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.

Clinical, serologic and magnetic resonance imaging of 3 cases of inflammatory myopathy with abundant macrophages in the Japanese population.

We report the first 3 cases of inflammatory myopathy with abundant macrophages (IMAM) to be found in an Asian country. Diagnosis of IMAM was based on the infiltration of CD68+ macrophages into biopsied specimens, particularly the fascia. Proximal skeletal muscle symptoms and signs, elevation of creatine kinase, and myogenic changes in electromyography were found in all of the cases, and magnetic resonance imaging clearly revealed thickening of the fascia. Since dermatomyositis (DM)-specific skin alterations were not found, none of the patients in this study fulfilled Bohan and Peter's criteria for DM; however, anti-PL-7 antibody was detected in case number 1. In addition, CD20+ B-cell infiltration into the fascia was also detected in all of the cases, indicating further transition to DM. Severe illness, namely macrophage activation syndrome and acute respiratory distress syndrome, occurred in case 1 but was resolved with intensive combination therapy. The other 2 cases also required glucocorticoids to achieve remission.

Graves' disease complicated by ventricular fibrillation in three men who were smokers.

BACKGROUND: Thyrotoxicosis is known to be associated with sinus tachycardia and supraventricular tachyarrhythmias, but rarely with ventricular fibrillation (Vf), which has only occurred in some patients with hypokalemic periodic paralysis or ischemic heart disease. PATIENT FINDINGS: We present three men who were transferred to our hospital with Graves' disease who developed idiopathic Vf. None of them had hypokalemic periodic paralysis or ischemic heart disease but all were smokers. None of other patients with thyrotoxicosis (587 females and 155 males) who were seen at our hospital, in the period during which the three men were seen, had idiopathic Vf. In our three men with thyrotoxicosis and idiopathic Vf, there was no identifiable underlying heart disease. One of the three patients died of hypoxic encephalopathy. The other two men did not have recurrent Vf after their thyroid function normalized. SUMMARY: These cases and a review of similar cases in the literature imply that improving thyrotoxicosis seems to be effective for treating idiopathic Vf in some patients. CONCLUSIONS: Our findings suggest that thyroid hormone excess might play a direct role in the development of Vf in susceptible individuals. Our experience with these three patients suggests that smoking men with thyrotoxicosis likely have an increased risk for Vf, even if they do not have other predisposing factors.

Acute stress response modified by modest inhibition of growth hormone axis: a potential machinery of the anti-aging effect of calorie restriction.

Calorie restriction (CR) may exert antiaging effects by inhibiting the growth hormone (GH)/IGF-1 axis. The present study investigated the effect of modest inhibition of GH signaling on stress response and compared it with the effect of CR. Heterozygous (tg/-) rats of a transgenic strain of male rats, whose GH signaling was inhibited by overexpression of the anti-sense GH gene, and wild-type (WT) rats were used. Rats were fed ad libitum (AL) or 30% CR diets from 6 weeks of age. At 6 months of age, rats were killed between 0 and 8h after lipopolysaccharide (LPS) injection to evaluate the acute phase stress response. tg/- rats had less tissue injury, indicated by blood aspartate aminotransferase (AST) concentrations, than WT rats. Successive waves of incremental plasma TNF-α, IL-6, and interferon (IFN)-γ levels were also attenuated in tg/- rats. Activation of NF-κB, a redox-sensitive transcription factor, was slightly diminished in tg/- rats, whereas the AP-1 activity was increased. Similar trends were also observed in the CR groups as compared to the AL groups. The present results suggest an involvement of the GH/IGF-1 axis in the effect of CR for stress response, even if CR does not act solely through the GH axis.

Manipulation of caloric content but not diet composition, attenuates the deficit in learning and memory of senescence-accelerated mouse strain P8.

Calorie restriction (CR) is an experimental intervention in laboratory animals that attenuates age-associated increases in morbidity, mortality, and functional impairment. It is characterized by mild ketosis, hypoinsulinemia and hypoglycemia. In this study, we examined whether metabolic simulation of CR by a diet of isocaloric ketogenic or hypoinsulinemic diets ameliorated the learning and memory deficit in a strain of senescence-accelerated prone mice (SAMP8), a mouse model of age-dependent impairments in learning and memory. Male SAMP8 mice were fed high carbohydrate (CHO), high fat (FAT), or high protein (PRO) diets after weaning, and calorie intake was adjusted to 95% (sub ad libitum, sAL) or 70% (CR) of the mean calorie intake of control mice. At 28 weeks of age, we found CR ameliorated the performance defects of SAMP8 mice in a passive avoidance task. Neither FAT nor PRO diets affected performance of the task when fed sAL level, although a diet of these compositions partially mimicked the serum parameters of CR mice. These results suggest restriction of calorie intake is important for the prevention of learning and memory deficits, and that the simulation of serum changes induced by CR is not sufficient to prevent the cognitive defects of SAMP8 mice.