In September 2008, the Austrian Agency for Health and Food Safety (AGES) learned of an outbreak of diarrheal illness that included a 71-year-old patient hospitalized for gastroenteritis with a blood culture positive for Listeria monocytogenes. Three stool specimens provided by seven of 19 persons attending a day trip to a foreign city, including a final break at an Austrian tavern, yielded L. monocytogenes. All isolates were of serovar 4b and had fingerprints indistinguishable from each other. A cohort study revealed that the outbreak of gastroenteritis occurred among 16 persons who had eaten dinner at the wine tavern on September 6. Of the 15 persons who ate from platters of mixed cold-cuts, 12 (80%) developed symptoms of febrile gastroenteritis within 24-48 h. The median age of those who became ill was 62 years. A 72-year-old patient recovered from gastroenteritis but was hospitalized with bacterial meningitis on day 19 after the dinner. The epidemiological investigation identified the consumption of mixed cold-cuts (including jellied pork) at the wine tavern as the most likely vehicle of the foodborne outbreak (P = 0.0015). This hypothesis was confirmed by microbiological investigation of jellied pork produced by the tavern owner on September 3. L. monocytogenes was isolated from leftover food in numbers of 3 x 10(3)-3 x 10(4) colony forming units/g and was indistinguishable from the clinical outbreak isolates. Symptoms reported by the 12 patients included unspecified fever (12x), diarrhea (9x), headache (5x), vomiting (4x), body aches (2x) and sore throat (1x). Active case finding identified one case of rhombencephalitis (female, age 48) among another group of four guests, among whom only the patient and her asymptomatic husband had eaten jellied pork on September 6. This is the first outbreak of L. monocytogenes-associated gastroenteritis reported in Austria. The occurrence of a secondary case of meningitis (diagnosed on day 19 after consumption of jellied pork) indicates a significant risk of systemic listeriosis among elderly patients with febrile gastroenteritis caused by L. monocytogenes; antibiotic therapy should therefore be considered in such cases of documented listerial gastroenteritis.

In May 2004, an Austrian scientific board started a hypertension project, LIIFE-IN-LIFE, to gain epidemiological data on hypertension in Austria and, based on the LIFE study results, to document antihypertensive regimen in daily practice. In 20,615 hypertensive patients, epidemiologic and clinical data of the typical Austrian hypertensive patient were evaluated and extensive risk management was initiated.The average hypertensive patient turned out to be overweight, was on average 66 years old, showed in more than 50 % at least one underlying cardiovascular disease and suffered from diabetes in 24 %; the mean LDL cholesterol level was 134 mg/dl. Mean systolic blood pressure was 158.3 +/- 18.9 mmHg and diastolic blood pressure 90.8 +/- 10.8 mmHg. According to the Framingham apoplexy score, the risk of apoplexy was estimated as 28.9 % in the studied population within 10 years. Less than one fifth (18.7 %) showed blood pressure values at goal according to the European criteria (ESC, EHC) despite antihypertensive combination therapy. Changing to an optimized, losartan-based therapy 7 of 10 (68.9 %) hypertensive patients reached the blood pressure goal and remained stable for one year.This largest-ever Austrian project in hypertensive patients proves the extensive cardiovascular risk profile in the project patients with, in general, inadequate antihypertensive therapy. LIIFE-IN-LIFE will show long-term data on more than 20,000 hypertensives in a follow-up period of up to 5 years (until 2008) and will evaluate intensified antihypertensive regimen with respect to endpoint data. First data over 12 months in 9000 patients document that 7 out of 10 hypertensive patients put on a losartan-based therapy reach and maintain their blood pressure target values.

The Austrian Hypertensive Patient in Daily Clinical Practice: A First Analysis of 20,615 Hypertensive Patients Included in the LIIFE-INLIFE-Project with Therapeutic Results of 12 Months in 9000 Patients. In May 2004, an Austrian scientific board started a hypertension project, LIIFE-IN-LIFE, to gain epidemiological data on hypertension in Austria and, based on the LIFE study results, to document antihypertensive regimen in daily practice. In 20,615 hypertensive patients, epidemiologic and clinical data of the typical Austrian hypertensive patient were evaluated and extensive risk management was initiated.

Vasodilating prostaglandins may be increased in patients with chronic congestive heart failure (CHF) to balance out the effects of vasoconstricting forces. Significant increases in plasma levels of bicycloprostaglandin E2 metabolite (PGEm), a chemically stable degradation product of the vasodilating prostaglandin E2, were found in response to captopril (39.4 +/- 7.8 vs. 46.2 +/- 8.2 pg/ml; p less than 0.01). With chronic captopril treatment bicyclo-PGEm remained elevated for 12 h after the last dose after 1 and 2 months (75.5 +/- 5.5; p less than 0.05 and 72.1 +/- 6.3 pg/ml; p less than 0.05, respectively). Upon readministration of captopril during chronic captopril treatment the significant increase of bicyclo-PGEm in response to captopril was sustained, as were changes in plasma renin activity, angiotensin II, and blood pressure. Plasma catecholamines were unchanged with captopril or decreased slightly, vasopressin remained moderately increased throughout. Taken together, the results suggest that vasodilating prostaglandin E2 production might play a part in captopril's beneficial action in chronic congestive heart failure.

In patients with arterial hypertension hemodynamic as well as humoral factors may influence the development of left ventricular hypertrophy. We therefore investigated in 23 patients with long standing hypertension (11 females, 12 males, age 50 +/- 13 years) wether left ventricular mass as determined by echocardiography interrelates with hemodynamic or humoral parameters. Left ventricular mass measured 161 +/- 51 g/m2 and correlated significantly with patients' age (r = 0.55, p less than 0.05) and systolic blood pressure (159 +/- 21 mm Hg, r = 0.51, p less than 0.05) but not with diastolic blood pressure (99 +/- 15 mm Hg, r = 0.23, not significant). Plasma renin activity was 0.6 +/- 0.6 ng/ml/h and plasma norepinephrine levels measured 371 +/- 168 ng/l. Neither of these humoral parameters correlated significantly with left ventricular mass. It is concluded that in long standing hypertension left ventricular hypertrophy is determined predominantly by the elevation of systolic blood pressure and the patients' age.

In hepatic cirrhosis neurohumoral vasoconstrictor systems are activated to compensate for circulatory disturbances. To study the renin-angiotensin-aldosterone system in more detail, angiotensin converting enzyme in 15 patients with advanced liver disease was inhibited with captopril after moderate sodium restriction.

1. Epoprostenol (prostacyclin, PGI2) has been evaluated in clinical trials in peripheral vascular disease and other conditions chiefly on the basis of its platelet inhibitory properties. These therapeutic evaluations have proceeded in the absence of evidence as to the optimum infusion regimen for epoprostenol and the choice of schedules of administration has been arbitrary. We have tried to establish an optimum infusion regimen in patients with peripheral vascular disease in terms of maximal inhibition of platelet deposition on atherosclerotic lesions in vivo together with maximal inhibition of platelet aggregation ex vivo. 2. One hundred and twenty three patients with atherosclerotic peripheral vascular disease and increased platelet uptake at atherosclerotic sites were selected. Epoprostenol was administered at a fixed dose of 5 mg kg-1 min-1 for 0.5-24 h daily for 3-7 days. 3. Infusion of epoprostenol for 6 h daily for up to 5 days caused maximum decrease in platelet uptake without tachyphylaxis and without loss of the inhibitory effect of epoprostenol on platelet aggregation responses. Longer daily infusion periods were associated with progressive loss of the anti-aggregatory effect of epoprostenol without any greater decrease in platelet uptake. Shorter daily infusion periods produced smaller decreases in platelet uptake.

Vasodilator prostaglandins may play a role in maintaining circulatory homeostasis in patients with congestive heart failure (CHF). Plasma levels of bicyclo-prostaglandin E2 metabolite (PGEm), a chemically stabilized degradation product of the vasodilator prostaglandin E2, were determined in 45 patients with chronic CHF (New York Heart Association class II, III or IV). Mean circulating levels of bicyclo-PGEm were significantly elevated in patients with functional class III (72 +/- 8 pg/ml) or IV CHF (77 +/- 10 pg/ml) compared with control subjects (49 +/- 3 pg/ml) and patients with functional class II CHF (49 +/- 4 pg/ml). Bicyclo-PGEm concentrations correlated with plasma renin activity (r = 0.68, p less than 0.001) and plasma angiotensin II (r = 0.56, p less than 0.001) and plasma noradrenalin levels (r = 0.34, p less than 0.05). An inverse correlation was found between serum sodium concentrations and levels of bicyclo-PGEm (r = 0.46, p less than 0.01) as well as plasma renin activity (r = 0.66, p less than 0.001). Thus, prostaglandin E2 levels in plasma are increased in patients with severe CHF.

Hemodynamic and hormonal actions of acute (50 mg) and chronic (150 mg/day) captopril were tested in 10 patients with essential hypertension. Under short-term conditions blood pressure was reduced, heart rate and plasma adrenaline did not change, plasma angiotensin II and plasma aldosterone decreased. Plasma renin activity, basal plasma noradrenaline and bicyclo-PGEm, a novel stable metabolite of prostaglandin E2, increased after captopril. With chronic captopril treatment blood pressure was reduced after 4 weeks before readministration of captopril, heart rate did not change, plasma renin activity and bicyclo-PGEm remained elevated for 12 h after the last captopril dose. Angiotensin II remained suppressed, aldosterone and plasma catecholamines did not change between doses. Readministration of captopril led to a further reduction in blood pressure. Angiotensin II and aldosterone were further suppressed, bicyclo-PGEm levels increased from a higher baseline. Heart rate and plasma catecholamines did not change. Taken together, the results suggest that prostaglandin E2 is involved in the acute and chronic hypotensive response of captopril in patients with essential hypertension.

The mechanism of action by which nitrates produce vasodilation has not been fully clarified so far. Experimental studies indicate a possible relationship to the prostaglandin system. This study describes the consequences of acute prostaglandin synthesis inhibition on the hemodynamic effects of nitroglycerin in patients with stable angina pectoris. Intravenous application of 1 g acetylsalicylic acid was associated with a small but significant blunting of the pressure decline in the pulmonary and systemic circulation following the sublingual administration of 0.8 mg nitroglycerin. Premedication with 75 mg indomethacin i.m. was followed by a decrease in pressure decline in the pulmonary artery during intravenous nitroglycerin infusion. Significant inhibition of prostaglandin synthesis was shown by a substantial decline in plasma levels of circulating prostaglandin metabolites in both experiments. These results indicate that the mechanism of action of nitroglycerin may be partially mediated by vasodilatory prostaglandins.

A high prevalence of left ventricular dysfunction in insulin-dependent (type-I) diabetics has been reported. However, the exact influence of metabolic control and/or the coexistence of early diabetic microangiopathy is unknown. Thus, we assessed left ventricular function by echophonocardiography in 50 type-I diabetics (mean age 26 +/- 7.9 years), who showed a fairly good metabolic long-term control (mean hemoglobin A1: 8.8%) after the introduction to intensified insulin therapy in comparison with 50 age- and sex-matched controls. Type-I diabetics did not differ from controls in their left ventricular internal diameters, mean wall thickness, ratio of pre-ejection period to left ventricular ejection time and systolic shortening fraction. Isovolumetric relaxation period reflecting an early diastolic event was slightly but significantly prolonged in diabetic subjects, independent of metabolic control status or existence of early microangiopathy. Isovolumetric relaxation period showed a statistically significant correlation to age in type-I diabetics, but not in controls. Possibly, the diabetic status--although well-controlled, but not normalized--may biochemically alter the myocardium and might influence its diastolic properties.