Startling hyperglycaemia with transient beta cell stunning in a patient with type 2 diabetes.

A 59-year-old woman unaware of having diabetes was transferred due to coma. Upon discovery at home, her consciousness on the Glasgow Coma Scale was E1V2M4, BP 95/84 mmHg, body temperature 34.7°C. On arrival at ER, height was 1.63 m, weight 97 kg, plasma glucose (PG) 1,897 mg/dL, HbA1c 13.6%, osmolality 421 mosm/kg, arterial pH 7.185, lactate 6.34 mmol/L, ß-hydroxybutyrate 7.93 mmol/L. With saline and regular insulin infusion, PG was lowered to 1,440 mg/dL at 2 hours and then to 250 mg/dL by Day 3, and consciousness normalized by Day 5. On admission, serum immunoreactive insulin (IRI) was undetectable (<0.03 U/mL), C-peptide immunoreactivity (CPR) undetectable (<0.003 ng/mL), and anti-glutamic acid decarboxylase antibody negative. Following the above-described treatment, fasting PG was 186 mg/dL and CPR 1.94 ng/mL, respectively, on Day 14; 2-h post-breakfast PG 239 mg/dL and CPR 6.28 ng/mL, respectively, on Day 18. The patient discharged on Day 18 with 1,800 kcal diet, 32 U insulin glargine and 40 mg gliclazide. Fifteen months later at outpatient clinic, her HbA1c was 6.9% and 2-h post-breakfast PG 123 mg/dL and CPR 5.30 ng/dL with 750 mg metformin, 10 mg gliclazide and 18 U insulin glargine. Transient, but total cessation of insulin secretion was documented in a patient with type 2 diabetes under severe metabolic decompensation. Swift, sustained recovery of insulin release indicated that lack of insulin at the time of emergency was due to secretory failure, i.e., unresponsive exocytotic machinery or depletion of releasable insulin, rather than loss of beta cells.

Incidence and mortality of acute myocardial infarction. A population-based study including patients with out-of-hospital cardiac arrest.

The in-hospital mortality rate of acute myocardial infarction (AMI) is improving. In Japan, little information exists concerning the incidence and mortality of AMI. Therefore, our population-based analysis examined the incidence and mortality rate in AMI cases in individuals that lived in the Matsumoto region in 2002. We studied 169 AMI patients who were admitted within 14 days after a non-out-of-hospital cardiac arrest (non-OHCA group) and 63 patients with an AMI-related out-of-hospital cardiac arrest (OHCA group). The in-hospital mortality rate of the non-OHCA group was 9.5% (reperfusion therapy [+] 3.4%, [-] 22.7%, P < 0.0001). The rate of return of spontaneous circulation and the survival rate were 21% and 1.6%, respectively, in the OHCA group. The incidence of AMI in the non-OHCA and OHCA groups combined was 55.2 to 63.1 events/100,000 people annually and the mean age of AMI patients was 70 ± 13 years. The population-based mortality rate of AMI was 34% to 42%. The mortality rate of AMI remains high, and most deaths occur outside of the hospital. Prehospital care may lower the mortality rate of AMI.

Painless acute aortic dissection. - Diagnostic, prognostic and clinical implications.-.

BACKGROUND: Acute aortic dissection (AAD) classically presents as sudden, severe chest, back, or abdominal pain. However, there have been several documented cases presenting with atypical features. The clinical characteristics and outcomes of patients with painless AAD were investigated. METHODS AND RESULTS: The study group comprised 98 patients (53 males, 45 females; 66 ± 12 years) with AAD admitted to hospital from 2002 to 2007: 16 patients (17%) had no pain (painless group) and 82 patients had pain (painful group). In 81% of the painless group and 70% of the painful group there was a type A dissection. The painless group more frequently had a persistent disturbance of consciousness (44% vs. 6%, P < 0.001), syncope (25% vs. 1%, P < 0.001) and a focal neurologic deficit (19% vs. 2%, P = 0.006) as presenting symptoms. Imaging study findings were not significantly different. Cerebral ischemia (50% vs. 1%, P < 0.001) and cardiac tamponade (38% vs. 13%, P = 0.01) were more frequent complications in the painless group. In-hospital mortality was not significantly different (19% vs. 15%). However, the painless group had a more unfavorable functional outcome on overall performance category (P < 0.001). CONCLUSIONS: Painless AAD may be more frequent than previously reported. Painless AAD patients often present with a disturbance of consciousness or a neurologic deficit, and have a higher morbidity than painful AAD patients.

A case of left atrial involvement of cardiac sarcoidosis manifesting as atrial flutter treated with corticosteroids.

The clinical diagnosis of cardiac sarcoidosis can be elusive, because the clinical manifestations are non-specific, and the sensitivity and specificity of diagnostic modalities are limited. A 60-year-old woman suffered atrial flutter and diffuse thickening of the left atrial wall accompanied with gallium-67 uptake, both of which were successfully treated with corticosteroid therapy. The diagnosis of cutaneous sarcoidosis had been made two years previously; therefore, we diagnosed the patient as having atrial involvement of cardiac sarcoidosis, and discuss here the importance of noninvasive evaluation of cardiac sarcoidosis using echocardiography.

Anti-beta 1-adrenoreceptor autoantibodies and myocardial sympathetic nerve activity in chronic heart failure.

BACKGROUND: The autoantibodies stimulate the beta1-adrenoreceptors on cardiac myocytes similar to norepinephrine, and are associated with reduced cardiac function. Iodine-123 metaiodobenzylguanidine ((123)I-MIBG) is metabolized similarly to norepinephrine. This study was undertaken to investigate the relationship between cardiac stimulation by anti-beta1-adrenoreceptor autoantibodies and myocardial sympathetic nervous activity in patients with chronic heart failure. METHODS: We screened for the anti-beta1-adrenoreceptor autoantibodies in 52 patients with chronic heart failure by conducting an enzyme-linked immunosorbent assay, and underwent (123)I-MIBG scintigraphy in 27 of the patients. Anterior planar images of (123)I-MIBG were obtained 15 min and 3 h after the injection. We determined the heart to mediastinum radioactivity ratio (H/M), and calculated the rate of washout of (123)I-MIBG from the heart. RESULTS: Patients with New York Heart Association functional class III or IV had higher levels of anti-beta1-adrenoreceptor autoantibodies than those with class I or II (p<0.01). The autoantibody level was significantly correlated with delayed H/M (r=-0.65, p<0.001) and washout rate (r=0.65, p<0.001). Sixteen patients with a cardiac event showed higher levels of the autoantibodies (p<0.05). Cardiac event-free survival was poorer in patients with the autoantibody levels >10 U/ml than that <10 U/ml (log-rank=12.1, p<0.001). CONCLUSION: The anti-beta1-adrenoreceptor autoantibodies are closely associated with cardiac sympathetic nervous activity assessed by (123)I-MIBG and cardiac event in patients with chronic heart failure.

Effective uptake of N-acetylglucosamine-conjugated liposomes by cardiomyocytes in vitro.

A drug delivery system (DDS) that targets the injured myocardium would serve as a novel therapeutic tool for cardiac diseases. To develop such a DDS, we investigated the interaction of 2 types of glycoside-conjugated liposomes containing a fluorescence substrate with cardiomyocytes. Flow cytometry revealed that cardiomyocytes adequately interact with N-acetylglucosamine-conjugated liposomes (GlcNAc-Ls). Furthermore, to confirm whether the agents encapsulated in GlcNAc-Ls affect the intracellular environment of cardiomyocytes, we prepared GlcNAc-Ls-containing pravastatin and examined the effect of pravastatin on cardiomyocytes. Pravastatin is a 3-hydroxy-3-methylglutaryl-CoA reductase inhibitor (statin) and is hydrophilic. It is reported that lipophilic statins enhance nitric oxide (NO) production and inducible nitric oxide synthase (iNOS) expression by interleukin-1beta (IL-1beta)-stimulated cardiomyocytes. The hydrophilic nature of pravastatin prevents its entry into cardiomyocytes; therefore, it cannot enhance both these processes. Treatment with GlcNAc-Ls-containing pravastatin specifically enhanced NO production and iNOS expression by IL-1beta-stimulated cardiomyocytes. Based on these results, we found that cardiomyocytes exhibit a high degree of interaction with GlcNAc-Ls, and GlcNAc-Ls-encapsulated agents can be effectively taken up by cardiomyocytes. We suggest that GlcNAc-Ls can be utilized therapeutically as a DDS for the injured myocardium.