| Abstrakt: |
For about 120 years we have been looking for the 'cause' of essential hypertension. It is possible that we have merely been wandering through its graveyard, looking at the pathogenetic mechanisms but never the actual cause? Here we pass the gravestone of increased sympathetic activity; there the gravestone of low renin activity. Here high endothelin; there low EDRF. Here high thromboxane A2; there low prostacyclin. It is possible that all these and so many other pathogenetic factors are all due to one basic defect? Is it possible that, in the dead of night while patients with EH have been sleeping, the villain has been lurking in their mouths, stuck somewhere at the back of their throats, hidden from view yet choking them hundreds of times a night. But this intermittent strangulation has not occurred silently. On the contrary, it has made its presence felt in the most irritating way, with snores, groans, grunts, gasps and frightening periods of total apnea. But we, their physicians, never asked about these symptoms, or, if we did, we never paid heed to them. This is clear from the fact that, most cases of OSA occur in association with EH yet are not diagnosed. Perhaps the next 'arousal response' should be the arousal of physicians' consciousness so that they can at long last wake up to the existence of the close connection between sleep-related breathing disorders and hypertension and breathe some new life into the treatment of two old diseases-essential hypertension and secondary hypertension. Early diagnosis and treatment of the sleep-related breathing disorders may not only make the patient feel much better, (something our antihypertensive medications do not always do), but may reduce the blood pressure and prevent the progression of renal and cardiovascular damage as well. [ABSTRACT FROM PUBLISHER] |
