Impact of Morning Onset on the Incidence of Recurrent Acute Coronary Syndrome and Progression of Coronary Atherosclerosis in Acute Myocardial Infarction.

BACKGROUND: The relationship between time of onset of acute myocardial infarction (MI) and long-term clinical outcome has not been completely understood. We hypothesized that morning onset acute MI may be associated with adverse cardiac events.Methods and Results:This study involved 663 patients who underwent primary percutaneous coronary intervention (PCI). The main outcome measures were cardiac death, recurrent acute coronary syndrome (ACS), and re-hospitalization for heart failure. Major adverse cardiac events (MACE) were defined as a composite of individual adverse outcomes. Morning onset acute MI occurred in 212 patients (32.0%); they had higher rates of recurrent ACS (13% vs. 8%, P=0.03) and MACE (21% vs. 14%, P=0.012) than the patients with other times of onset. The PCI rate for progressive lesions was also higher than for patients with other times of onset (23% vs. 14%, P=0.013). On multivariate Cox regression analysis, morning onset was an independent predictor of recurrent ACS, MACE, and PCI for progressive lesions, with adjusted hazard ratios of 1.34 (95% CI: 1.06-2.92, P=0.030), 1.51 (95% CI: 1.02-2.23, P=0.038), and 1.58 (95% CI: 1.03-2.42, P=0.037), respectively. CONCLUSIONS: Morning onset may be associated with increased risk of recurrent ACS and coronary atherosclerosis progression.

Impact of obstructive sleep apnea on myocardial tissue perfusion in patients with ST-segment elevation myocardial infarction.

BACKGROUND: 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). METHODS AND RESULTS: 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). CONCLUSIONS: OSA may impair myocardial tissue perfusion following primary PCI.

Sotalol-induced coronary spasm in a patient with dilated cardiomyopathy associated with sustained ventricular tachycardia.

A 54-year-old man with severe left ventricular dysfunction due to dilated cardiomyopathy was referred to our hospital for symptomatic incessant sustained ventricular tachycardia (VT). After the administration of nifekalant hydrochloride, sustained VT was terminated. An alternate class III agent, sotalol, was also effective for the prevention of VT. However, one month after switching over nifekalant to sotalol, a short duration of ST elevation was documented in ECG monitoring at almost the same time for three consecutive days. ST elevation with chest discomfort disappeared since he began taking long-acting diltiazem. Coronary vasospasm may be induced by the non-selective beta-blocking properties of sotalol.