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Background: NYHA classification is mostly used for graduation of clinical limitation due to cardiac failure. Right heart catheterization is not generally used to evaluate hemodynamics and to define the effects of drugs in patients with chronic cardiac failure. Clinical data and results from echocardiography, stress tests or nuclear cardiology seem to be sufficient. Our aim was to demonstrate subjectivity of a classification system (NYHA) comparing the graduation done by physicians and by patients and to represent the difficulty to prognosticate hemodynamic data of patients with heart failure., Patients and Methods: Limitation of 53 patients with heart diseases was classified by physicians and patients using NYHA classification. Pulmonary capillary wedge pressure (PCWP), stroke volume (SV) and cardiac output were predicted by physicians; they were allowed to utilize all examination data they could get. Predicted hemodynamic data were compared with the results of measurement at rest and during exercise., Results: Patients classified themselves significantly worse than physicians did: 2.68 +/- 0.64 vs. 2.23 +/- 0.74 (p = 0.0012). Similarity in NYHA classification was found in 29/53 cases. Correlation of predicted and measured hemodynamic data was low: PCWP (at rest) r = 0.346; PCWP (during exercise) r = 0.232; SV (at rest) r = 0.476; SV (during exercise) r = 0.445; HMV (at rest) r = 0.412; HMV (during exercise) r = 0.538., Conclusion: Clinical classification systems like NYHA are subjective, classification by physicians differs significantly from classification by patients. Prediction of hemodynamics is not possible despite all examination data had been available. Right heart catheterization is necessary to define hemodynamics at rest and during exercise.

The aim of the study was to examine the effects of maintenance molsidomine therapy on portal and cardiac haemodynamics in patients with confirmed alcoholic or nonalcoholic liver cirrhosis and portal hypertension. Molsidomine is a selective reducer of preload without development of tolerance. 16 patients with portally decompensated cirrhosis of the liver following an initial or recurrent episode of bleeding form oesophageal/fundal varices were on long-term treatment (4-24 months) with 2 or 3 x 8 mg molsidomine/day (Corvaton retard). They were followed up after 3-6 months. 6 of the 16 had been treated previously with propranolol for haemorrhage prophylaxis over 11 +/- 15 months. In a total of 70 treatment months with propranolol, 10 recurrent bleeds had occurred. During 166 treatment months with propranolol, 10 recurrent bleeds had occurrences of bleeding. This long-term treatment showed reductions in hepatic venous pressure gradient of 24.8% (n = 8) (p < 0.05), variceal pressure of 28.7% (n = 7) (p < 0.05) and size of varices of 17% (n = 8). This occurred without any clinically relevant impairment of systemic cardiovascular regulation. Therefore long-term therapy with molsidomine may be suitable for prophylaxis of haemorrhage of oesophageal varices.

We studied nine patients (56 +/- 7 years) with complete AV-block and permanent dual-chamber pacemaker (DDD) under different pacing modes: ventricle pacing (VVI) 70 bpm, DDD 106 +/- 4 bpm, rate adaptive pacing (VVI-FA) 108 +/- 3 bpm. Exercise was performed supine on the bicycle ergometer at 50 watts for 5 min at each setting. DDD-paced patients showed significantly higher mixed venous oxygen saturation, being 45 +/- 2% after the fourth minute, (VVI 38 +/- 2%, p less than 0.01 and VVI-FA paced patients 40 +/- 1%, p less than 0.01). Pressures were normal under DDD pacing during exercise (RAP 7 +/- 2 mm Hg; PCP 14 +/- 3 mm Hg) and showed further increase to abnormal levels during VVI (RAP 13 +/- 2 mm Hg, p less than 0.01; PCP 21 +/- 3 mm Hg, p less than 0.02) and VVI-FA pacing (RAP 10 +/- 2 mm Hg, p less than 0.05; PCP 20 +/- 3 mm Hg, p less than 0.01). Stroke volume increased from 71 +/- 5 ml to 105 +/- 7 ml during VVI and from 64 +/- 7 ml to 81 +/- 7 ml during DDD pacing. Stroke volume remained unchanged (69 +/- 5 ml) during VVI-FA pacing. The peak levels of ANP during and after exercise were significantly higher under VVI (951 +/- 248 pg/ml) than under DDD pacing (650 +/- 140 pg/ml, p less than 0.01) and were not different between DDD and VVI-FA pacing (677 +/- 97 pg/ml). These results show that VVI pacing effects a more pronounced increase of ANP level than other pacing modes. Under moderate exercise, rate-responsive pacing compared to VVI pacing showed no differences in mixed venous oxygen saturation and in atrial pressures. Only DDD pacing showed higher oxygen saturation and a normalization of atrial pressures when compared to other types of single chamber pacing.