Clinically suspect ischemic heart disease not corroborated by demonstrable coronary artery disease

Myocardial Synthesis of Prostaglandin‐like Substances and Coronary Reactions to Cardiostimulation and to Hypoxia

“…The excess cardiac synthesis of prostaglandins or lack of its metabolic degradation, could lead to a diminished adenylate cyclase activation and subsequent reduced levels of cyclic AMP necessary to trigger the mechanism responsible for MCD reactions (Sen et al, 1976;Sen et al, 1977). Thus, abnormally high levels of prostaglandin might be, at least in part, the underlying mechanism of coronary insufficiency reported in humans with normal coronary arteriogram (Neill, Judkins, Dhindsa, Metcalfe, Kassebaum & Kloster, 1972;Bamrah, Bahler and Rakita, 1974;Rocher, Fayard, Manin, Bens, Guermonprez, Vagner, Leclerc, Ourbak & Maurice, 1974;Lawson, Rosch & Rahimtoola, 1976;Rosenblatt & Selzer, 1977;Oliva & Breckinridge, 1977;Selzer, 1977). Since patients with 'normal' coronary arteries may show angina pectoris, with abnormal myocardial lactate metabolism, the diagnosis of 'small vessel disease' with changes in structure or dysfunction of structurally normal small arteries has been suggested (Schaper & Schaper, 1977); the lack of evidence nevertheless inclined other authors to revive the hypothesis of neurogenic vasospasm as a mechanism of coronary insufficiency (Yasue, Touyama, Shimamoto, Kato, Tanaka & Akiyama, 1974;Johnson & Detwiler, 1977;Hellstrom, 1977).…”

Acute effects of nitrates on exercise testing in patients with syndrome X. Clinical and pathophysiological implications.

“…Compared with the control test, the main differences in the two groups observed during the exercise test after administration of ISDN were (1) heart rate at 1-mm ST-segment depression was higher (126±25 versus 104±15 beats per minute [bpm], P<.01) in group C, whereas it was not different (125±15 versus 126±16 beats per minute) in group X; (2) the rate-pressure product at 1-mm ST-segment depression, the time to 1-mm ST-segment depression, and the exercise duration were significantly imSyndrome X is diagnosed in patients with effort angina and ST-segment depression on the exercise ECG who are found to have normal epicardial coronary arteries at angiography.1"2 Myocardial ischemia caused by abnormalities in the function of small coronary arterial vessels has been hypothesized to be the cause of the syndrome.2'3 Indeed, a reduced coronary flow reserve, as indicated by an impaired response to vasodilator stimuli, has been demonstrated in a group of such patients,3-5 although the mechanism(s) of the microvascular abnormality are not known for the moment. Chest pain in patients with syndrome X is often indistinguishable from that occurring in patients with stable angina and atherosclerotic coronary disease. 6 Also, the accurate analysis of noninvasive tests such as ECG exercise testing,7-9 Holter monitoring,10 and radionuclide techniques"l-" does not allow a reliable prediction of coronary stenosis in patients coming to medical attention because of effort anginal pain.…”

Heart Disease Indicators in Patients with Aortocoronary Bypass Operation

“…Some of these patients may have belonged to the increasing group of individuals who were reported to have angina, or even myocardial infarcts, in the absence of any demonstrable serious coronary blood flow impairment [9,16,20], However, a more detailed study of our patients has shown that most of them had a single vessel disease. The frequent finding of chest pain in patients with relatively unremarkable coronary artery blood impairment stresses again the need for more detailed and definitive characterization of this symptom into anginal and nonanginal type and classification of its severity in order to assess its predictive or diagnostic value [4,10].…”