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        New Message Board Archives >> Medications, Treatments, Therapies 2004 >> Fresh Research on Nitrates and CH
        
(Message started by: floridian on Jun 28^th, 2004, 9:48pm)

Title: Fresh Research on Nitrates and CH
Post by floridian on Jun 28^th, 2004, 9:48pm

Everybody here knows that nitroglycerin and other nitrate containing medicines can trigger clusters. The most popular theory is that the nitrates increase nitric oxide production. Another theory mentioned in this research is that nitrates trigger by reducing oxygen saturation of the blood. (Ever hear of 'blue-baby' syndrome? Its caused by nitrate poisoning, and the amount of oxygen drops so low that the infant literally turns blue).

The oxygen saturation idea also could explain part or all of the link between smoking and clusters - carbon monoxide lowers the oxygen carrying capacity of blood, and lung damage from particulates also reduces oxygenation. This theory suggests that nicotine itself may not be the bad actor in CH, but rather the toxic by-products from the burning leaf. It would also suggest that aerobic exercise may be beneficial for some, and that other creative strategies should be tested (blood packing, or the use of erythropoetin, the hormone that stimulates red blood cell production).

Quote:

Ekbom K, Sjostrand C, Svensson D, Waldenlind E. Periods of cluster headache induced by nitrate therapy and spontaneous remission of angina pectoris during active clusters. Cephalalgia. 2004;24:92-98.

Glyceryl trinitrate (GTN) is known to induce single extra attacks of cluster headache (CH) during active cluster periods, most probably via actions of nitric oxide (NO). Induction of whole periods of CH by organic nitrates has, however, attracted little attention in the literature. We report on eight patients with episodic CH and coexistent effort-induced angina pectoris. Cases 1 to 6 had been free of their headaches for many years but got recurrence of CH within a few weeks after the administration of long-acting organic nitrates (isosorbide-dinitrate, isosorbide-5-mononitrate, or slow-release GTN) aimed at treating their chest pains. These nitrate-induced headache periods were more severe and had a longer duration than the previous spontaneous ones. Furthermore, one of the subjects and two additional cases experienced a marked reduction of their anginal attacks during successive CH periods. Exercise time to effort-induced angina was increased in all three patients and one of them revealed a markedly elevated threshold for eliciting ischemic cardiac symptoms by standardized physical exercise on a cycle ergometer. We hypothesize whether extra CH periods elicited by sustained nitrate therapy and remission of angina pectoris during active clusters are caused by central mechanisms involving inhibition of sympathetic tone and effects on both cranial vessels and cardiac functions. Comments: The GTN may be a vehicle for delivering NO, thus triggering the cluster attacks, however, it is worth remembering that Dr. Lee Kudrow, one of the most prominent cluster specialists of the last 20 years and also a former editor of this journal, felt that GTN triggered attacks by lowering oxygen saturation, thus tying in the higher prevalence of cluster in smokers (Kudrow L, Kudrow DB. The role of chemoreceptor activity and oxyhemoglobin desaturation in cluster headache. Headache. 1993;33:483-484). Stewart J. Tepper