Haruki Musha

Left Ventricular Rupture Associated With Takotsubo Cardiomyopathy

A 70-year-old woman was admitted to the hospital with chest discomfort after quarreling with her neighbors. Electrocardiography revealed ST-segment elevation in leads I, II, III, aVL, aVF, and V2 through V6. Coronary angiography demonstrated normal arteries, but left ventriculography showed apical akinesis and basal hyperkinesis. Takotsubo cardiomyopathy was diagnosed on the basis of these characteristic findings. The creatine kinase and creatine kinase-MB concentrations were elevated at admission and reached maximum levels 6 hours after admission. The plasma level of brain natriuretic peptide was 10.7 pg/mL (reference range, <18.4 pg/mL) on the first hospital day. ST-segment elevation in leads I, II, III, aVL, aVF, and V2 through V6 persisted at 72 hours after admission. On the third hospital day, sudden rupture of the left ventricle occurred, and despite extensive resuscitation efforts, the patient died. Takotsubo cardiomyopathy presents in a manner similar to that of acute myocardial infarction, but ventricular systolic function usually returns to normal within a few weeks. To our knowledge, this is the first reported case of fatal left ventricular rupture associated with takotsubo cardiomyopathy. We suggest that takotsubo cardiomyopathy may be a newly recognized cause of sudden cardiac death.

Reversible ventricular dysfunction takotsubo cardiomyopathy

Recently, many cardiologists have recognized the existence of a rapidly reversible form of heart failure of unknown origin characterized by a takotsubo‐shaped, dyskinetic left ventricle on left ventriculography.

Impact of Contrast-Induced Nephropathy and Cardiovascular Events by Serum Cystatin C in Renal Insufficiency Patients Undergoing Cardiac Catheterization

We assessed the usefulness of serum cystatin C for predicting contrast-induced nephropathy (CIN) in patients (n = 100) undergoing coronary catheterization. After a 12-month follow-up, the incidence of CIN was 8.3% (n = 5) in patients with mild renal insufficiency (estimated glomerular filtration rate [eGFR] 60-89 mL/min per 1.73 m2), 34.4% (n = 10) in those with moderate renal insufficiency (eGFR 30-59 mL/min per 1.73 m2), and 100% (n = 3) in those with severe renal insufficiency (eGFR 15-29 mL/min per 1.73 m2). The sensitivity was 81.8% and specificity was 90.9% at the cutoff level of serum cystatin C >1.18 mg/L. Serum cystatin C levels were significantly (P < .001) higher in the patients with moderate renal insufficiency in the CIN group than those in the non-CIN group. Multivariate logistic regression analysis demonstrated that baseline serum cystatin C independently predicted short-term mortality (odds ratio [OR], 0.311; 95% confidence interval [CI] 0.058-0.538; P = .026). Baseline serum cystatin C significantly predicted the occurrence of CIN in the patients with moderate renal insufficiency.

Three-month exercise and weight loss program improves heart rate recovery in obese persons along with cardiopulmonary function.

OBJECTIVE Heart rate recovery (HRR) after exercise is an independent risk factor for cardiovascular disease and mortality, and it is well known to be modifiable by weight loss. We investigated whether HRR was mainly improved by better cardiopulmonary function or by alteration of the metabolic profile. METHODS The weight loss program included 2h of group exercise per week and individual dietary instruction by a qualified dietician every week. Clinical assessment (including HRR) was done before and after the 3-month program. PATIENTS The subjects were 125 obese persons without a past history of stroke, cardiovascular events, or use of medications who participated in and completed our exercise plus weight loss program. RESULTS HRR (35.61+/-12.83 to 45.34+/-13.6 beats/min, p<0.0001) was significantly faster after the program. The change in HRR was significantly correlated (p<0.05) with the changes in body weight, body mass index, percent body fat, waist circumference, hip circumference, resting heart rate, peak exercise heart rate, exercise time, maximal work load, physical working capacity divided by body weight (PWC75%HRmax/weight), subcutaneous fat area, visceral fat area, low-density lipoprotein cholesterol, and leptin. Multivariate analysis showed that the change in HRR was significantly correlated (p<0.05) with the changes in resting heart rate, peak exercise heart rate, and PWC75%HRmax/weight. CONCLUSIONS Our data demonstrated that HRR can be improved in obese subjects by a 3-month exercise and weight loss program. Improvement in cardiopulmonary function by exercise seems to be the main contributor to the increment of HRR.

Cystatin C: a better marker to detect coronary artery sclerosis.

BACKGROUND Nowadays, early detection and treatment can often keep chronic kidney disease patients from getting worse and prevent the occurrence of cardiovascular disease. Cystatin C (Cys-C) is a new marker for renal dysfunction. This study investigated whether Cys-C played an important role for screening coronary artery disease. METHODS The consecutive 88 outpatients (51 males and 37 females), who were suspected of having effort angina pectoris or asymptomatic ischemic heart disease, were enrolled. Serum Cys-C, which was obtained within 3 months before coronary angiography, was assessed with the presence or absence of coronary arteriosclerosis, the number of culprit arteries, and blood biochemical parameters. RESULTS Mean serum Cys-C was 0.82+/-0.29 mg/l. Significant differences in the estimated creatinine clearance (p=0.036), hemoglobin A1c (p=0.01), left ventricular ejection fraction (p=0.01), creatinine (p=0.007), Cys-C (p=0.006), and high-density lipoprotein (HDL) cholesterol (p=0.001) were observed between the patients with or without coronary arteriosclerosis. Serum Cys-C was significantly greater in the multi-vessel disease (MVD) group than the 0 vessel disease (0VD) group (p<0.001). HDL cholesterol was significantly lower in the MVD group than the 0VD and single-vessel disease groups (p=0.002 and p=0.005, respectively). CONCLUSION The results of this study suggest Cys-C might be one of the risk factors for coronary arteriosclerosis in the patients with suspected ischemic heart disease without any history of coronary artery disease. Cys-C was a useful marker to detect coronary artery disease and the level of Cys-C could reflect the severity of coronary arteriosclerosis.

Myocardial injury in a 100-km ultramarathon

Abstract Impaired cardiac function after strenuous exercise, such as an ultramarathon or triathlon, has been ascribed to “cardiac fatigue.” However, a reduction of cardiac function in strenuous sports in the absence of coronary artery disease might also be based on myocardial injury because of excess catecholamines. We studied the cardiac injury in runners of a 100-km ultramarathon by determination of levels of serum troponin T, which is highly specific for myocardial injury. Blood was collected from 13 healthy adult men before, immediately after, and the next morning after participation in a 100-km ultramarathon. Creatine kinase (CK), isozyme of CK with muscle and brain subunits (MB), and cardiac troponin T levels were determined. Creatine kinase levels were 207 ± 108 IU/L before the marathon, 10,313 ± 10,273 IU/L immediately after, and 10,799 ± 6593 IU/L on the next day. Creatine kinase MB levels at the same time points were 12 ± 14 IU/L, 197 ± 170 IU/L, and 166 ± 108 IU/L, respectively. Cardiac troponin T level was ⩽0.1 ng/mL in all subjects before the marathon and increased significantly to a mean of 0.68 ± 0.73 ng/mL immediately after, exceeding the normal limit in seven subjects. It then returned to normal (0.15 ± 0.07 ng/mL) on the next day, while CK, which referred to skeletal muscle damage, was still elevated at a high level. Because cardiac troponin T levels increased after the ultramarathon, myocardial injury was considered to have occurred.

The DNA Repair Enzyme Apurinic/Apyrimidinic Endonuclease (Apex Nuclease) 2 Has the Potential to Protect against Down-Regulation of Chondrocyte Activity in Osteoarthritis

Apurinic/apyrimidinic endonuclease 2 (Apex 2) plays a critical role in DNA repair caused by oxidative damage in a variety of human somatic cells. We speculated that chondrocyte Apex 2 may protect against the catabolic process of articular cartilage in osteoarthritis (OA). Higher levels of Apex 2 expression were histologically observed in severely compared with mildly degenerated OA cartilage from STR/OrtCrlj mice, an experimental model which spontaneously develops OA. The immunopositivity of Apex 2 was significantly correlated with the degree of cartilage degeneration. Moreover, the OA-related catabolic factor interleukin-1β induced the expression of Apex 2 in chondrocytes, while Apex 2 silencing using small interfering RNA reduced chondrocyte activity in vitro. The expression of Apex 2 in chondrocytes therefore appears to be associated with the degeneration of articular cartilage and could be induced by an OA-related catabolic factor to protect against the catabolic process of articular cartilage. Our findings suggest that Apex 2 may have the potential to prevent the catabolic stress-mediated down-regulation of chondrocyte activity in OA.

The NAD-Dependent Deacetylase Sirtuin-1 Regulates the Expression of Osteogenic Transcriptional Activator Runt-Related Transcription Factor 2 (Runx2) and Production of Matrix Metalloproteinase (MMP)-13 in Chondrocytes in Osteoarthritis.

Aging is one of the major pathologic factors associated with osteoarthritis (OA). Recently, numerous reports have demonstrated the impact of sirtuin-1 (Sirt1), which is the NAD-dependent deacetylase, on human aging. It has been demonstrated that Sirt1 induces osteogenic and chondrogenic differentiation of mesenchymal stem cells. However, the role of Sirt1 in the OA chondrocytes still remains unknown. We postulated that Sirt1 regulates a hypertrophic chondrocyte lineage and degeneration of articular cartilage through the activation of osteogenic transcriptional activator Runx2 and matrix metalloproteinase (MMP)-13 in OA chondrocytes. To verify whether sirtuin-1 (Sirt1) regulates chondrocyte activity in OA, we studied expressions of Sirt1, Runx2 and production of MMP-13, and their associations in human OA chondrocytes. The expression of Sirt1 was ubiquitously observed in osteoarthritic chondrocytes; in contrast, Runx2 expressed in the osteophyte region in patients with OA and OA model mice. OA relating catabolic factor IL-1βincreased the expression of Runx2 in OA chondrocytes. OA chondrocytes, which were pretreated with Sirt1 inhibitor, inhibited the IL-1β-induced expression of Runx2 compared to the control. Since the Runx2 is a promotor of MMP-13 expression, Sirt1 inactivation may inhibit the Runx2 expression and the resultant down-regulation of MMP-13 production in chondrocytes. Our findings suggest thatSirt1 may regulate the expression of Runx2, which is the osteogenic transcription factor, and the production of MMP-13 from chondrocytes in OA. Since Sirt1 activity is known to be affected by several stresses, including inflammation and oxidative stress, as well as aging, SIRT may be involved in the development of OA.

Influence of gender and types of sports training on QT variables in young elite athletes

Abstract Influence of gender and sports training on QT variables such as QT interval and dispersion (QT dispersion: QTD) in young elite athletes were evaluated. Subjects included 104 male and 97 female Japanese elite athletes (mean age 21.6 years). Sports included basketball, fencing, gymnastics, judo, swimming, tennis, track and field and volleyball. Age-matched healthy non-athletes (32 men and 20 women) were enrolled as controls. QT measurements were manually obtained from a 12-lead resting electrocardiogram and QTD was calculated as the difference between the longest and shortest QT intervals. A corrected QT interval (QTc) was obtained using Bazetts formula. Subjects were divided into two groups; an endurance training group and a static training group on the basis of their training types. Results: Maximum and minimum QTc were significantly longer in female athletes than in male athletes (max: 414.2 vs. 404.5 ms, min: 375.1 vs. 359.2 ms, p<0.0001 respectively), whereas QTc dispersion (QTcD) was shorter in female athletes than in male athletes (39.2 vs. 45.3 ms, p<0.0001). QTcD was significantly shorter in female athletes than in the female control group (39.2 vs. 45.2 ms, p<0.05). However, no statistically significant difference was observed between male athletes and the male control group. Male gymnasts exhibited significantly longer QTcD than the control group (p<0.01), but female gymnasts had significantly shorter QTcD than the control group (p<0.05). Maximum QTc intervals were prolonged in the male static training group compared with non-athletes, and QTcDs in the static training group were prolonged compared with the endurance training group. However, no significant difference was observed in the female group. In conclusion, both gender and different characteristics of sports training may affect QT variables even in young elite athletes. Vigorous static exercise training may independently prolong QT variables.

123I-BMIPP delayed scintigraphic imaging in patients with chronic heart failure

ObjectiveThe objective of the present study was to clarify the ability of 123I-beta-methyl-iodophenylpentadecanoic acid (123I-BMIPP) to evaluate the heart-to-mediastinum (H/M) ratio and myocardial global washout rate (WR) in patients with chronic heart failure (CHF).MethodsThe severity of CHF was evaluated on the basis of the New York Heart Association (NYHA) classification. Twenty patients with CHF (13 with idiopathic dilated cardiomyopathy and 7 with ischemic cardiomyopathy) and 11 age-matched controls underwent myocardial radionuclide imaging. Scintigraphic images were obtained from each participant at the early (30 min following radio-isotope injection) and late (4 h) phases using 123I-BMIPP. The H/M ratio and WR were calculated from planar images. Concentrations of plasma brain natriuretic peptide (BNP) were measured prior to the scintigraphic study.ResultsThe 123I-BMIPP uptake of early H/M and global WR did not significantly differ among groups, but uptake of delayed H/M was significantly lower in patients with NYHA class III than in controls (control 2.47 ± 0.39; class III 1.78 ± 0.28, P < 0.05). The uptake of delayed H/M and global WR correlated with plasma log BNP in all participants (r = −0.38, P < 0.05; 0.43, P < 0.05, respectively).ConclusionsThese data suggest that 123I-BMIPP uptake of delayed H/M enhances the image of CHF severity. The myocardial WR of 123I-BMIPP also effectively depicted the severity of CHF.