Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of this study was to assess the safety of continuous subcutaneous therapy with treprostinil sodium (Remodulin), a prostacyclin analog, and its effect on ischemic rest pain and ischemic wound healing in subjects with critical limb ischemia (CLI) and no planned revascularization procedure. This was a 12-week, open-label, single-center pilot study enrolling 10 subjects (mean age 82.4 years) with Fontaine stage III to IV (Rutherford class 4-6) peripheral arterial disease and ankle brachial indices less than 0.55. The primary end point was safety, and the secondary end points were the effects of treatment on ischemic rest pain, limb salvage, and wound healing. There was a 62% reduction in mean worst rest pain and a 57% reduction in mean average rest pain at week 12, with most subjects using less pain medication. Three subjects experienced complete healing of their wounds. No subject developed a new wound during the trial. Treprostinil was generally well tolerated. Subcutaneous infusion-site pain was the most frequently reported side effect, with one subject withdrawing from the study as a result. Jaw pain was reported by two subjects. One subject experienced two serious adverse events considered unrelated to treprostinil (cholecystitis and congestive heart failure). This study demonstrates that chronic, continuous subcutaneous treprostinil is safe and can be useful in the treatment of ischemic pain and wounds in subjects with CLI. Future controlled studies are needed to evaluate these effects and determine appropriate patient selection.
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PMID:Treprostinil sodium (Remodulin), a prostacyclin analog, in the treatment of critical limb ischemia: open-label study. 1695 86

Serotonin (5-hydroxytryptamine)(1B/1D) agonists are vasoconstrictors that can affect coronary and cerebral arteries. Retrosternal chest, arm, and jaw pain following triptan use is generally attributed to "triptan sensations" and dismissed as noncardiac. However, triptans narrow normal coronary arteries and occasionally trigger vasospasm. They are contraindicated in atherosclerotic vascular disease. Part 1 of this review examines the relationship of medications used in migraine with the likelihood of causing vasospasm or vasoconstriction, and the triggering of cardiac arrhythmias. We report an illustrative case of polymorphic ventricular tachyarrhythmia, electrocardiogram changes consistent with cardiac ischemia, and acquired corrected QT interval lengthening following oral sumatriptan in a 53-year-old migraineur without risk factors for coronary artery disease (CAD). Extensive evaluation revealed insignificant single coronary vessel atherosclerosis and coronary artery vasospasm on ergonovine challenge. The report highlights the hidden risk that may underlie a "triptan sensation" and the possible association of the vasospastic features of Raynaud's phenomenon, migraine headaches, and coronary vasospasm. Part 1 discusses the risks for Torsade de Pointes, vasospasm, and ischemia, with a review and discussion of case reports of triptan-associated cardiovascular events in migraineurs with and without CAD risk factors or documented CAD; of the epidemiology and studies of triptans, vasospasm, and cardiovascular morbidity; and of the relationship of variant angina, migraine, and vasospastic disease. In the second part of this review, headache medications and their propensity for corrected QT prolongation will be summarized.
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PMID:QT prolongation, Torsade de Pointes, myocardial ischemia from coronary vasospasm, and headache medications. Part 1: review of serotonergic cardiac adverse events with a triptan case. 2321 17

Acute coronary syndrome usually presents with retrosternal chest pain, nausea, vomiting, sweating, and jaw and arm pain. Some patients only present with neck, epigastric, or ear discomfort. A 47-year-old male with a history of hypertension and coronary artery disease presented to the emergency department complaining of bilateral otalgia. He never felt chest pain, jaw pain, nausea, diaphoresis, or shortness of breath. He had a history of 2 acute coronary events and had a stress test 2 months prior to admission, which was unremarkable. The initial electrocardiography was sinus rhythm with Q-waves in the inferior leads and nonspecific ST changes in the lateral leads. His troponin on admission was normal but subsequently elevated to 20.00 mg/mL after 24 hours. He underwent left heart catheterization, which found significant occlusive disease of the second and fourth obtuse marginal branches and 2 drug-eluting stents were placed. His ear pain resolved soon after cardiac catheterization. The pathophysiology of this referred pain is thought to be related to the neuroanatomy of the nerves innervating the heart and ear. The auricular nerve branch of the vagus nerve supplies the inner portion of the external ear. Only a few cases with the complaint of otalgia have been reported. Patients were older, more frequently women, and with diabetes or heart failure. Clinicians should be aware of the atypical presentation of angina that may be life-threatening cardiac ischemia. Ear pain and fullness could be the sole presenting symptom in a patient with acute coronary syndrome.
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PMID:Myocardial Infarction Presenting as Ear Fullness and Pain. 2955 70