ABSTRACT
A magnitude da resolução do supradesnivelamento do segmento ST é um marcador de reperfusão miocárdica em pacientes com infarto agudo do miocárdio. A resolução incompleta do supradesnivelamento do segmento ST foi identificada como preditor de resultados desfavoráveis em pacientes com infarto agudo do miocárdio após terapia de reperfusão. Este estudo teve como objetivos descrever a frequência de resolução incompleta do supradesnivelamento do segmento ST em um registro contemporâneo de pacientes submetidos a angioplastia primária e fazer uma comparação de seus resultados hospitalares com pacientes que apresentaram resolução completa do supradesnivelamento do segmento ST. Método: Entre julho de 2008 e fevereiro de 2009, foram incluídos 183 pacientes consecutivos com infarto agudo do miocárdio (< 24 horas) de oito centros na Argentina em um registro prospectivo de infarto agudo do miocárdio com supradesnivelamento do segmento ST foi definida como redução < ou igual 70 por cento do supradesnivelamento do segmento ST no eletrocardiograma...
Subject(s)
Humans , Angioplasty, Balloon, Coronary , Myocardial Infarction/diagnosis , Reperfusion , Thrombolytic Therapy , Aspirin , Electrocardiography/methods , ElectrocardiographyABSTRACT
BACKGROUND: In vitro, octreotide potentiates vasoconstriction in isolated, preconstricted, mesenteric arterial vessels. In cirrhotic patients, portal pressure (HVPG) reduction induced by propranolol is partly due to splanchnic vasoconstriction. AIM: To evaluate HVPG effects of octreotide administration in cirrhotic patients receiving long-term propranolol. PATIENTS AND METHODS: A randomized, controlled trial. First study: a total of 28 patients were studied at baseline and 30 and 60 minutes after octreotide (200 mug) (N = 14) or placebo (N = 14) and then treated with propranolol for approximately 30 days (106 +/- 5 mg/day). Second study: after baseline evaluation patients received octreotide or placebo as they were assigned to in the first study and measurements repeated 30 and 60 minutes later. RESULTS: In the first study baseline HVPG was 18.7 +/- 0.9 mmHg and decreased to 17.1 +/- 1.1 mmHg and 17.1 +/- 1.0 mmHg (both P < 0.05 vs baseline) at 30 and 60 minutes after octreotide, respectively. Eight patients decreased their HVPG after octreotide. In the second study baseline HVPG was 15.6 +/- 1.3 mmHg (P < 0.01 vs baseline HVPG in first study) and decreased to 14.1 +/- 1.2 mmHg and 14.1 +/- 1.3 mmHg (25.7 +/- 5% lower than baseline HVPG in the first study, P < 0.01) (both P < 0.05 vs baseline) at 30 and 60 minutes after octreotide, respectively. Nine patients (2 responders/7 nonresponders to propranolol) decreased their HVPG after octreotide. Octreotide effects may be mediated by potentiation and additive mechanisms. CONCLUSIONS: Octreotide enhances HVPG reduction induced by propranolol in cirrhotic patients.
Subject(s)
Gastrointestinal Agents/pharmacology , Liver Cirrhosis/physiopathology , Octreotide/pharmacology , Portal Pressure/drug effects , Adrenergic beta-Antagonists/administration & dosage , Adrenergic beta-Antagonists/pharmacology , Drug Administration Schedule , Esophageal and Gastric Varices/complications , Esophageal and Gastric Varices/physiopathology , Female , Follow-Up Studies , Gastrointestinal Agents/administration & dosage , Heart Rate/drug effects , Humans , Liver Cirrhosis/complications , Male , Middle Aged , Octreotide/administration & dosage , Propranolol/administration & dosage , Propranolol/pharmacologyABSTRACT
BACKGROUND & AIMS: Postprandial increases in portal pressure may influence esophageal variceal rupture. The effects of chronic propranolol and octreotide (100 and 200 microg subcutaneously in a single dose) on postprandial hemodynamics were evaluated. METHODS: FIRST STUDY: 36 cirrhotic patients were studied at baseline and 30 and 60 minutes after a standard meal and then treated with propranolol (139 +/- 9 mg/d during 39 +/- 2 days). SECOND STUDY: After baseline measurements, patients were randomized into 3 groups: (1) placebo, (2) octreotide (100 microg), or (3) octreotide (200 microg) (n = 12 for each group). Thirty minutes postinjection a new baseline was established and measurements were repeated 30 and 60 minutes after the meal. RESULTS: First study: Baseline portal pressure was 18.1 +/- 1.2 mm Hg, 30 and 60 minutes after the meal it was 21.5 +/- 0.8 mm Hg and 20.5 +/- 0.8 mm Hg, respectively (both P < 0.01 vs. baseline). Cardiac index (CI) was 4.5 +/- 0.2, 4.8 +/- 0.2, and 4.9 +/- 0.2 L x min(-1) x m(-2), respectively (both P < 0.05 vs. baseline). Peripheral vascular resistance was 1012 +/- 56, 902 +/- 51 (P = NS), and 884 +/- 49 dynes x sec x cm(-5) (P< 0.05 vs. baseline), respectively. Second study: Propranolol and placebo did not blunt postprandial increase in portal pressure. Octreotide (100 microg) partially ameliorated postprandial increase in portal pressure. Octreotide (200 microg) significantly enhanced the portal hypotensive effect of propranolol and blunted the postprandial increase in portal pressure. CONCLUSIONS: Octreotide blunts postprandial increase in portal pressure not prevented by long-term propranolol administration.
