Effects of moderate-to-severe obstructive sleep apnea on the clinical manifestations of plaque vulnerability and the progression of coronary atherosclerosis in patients with acute coronary syndrome.

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.

Obstructive sleep apnoea increases the incidence of morning peak of onset in acute myocardial infarction.

AIMS: There exists a discrepancy regarding the relationship between obstructive sleep apnoea (OSA) and circadian variation during the onset of acute myocardial infarction (MI). We hypothesized that OSA patients show a characteristic circadian variation and that the severity of OSA significantly affects this variation. METHODS AND RESULTS: The present study included 288 patients with first acute MI who underwent percutaneous coronary intervention within 12 h of symptom onset. The diagnosis of OSA required an apnoea-hypopnoea index (AHI) of ≥5 events/h. A total of 216 patients fulfilled the OSA criteria. The incidence of MI onset between 06:00 and 11:59 hours was significantly higher in OSA patients than in control patients (38 vs. 25%, p=0.039). Circadian variation in the morning peak of MI onset was attenuated in mild OSA (as defined by AHI, 5.0-14.9 events/h; 33 vs. 25%, p=0.240). Moderate-to-severe OSA (as defined by AHI ≥15.0 events/h) clearly increased the incidence of MI onset between 06:00 and 11:59 hours (43 vs. 25%, p=0.014). Multiple logistic regression adjusting for AHI (≥15.0 events/h), age, body mass index, hypertension, and current smoking showed that moderate-to-severe OSA significantly contributed to MI onset between 06:00 and 11:59 hours (odds ratio 2.00, p=0.010). CONCLUSIONS: OSA showed a morning peak with regard to MI onset, and moderate-to-severe OSA significantly enhanced this circadian variation.

Successive immunosuppressive treatment of fulminant myocarditis that is refractory to mechanical circulatory support.

BACKGROUND: Long-term prognosis in patients with fulminant myocarditis can be favorable; however, for 32-36% of patients, this condition becomes fatal during the acute stages despite the use of mechanical circulatory support. Other therapeutic options may be needed for patients in whom these conditions are resistant to aggressive management. CASE REPORT: We present a case of fulminant myocarditis that rapidly progressed to cardiogenic shock and in-hospital cardiac arrest in a 46-year-old male. The patient promptly received inotropic agents, intra-aortic balloon pump therapy, and extracorporeal membrane oxygenation. However, creatinine kinase (CK), C-reactive protein (CRP), and QRS width increased significantly between days 1 and 3 of treatment; the patient's hemodynamic profile deteriorated despite this treatment regimen. Intravenous methylprednisolone was initiated on day 3 at a dose of 1,000 mg/day and maintained for an additional three days. Less than 24 h after methylprednisolone administration, the QRS width decreased significantly from 0.44 s to 0.18 s. In addition, CK and CRP levels declined sharply, which is associated with hemodynamic improvement. CONCLUSIONS: High doses of intravenous methylprednisolone may be considered a therapeutic option for patients with fulminant myocarditis that is refractory to usual management practices.