Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The cardiovascular effects of ranitidine were studied in 12 children with congenital heart disease who had been given tolazoline as a pulmonary vasodilator. Ranitidine was given as prophylaxis against gastrointestinal haemorrhage induced by tolazoline. Tolazoline 1-2 mg/kg caused significant falls in pulmonary and systemic vascular resistances and a rise in heart rate. After intravenous administration of ranitidine 3 mg/kg both resistances rose again and neither resistance then differed significantly from baseline levels. Heart rate also fell and the final heart rate was significantly below baseline levels. We conclude that there may be H2 receptors within the pulmonary and systemic circulations and that tolazoline may mediate some of its effects through these H2 receptors rather than by alpha adrenergic receptor blockade. The safety of H2 blockade in children, particularly those with pulmonary hypertension, needs further investigation.
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PMID:Cardiovascular effects of tolazoline and ranitidine. 356 16

Ranitidine may cause liver injuries ranging from transient, subclinical serum transaminases increase every 100-1,000 treated patients to cholestatic hepatitis in less than 1/100,000. Other H2-receptor antagonists are more dangerous: 11 toxic hepatitis cases have been reported as adverse effect after 1 year of marketed ebrotidine. A 75-year-old male with ischemic cardiopathy history was started on an 8 days treatment of oral ranitidine due to pirosis, without any other changes of therapy; 48 h after drug withdrawal, light-coloured stools, dark urine and icteric scleras developed. On hospital admission, 10 days later, physical examination showed slight hepatomegaly and severe jaundice with skin excoriations followed by serum mixed bilirubin further increase and aminotransferases activities mild rise. Total bilirubin peaked at 381.33 mmol/l (5.1-17.1) and progressively returned to normal, after discharge home, in 3 months and now, 1 year later, there is no sign of liver disease. Ultrasonographic biliary anomalies and the most frequent causes of liver damage were excluded. Liver biopsy confirmed ranitidine as the most likely cause of liver toxicity since histological and ultramicroscopical study revealed a drug-induced picture. We report a rare case of intrahepatic cholestasis jaundice related to ranitidine, a widely used drug. Diagnosis would need an ethically unacceptable rechallange test.
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PMID:Intrahepatic cholestatic jaundice related to administration of ranitidine. A case report with histologic and ultramicroscopic study. 1578 90

In patients with structural heart disease, occurrence of an electrical storm (ES) is associated with increased mortality acutely and during medium term follow-up. Depending on the underlying heart disease and baseline type of arrhythmia, different clinical pathways have to be followed to reach sustained freedom from ventricular arrhythmia recurrences. Trigger elimination, sympathetic blockade (initially using betablockers and sedation), antiarrhythmic therapy with amiodarone and catheter ablation, treatment of heart failure and invasive hemodynamic support are cornerstones of the treatment. We present an algorithm which may help to organize an optimized treatment for each ES patient, implementing invasive treatment options like coronary angioplasty, catheter ablation and invasive circulatory support. Further studies are necessary to evaluate medium term outcome of such a structured therapy.
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PMID:[Electrical storm in the emergency room: clinical pathways]. 2489 90