Archives

  • 2018-07
  • 2019-04
  • 2019-05
  • 2019-06
  • 2019-07
  • 2019-08
  • 2019-09
  • 2019-10
  • 2019-11
  • 2019-12
  • 2020-01
  • 2020-02
  • 2020-03
  • 2020-04
  • 2020-05
  • 2020-06
  • 2020-07
  • 2020-08
  • 2020-09
  • 2020-10
  • 2020-11
  • 2020-12
  • 2021-01
  • 2021-02
  • 2021-03
  • 2021-04
  • 2021-05
  • 2021-06
  • 2021-07
  • 2021-08
  • 2021-09
  • 2021-10
  • 2021-11
  • 2021-12
  • 2022-01
  • 2022-02
  • 2022-03
  • 2022-04
  • 2022-05
  • 2022-06
  • 2022-07
  • 2022-08
  • 2022-09
  • 2022-10
  • 2022-11
  • 2022-12
  • 2023-01
  • 2023-02
  • 2023-03
  • 2023-04
  • 2023-05
  • 2023-06
  • 2023-07
  • 2023-08
  • 2023-09
  • 2023-10
  • 2023-11
  • 2023-12
  • 2024-01
  • 2024-02
  • 2024-03
  • 2024-04

    • br ACh and ER tests hereafter

    2024-03-08


    ACh and ER tests hereafter Spasm provocation tests have self-limitations to document coronary artery spasm during daily life. In the past reports, ST elevation was reproducible in some patients with variant trans-AUCB by the administration of ACh or ER. However, we now employ the ER and ACh spasm provocation tests in patients with not only variant angina but also non-variant angina. In patients with low disease activity, we may not obtain positive spasm even by performing either single ER or ACh test. As shown in Fig. 1, we recommend the supplementary use of pharmacological spasm provocation tests if patients had no provoked spasm by the single ACh or ER test. Moreover, if we could not obtain the typical positive spasm in patients with strongly suspected coronary spasm by the supplementary method, we may select to perform the sequential spasm provocation tests: first, ACh test, second, ER tests, and last, adding intracoronary ACh after ER tests [60]. Goto et al. also reported the usefulness of adding intracoronary injection of ACh following the intravenous infusion of ER when intravenous administration of ER 0.4mg showed negative spasms [61]. We also reported that the sensitivity and specificity of the combined sequential spasm provocation tests was more than 90%. Hereafter, if we could not obtain positive spasm in patients with strongly suspected coronary spasm, we should perform the supplementary use of ER and ACh and combined sequential tests. By performing the above tests, we will obtain the real truth in the clinic [62]. However, we should also take care of the pseudo-positive response during the supplementary and sequential methods.
    Conclusions We could perform the pharmacological spasm provocation tests without irreversible complications. Prior ACC/AHA guidelines support limited use of the pharmacological spasm provocation testing for spasm; however, current guidelines do not address the provocative testing [63]. We hope that ACC/AHA guidelines and ESC guidelines give spasm provocation testing a Class I indication similar to the JCS guidelines and the COVADIS group. We should perform the pharmacological spasm provocation tests routinely when we undertake coronary angiography as much as possible. If we performed the routine pharmacological spasm provocation tests in the cardiac catheterization laboratory, we will learn many things in the future. The era in which cardiologists investigate the presence of coronary artery stenosis in the cardiac catheterization laboratory has passed, because we could obtain the clear coronary trees by using other modalities such as coronary computed tomography or magnetic resonance imaging. Cardiologists are now in the next stage in which they should strictly diagnose patients without significant stenosis and medicate these patients appropriately, because patients without obstructive coronary artery disease are not always normal. Patients with normal coronary arteriogram may have variant angina, severe triple vessel spasms, or microvascular spasm/angina. These states may lead to sudden cardiac death/acute coronary syndrome or poor prognosis in the future.
    Funding
    Conflicts of interest
    Acknowledgments
    Introduction Nicotinic acetylcholine receptors (nAChRs) are neurotransmitter-gated ion channels that mediate fast cholinergic synaptic transmission in both vertebrates and invertebrates [6], [24]. In insects, nAChRs play important roles in the insect central nervous system (CNS) due to their great abundance, where acetylcholine is the major excitatory neurotransmitter [2]. Insect nAChRs are the action site of compounds extensively used in crop protection and animal health, such as neonicotinoid insecticides [17]. NAChRs are pentameric complexes assembled from a variety of distinct subunits [6], [12]. Through molecular cloning and genome sequencing, 10 nAChR subunits (Dmα1-Dmα7 and Dmβ1-Dmβ3) have been identified and characterized in the fruit fly Drosophila melanogaster[6], [18], and a similar number of nAChR subunits have been identified in other insect species [6], [17]. More than 10nAChR subunits from one insect species give many possibilities to comprise different nAChRs with distinct properties. In some insect species, alternative splicing frequently occurs in nAChR subunits, which would comprise more nAChRs with further diverse properties in function and pharmacology [4], [8], [9], [11], [22], [23], [28]. Although many nAChR subunits and their alternative splicing have been characterized in insects, it is unsuccessful to heterologously express insect nAChRs without any help from chaperon proteins from insects or other subunits from vertebrates [19], [20]. Even with vertebrate nAChR subunits, such as the rat (Rattus norvegicus) β2 subunit, few insect subunits were successfully co-expressed in heterologous systems [14], [20], [36].