["Can high fluid intake prevent cerebral and myocardial infarction?" Systematic review].

OBJECTIVES: We performed a systematic review about whether high fluid intake can prevent cerebral and myocardial infarction. MATERIALS AND METHODS: Previously published papers were searched for in PubMed using the combined terms of dehydration, hydration, water intake, fluid intake, cerebral infarction, cerebrovascular disease, apoplexy, myocardial infarction, angina pectoris, ischemic heart disease, blood viscosity and hemorheology. RESULTS: Of 611 papers searched, twenty-two were selected. There was one prospective randomized study, four prospective non-randomized studies, eight epidemiologic (cohort or case-control) studies and nine retrospective descriptive studies, presenting the following points. Dehydration, which increases blood viscosity, is one of the causes of cerebral or myocardial infarction. Important factors other than dehydration can cause an increase in viscosity. Drinking water during the night can protect an increase in blood viscosity but there has been no evidence that drinking excessive amount of water prevents cerebral infarction. There was one report that the risk of myocardial infarction was lower in people drinking more than 5 glasses of water than those drinking less than 2. CONCLUSION: Since cerebral and myocardial infarction are primarily caused by atherosclerosis and atheroma plaque, it is essential to adjust life style for prophylaxis. There has been no direct evidence that decrease in viscosity due to high fluid intake can prevent cerebral infarction. Further studies regarding the relationship between fluid intake and ischemic diseases, and the appropriate fluid intake for the elderly to improve their QoL are needed.

Myocardial ischemia during percutaneous transluminal coronary angioplasty in patients with rich collateral circulation of the target lesion.

Although it is commonly believed that ischemia does not develop during coronary intervention in patients with rich collateral circulation to the target vessel, ST changes are often observed, the study group comprised 40 consecutive patients who underwent elective percutaneous coronary angioplasty and who had rich collateral vessels to the target lesions. None had side branches in the target vessel that would be occluded by the angioplasty balloon. During the intervention, the 12-lead electrocardiogram was monitored for any change in the ST-T segment and 13 (32.5%) showed significant ST changes. Of these, 3 had ST changes with every balloon inflation and the remaining 10 patients had ST changes with the second or subsequent inflations. Myocardial ischemia caused by balloon inflation is not uncommon during coronary angioplasty in patients with rich collaterals to the target vessel. The collateral circulation may stop functioning very early after improvement in the forward flow of the target vessel.