Background: Diabetes mellitus is well known as a significant predictor of silent myocardial ischemia. The incidence rates of silent events with newly developed Q waves, (especially, silent myocardial infarction (SMI)) in diabetic patients, have yet to be elucidated. We sought to evaluate the prevalence and predictors of SMI in type 2 diabetic patients without a history of atherosclerotic events. Methods: The Japanese primary prevention of atherosclerosis with aspirin for diabetes (JPAD) trial was performed to examine the efficacy of low-dose aspirin therapy for the primary prevention of atherosclerotic events in type 2 diabetes patients. Initially, there were no Q waves in any electrocardiograms (ECGs). The JPAD trial was a multicenter, prospective, randomized, open label, blinded, end-point study done from 2002 to 2008. After completion of the JPAD trial, we followed up the patients until 2015. ECGs of 1648 patients were re-examined to discover SMI in 2013 and 2015. We compared predictive factors for SMI to those for acute myocardial infarction (AMI). Results: During follow up of a median of 10.3 years, 64 patients suffered from a first AMI and 51 patients suffered from a first SMI. We novelly demonstrated that the incidence rate of SMI is comparable to that of AMI in diabetic patients (Figure). Age, smoking, dyslipidemia, and HbA1c ≥ 7.2 % were all associated with AMI. Hypertension was associated with SMI. Cox proportional hazards model analysis revealed that age ≥ 65 years and HbA1c ≥ 7.2 % were independent factors for AMI (P=0.0003, 0.0214, respectively, Figure). On the other hand, there were no significant independent factors for SMI. Conclusions: Our study demonstrates that age ≥ 65 years and HbA1c ≥ 7.2 % were independently associated with the incidence rate of AMI, but they were not associated with the incidence rate of SMI. Clinically, diabetic patients should frequently get ECGs for the detection of SMI because the rate of SMI is similar to AMI rates.
This study examined the direct response of smooth muscle of coronary spasm sites to α1-adrenergic stimulation in patients with coronary spastic angina. Phenylephrine (1 μM in the coronary circulation, for 5 min), a stimulator of α1-adrenoreceptors, was directly infused into coronary arteries with spasm in 10 patients with coronary spastic angina and into normal coronary arteries in 10 control patients. The luminal diameter of epicardial coronary arteries was determined by computer-assisted quantitative angiography. The constrictor response to intracoronary injection of acetylcholine (ACh; 50 μg) was greater in spastic arteries than in control arteries (decrease from baseline, 48 ± 2% vs. 12 ± 2%, respectively; p < 0.001). ACh (50 or 100 μg) induced coronary spasm associated with myocardial ischemia in all of patients with coronary spastic angina but not in any control patients. On the other hand, phenylephrine infusion did not induce coronary spasm in any of patients with coronary spastic angina or in control subjects. The constrictor response to phenylephrine infusion was comparable between spasm and control coronary arteries (decrease from baseline, 11 ± 2% vs. 9 ± 2%, respectively; p = NS). The results indicate that smooth muscle of spastic coronary arteries does not exhibit enhancement of constrictor response to direct stimulation of α1-adrenoreceptor on coronary smooth muscle. There may be receptor-specific enhancement of constrictor response to agonists in smooth muscle of spastic coronary arteries in patients with coronary spastic angina.
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