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Biomedical subjects

R L Koller

Publications and source records attributed to R L Koller.

5 recordsLinked to original sources

Intravenous thrombolytic therapy for acute ischemic stroke. Weighing the risks and benefits of tissue plasminogen activator.

The use of intravenous tPA within 3 hours after acute ischemic stroke has been proved to increase the number of good outcomes. However, tPA is a toxic therapy that carries a substantial risk of intracerebral hemorrhage. To decrease the risk, tPA use must be restricted to a carefully selected patient population. Treatment must be administered in an intensive care setting and directed by physicians with expertise in diagnosing and managing stroke.

Acute Disease↗

Prevention of recurrent ischemic stroke.

Treatment after an ischemic stroke or transient ischemic attack (TIA) should target the presumed cause of the initial episode to facilitate focused prophylaxis. In the majority of ischemic strokes, degenerative large- and small-vessel disease is the cause. In these patients, attention to modifiable risk factors is an important priority. However, uncertainty and controversy remain regarding therapy, although issues are gradually being settled. There are now strong scientific data to support the use of carotid endarterectomy in patients with 70% to 99% stenosis and an ipsilateral TIA or nondisabling stroke. Aspirin is accepted as standard preventive therapy and should be used in all patients with a TIA or stroke, including those who undergo endarterectomy. Although the dose most commonly used in clinical trials is 1,300 mg/day, a daily dose of 325 mg is probably equally effective with less gastrotoxicity. Given present evidence, use of dipyridamole (Persantine) is not warranted. The role of ticlopidine hydrochloride (Ticlid) in stroke prophylaxis is not well defined. Its superiority over aspirin demonstrated in one study may make it the drug of first choice despite its expense and side effects. The efficacy of warfarin sodium (Coumadin, Panwarfin, Sofarin) or heparin in ischemic stroke caused by degenerative cerebrovascular disease is not supported by scientific data, but no prospective controlled studies have demonstrated that these agents are ineffective. Therefore, it seems prudent to reserve anticoagulant therapy for situations in which an ongoing thrombotic process is likely (eg, progressing stroke). Heparin therapy in the immediate post-TIA period is not warranted on the basis of current scientific evidence.

Anticoagulants↗

Cervical bruits: clinical correlates of stenosis.

To analyze the relationship among characteristics of buits, degree of underlying stenosis, and neurologic symptom complexes, the authors studied 157 patients with bruits undergoing digital subtraction angiography. Symptom status assignment (definite lateralizing, possible lateralizing, vertebrobasilar, diffuse, and asymptomatic) and cervical auscultation for location, duration, and other bruit characteristics were performed independently. Bruit occurrence was associated with stenosis of greater than or equal to 50% of the underlying vessel with the association being no stronger at higher levels of stenosis (greater than or equal to 80%). No relationship existed between the side of bruit and side of symptoms in those with lateralized symptoms. The authors found more severe degrees of carotid stenosis in two symptomatic groups (vertebrobasilar insufficiency [VBI] and definite lateralized) compared with asymptomatic patients. Those with VBI had more high-grade stenosis, whereas those with lateralized symptoms had more occlusions, which tended to be ipsilateral to the symptoms.

Aged↗

Recurrent embolic cerebral infarction and anticoagulation.

A retrospective review of the hospital course of 44 patients with embolic cerebral infarction was carried out. Eleven patients (25%) suffered recurrent embolic infarction. Three of the recurrences were fatal. Two patients suffered a recurrence within 48 hours of the initial event, and an additional patient suffered a recurrence 6 days after the initial event. Sixteen embolic infarctions were managed with therapeutic anticoagulation within 48 hours without adverse effect. The clinical and experimental data concerning early anticoagulation after embolic infarction were reviewed. It appears that the risk of early anticoagulation is less than the risk of recurrent embolic infarction.

Adult↗