Potential Effects of Ischemic Postconditioning and Changes in Heat Shock Protein 72 in Patients with Acute Myocardial Infarction without Prodromal Angina.

The effectiveness of ischemic postconditioning (iPoC) in patients with ST-elevation myocardial infarction (STEMI) without ischemic preconditioning has not been determined. Therefore, we investigated the impact of iPoC and its potential mechanism related to heat shock protein 72 (HSP72) induction on myocardial salvage in patients with STEMI without prodromal angina (PA).We retrospectively analyzed data from 102 patients with STEMI with successful reperfusion among 323 consecutive patients with acute coronary syndrome. Among these, 55 patients with iPoC (iPoC (+) ) underwent 4 cycles of 60-second inflation and 30-second deflation of the angioplasty balloon. Both the iPoC (+) and iPoC (-) groups were divided into 2 further subgroups: patients with PA (PA (+) ) and those without (PA (-) ). We analyzed HSP72 levels in neutrophils, which were measured until 48 hours after reperfusion. I-123 ß-methyl-p-iodophenyl-pentadecanoic acid (BMIPP) scintigraphy was performed within a week of reperfusion therapy. In 64% of patients, thallium-201 (TL) scintigraphy was performed 6-8 months after STEMI onset.Using BMIPP and TL, in the PA (-) subgroups, the iPoC (+) group had a significantly greater myocardial salvage ratio than the iPoC (-) group. iPoC was identified as an independent predictor of the myocardial salvage ratio. The HSP72 increase ratio was significantly elevated in the iPoC (+) PA (-) group. Importantly, the myocardial salvage effect in patients without PA was significantly correlated with the HSP72 increase ratio, which was greater in patients with iPoC.These results suggest the potential impact of iPoC via HSP72 induction on myocardial salvage; however, the effects may be limited to patients with STEMI without PA.

A Carbamazepine-induced Brugada-type Electrocardiographic Pattern in a Patient with Schizophrenia.

We report the case of a 61-year-old man with schizophrenia who was treated with carbamazepine, in whom electrocardiography showed transient Brugada-type ST elevation. He had been hospitalized our hospital's Department of Psychiatry and had been diagnosed with pneumonia. On the following day, electrocardiography showed coved-type ST elevation in the right precordial leads and a blood examination revealed that the patient's carbamazepine concentration was at the upper limit of the standard range, as well as hypothyroidism. The patient's electrocardiogram normalized after the withdrawal of carbamazepine. We demonstrated that the patient's carbamazepine concentration-and not hypothyroidism-was associated with the serial electrocardiographic changes by monitoring the patient's blood concentration of carbamazepine and his thyroid function.

Association between microalbuminuria predicting in-stent restenosis after myocardial infarction and cellular senescence of endothelial progenitor cells.

OBJECTIVE: Relationship between microalbuminuria and worse outcome of coronary artery disease patients is discussed, but its underlying pathophysiological mechanism remains unclear. We investigated the role of microalbuminuria to the function of endothelial progenitor cells (EPCs), that might affect to outcome of acute myocardial infarction (AMI) patients. METHODS: Forty-five AMI patients were divided into two groups according to their urinary albumin excretion: normal (n = 24) and microalbuminuria (>30 mg/day, n = 21). At day-2 and day-7 after AMI onset, circulating-EPCs (CD34+ Flk1+) were quantified by flow cytometry. The number of lectin-acLDL-positive cultured-EPCs immobilized on fibronectin was determined. To assess the cellular senescence of cultured-EPCs, the expression level of sirtuin-1 mRNA and the number of SA-ß-gal positive cell were evaluated. Angiographic late in-stent loss after percutaneous coronary intervention (PCI) was evaluated at a six-month follow-up. RESULTS: No significant differences in coronary risk and the extent of myocardial damage were observed between the two groups. Late in-stent loss at the six-month follow-up was significantly higher in the microalbuminuria group (normal:microalbuminuria = 0.76±0.34:1.18±0.57 mm, p=0.021). The number of circulating-EPCs was significantly increased in microalbuminuria group at day-7, however, improved adhesion of EPCs was observed in normal group but not in microalbuminuria group from baseline to day-7 (+3.1±8.3:-1.3±4.4%: p<0.05). On the other hand, in microalbuminuria group at day-7, the level of sirtuin-1 mRNA expression of cultured-EPCs was significantly decreased (7.1±8.9:2.5±3.7 fold, p<0.05), which was based on the negative correlation between the level of sirtuin-1 mRNA expression and the extent of microalbuminuria. The ratio of SA-ß-gal-positive cells in microalbuminuria group was increased compared to that of normal group. CONCLUSIONS: Microalbuminuria in AMI patients is closely associated with functional disorder of EPCs via cellular senescence, that predicts the aggravation of coronary remodeling after PCI.

Dipstick proteinuria as a surrogate marker of long-term mortality after acute myocardial infarction.

BACKGROUND: Proteinuria and reduced estimated glomerular filtration rate (eGFR) are associated with an increased risk of mortality from acute myocardial infarction (AMI). However, it is unknown whether there is a difference in prognostic value for all-cause mortality between proteinuria and eGFR during post-AMI. METHODS: A consecutive series of 101 patients admitted with AMI who received angioplasty were enrolled. Dipstick proteinuria and eGFR were assessed on admission: (i) the patients were divided into 2 groups according to the presence of proteinuria (proteinuria, n=25), or not (negative, n=76), (ii) the patients were divided into 2 groups according to lower eGFR (GFR<60mL/min/1.73m(2), n=31) or higher (GFR>60mL/min/1.73m(2), n=70). Clinical characteristics and 3-year all-cause mortality estimated by Kaplan-Meier method were evaluated in each group. Additionally, a multivariate Cox proportional hazards model was applied to evaluate which factor was associated with all-cause mortality. RESULTS: Mean follow-up period was 914 days. Higher brain natriuretic peptide (BNP) levels were shown in the proteinuria and lower eGFR groups, respectively (proteinuria, 301±324pg/mL; negative, 146±159pg/mL; p=0.02; lower eGFR, 294±305pg/mL; higher eGFR, 142±161pg/mL; p=0.02). Three-year all-cause mortality was higher in the proteinuria group than in the normal group (p<0.001) and in the lower eGFR group than in the higher group (p=0.006). In a Cox proportional hazards model, the presence of proteinuria [hazard ratio (95% confidence interval), 4.51 (1.07-18.96); p=0.04] was selected as one of the predictors for all-cause mortality. CONCLUSIONS: Dipstick proteinuria and lower eGFR in the early phase of AMI follow-up were related to increased plasma BNP level during the sub-acute phase and long-term adverse outcome. Dipstick proteinuria may be a prognostic marker for long-term all-cause mortality.

Impaired ventricular repolarization dynamics in patients with early repolarization syndrome.

INTRODUCTION: Almost all current investigations on early repolarization syndrome (ERS) have focused on the J-wave characteristics and ST-segment configuration; however, few have reported on ventricular repolarization indexes in ERS. METHODS AND RESULTS: A total of 145 subjects were enrolled: 10 ERS patients, 45 uneventful ER pattern (ERP) subjects, and 90 healthy controls without J waves or ST-segment elevation. Ambulatory ECG-derived parameters (QT, QTc(B), QTc(F), T peak-Tend(Tpe), and QT/RR slope) were measured and statistically compared. Among the groups, there was no significant difference in the average QT and QTc(B); however, ERS patients had the shortest QTc(F) and longest Tpe (QTc(F): 396.2 ± 19 vs 410.4 ± 20 vs 419.2 ± 19 milliseconds, P = 0.036, Tpe: 84.9 ± 12 vs 70.4 ± 11 vs 66.9 ± 15 milliseconds, P < 0.001, for the ERS, ERP, and control groups, respectively). Importantly, the 24-hour QT/RR slope was significantly smaller in the ERS than ERP and control groups (QT/RR: 0.105 ± 0.01 vs 0.154 ± 0.02 vs 0.161 ± 0.03, respectively; P < 0.001). When analyzing the diurnal and nocturnal QT/RR slopes, ERS patients had small diurnal and nocturnal QT/RR slopes while the ERP and control groups had large diurnal and small nocturnal QT/RR slopes (diurnal QT/RR: 0. 077 ± 0.01 vs 0.132 ± 0.03 vs 0.143 ± 0.03, P < 0.001; nocturnal QT/RR: 0.093 ± 0.02 vs 0.129 ± 0.03 vs 0.130 ± 0.04, P = 0.02 in the ERS, ERP, and control groups, respectively). CONCLUSION: ERS patients had a continuously depressed diurnal and nocturnal adaptation of the QT interval to the heart rate. Such abnormal repolarization dynamics might provide a substrate for reentry and be an important element for developing ventricular fibrillation in the ERS cohort.

Site of transmural late gadolinium enhancement on the cardiac MRI coincides with the ECG leads exhibiting terminal QRS distortion in patients with ST-elevation myocardial infarctions.

Large infarcts are associated with a terminal QRS-distortion in ST-elevation myocardial infarction (STEMI) patients. Late gadolinium enhancement (LGE) on the cardiac MRI (CMR) can depict an infarct distribution. However, less is known about the relationship between the LGE findings and QRS-distortion on admission, including the best ECG-lead location to reveal the QRS-distortion (DIS-lead) in STEMI patients. Fifty STEMI patients successfully treated with percutaneous coronary intervention were classified into two groups according to whether the QRS-distortion was positive (+) or negative (-). The LGE on a recent CMR was classified into 12 left ventricular segments (Basal-Middle-Apical × Anterior-Septal-Inferior-Lateral). The coincidences between the segmental LGE scores and DIS-lead were investigated. All patients were divided into 23 QRS-distortion (+) and 27 QRS-distortion (-) groups. The total LGE score was significantly greater in the QRS-distortion (+) group (14.7 ± 6.8 versus 9.6 ± 6.2, P < 0.01). The highest LGE score in 96% of QRS-distortion (+) patients was 4, and a score 4 segment indicated a good selection of the DIS-lead (86.4%). QRS-distortion in the ECG on admission represents severe transmural infarction in the LGE using CMR, which represents large infarcts in STEMI patients.

Clinical and genetic investigation of a Japanese family with cardiac fabry disease. Identification of a novel α-galactosidase A missense mutation (G195V).

Fabry disease is an X-linked lysosomal storage disorder caused by mutations of the α-galactosidase A gene (GLA), and the disease is a relatively prevalent cause of left ventricular hypertrophy mimicking idiopathic hypertrophic cardiomyopathy. We assessed clinically 5 patients of a three-generation family and also searched for GLA mutations in 10 family members. The proband had left ventricular hypertrophy with localized thinning in the basal posterior wall and late gadolinium enhancement (LGE) in the near-circumferential wall in cardiovascular magnetic resonance images and her sister had vasospastic angina pectoris without organic stenosis of the coronary arteries. LGE notably appeared in parallel with decreased α-galactosidase A activity and increased NT-pro BNP in our patients. We detected a new GLA missense mutation (G195V) in exon 4, resulting in a glycine-to-valine substitution. Of the 10 family members, 5 family members each were positive and negative for this mutation. These new data extend our clinical and molecular knowledge of GLA gene mutations and confirm that a novel missense mutation in the GLA gene is important not only for a precise diagnosis of heterozygous status, but also for confirming relatives who are negative for this mutation.

Recovery of advanced atrioventricular block by cilostazol.

We describe a case of advanced atrioventricular (AV) block, in which treatment with cilostazol was effective in recovering the AV conduction. The patient was referred to our hospital for close examination of the advanced AV block and permanent pacemaker implantation. Although the patient had experienced third-degree AV block with occasional AV synchrony for more than two days, the AV conduction completely recovered after treatment with oral cilostazol at 200 mg/day. Here we discuss the possible mechanism of the improvement in the AV conduction by cilostazol.

A case of idiopathic systemic capillary leak syndrome with high serum levels of G-CSF on exacerbation.

Systemic capillary leak syndrome (SCLS) is a life-threatening disorder which presents with periodic episodes of hypovolemic shock, due to plasma leakage to the extra-vascular space reflected by accompanying hypoalbuminemia, hemoconcentration and edema often with associated monoclonal gammopathy. We describe a 28-year-old woman with SCLS who required aggressive fluid resuscitation and was successfully treated with corticosteroid, terbutaline, and theophylline. At exacerbation, the levels of serum granulocyte colony-stimulating factor (G-CSF) were increased. Thus, G-CSF might play an important role and can be a useful biomarker for the severity of attacks in SCLS.

Spontaneous resolution of an accidental total coronary occlusion.

In December 2007, a woman was involved in a traffic accident. At first, her vital signs were normal, but electrocardiogram showed ST-segment elevation in the inferior leads. She was diagnosed as a blunt chest trauma-induced myocardial infarction. Her right coronary angiography showed total occlusion. She underwent an emergency coronary artery bypass surgery; 64-multi-detector-row computed tomography (64-MDCT) demonstrated an intravascular protruding lesion, which suggested subintimal hematoma. One month later, repeat coronary angiogram showed spontaneous recanalization, and 64-MDCT showed no discontinuous vessel wall. Coronary artery occlusion secondary to blunt chest trauma is rare, and it's even rarer to have spontaneous recanalization.

Brugada syndrome case: difficult differentiation between a concealed form and tricyclic antidepressant-induced Brugada sign.

We describe a case of Brugada syndrome, in which recurrent syncope with convulsive seizures was induced after antidepressant treatment. The patient had been treated with five kinds of psychotropic drugs. The twelve-lead ECG after the syncope exhibited an RSR'-pattern in the precordial leads, however, a coved type ST-segment elevation was induced by a pilsicainide test. Although ventricular fibrillation was not induced in the electrophysiologic study, an ICD implantation was considered as the recommended therapy since Brugada syndrome unmasked by antidepressants could not be ruled out. The possible contribution of antidepressants to Brugada type ST-segment changes is discussed.

Brugada syndrome whose ST-segment changes were enhanced by antihistamines and antiallergenic drugs.

We describe a case of Brugada syndrome, in which a coved type ST-segment elevation was enhanced by antihistamines and antiallergenic drugs. The patient had been treated with four kinds of antihistamines and antiallergenic drugs. The twelve-lead ECG exhibited a coved type ST-segment elevation in leads V(1) and V(2), and their enhancement was induced by pilsicainide. After discontinuing those drugs, the ST segment elevation in leads V(1) and V(2) became reduced. An ICD implantation was selected for the therapy since ventricular fibrillation was induced. Our report discusses the possible contribution of antihistamines and antiallergenic drugs to the Brugada type ST-segment changes.