Terapevticheskii arkhiv · 2006
[The course of gastroesophageal reflux disease in elderly patients with concomitant ischemic heart disease].
Сравнительное исследованиеАннотация на английскомСтатьяНазвание и аннотация: Перевод в очереди
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Zvenigorodskaia L A, Taranchenko Iu V
Аннотация
AIM: To study basic functional and pathogenetic features of the course of gastroesophageal reflux disease (GERD) in elderly patients with concomitant coronary heart disease (CHD).
MATERIAL AND METHODS: Esophagogastroduodenoscopy, 24-h pH-metry, simultaneous 24-h pH- and ECG-monitoring, omeprasol test were made in 126 patients: 74 GERD patients with CHD and 52 patients with GERD alone.
RESULTS: Mean number of refluxes for 24 hours in isolated GERD was maximal at stages IIa and IIb (74%). In CHD patients (77%) there was a trend to a rise in this number. Only patients with associated CHD demonstrated a clinically significant depression of ST segment related to reflux, a significantly more frequent occurrence of supraventricular and ventricular extrasystoles.
CONCLUSION: The acid component of gastric content pushed into the esophagus is not a leading factor of esophageal mucosa lesion in GERD patients with CHD. Pathological gastroesophageal refluxes may trigger mechanisms provoking new attacks of angina pectoris.
MATERIAL AND METHODS: Esophagogastroduodenoscopy, 24-h pH-metry, simultaneous 24-h pH- and ECG-monitoring, omeprasol test were made in 126 patients: 74 GERD patients with CHD and 52 patients with GERD alone.
RESULTS: Mean number of refluxes for 24 hours in isolated GERD was maximal at stages IIa and IIb (74%). In CHD patients (77%) there was a trend to a rise in this number. Only patients with associated CHD demonstrated a clinically significant depression of ST segment related to reflux, a significantly more frequent occurrence of supraventricular and ventricular extrasystoles.
CONCLUSION: The acid component of gastric content pushed into the esophagus is not a leading factor of esophageal mucosa lesion in GERD patients with CHD. Pathological gastroesophageal refluxes may trigger mechanisms provoking new attacks of angina pectoris.