Kentarou Amenomori

Nagasaki University Hospital, Nagasaki, Nagasaki, Japan

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Publications (3)19.14 Total impact

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    ABSTRACT: Aims: It is unclear whether obstructive sleep apnea (OSA) increases the recurrence of acute coronary syndrome (ACS) in patients with acute myocardial infarction (MI). We hypothesized that moderate-to-severe OSA increased the number of adverse cardiovascular events in patients who underwent primary percutaneous coronary intervention (PCI). Methods and results: This study included 272 patients with acute MI. Polysomnography at first admission determined that 124 patients suffered from moderate-to-severe OSA. The main study outcome measures were cardiac death, recurrence of ACS, and re-admission for heart failure. Major adverse cardiac events (MACEs) were defined as composite end points of individual clinical outcomes. Follow-up coronary angiograms were obtained in 222 patients. PCI-related measures were target vessel revascularization and newly necessitated PCI for progressive lesions. The moderate-to-severe OSA patients had increased ACS recurrence and MACEs compared with patients with mild OSA or without sleep apnea (16% vs. 7%, p = 0.014; 22% vs. 11%, p = 0.014, respectively). PCI for progressive lesions was also higher in the moderate-to-severe OSA patients (28% vs. 15%, p = 0.015). Cox regression analysis showed that moderate-to-severe OSA was an independent predictor of ACS recurrence (hazard ratio = 2.30, p = 0.040). In addition, moderate-to-severe OSA was an independent predictor of PCI for progressive lesions, with a hazard ratio of 2.38 (p = 0.015). Conclusions: Moderate-to-severe OSA increased the risk of ACS and the incidence of PCI for progressive lesions. Increased plaque vulnerability might be related to these clinical manifestations.
    European Heart Journal: Acute Cardiovascular Care 05/2014; 4(1). DOI:10.1177/2048872614530865
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    ABSTRACT: Vascular endothelial dysfunction has been recognized as an essential feature of obstructive sleep apnea (OSA). This study was designed to examine the hypothesis that OSA may impair the coronary microcirculation in patients with ST-segment elevation myocardial infarction (STEMI). The present study included 100 patients with a first STEMI who underwent primary percutaneous coronary intervention (PCI) within 12h from onset. Coronary flow velocity at baseline and at maximum hyperemia was measured using a Doppler guidewire following PCI. Total ST-segment elevation was calculated at baseline and 30 min after PCI. All patients underwent polysomnography at 14 days to diagnose OSA. Coronary flow velocity reserve (CFVR) was used for quantitative analysis of myocardial tissue perfusion. Systolic retrograde flow (SRF) and ST-segment resolution (STR) <50% were used as an index of microvascular injury. Forty-eight patients presented with OSA. CFVR was comparable between the 2 groups. The incidence of SRF was higher in OSA patients than in the control patients (6% vs. 31%, P=0.005). Patients with OSA had a higher incidence of STR <50% (31% vs. 60%, P=0.003). Multiple logistic regression showed that OSA was an independent positive predictor of SRF and STR <50% (odds ratio=4.46, P=0.044; odds ratio=3.79, P=0.010). OSA may impair myocardial tissue perfusion following primary PCI.
    Circulation Journal 02/2011; 75(4):890-6. DOI:10.1253/circj.CJ-10-0768 · 3.94 Impact Factor
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    ABSTRACT: It has been suggested that obstructive sleep apnoea syndrome (OSA) may be a direct cause of left ventricular (LV) systolic dysfunction. This study was designed to examine our hypothesis that OSA inhibits the recovery of LV function in patients with acute myocardial infarction (AMI). Our 86 consecutive first-AMI patients underwent primary percutaneous coronary intervention (PCI). All patients underwent polysomnography and OSA was defined as an apnoea-hypoapnoea index (AHI) > or =15 events/h, of which more than 50% were obstructive. Left ventriculograms immediately after PCI and at 21 days were used to evaluate LV ejection fraction (LVEF), LV end-diastolic volume index, and regional wall motion (RWM) within the infarct area. OSA was observed in 37 patients (43%). All three indices of LV function after primary PCI were comparable between the two groups. Increases in LVEF and RWM during admission were significantly lower in OSA patients than those without OSA (delta LVEF: -0.3+/-9.6 vs. 7.4+/-7.2%, P < 0.001; delta RWM: 0.26+/-1.04 SD/chord vs. 1.16+/-1.20 SD/chord, P = 0.002). Multiple regression analysis showed that AHI correlated negatively with delta LVEF and delta RWM. The novel finding is that OSA may inhibit the recovery of LV function in patients with AMI.
    European Heart Journal 11/2006; 27(19):2317-22. DOI:10.1093/eurheartj/ehl219 · 15.20 Impact Factor