By Gerald C. Timmis
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Additional resources for Cardiovascular Review 1984
Hooper et a l . (JAMA 244:1960, 80) showed t h a t zinc a d m i n i s t r a t i o n could be c o u n t e r p r o d u c t i v e in man s i n c e i t may produce a sharp r e d u c t i o n in high-density lipoprotein. Singh et a l . (Angiology 3 4 : 2 1 5 , 83) r e p o r t e d t h a t a f a l l in plasma zinc l e v e l s below 65 ug/dL, t h e lower l i m i t of n o r m a l , w i t h i n t h e f i r s t t h r e e d a y s a f t e r a c u t e MI was an ominous p r o g n o s t i c sign because a l l t h e i r c a s e s below t h i s l e v e l expired.
Eighty-six percent of p o s i t i v e responders were found to develop angina within one year of MI; infarction f a i l e d to abolish angina in 96% of p a t i e n t s with a p o s i t i v e low-level t e s t (Am J Med 66:991, 7 9 ) . Thus, angina following infarction i s more l i k e l y a s s o c i a t e d w i t h p r e i n f a r c t i o n a n g i n a , and t e n d s t o increase at a rate of approximately 5% per year. Disappearance of angina i s exceptional (Clin Cardiol 1:31, 78) and i s decidedly l e s s than the 30% spontaneous remission rate seen in p a t i e n t s who have not infarcted (AJC 44:53, 7 9 ) .
However, Wilson et al. (Chest 82:416,82) found that patients with unstable angina had more severe regional myocardial ischemia due to reduced collateralization than patients with exertional angina, while the severity of coronary stenoses was similar between groups. Borer (NEJM 302:1200, 80) views the pathophysiology of unstable angina not necessarily as a result of a transient increase in oxygen demand but rather (or also) a reflection of a transient decrease in oxygen supply. Variability in the angina threshold on serial exercise testing reflects fluctuations in coronary arterial tone superimposed on increased myocardial oxygen requirements (AJC 51:397, 83).