Preclinical impairment of myocardial function in rheumatoid arthritis patients. Detection of myocardial strain by speckle tracking echocardiography.

OBJECTIVES: The incidence of heart failure is higher in patients with rheumatoid arthritis (RA) than in the general population and contributes to elevated cardiovascular mortality and morbidity rates. Impaired myocardial function can be detected by a novel echocardiographic method, speckle tracking echocardiography (STE), when conventional methods have yielded normal findings. The aim of our study was to investigate the effect of disease duration on myocardial strain and strain rate parameters in patients with RA. METHODS: This cross-sectional study included 37 RA patients [n=16, female gender n=16, mean age, 45.7 ± 9 years in the early-stage disease (ESD); n= 21, female gender n=19, 45.7 ± 16.8 years in the advanced-stage disease (ASD) group] who were compared according to early disease duration and advanced-stage disease (2.8 ± 1.2 vs. 14.6 ± 6.8 years, respectively). Hypertension, diabetes mellitus, and other cardiovascular risk factors were excluded. Offline analysis of STE was performed and data between the two groups were compared. RESULTS: RS, RSR-E, and RSR-E/A values were statistically significantly lower in patients with ASD. Circumferential strain and strain rate were similar between the two groups. Except for LSR-E/A values, LS, LSR-S, LSR-E, and LSR-A values were decreased in patients with ASD. CONCLUSION: RA patients without clinical evidence of cardiovascular disease and in the absence of traditional cardiovascular risk factors can be followed up with STE. In this way, early impairment of myocardial deformation can be detected before the appearance of any clinical evidence of cardiac involvement.

Impact of D-dimer level on postinterventional coronary flow and in-hospital MACE in ST-segment elevation myocardial infarction.

OBJECTIVE: Preintervention thrombus burden in the infarct-related artery is an independent predictor of no-reflow and adverse outcomes in coronary artery disease. The role of D-dimers in the acute phase of ST-elevated myocardial infarction (STEMI) during primary percutaneous coronary intervention (PCI) has not been fully elucidated. We aimed to investigate the predictive value of serum D-dimer levels on the outcome of patients with STEMI. METHODS AND RESULTS: A total of 266 consecutive patients presenting with STEMI within the first 12 h of symptom onset were included in this study. Patients were divided into two groups based on the postinterventional Thrombolysis In Myocardial Infarction (TIMI) flow grade score. Postinterventional TIMI grades of 0, 1, or 2 were defined as no-reflow (group 1) and angiographic success was defined as TIMI 3 flow (group 2). D-dimer levels were significantly higher in patients with postinterventional no-reflow than in patients with postinterventional TIMI grade 3 flow (686 ± 236 µg/ml-418 ± 164 µg/ml, p < 0.001). Multivariate logistic regression analysis showed that D-dimer level was an independent predictor of postinterventional no-reflow (OR: 1.005; 95 % CI: 1.003-1.007; p < 0.001) and in-hospital major adverse cardiovascular events (MACE; OR: 1.002; 95 % CI: 1.000-1.004; p = 0.029). Receiver operator characteristics analysis provided a cut-off value of 549 µg/ml for D-dimer for predicting no-reflow with an 83 % sensitivity and an 81 % specificity, and 544 µg/ml for predicting in-hospital MACE with a 69 % sensitivity and a 67 % specificity. CONCLUSION: In conclusion, D-dimer levels measured on admission may be an independent predictor of no-reflow, which is also a predictor of adverse outcomes in patients with STEMI.

A multi-center, open label, crossover designed prospective study evaluating the effects of lipid lowering treatment on steroid synthesis in patients with Type 2 diabetes (MODEST Study).

OBJECTIVE: It has been suggested that lipid-lowering treatment with the use of statins adversely affects the steroid hormones. However, the safety of lipid lowering treatment targeting very low levels of LDL with respect to the steroid hormones has not been established. RESEARCH DESIGN AND METHODS: A prospective, randomized, multicenter trial was conducted involving 98 patients. The patients were randomized into 2 groups: group-I received 10 mg of atorvastatin plus 10 mg of ezetimibe and group-II 80 mg of atorvastatin for the first 3 months. After crossover, the first group received 80 mg of atorvastatin and the second group 10 mg of atorvastatin plus 10 mg of ezetimibe for the following 3 months. Cortisol, DHEAS, testosterone, and estradiol levels were measured at the enrollment and at the end of the 1st, 2nd, 3rd, and 6th months. RESULTS: Along with a decrease in LDL level, the levels of DHEAS, testosterone, and estradiol decreased in both groups (p<0.001). While cortisol levels were maintained in the group given 10 mg of atorvastatin plus 10 mg of ezetimibe, it decreased significantly after the crossover to 80 mg of atorvastatin (p<0.001). The group initially given 80 mg of atorvastatin measured a lower level of cortisol for the first 3 months and it returned to normal levels after switching to 10 mg of atorvastatin plus 10 mg of ezetimibe. CONCLUSION: Eighty milligrams of atorvastatin decreased all adrenal and gonadal steroids, whereas 10 mg of ezetimibe combined with 10 mg of atorvastatin had at least no impact on cortisol levels.

Effect of diabetes mellitus on formation of coronary collateral vessels.

BACKGROUND: Although myocardial ischemia is known to be significantly related to the development of coronary collateral vessels (CCVs), there is considerable variation between patients with ischemic heart disease in the presence of collateral development. The nature of this variability is not well known. Likewise, it remains unclear whether diabetes mellitus (DM) has any effect on CCVs. The aim of this study was to evaluate the effect of DM on CCVs. METHODS AND RESULTS: Of the patients who underwent coronary angiography during the interval between March 1, 1993, and June 20, 1998, in our institution, 306 were diabetic. Those patients in whom coronary angiography is normal or severity of coronary artery stenosis is thought not to be sufficient for the development of CCVs (<75%) were excluded from the study. A total of 205 patients (mean age, 59+/-8 years) met the criteria for the DM group. For case-control matching, 205 consecutive nondiabetic patients (mean age, 58+/-9 years) who had >/=1 diseased vessel with >75% stenosis were included in the control group. The CCVs were graded according to the Rentrop scoring system, and the collateral score was calculated by summing the Rentrop numbers of every patient. There was no statistical difference between patients with and without DM in clinical baseline characteristics. The mean number of diseased vessels in the DM group (1.58+/-0.68) was higher than that in the nondiabetic group (1.42+/-0.65, P=0.005). The mean collateral score was 2.41+/-2.20 in the DM group and 2.60+/-2.39 in the control group. After confounding variables were controlled for, the collateral score in the diabetic group was significantly different from that in the nondiabetic group (P=0.034). CONCLUSIONS: Our findings suggest that CCV development is poorer in patients with than in patients without DM. Thus, we can speculate that DM is an important factor affecting CCV development.