependent on the clinical severity of coronary artery disease (AMI vs. SAP: ET and BET p0.001; AMI vs. IAP: BET p0.05; IAP vs. SAP: ET p0.05; BET p0.01). Twelve of 15 patients with big endothelin concentrations over 3 fmol/ml suffered acute myocardial infarction. Seven of 12 patients with AMI showed elevated ET and BET concentrations before the increase of creatinecinase. There was no correlation between number of risk factors per patient, cholesterin and subfractions, severity of CAD classified in one-two-three-vessel disease or coronary score according to modified criteria of the American Heart Association (AHA). We conclude that in patients with coronary artery disease endothelin and big endothelin levels are elevated and related to the clinical and not to the morphological severity of coronary artery disease. Big endothelin is the more sensitive parameter in comparison to endothelin and indicates a severe course of myocardial ischemia in patients with unstable angina. The development of assays with the possibility of a quick determination of the peptides may be valuable for risk stratification of acute coronary events.

There was an unusually high incidence of atypical pneumonias in the catchment area of the Rhine river near the university of Düsseldorf in July 1994 during a long period of hot and dry weather. The 18 patients described in this paper (5 women and 13 men) complained of sudden onset of fever up to over 40 degrees C, often associated with severe headache and dry cough. Almost all of these patients had previously been healthy and active and of young to middle age (average 38 years) without any bronchopulmonary anamnesis. Radiology revealed that all the patients had in most cases defined pulmonary infiltrates without any specific preference for a particular site. Serology was initially negative, but four weeks later the complement fixation reaction titre was positive for Coxiella burnetii antibodies in 14 patients (78%). All patients became symptom-free within a few days'time when treated with a combination of antibiotics which included doxycycline, whereas the infiltrates receded completely only after several weeks. The occurrence of pulmonary Q-fever in a large northern German conurbation had been rare at that time. Such epidemics, however, were also noted in Berlin (1992) and in Dortmund (1993). The epidemic reported in this article probably originated from one of the frequent flocks of sheep grazing along the banks of the Rhine river near Düsseldorf. The infections were probably acquired by inhalation of airborne organisms in infected aerosols derived from infected sheep, promoted by the long-term very hot and dry weather which was at the same time very windy, leading to an unusually extensive spreading of the pathogens throughout a very large infected aerosol area.