Comparison of Framingham risk score and atherogenic indices as a predictor of atherosclerosis in patients with myocardial bridge in left anterior descending artery.

BACKGROUND: Myocardial bridge (MB) is generally considered as a benign condition, but it may trigger atherosclerosis, especially in the adjacent proximal coronary artery segment. In this study, we aimed to investigate whether the Framingham risk score (FRS) or atherogenic indices are risk factors for coronary atherosclerosis in patients with MB in the left anterior descending coronary artery (LAD). METHODS: We performed a retrospective study evaluating 155 patients who have MB in LAD. The patients were evaluated in two groups according to the presence of atherosclerosis (74 patients in atherosclerotic group vs. 81 patients in non-atherosclerotic group). Baseline characteristics, FRS and atherogenic indices were reviewed between groups. Significant independent risk factors for coronary atherosclerosis were investigated by logistic regression analysis. RESULTS: Patients in atherosclerotic group were significantly older (58.15 ± 10.04 vs. 50.22 ± 9.27 years, p < .001) and 74.3% of the patients were male. While the mean FRS in the atherosclerotic group was 21.20 ± 8.81, it was 12.79 ± 8.61 in the non-atherosclerotic group (p < .001). Among the atherogenic indices, only LDL-c/HDL-c ratio was significantly higher in the atherosclerotic group (3.49 ± 1.2 vs. 3.11 ± 0.98, p:.033). Multivariable analysis showed that age (OR: 1.08, 95% CI 1.03-1.13, p < .001) and FRS (OR: 1.06, 95% CI 1.01-1.11, p:.012) were independently associated with the presence of atherosclerotic lesion. CONCLUSIONS: FRS is an easily applicable predictor in clinical practice that indicates the presence of coronary atherosclerosis in patients with MB in LAD.

Fragmented QRS is a marker of mortality in patients with severe COVID-19: A retrospective observational study.

OBJECTIVE: In this study, we aimed to investigate the association of fragmented QRS (f-QRS) with in-hospital death in patients with severe novel coronavirus disease 2019 (COVID-19). METHODS: This was a retrospective and observational study. A total of 201 consecutive patients with severe COVID-19 were enrolled. Demographic data, laboratory parameters, medications, electrocardiographic (ECG) findings, and clinical outcomes were recorded. Patients with and without f-QRS were compared, and predictors of all-cause in-hospital mortality were analyzed. RESULTS: A total of 135 patients without f-QRS (mean age of 64 years, 43% women) and 66 patients with f-QRS (mean age of 66 years, 39% women) were included. C-reactive protein (CRP), D-dimer, troponin I, ferritin levels, and CRP to albumin ratio were significantly higher in patients with f-QRS. The need for invasive mechanical ventilation (63.6% vs. 41.5%, p=0.003) and all-cause in-hospital mortality [54.5% vs. 28.9%, log rank p=0.001, relative risk 1.88, 95% confidence interval (CI) 1.16-4.78] were significantly higher in patients with f-QRS. A number value of f-QRS leads ≥2 yields sensitivity and specificity (85.3% and 86.7%, respectively) for predicting in-hospital all-cause mortality. Multivariable analysis showed that f-QRS (odds ratio: 1.041, 95% Cl: 1.021-1.192, p=0.040) were independently associated with in-hospital death. CONCLUSION: This study revealed that the presence of f-QRS in ECG is associated with higher in-hospital all-cause mortality in patients with severe COVID-19. f-QRS is an easily applicable simple indicator to predict the risk of death in these patients.

Peripheral polyneuropathy in patients receiving long-term statin therapy.

OBJECTIVE: Peripheral neuropathy is an important potential side effect of statin use. This study was an investigation of the incidence of peripheral neuropathy in patients taking atorvastatin or rosuvastatin for hypercholesterolemia and the relationship to the dose and duration of the treatment. METHODS: In all, 50 patients using a statin treatment and 50 healthy controls matched for age and gender who had never taken a statin were included in the study. Polyneuropathy was assessed with a neurological examination and electroneuromyography (ENMG). RESULTS: While no polyneuropathy was detected in the control group, polyneuropathy was seen in 33 (66%) of the patients in the statin group (p<0.01). There was no significant difference between the 2 statin groups in the results of the neurological examination or the ENMG findings regarding the incidence of polyneuropathy (p=0.288 and p=0.720, respectively). Neuropathy was observed in a neurological examination performed within the first year in 50% of the rosuvastatin users and 18% of those taking atorvastatin. The severity of the polyneuropathy increased with the duration of the treatment in the atorvastatin group (p=0.030). CONCLUSION: This study revealed an increased risk of peripheral neuropathy with long-term statin use (>1 year). Electrodiagnostic changes have been detected in motor and sensory nerves in nerve conduction studies of patients on long-term statin treatment. The assessment of neurological symptoms, like tingling, numbness, pain and tremor in the hands and feet, and unsteadiness during walking associated with peripheral neuropathy may be useful in the follow-up of the patients on long-term statin treatment. Early detection of peripheral neuropathy and changing hypercholesterolemia treatment may prevent permanent nerve damage.

Strenuous exercise induced syncope due to coronary artery anomaly.

Coronary artery anomalies are among the neglected topics in cardiology. Anomalous origin of the left main coronary artery from the right sinus of valsalva is a rare coronary anomaly observed in 0.15% of patients. During exercise, the distended aorta and pulmonary artery with increased blood flow may squeeze the Left Main Coronary Artery (LMCA) between them. Even though arrhythmias are common causes of syncope, one should also think about aberrant coronary artery in the patients with syncope of unexplained origin. Patients experiencing exercise induced syncope accompanied by symptoms of coronary ischemia (typically: chest pain, ischemic findings on ECG, and raised cardiac markers) should be referred to diagnostic coronary angiography.

The effect of long-term continuous positive airway pressure treatment on systolic and diastolic function in patients with obstructive sleep apnoea syndrome: a five year observational study.

OBJECTIVE: Evaluation of the long-term effects of continuous positive airway presure (CPAP) on mean heart rate and left ventricular systolic and diastolic parameters in obstructive sleep apnea syndrome (OSAS) using conventional and tissue Doppler techniques. METHODS: This prospective cohort study is designed to evaluate the long-term effects of CPAP treatments in normotensive OSAS patients. Initially 40 patients aged from eighteen to fifty five with documented OSAS syndrome were evaluated within one month of CPAP treatment. All had high self-reported compliance with treatment. From the latter, 21 patients with uninterrupted CPAP therapy (for at least 5 years, 5 hours per day) were included in the study and further evaluated with treatment. The left ventricular systolic function was assessed on apical four- chamber view using modified Simpson method and diastolic function was evaluated with classic transmitral pulsed and tissue Doppler techniques. Paired t test and Wilcoxon signed rank test had been used to compare the clinical and echocardiography data before and after treatment period. RESULTS: A comparison of values assessed after one month and after 5 years of CPAP therapy, revealed a significant increase in the acceleration time(AT) Em/Am ratio and ejection time (ET) (AT: p=0.04; Em/Am ratio p=0.03 ET: p=0.04) while a significant decrease was observed on deceleration time (DT), isovolumetric relaxation time (IRT), myocardial performance index (MPI), mitral regurgitation (MR) and 24 hour mean heart rate (HR) in all subjects (DT: p=0.02; IVRT: p=0,04; MPI: p=0,01; MR: p≤0.001; HR: p=0.004). CONCLUSION: We observed a significant improvement in the left ventricular systolic and diastolic function and a significant decrease of 24-hour heart rate and mitral regurgitation with unchanged ejection fraction of the left ventricle with long-term CPAP treatment similar to short-term treatment studies. The long-term maintenance of the beneficial effect of CPAP throughout the 5 year long-term treatment can be one of the pathophysiologic mechanisms that may explain the decrease of cardiovascular mortality observed with long-term CPAP therapy in OSAS patients.

The association of apolipoprotein E polymorphism and lipid levels in children with a family history of premature coronary artery disease.

BACKGROUND: Polymorphisms in the apolipoprotein E (apoE) gene may modulate lipoprotein metabolism and influence plasma lipid levels. Thus, they have been associated with relative risk of coronary artery disease (CAD). OBJECTIVE: To evaluate the association of apolipoprotein E polymorphism and lipid levels in children with family history of premature coronary artery disease. METHODS: The apoE genotypes, allele frequencie,s and plasma lipid levels were analyzed in 137 children. Among these children, 70 (study group) had and 67 (control group) did not have a parental history of premature CAD RESULTS: Total cholesterol (Tc) levels were greater in the study group (P = .04). The frequencies of ɛ3ɛ4 genotype and ɛ4 allele were significantly greater in the study group (P = 005 for both), Thɛ ɛ2 allele correlated negatively with Tc and low-density lipoprotein cholesterol levels, and ɛ4 had a positive correlation with Tc and low-density lipoprotein cholesterol levels. CONCLUSIONS: Tc levels are influenced by apoE genotypes in childhood. Also, the frequency of the ɛ4 allele is greater in children with family history of premature CAD. The ɛ4 allele may be associated with an increased risk for development of atherosclerosis by elevated levels of Tc in children with family history of CAD. The evaluation of apoE gene polymorhisms may contribute to the assessment of cardiovascular risk in children with a family history of CAD.

The effect of anti-tumor necrosis factor (TNF)-alpha therapy with etanercept on endothelial functions in patients with rheumatoid arthritis.

OBJECTIVE: To investigate the effects of tumor necrosis factor (TNF)- alpha antagonism with etanercept (ENC) on endothelial functions in patients with active rheumatoid arthritis (RA). METHODS: A total of 21 patients with RA were enrolled in this prospective study. Eleven of them (8 women, 3 men mean age 47.0+/-10.1 years) with high disease activity despite the conventional treatment were assigned to Group 1 and were given ENC treatment twice a week (25 mg SC injection) for 12 weeks. Ten patients with RA (8 women, 2 men mean age 55.0+/-6.4 years) under conventional methotrexate and prednisone therapy were assigned as Control group (Group 2). Endothelium-dependent and -independent vasodilator responses of the brachial artery were assessed by high-resolution ultrasound. Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) were also measured at baseline and at the post treatment period. Mann-Whitney U and Wilcoxon tests were used to compare the data and correlation analysis was performed using Pearson correlation test. RESULTS: Endothelium-dependent vasodilatation improved from 5.2+/-0.8% to 7.9+/-1.3% (p=0.04) in ENC group, while no significant change was observed in the control group (from 6.6+/-1.1% to 7.0+/-1.8% p=0.67). No significant changes were found in endothelium-independent vasodilatation and baseline brachial artery diameters in both groups. A significant reduction in ESR and CRP were observed in patients receiving ENC (from 16.2+/-6.8 to 9.2+/-5.1 mm/h, p=0.003 and from 14.68+/-3.4 to 9.25+/-3.7 mg/L, p=0.003, respectively). CONCLUSION: Treatment with ENC for 12 weeks significantly improved endothelial function in patients with active RA compared to those under conventional therapy. The findings of the present study support the hypothesis that the use of TNF-alpha blockers in patients with active RA may reduce the high incidence of cardiovascular complications.

The factor V G1691A, factor V H1299R, prothrombin G20210A polymorphisms in children with family history of premature coronary artery disease.

Atherosclerosis, the major cause of coronary artery disease (CAD), has a very long asymptomatic development phase, which begins in childhood. In this study, we describe the factor V G1691A, factor V H1299R and prothrombin G20210A gene polymorphisms in children with a family history of premature CAD. Evidence of these polymorphisms in these children may predict the probability of having atherosclerosis in the future. Our study included a total of 140 children, 72 males and 68 females between the ages of 4.9 and 15.7 years. Among these children, 73 had a parental history of premature CAD and the remaining 67 belonged to our control group. The participants were screened for the mutations factor V G1691A, factor V H1299R and prothrombin G20210A by polymerase chain reaction amplified DNA products with specific oligonucleotide probes. Our results suggested that frequencies of the mutated allele of factor V G1691A and prothrombin G20210A are higher in children with a parental history of premature CAD. In conclusion, factor V G1691A and prothrombin G20210A polymorphisms which were detected in higher frequencies in children with a parental history of premature CAD may indicate a risk for developing atherosclerosis and might be useful in screening for CAD in children; however, large population-based research is necessary to investigate further genetic risk assessment for CAD.

Increased serum leptin concentrations in patients with chronic stable angina pectoris and ST-elevated myocardial infarction.

Leptin is an adipocytokine that is produced mainly by adipose tissue; it is also identified in atherosclerotic lesions in human coronary atherosclerosis. However, the relation of serum leptin concentrations to ischemic heart disease (IHD) is still obscure. The aims of the present study were to investigate serum leptin concentrations in patients with ST-elevated myocardial infarction (STEMI) and with chronic stable angina pectoris (CSAP) and to evaluate the possible correlations of leptin to other atherosclerotic risk factors; including serum high sensitive C-reactive protein (Hs-CRP), serum homocysteine, and fibrinogen concentrations. For this purpose, 35 patients with CSAP, 40 with acute STEMI, and 30 control subjects with normal findings from coronary angiography were taken into the study prospectively. Serum leptin concentrations were significantly higher in patients with CSAP and STEMI compared to the control group (7.74 +/-1.34 vs 6.37 +/-1.85 ng/mL, p=0.021 and 8.22 +/-3.13 vs 6.37 +/-1.85 ng/mL, p=0.023, respectively). In addition, serum homocysteine concentrations were significantly increased in patients with CSAP (15.23 +/-5.96 vs 11.40 +/-2.11 micromol/L, p=0.025) and patients with STEMI (15.90 +/-5.02 vs 11.40 +/-2.11 micromol/L, p=0.012) compared to the control group. Serum fibrinogen concentrations were significantly increased only in the CSAP group as compared to controls (4.15 +/-1.39 vs 3.45 +/-1.19 g/L, p=0.025). No significant correlation was found between leptin levels and selected risk factors. In conclusion, serum leptin concentrations were significantly higher in both the CSAP and STEMI groups. However, owing to the lack of correlation between the leptin levels and selected classical coronary risk factors, it may be considered that leptin can be evaluated as one of the independent risk factors for IHD. Further randomized and controlled studies will be required to determine the pathophysiological meaning of the increased leptin levels and the central role between adipocyte function and atherosclerosis.

Effects of Angiotensin-converting enzyme inhibition and statin treatment on inflammatory markers and endothelial functions in patients with longterm rheumatoid arthritis.

OBJECTIVE: To investigate the effects of angiotensin-converting enzyme (ACE) inhibitors and statins (hydroxy-methyl-glutaryl-CoA reductase inhibitors) on inflammatory markers and endothelial functions in patients with rheumatoid arthritis (RA). METHODS: A total of 45 patients with longterm RA were randomized into 3 groups to receive 8 weeks of treatment with placebo (n = 15), simvastatin (20 mg/day, n = 15), or quinapril (10 mg/day, n = 15) as an adjunct to existing antirheumatic drug treatment. Factors with a role in the development of endothelial dysfunction, such as C-reactive protein (CRP), fibrinogen, nitric oxide (NO), and serum cytokine concentrations including interleukin 1beta (IL-1beta), IL-6, and tumor necrosis factor-alpha (TNF-alpha) were measured at baseline and in the posttreatment period. Brachial artery vasodilator responses were assessed by high resolution ultrasound to evaluate endothelial functions. RESULTS: Simvastatin treatment significantly decreased serum CRP and TNF-a [from 14 +/- 6 to 7 +/- 3 mg/l (p = 0.025) and 30 +/- 5 to 16 +/- 4 pg/ml (p = 0.012), respectively], while quinapril had no significant changes in these 2 measures. IL-1beta and IL-6 showed insignificant changes in patients in the 2 drug groups. Endothelium-dependent vasodilatation was improved significantly in the simvastatin group [from 5.3 +/- 1.1% to 8.9 +/- 1.4% (p = 0.025)], while there was no difference in endothelium-independent vasodilatation [9.0 +/- 1.8% to 11.2 +/- 2.5% (p = 0.17)]. The quinapril group showed no significant changes in both types of vasodilation although there was a tendency to an increase in endothelium-dependent vasodilatation [from 6.1 +/- 0.8% to 7.8 +/- 0.7% (p = 0.06)]. Treatment with the 2 drugs had no significant effects on resting arterial diameter. CONCLUSION: We show that simvastatin 20 mg daily improves endothelial function in patients with RA. Its beneficial effect may be attributed to lowering CRP and TNF-alpha concentrations. ACE inhibition with daily 10 mg quinapril was found to have no significant effects on inflammatory markers and endothelial vasodilator response.

Endothelial dysfunction in patients with primary Sjögren's syndrome.

The aim of this study was to determine the endothelial function in patients with primary Sjögren's syndrome (SS). We also aimed to determine whether endothelial (dys)function correlates with extraglandular manifestations, specific autoantibodies and the severity of salivary gland involvement of SS. Endothelium-dependent vasodilation and endothelium-independent vasodilation of the brachial artery were assessed by a high-resolution ultrasound on 25 patients with primary SS and on 29 healthy controls. Patients with primary SS had significantly less mean endothelium-dependent vasodilation than did controls (3.0 +/- 0.4% vs 4.2 +/- 0.3%; p = 0.012). Endothelium-independent vasodilation induced by sublingual glycerol trinitrate was not different between the two groups (12.9 +/- 1.4% vs 14.1 +/- 1.2%; p = 0.86). We concluded that endothelium-dependent vasodilation was impaired in primary SS patients, in particular those presenting with Raynaud's phenomenon, when compared with the healthy controls and this impairment was not associated with the presence of RF, ANA, anti-Ro/SS-A, anti-La/SS-B and with the other extraglandular manifestations of the disease.

Selective COX-2 inhibition with different doses of rofecoxib does not impair endothelial function in patients with coronary artery disease.

In this study, we investigated the effects of both 25 and 50 mg daily doses of rofecoxib on the endothelial functions of patients with coronary artery disease (CAD). For this purpose, 34 patients with documented severe CAD and who were under aspirin treatment (300 mg/day) were randomized to receive 4 weeks of treatment with a placebo (n = 10, group I), rofecoxib 25 mg/day (n = 12, group II), and rofecoxib 50 mg/day (n = 12, group III). Brachial artery vasodilator responses were measured in order to evaluate endothelial function. The percentage of change in endothelial-dependent vasodilation in groups I, II, and III were similar at the baseline level and showed no significant change after treatment (6.2+/-3.9% vs. 5.9+/-3.1% and 5.8+/-3.3% vs. 5.6+/-3.8% and 6.1+/-4.5% vs. 5.8+/-4.1%, respectively; P > 0.05). Compared with the baseline, endothelium-independent vasodilatation, as assessed by nitroglycerine (NTG), remained unchanged after the treatment period (11.2+/-6.9% vs. 10.3+/-7.1% and 11.2+/-6.3% vs. 9.9+/-5.1% and 9.5+/-4.9% and 8.8+/-4.6%, respectively; P> 0.05). Treatment with both doses also showed no significant effects on high-sensitivity C-reactive protein (hs-CRP) levels and resting arterial diameters (P > 0.05). In conclusion, 4 weeks of treatment with standard and high doses of rofecoxib showed no significant effects on either endothelial-dependent or independent vasodilator response or plasma hs-CRP levels in patients with severe CAD taking concomitant aspirin.

Effects of simvastatin on bone mineral density and remodeling parameters in postmenopausal osteopenic subjects: 1-year follow-up study.

Observational studies suggest that statin use may be associated with lower incidence of fracture. However, there are conflicting data for their effects on bone remodeling parameters and bone mineral density (BMD). In the present study, we aimed to investigate the effects of simvastatin on bone metabolism and BMD in subjects with hypercholesterolemia (>240 mg/dl). For this purpose, 32 postmenopausal osteopenic subjects who were given simvastatin treatment (20 mg/day) and not on osteoporosis treatment were included in the study. During the 1-year follow-up period, the total cholesterol level decreased from 262.1+/-30.9 to 202.2+/-30.1 mg/dl (p<0.0001). At a period as early as the 3rd month, levels of the anabolic markers, e.g., bone-specific alkaline phosphatase (BSAP) and osteocalcin (OCL), were found to be significantly increased (from 120.8+/-56.6 to 149.5+/-57.6 IU/l, p=0.008, and from 20.8+/-12.6 to 34.7+/-18.4 microg/l, p=0.015, respectively) while no significant change was observed in the resorptive marker of serum N-telopeptide of type I collagen (CTX). At the 6th and 12th month, BSAP and OCL were both found to be decreased below the pretreatment values. While a significant reduction was found in BSAP levels (from 120.8+/-56.6 to 55.9+/-18.8 IU/l, p<0.001), no significant change was observed in CTX levels after the 6-month treatment period. Parathyroid hormone showed a gradual profound increase during the follow-up period (from 62.7+/-41.5 to 108.4+/-51.7 pg/ml, p<0.001). No significant change was found in BMD levels at the spine, femoral neck, Ward's triangle, and trochanter at the end of the 1-year follow-up period. In conclusion, simvastatin treatment showed a short-lasting anabolic effect on bone metabolism. However, this effect was lost by prolongation of therapy. The decrease in both anabolic and resorptive markers at the 6th and 12th month suggests that simvastatin affects bone metabolism mostly in favor of inhibition of the bone turnover in a long-term observation period although this inhibitory effect was not reflected in BMD.

[Evaluation of diastolic function by transmitral color M-mode flow propagation velocity in hypertensive patients]. / Hipertansif olgularda transmitral renkli M-mod akim yayilma hizi ile diyastolik fonksiyonlarin degerlendirilmesi.

OBJECTIVE: Diastolic dysfunction is considered as the most important cause of heart failure and morbidity in hypertensives. This study was designed to evaluate the relationship between the transmitral diastolic color M-mode flow propagation velocity (FPV) and left ventricular relaxation by using Doppler echocardiography. METHODS: In the present study, thirty-nine patients (21 male, 58.3%, age mean 52.7+/-5.9 years) with hypertension stage-I and over, were included. Transmitral diastolic E and A velocities, E-deceleration time (DT) and isovolumic relaxation time (IVRT) were measured by pulse Doppler method. We performed color M-mode technique for measurement of FPV of transmitral diastolic flow in the apical four-chamber view. We measured slope of aliasing velocity (blue aliasing) determined by color M-mode images. RESULTS: Flow propagation velocity values were not statistically related with age and gender, whereas differentiation of age groups were estimated as poor parabolic relationship, specially in patients over fifty years, FPV is estimated to be decreasing. Color M-mode FPV is correlated with DT, (r=-0.715, p<0.01), IVRT (r=-0.736, p<0.01) and interventricular septum thickness (r=-0.498, p<0.01), but not correlated with E/A ratio. CONCLUSION: Color M-mode FPV is correlated with DT and IVRT, which are important parameters for evaluation of diastolic function in hypertensive patients. This parameter is related with left ventricular relaxation and should be considered as a routine echocardiographic evaluation, because it is not affected by minimal changes in left ventricular filling pressure.

[The effects of clarithromycin treatment on cardiac events in acute coronary syndrome patients]. / Akut Koroner Sendromlu Hastalarda Klaritromisin Tedavisinin Kardiyak Olaylar Uzerine Etkisi.

OBJECTIVE: The assessment of short duration early clarithromycin treatment on major cardiac events in acute coronary syndrome patients. METHODS: One hundred and thirteen patients with acute coronary syndrome had been enrolled in the study in a prospective manner. Fifty-seven of 113 patients received peroral clarithromycin 1g/day for 14 days in addition to standard therapy. The remaining 56 patients were considered as control group. The treatment and control groups had similar major cardiac risk factors such as diabetes, hypertension, dyslipidemia and smoking habits. The occurrence of unstable angina pectoris, non-ST elevation myocardial infarction and ST elevation myocardial infarction was comparable in both groups. The use of thrombolytic therapy and glycoprotein IIb/IIIa receptor blockers administration was also similar in both groups. The patients were followed for major cardiac events for 6 months. RESULTS: During the follow-up, no difference was observed between groups in the occurrence of unstable angina pectoris, myocardial infarction, the need for revascularization with percutaneous coronary intervention or cardiac surgery and cardiac death. We observed a reduction of myocardial infarction and cardiac death occurrence and an increase in the necessity of percutaneous interventions in the treatment group even though this difference did not reach statistical significance. CONCLUSION: No benefit of short duration early clarithromycin therapy was observed in the occurrence of major cardiac events in acute coronary syndromes. Studies with longer treatment and follow-up period using different antibiotics are necessary to elucidate the possible effect of antibiotics on major cardiac events in patients with acute coronary syndrome.

The effect of simvastatin on serum cytokine levels and bone metabolism in postmenopausal subjects: negative correlation between TNF-alpha and anabolic bone parameters.

In this prospective study, we aimed to evaluate the effect of simvastatin on bone metabolism and the correlation between changes in bone turnover parameters and serum cytokine levels. For this purpose, 38 postmenopausal subjects with hypercholesterolemia (>240 mg/dl), not on osteoporosis treatment, were studied. Simvastatin was started at a dose of 20 mg daily and continued for 3 months. Six patients were excluded from the study during the follow-up period. Pre- and post-treatment samples were analyzed for bone alkaline phosphatase (BAP) and osteocalcin (OCL), as markers of bone formation; for carboxyterminal telopeptide of collagen I (CTX), as a marker of bone resorption; and for interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) cytokine levels. Total cholesterol level was decreased from 262.1 +/- 30.9 to 210.2 +/- 35.6 mg/dl after simvastatin treatment (P < 0.0001). While no significant change was observed in serum CTX level, BAP and OCL levels were significantly increased (from 120.8 +/- 56.6 to 149.5 +/- 57.6 IU/l [P = 0.008], and from 20.8 +/- 12.6 to 34.7 +/- 18.4 microg/l [P = 0.015], respectively). In the analysis of cytokines, while no significant change was observed in IL-6 levels, the TNF-alpha level was found to be significantly decreased after simvastatin treatment (from 77.9 +/- 31.6 pg/ml to 23.5 +/- 12.6 pg/ml [P = 0.021]). Individual changes in TNF-alpha levels showed a moderate negative correlation with the individual changes in BAP and OCL levels (r = -0.550 [P = 0.001], and r = -0.497 [P = 0.004], respectively). In conclusion; 20-mg daily simvastatin treatment for 3 months significantly increased BAP and OCL levels (markers of bone formation) in hypercholesterolemic postmenopausal subjects, without affecting bone resorption. These findings support the idea that simvastatin has an anabolic effect on bone formation. Additionally, the presence of a negative correlation between TNF-alpha levels and the anabolic bone parameters suggests that a cytokine-lowering effect of simvastatin may also be involved in the remodeling process and could exert some additive beneficial effect on bone metabolism.

[Doppler index of myocardial performance and its relationship with mitral E wave deceleration time in acute Q-wave myocardial infarction]. / Akut Q-Dalgali Miyokard Infarktüsünde Miyokardiyal Performans Indeksi ve Mitral E Dalga Deselerasyon Zamani Arasindaki Iliski.

OBJECTIVE: The objectives of the study were to assess myocardial systolic and diastolic functions by myocardial performance index (MPI) and its relationship with E - wave deceleration time (DT) in early phase of acute Q-wave myocardial infarction (MI). METHODS: We performed nongeometric Doppler-derived echocardiography to assess combined systolic and diastolic functions using myocardial performance index in 50 patients with acute Q-wave MI at early phase of events, (25 pts with anterior MI and 25 pts with inferior MI). The index is defined as the sum of the isovolumic contraction and isovolumic relaxation times divided by ventricular ejection time and was obtained by Doppler measurement from the diastolic mitral inflow and left ventricular outflow velocity-time intervals. RESULTS: As a result, the index was 0.54+/-0.1 in all patients with MI. We also estimated the higher MPI and DT values in anterior than in inferior MI (MPI: 0.61+/-0.07 vs. 0.46+/-0.06, p<0.001; DT: 244+/-64 msec vs. 204+/-31.2 msec, p=0.005, respectively). Myocardial performance index was positively correlated with DT in inferior MI (r=0.42, p<0.035) and negatively correlated with anterior MI; (r=- 0.72, p=0.0001). CONCLUSION: These data suggest that Doppler-derived MPI reflects severity of global left ventricular dysfunction in early phase of acute MI and may be a useful parameter in these patients.