The haematocrit--an important factor causing impaired haemostasis in patients with cyanotic congenital heart disease.

BACKGROUND: Patients with cyanotic congenital heart disease(CCHD) have haemostatic abnormalities, which result in an increased risk of bleeding. The cause is unknown, but recent studies have indicated that an elevated haematocrit, which is present in cyanotic patients, could be an important factor. The aim of this study was to characterize the haemostatic profile, examine how changes in haematocrit affect the haemostatic profile, and whether a haematocrit reduction could terminate bleeding in CCHD patients. METHODS: This was a prospective, multicenter study. The haemostatic profile consisting of haematocrit, platelet count and thrombelastography(TEG) was characterized in ninety-eight CCHD patients. To evaluate the influence of haematocrit on the haemostatic profile, 21 of the patients underwent phlebotomy and 16 patients received treatment with an iron supplement. Furthermore ten patients with haemoptysis underwent phlebotomy. The haemostatic profile was reevaluated after interventions. RESULTS: TEG revealed that patients with CCHD and elevated haematocrit were hypocoagulable due to reduced clot formation and strength. Furthermore a positive correlation between elevated haematocrit and hypocoagulability was present. Interventions such as phlebotomy and treatment with supplemental iron causing significant haematocrit changes confirmed the correlation between haematocrit and the haemostatic profile. Finally a haematocrit reduction by phlebotomy successfully terminated haemoptysis in ten CCHD patients. CONCLUSION: Patients with CCHD and elevated haematocrit are hypocoagulable. The hypocoagulable haemostatic profile is positively correlated to increasing haematocrit. An intervention, which increases or decreases haematocrit, changes the haemostatic profile. A haematocrit reduction seems to improve the haemostatic profile, and may thereby terminate bleeding. However, these results warrant further studies.

Atrial myocardial pathoelectrophysiology in adults with a secundum atrial septal defect is unaffected by closure of the defect. A study using high resolution signal-averaged orthogonal P-wave technique.

BACKGROUND: In patients with atrial septal defect (ASD) the P-wave is prolonged as a marker of delayed atrial conduction which is associated with atrial fibrillation. The study aim was to analyse the impact of ASD closure in adults on P-wave duration and morphology by means of signal-averaged P-waves (PSA-ECG) and to investigate potential mechano-electrical interactions. METHODS: PSA-ECG was obtained before and 8+/-6 months after ASD closure in 35 adult patients (age 53+/-15 years). Heart chamber sizes and pulmonary artery pressure levels were assessed by echoDopplercardiography. RESULTS: P-wave duration and morphology did not change after ASD closure (148+/-16 vs 144+/-16 ms, P=0.07). P-wave duration did not relate to age at repair, preclosure atrial sizes or pulmonary artery pressure. Pre- or postclosure atrial fibrillation propensity was associated with longer P-wave duration both before and after ASD closure. CONCLUSION: Atrial conduction disturbances in middle-aged patients with ASD, manifested as a prolonged P-wave duration, do not change after ASD closure and are not related to the dilatation of the right and left atria. It is suggestive that atrial conduction disturbance associated with ASD develop early and early intervention is required to prevent the development of late atrial fibrillation.

Antihypertensive effect of felodipine combined with beta-blockade. A comparison between 2 and 3 daily dosages.

24 hypertensive patients, who were not satisfactorily controlled (diastolic blood pressure greater than 95 mm Hg) with beta-blockers alone were randomised to 2 treatment groups where felodipine was administered for 2 weeks in a total daily dose of 15 mg divided in 2 or 3 doses. Following a 2-week placebo washout period, the patients were switched to the alternative dose regimen in a double-blind crossover manner. Blood pressure was measured with standard techniques and was also non-invasively monitored for 24 hours at the end of each dose regimen period and at the end of the intermediate placebo period. Mean arterial blood pressure at the end of the placebo run-in period was 169/105 mm Hg. Felodipine 5 mg thrice daily reduced blood pressure by 20/9 mm Hg and felodipine 7.5 mg twice daily by 17/9 mm Hg (p less than 0.05). The difference between the 2 dose regimens was not statistically significant. When 24-hour blood pressure measurements for the 2 dose regimens were compared, there were no statistically significant differences. Both regimens reduced the 24-hour blood pressure significantly compared with placebo. Two patients were withdrawn during the study, 1 before felodipine treatment started and the other due to diarrhoea and flushing related to felodipine. Otherwise felodipine was generally well tolerated.