Successful screening of sleep-disordered breathing using a pacemaker-based algorithm in Japan.

BACKGROUND: Recent pacemakers with transthoracic impedance sensors have a specific algorithm identifying sleep apnea (SA). Our aim was to evaluate the algorithm in Japanese patients. METHODS: Consecutive patients implanted with a pacemaker with sleep apnea monitoring algorithm at our hospital were enrolled prospectively. After implantation, patients underwent polysomnography (PSG). The respiratory disturbance index measured by pacemaker (RDI-PM) was extracted in the morning after PSG. RESULTS: Forty-five patients were recruited; 78% of patients underwent overnight PSG completely, and among them RDI-PM was invalid for one patient. Then the analysis was performed in 34 patients. Moderate/severe SA (apnea hypopnea index, AHI≥15events/h) and severe SA (AHI≥30events/h) by PSG were diagnosed in 65% and 41% of patients. The mean AHI-PSG and RDI-PM were 30.4±22.6 and 21.7±14.2events/h, respectively. There was a significant positive correlation between AHI-PSG and RDI-PM (r=0.543; p=0.001). The correlation was stronger in the severe SA group (r=0.664; p=0.010), in a group whose apnea index was higher than hypopnea index (r=0.822; p=0.002), and in a group whose central sleep apnea (CSA) index was higher than obstructive sleep apnea index (r=0.977; p<0.001). RDI-PM cut-off value for identifying severe SA was 22 (area under the curve, 0.682; sensitivity, 64%; specificity, 75%). CONCLUSIONS: The pacemaker-based algorithm is a useful screening tool for SA in Japanese individuals, especially in the severe SA group, apnea-dominant group, and CSA-dominant group.

Intravascular ultrasound assessment of the association between spatial orientation of ruptured coronary plaques and remodeling morphology of culprit plaques in ST-elevation acute myocardial infarction.

The aim of this study was to assess the association between the spatial location of plaque rupture and remodeling pattern of culprit lesions in acute anterior myocardial infarction (MI). Positive remodeling suggests a potential surrogate marker of plaque vulnerability, whereas plaque rupture causes thrombus formation followed by coronary occlusion and MI. Intravascular ultrasound (IVUS) can determine the precise spatial orientation of coronary plaque formation. We studied 52 consecutive patients with acute anterior MI caused by plaque rupture of the culprit lesion as assessed by preintervention IVUS. The plaques were divided into those with and without positive remodeling. We divided the plaques into three categories according to the spatial orientation of plaque rupture site: myocardial (inner curve), epicardial (outer curve), and lateral quadrants (2 intermediate quadrants). Among 52 plaque ruptures in 52 lesions, 27 ruptures were oriented toward the epicardial side (52%), 18 toward the myocardial side (35%), and 7 in the 2 lateral quadrants (13%). Among 35 plaques with positive remodeling, plaque rupture was observed in 21 (52%) on the epicardial side, 12 (34%) on the myocardial side, and 2 (6%) on the lateral side. However, among 17 plaques without positive remodeling, plaque rupture was observed in 6 (35%), 6 (35%), and 5 (30%), respectively (p = 0.047). Atherosclerotic plaques with positive remodeling showed more frequent plaque rupture on the epicardial side of the coronary vessel wall in anterior MI than those without positive remodeling.

Impact of plaque rupture on infarct size in ST-segment elevation anterior acute myocardial infarction.

OBJECTIVES: We sought to assess whether coronary plaque rupture at culprit lesions is associated with infarct size in patients with anterior acute myocardial infarction (AMI). BACKGROUND: Some patients with AMI have large infarcts despite early reperfusion. Whether culprit plaque morphology impacts infarct size or not remains unknown. METHODS: Patients who had a first anterior AMI with reperfusion within 6 hours after onset were enrolled and divided into 2 groups according to the presence or absence of plaque rupture at the culprit lesion as defined by preintervention intravascular ultrasound (IVUS): patients with rupture (n = 54) and without rupture (n = 37). RESULTS: Patients with plaque rupture had a higher incidence of no-reflow phenomenon (15% vs. 3%; p = 0.08) and a lower myocardial blush grade (1.5 vs. 2.3; p < 0.05) after percutaneous coronary intervention. The IVUS analysis showed that patients with plaque rupture had a higher incidence of soft plaque and positive remodeling. Peak creatine kinase levels were higher (4,707 vs. 2,309 IU/l; p < 0.0001) and left ventricular ejection fraction in the chronic phase was lower (54% vs. 63%; p < 0.01) in patients with plaque rupture. A multivariate logistic regression analysis revealed that plaque rupture and the proximal lesion site correlated with a left ventricular ejection fraction of <50% in the chronic phase (odds ratios 6.5 and 17.5, respectively; p < 0.05). CONCLUSIONS: Plaque rupture is associated with morphologic characteristics of vulnerable lesions, as well as with larger infarcts and a higher incidence of no-reflow phenomenon, suggesting that plaque embolism contributes to the progression of myocardial damage in patients with anterior AMI.