Myocardial dysfunction in patients with type 2 diabetes mellitus: role of endothelial progenitor cells and oxidative stress.

BACKGROUND: Endothelial progenitor cells (EPCs) are responsible for angiogenesis and maintenance of microvascular integrity, the number of EPCs is correlated with oxidative stress. Their relation to myocardial dysfunction in patients with type 2 diabetes mellitus (T2DM) is nonetheless unknown. METHODS: Eighty-seven patients with T2DM and no history of coronary artery disease were recruited. Transthoracic echocardiography and detailed evaluation of left ventricular (LV) systolic function by 2-dimensional (2D) speckle tracking derived strain analysis in 3 orthogonal directions was performed. Four subpopulations of EPCs, including CD34+, CD133+, CD34+/kinase insert domain-containing receptor (KDR) + and CD133+/KDR + EPCs, were measured by flow cytometry. Oxidative stress was assessed by superoxide dismutase (SOD). RESULTS: The mean age of the patients was 62 ± 9 years and 39.6% were male. Those with an impaired longitudinal strain had a lower number of CD34+ EPCs (2.82 ± 1.87% vs. 3.74 ± 2.12%, P < 0.05) than those with preserved longitudinal strain. When compared with those with preserved circumferential strain, patients with an impaired circumferential strain had a lower number of CD34+ EPCs (2.63 ± 1.80% vs. 3.87 ± 2.10%, P < 0.01) and SOD level (0.13 ± 0.06U/ml vs. 0.20 ± 0.08U/ml, P < 0.01). Patients with an impaired radial strain nonetheless had a lower number of CD34+ EPCs (2.62 ± 2.08% vs. 3.69 ± 1.99%, P < 0.05). Multivariate analysis demonstrated that only impaired global circumferential strain remained significantly associated with CD34 + EPCs and SOD. CONCLUSIONS: LV global circumferential strain was independently associated with number of CD34+ EPCs and SOD. These findings suggest that myocardial dysfunction in patients with T2DM is related to depletion of EPCs and increased oxidative stress.

Case report: Dual atrioventricular nodal non-reentrant tachycardia with six types of ECG patterns leading to tachycardia-induced cardiomyopathy in a 51-year-old man.

More than three types of ECG manifestations in one patient with dual atrioventricular nodal non-reentrant tachycardia (DAVNNT) are rare. We report a 51-year-old male patient with DAVNNT consisting of six types of ECG patterns leading to tachycardia-induced cardiomyopathy. After radiofrequency ablation of the slow pathway, DAVNNT was eliminated and cardiac function was restored.

An acute model for atrial fibrillation arising from a peripheral atrial site: evidence for primary and secondary triggers.

BACKGROUND: We previously demonstrated that acetylcholine (Ach) injected into cardiac ganglionated plexi (GP) causes pulmonary vein (PV) ectopy initiating atrial fibrillation (AF). OBJECTIVE: To determine the effects of Ach applied at non-PV sites. METHODS: Overall, 54 dogs were anesthetized with Na-pentobarbital. A right and left thoracotomy allowed the placement of multielectrode catheters to record from the superior PVs, mid portion of the atrium and the atrial appendages (AA). A monophasic action potential (MAP) was recorded from the AA. Ach (1, 10, 100 mM) was applied sequentially to the AA. RESULTS: In 19 of 26 animals, Ach 100 mM on the right (n = 15) or left (n = 4) AA induced focal, sustained AF (>or=10 minutes) with rapid regular firing (cycle length = 37 +/- 7 ms) at the AA. A clamp with teeth placed across the AA caused arrest in the AA. However, AF was sustained only when PV sites adjacent to the GP manifested complex fractionated atrial electrograms (CFAE). Clamping the AA prior to Ach (100 mM) application resulted in focal AF arising at the PVs but not at the AA. When a clamp without teeth was applied prior to Ach application, no AF at either AA or PV site could be induced. CONCLUSION: Isolation of the focal AF at the AA (primary trigger) by clamping caused cessation of activity in the AA, but AF continued due to secondary triggers arising from PVs. The possible mechanism(s) responsible for these findings are discussed, and various ancillary experiments (n = 28) were added to help elucidate mechanisms.

Association between obesity and trastuzumab-related cardiac toxicity in elderly patients with breast cancer.

PURPOSE: Trastuzumab can improve the prognosis for patients with breast cancer, but its related cardiac toxicity is concerning. This study aimed to identify the risk factors associated with trastuzumab-related cardiac toxicity in elderly patients with HER2-positive breast cancer. PATIENTS AND METHODS: A total of 133 elderly (≥ 65 years) patients who were diagnosed with breast cancer between June 1, 2007, and January 31, 2016, and received trastuzumab treatment were retrospectively reviewed. Cardiac events were defined as: (1) LVEF reduction of >10% from baseline echocardiography, (2) reduction of LVEF to <50%, and (3) signs and symptoms of heart failure as defined by the Common Terminology Criteria for Adverse Events (CTCAE) accompanied by a decrease in the LVEF. Univariate and multivariate regression analyses were used to determine the contribution of different clinical variables to trastuzumab-related cardiac events. RESULTS: The median age of the cohort was 71.0 years (range, 65-81 years). The median follow-up period for measurement of left ventricular ejection fraction was 11.0 months (range, 2-71 months). Fifteen patients (11.2%) experienced cardiac events during the follow-up. Multivariate regression analysis revealed that obesity (odd ratio[OR], 4.706; 95% CI, 1.984-10.147; P = 0.002) was a statistically significant risk factor associated with cardiac events. CONCLUSION: Obesity is an independent risk factor for trastuzumab-related cardiac toxicity in elderly patients with breast cancer, receiving trastuzumab. Further studies are needed to establish the independent predictive value of obesity on cardiotoxicity in these patients.

Early diagnosis of rats with acute myocardial infarction by measurement of brain natriuretic peptide.

The aim of this study was to detect early changes (within 1-4 h) in the brain natriuretic peptide (BNP) levels of rats with acute myocardial infarction (AMI). A total of 35 Wistar rats were established as models of AMI and 30 sham-operated rats were used as the control group. The myocardia of the two groups were observed using a transmission electron microscope (TEM) prior to and following surgery. A double-antibody sandwich enzyme-linked immunosorbent assay (ELISA) was used to detect the serum BNP and cardiac troponin I (cTnI) concentrations before and 1-4 h after surgery. Following the successful establishment of the AMI models, serum BNP concentrations were significantly increased within 1-4 h compared with the values prior to surgery and with those of the control group (all P<0.01). The serum BNP concentration reached its highest level 2 h after AMI (532.25±15.16 ng/l). No significant changes were observed in the cTnI serum levels of the AMI group within 1-4 h compared with the values before AMI and those in the control group (all P>0.05). In the 1-4 h following the establishment of the AMI model, significant positive correlations were identified between the serum BNP concentrations and the size of the AMI and the most marked correlation occurred 2 h after AMI (r=0.72, P<0.05). No significant differences were noted in the serum concentrations of BNP and cTnI in the control group prior to and following the sham surgery (all P>0.05). BNP may be used as a blood marker for the early diagnosis of AMI, particularly 1-4 h after the onset of AMI, and to predict the size of the infarct area.