Adalat® in the Asian Pacific Region by Y. Nakamura, H. Miyashita, O. Iimura, K. Ueda, T. Sugimoto,

By Y. Nakamura, H. Miyashita, O. Iimura, K. Ueda, T. Sugimoto, Y. Toyama (auth.), Prof.Dr. David T. Kelly (eds.)

These are the lawsuits of the 3rd Asian Pacific Adalat Symposium. the 1st was once held in Tokyo in 1982 and the second one in Sydney in 1985. We have been honoured that the past due Dr. Sukaman and his colleagues have been in a position to host this 3rd symposium in Jakarta. This assembly was once designed to give a contribution to and to advertise foreign collaboration in cardiovascular examine, and to aid advertise additional wisdom and figuring out concerning the remedy of vascular disorder within the Asian Pacific zone. Nifedipine used to be initially investigated within the mid-1960s by means of Prof. Fleckenstein. His first effects confirmed this drug used to be a robust calcium antagonist which altered excitation contraction. at the present, there has been a speedy improvement of information in regards to the pathophysiology of ischaemic middle affliction, and therefore the real pharmacological paintings on calcium antagonists similar to nifedipine paralleled and complimented the more moderen realizing of coronary body structure in guy. very quickly such a lot treatment used to be designed to lessen myocardial oxygen intake and demand.

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The mechanism of the beneficial effects of nifedipine in myocardial ischemia has been attributed by Lorell and coworkers, as well as by others, to a decrease in oxygen demand secondary to its unloading effect (Emanuelsson and Holmberg 1983; Nelson et al. 1984; Tiefenbrunn et al. 1983), an increase in oxygen supply due to its vasodilating effect (Henry et al. 1978; Malacoff et al. 1982; Zacca et al. 1982) and to direct protection from ischemic myocardial damage (Henry et al. 1977). Although it did not reach statistical significance, the LVPF showed a tendency to increase with nifedipine during ischemia.

On exercise an increased rate-pressure product greater than the diastolic pressure time index may result in subendocardial ischemia provided subendocardial coronary reserve is exhausted [37]. As epicardial vessels dilate in response to metabolic demands, coronary pressure distal to a proximal stenosis decrease and may cause hypoperfusion of the subendocardium [38-39]. After myocardial infarction, ST-segment depression detected on exercise testing predicts cardiac deaths within 1 year. Thus, ST depression as a reflection of induceable ischemia warrants cardiac catheterization since these EeG .

Findings help identify high-risk cases or multivessel coronary artery disease [36, 40-47]. Although angina following myocardial infarction with ST depression could also be caused by coronary spasm [48], there is little angiographic evidence that spasm plays a role in postinfarction angina [49-50]. If angiographic findings do not adequately explain patients' symptoms, ergonovineinduced coronary spasm may be seen in postinfarction cases [20]. However, there is reluctance to use ergonovine maleate provocation in postinfarction patients for fear of unresponsiveness of ergonovine-induced spasm to nitroglycerin [51].

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