Nitrates for XXXX .

@entity1 @entity662 @entity583 @entity731 @entity3362 @entity1242 @entity117 @entity5135 @entity3361 @entity1459 @entity951 @entity715 @entity922
The term @entity1459 encompasses @entity922 . Fissuring of an @entity731 coronary artery plaque with superimposed platelet deposition, with or without additional @entity715 formation, is invariably responsible for a prolonged episode of @entity951 at rest, increasing frequency of @entity951 at rest, or with minimal exertion of less than 4 weeks in duration and early postinfarction @entity951 . Plaque progression, rather than plaque fissuring, is the most likely mechanism for progressive reduction in walking distance due to @entity951 in @entity1 who previously have stable @entity951 . @entity3361 is responsible for @entity5135 , but its exact role in other forms of @entity1459 is unknown. The mainstay of treatment of @entity1459 (prolonged episode of @entity951 at rest and recent onset @entity951 at rest, or with minimal exertion with a crescendo pattern) is @entity117 , heparin, or both. Both @entity117 and intravenous (i.v.) heparin or their combination reduce early mortality and the incidence of @entity583 in @entity1 hospitalized with @entity1459 . However, these agents do not promptly relieve @entity662 . There are no placebo-controlled studies evaluating the usefulness of @entity3362 in @entity1459 . In open-label studies, continuous therapy with i.v. @entity1242 (NTG) for 24 hours or longer has been shown to relieve @entity662 in @entity1 with @entity1459 refractory to therapy with other antianginal agents, including long-acting nitrates. Recurrence of @entity662 in @entity1 receiving i.v. NTG is a common problem and probably represents development of pharmacologic tolerance, but this can be overridden by dose escalation; protracted tolerance during short-term use of i.v. NTG is usually not a problem.(ABSTRACT TRUNCATED AT 250 WORDS)
