Relationship between Retinal Nerve Fiber Layer Thickness and Aortic Distensibility in Peripheral Arterial Disease Patients.

AIM AND OBJECTIVE: To evaluate the relationship between aortic distensibility (AD) and aortic stiffness B index (ASBI) with retinal nerve fiber layer (RNFL) thickness measured with HD-OCT in peripheral arterial disease (PAD) patients. MATERIALS AND METHODS: Twenty-six PAD patients and 22 age-matched healthy control were enrolled. Subjects with PAD were classified into two groups. Patients with diabetes (DM) or hypertension (HT) comprised group I (n = 18) and without DM or HT comprised group II (n = 8). Color Doppler imaging was performed on all patients and PAD was diagnosed by using the ankle-brachial index (ABI). Retinal nerve fiber layer thickness values between control and PAD patients and correlations between RNFL thickness and aortic stiffness parameters (AD and ASBI) were evaluated. RESULTS: The inferior-nasal and inferior-temporal quadrant were the thickest in healthy subjects and the PAD group. Retinal nerve fiber layer thickness significantly decreased in superior-nasal, temporal, inferior-nasal quadrants in group I than healthy subjects (p < 0.001, p = 0.005, p < 0.001). Temporal and inferior-nasal quadrant thicknesses were statistically significantly thinner in group II than controls (p = 0.02, p < 0.001). The nasal RNFL quadrant was significantly thinner in group I than group II (p = 0.014). The correlation between RNFL thickness and aortic elasticity parameters in each group was not found to be significant. CONCLUSION AND CLINICAL SIGNIFICANCE: Isolated PAD without DM or HT may lead to localized RNFL loss in temporal and inferior-nasal quadrants. Aortic elasticity parameters did not seem to be correlated with RNFL thickness in PAD. HOW TO CITE THIS ARTICLE: Kumova D, Aktas Z, Eyiol A, et al. Relationship between Retinal Nerve Fiber Layer Thickness and Aortic Distensibility in Peripheral Arterial Disease Patients. J Curr Glaucoma Pract 2021;15(2):86-90.

High incidence of co-existing factors significantly modifying the phenotype in patients with Fabry disease.

Fabry disease results from deficiency of the lysosomal enzyme alpha-galactosidase A. The families of 11 index cases were screened by enzyme and molecular assays. Further clinical and laboratory investigations were carried out in all cases. Including 33 new patients, a total of 28 females (Age 25,82 ±â€¯12,1 Range 8-46) and 16 males (Age 24,56 ±â€¯15,04 Range 2-48) were investigated. Ten different disease-causing variants were found two of them being novel. One patient had co-existing familial mediteranian fever, one had celiac disease and three had rheumatological disorders. Lipoprotein (a) levels were elevated in 17,6%, homocysteine in 22,2%, total and low density cholesterol in 12% and antithrombin 3 levels were elevated in 13,3%. One patient was found to be heterozygous for prothrombin p.G20210A disease-causing variant (5,8%) and two for factor V Leiden disease-causing variant (11,7%). Anticardiolipin IgM antibody was found to be positive in 11,7%. The patients with abnormal cranial imaging were also noticed to have additional risk factors for thrombosis. This study provides the largest data about Fabry patients from Turkey and implies that co-existing risk factors unrelated to Fabry Disease have significant association with the presence of clinical symptoms in females and might cause an early and severe clinical course in males.

Relationship of serum HLA-B alleles and TNF-α with rheumatic heart disease

Background/aim: Acute rheumatic fever and rheumatic heart disease are major causes of morbidity and mortality in developing countries. Genetic studies have determined that the immune response in rheumatic heart disease is genetically controlled and that there is a close relationship between the gene of concern and the class II human leukocyte antigen (HLA) gene. The aim of this study was to evaluate the relationship of serum HLA-B alleles and tumor necrosis factor alpha (TNF-α) with rheumatic heart disease. Materials and methods: A total of 50 consecutive patients with rheumatic heart disease and 50 controls were enrolled in the study. HLA alleles were analyzed using sequence-specific primer-polymerase chain reaction and nucleotide sequencing. Results: The HLA-B35 allele was significantly more common in patients with rheumatic heart disease than the control group (P = 0.043). The HLA-B44 allele was significantly more common in control patients than in patients with rheumatic heart disease (P = 0.014). There was a significant inverse correlation between high-sensitivity C-reactive protein and mitral valve area (P = 0.001). There was no correlation between TNF-α levels and mitral valve area (P = 0.066). Conclusion: Our findings confirmed the association between HLA-B alleles and rheumatic heart disease.

The Relationship between Pre-Infarction Angina and Serum Sphingosine-1-Phosphate Levels.

BACKGROUND: Pre-infarction angina reduces myocardial infarct size by preventing the myocardium from being subjected to ischemia reperfusion (I/R) injury. Ischemic preconditioning is the proposed mechanism for this effect. Sphingosine 1 phosphate (S1P) activates ischemic preconditioning pathways and may play a role in the presence of cardioprotective effects of pre-infarction angina. Therefore, we evaluated the relationship between pre-infarction angina and serum S1P levels. METHODS: Between May 2011 and January 2012, 79 patients with acute myocardial infarction were included in the study. In addition to taking routine medical histories, all of the patients were questioned as to whether or not they had pre-infarction angina. We determined patients serum levels of S1P at admission and discharge, and peak creatine kinase MB and troponin levels were also measured in the pre-infarction angina positive and negative groups. RESULTS: Of the 79 patients included in the study, 36 had pre-infarction angina and 43 had not. Baseline characteristics were similar between the groups. The median level of serum S1P in patients with pre-infarction angina was significantly higher than in those without pre-infarction angina both at admission and discharge [0.54 (0.14-1.35) vs. 0.26 (0.12-0.62) p = 0.014/0.51 (0.20-1.81) vs. 0.30 (0.13-0.68) p = 0.010]. Serum high sensitive troponin levels were significantly lower in patients with pre-infarction angina [0.97 (0.39-3.07) vs. 2.56 (0.9-6.51) p = 0.034]. Serum S1P levels both at admission and discharge tended to be higher in patients with more angina episodes, but the differences between these subgroups were not statistically significant. CONCLUSIONS: Patients who experienced pre-infarction angina had higher serum S1P levels than patients without pre-infarction angina. This study supported our hypothesis that the cardioprotective effects of pre-infarction angina may in part be mediated by S1P. KEY WORDS: Ischemic preconditioning; Pre-infarction angina; Sphingosine 1 phosphate.

Troponin elevation in conditions other than acute coronary syndromes.

Acute coronary syndromes comprise a large spectrum of clinical conditions ranging from unstable angina pectoris to acute ST-elevation myocardial infarction. Chest pain is usually the major symptom of atherosclerotic heart disease; however, it may be challenging to diagnose correctly, especially in the emergency department, because of the ambiguous way that pain is characterized by some patients. Cardiac troponins are sensitive and specific biomarkers used in the diagnosis of myocardial infarction that are released into the bloodstream when cardiac myocytes are damaged by acute ischemia or any other mechanism. They are the cornerstone for the diagnosis, risk assessment, prognosis, and determination of antithrombotic and revascularization strategies. However, troponin elevation indicates the presence, not the mechanism, of myocardial injury. There are many clinical conditions other than myocardial infarction that cause troponin elevation; thus, the physician should be aware of the wide spectrum of disease states that may result in troponin elevation and have a clear understanding of the related pathophysiology to effectively make a differential diagnosis. This review focuses on causes of troponin elevation other than acute coronary syndromes.

The particular interactions of the traditional cardiovascular risk factors with different circulating specific leukocyte subtype counts in blood: an observational study.

OBJECTIVE: The pathogenesis of atherosclerosis is multifactorial, however the impact of inflammatory cells in this process is well known. Different traditional cardiovascular risk factors (CVRFs) may have specifically different effects on leukocyte subtype. Thus, these special interactions may induce different vascular involvement forms due to the altered endothelial damage and vascular repair mechanisms. The aim of the present study was to investigate whether there is any specific relationship between the leukocyte subtypes and the traditional CVRFs and to evaluate the independency of possible relationships. METHODS: The study had a cross-sectional observational design. The study population consisted of the patients who underwent coronary angiography with a suspicion of coronary artery disease (CAD) at our institution in an outpatient manner. We enrolled 677 consecutive eligible patients with CAD or normal coronary arteries (NCA) and investigated the associations of traditional CVRFs, demographic properties and biochemical parameters including fasting plasma glucose (FPG), creatinine, serum uric acid level (SUA) and lipids with total circulating inflammatory cell (WBC, leukocytes) and subtype counts including neutrophils (N), lymphocytes (L) and monocytes (M). As a dependent variable, total leukocyte count and subtypes, and neutrophil/lymphocyte ratio (N/L ratio) which has been found to being related with increased vascular risk and events were investigated in the groups determined by the presence or absence of CVRFs and CAD by the univariate analyses and then multiple linear regression analyses. RESULTS: When we performed multiple linear regression analyses to determine the independent associations of inflammatory cell subtypes, we have found that FPG had an independent incremental association with WBC (ß±SE:4.2±1.4, p=0.004) and N (ß±SE:4.2±1.2, p=0.001). Current smoking had an independent incremental association with WBC and all cell subtypes (for WBC, N, L, and M: ß±SE: 748±161, p<0.001; ß±SE: 556±136, p<0.001; ß±SE: 185±69, p=0.007; ß±SE: 38±20, p=0.061, respectively) and SUA had an independent incremental association with WBC (ß±SE: 115±43, p=0.008), N (ß±SE: 107±38, p=0.005) and M (ß±SE: 26±6, p<0.001). Hypertension had an independent incremental association with WBC (ß±SE: 431±140, p=0.002) and N (ß±SE: 315±118, p=0.008). Male gender had an independent incremental association with only M (ß±SE: 52±20, p=0.010). Family history of CAD had an independent decremental association with WBC (ß±SE: -327±139, p=0.019) and N (ß±SE: -326±121, p=0.007). Finally, age had an independent decremental association with WBC (ß±SE: -32±7, p<0.001) and L (ß±SE: -16±3, p<0.001). The N/L ratio was independently related with increased age (p<0.001), FPG (p=0.003) and SUA (p=0.012). CONCLUSION: Our study results demonstrate that leukocyte subtypes have different specific associations with traditional CVRFs. We found that FPG affects specifically N while SUA affects specifically N and M, and current smoking affects nonspecifically on all cell subtypes. While hypertension with N and male gender with M were specifically related, age and family history of CAD were only related to L. These different interactions may lead to different endothelial damage and vascular repair mechanisms.

The evaluation of diastolic dysfunction with tissue Doppler echocardiography in women with subclinical hypothyroidism and the effect of L-thyroxine treatment on diastolic dysfunction: a pilot study.

Background. Subclinical hypothyroidism (SH) predominantly affects women. The necessity of treatment in SH is controversial. Objective. We aimed to investigate the response of diastolic dysfunction to thyroid hormone replacement therapy (THRT) in women. Methods and Results. Twenty-two female subjects with SH and 20 euthyroid female controls were enrolled. Baseline and follow-up biochemical, hormonal, and echocardiographic evaluations were performed. Repeat echocardiograms were performed three months after the achievement of a euthyroid status with THRT. Mean baseline myocardial performance index (MPI) was 0.27 ± 0.08 in the SH group, and 0.22 ± 0.06 in the control group (P = 0.03). MPI did not change significantly after THRT. Pulsed-wave Doppler findings were not different among the groups. However, tissue Doppler-derived mitral annular E' velocities were significantly lower in the SH group. A moderate but significant improvement was observed in E' velocities after THRT (13.2 ± 3.87 versus 14.53 ± 2.75, P = 0.04). We also observed left ventricular concentric remodeling in SH patients which was reversible with THRT. Conclusions. Tissue Doppler echocardiography may be a useful tool for monitoring the response of diastolic dysfunction to thyroid hormone replacement therapy in patients with SH. Our findings suggest that THRT may reverse diastolic dysfunction in women with SH.

Relationship Between MMP-1, MMP-9, TIMP-1, IL-6 and Risk Factors, Clinical Presentation, Extent and Severity of Atherosclerotic Coronary Artery Disease.

BACKGROUND: Matrix metalloproteinases (MMPs) and Tissue Inhibitor of Matrix Metalloproteinases (TIMPs) may be associated with atherogenesis and plaque rupture. We evaluated the relationship between MMP-1, MMP-9, TIMP-1 and IL-6 levels and risk factors, presentation, extent and severity of atherosclerotic coronary artery disease (CAD). METHODS: Consecutive patients who underwent coronary angiography were randomly included. The serum concentrations of MMP-1, MMP-9, TIMP-1 and IL-6 were analyzed with ELISA method in 134 patients. Participants were divided into 5 groups; stable angina pectoris (SAP; n= 34), unstable angina pectoris (USAP; n=29), non-ST elevation myocardial infarction (NSTEMI; n=16), acute ST elevation myocardial infarction (STEMI; n=25) and controls (n=30). Coronary angiographic Gensini score was calculated. RESULTS: MMP-1 levels were higher in STEMI and NSTEMI groups compared with USAP, SAP and control groups (STEMI vs USAP p=0.005; STEMI vs SAP p=0.001; STEMI vs control p<0.001; NSTEMI vs USAP p=0.02; NSTEMI vs SAP p=0.027; NSTEMI vs control p<0.001). In STEMI group, MMP-9 levels were higher than USAP and control groups (p=0.002; p<0,001). TIMP-1 levels were not significantly different within all 5 groups. MMP-1 levels were found to be elevated in diabetic patients (p=0.020); whereas MMP-9 levels were higher in smokers (p=0.043). Higher MMP-1, MMP-9 and IL-6 levels were correlated with severe Left Anterior Descending artery (LAD) stenosis and higher angiographic Gensini Score (for severe LAD stenosis; r = 0.671, 0.363, 0.509 p<0.001; for Gensini score; r = 0.717, 0.371, 0.578 p<0.001). CONCLUSIONS: Serum levels of MMP-1, MMP-9, and IL-6 are elevated in patients with CAD; more so in acute coronary syndromes. MMP-1, MMP-9 and IL-6 are associated with more extensive and severe CAD (as represented by Gensini score).

Endothelial progenitor cells (CD34+KDR+) and monocytes may provide the development of good coronary collaterals despite the vascular risk factors and extensive atherosclerosis.

OBJECTIVE: Endothelial progenitor cells (EPC) have a regenerative role in the vascular system. In this study, we aimed to evaluate simultaneously the effects of EPC and inflammatory cells on the presence and the extent of coronary artery disease (CAD) and the grade of coronary collateral growth in patients with clinical suspicion of CAD. METHODS: This study has a cross-sectional and observational design. We enrolled 112 eligible patients who underwent coronary angiography consecutively (mean age: 59±9 years). The association of circulating inflammatory cells and EPC (defined by CD34+KDR+ in the lymphocyte and monocyte gate) with the presence, severity and extent of CAD and the degree of collateral growth were investigated. Logistic regression analysis was used to define the predictors of collateral flow. RESULTS: Of 112 patients 30 had normal coronary arteries (NCA, 27%, 55±9 years) and 82 had CAD (73%, 61±8 years). Among the patients with CAD, the percent degree of luminal stenosis was <50% in 12 patients; 50-90% in 35 patients; and ≥90% in the other 35 patients. Circulating inflammatory cells were higher (leukocytes, 7150±1599 vs 8163±1588 mm(-3), p=0.001; neutrophils, 4239±1280 vs 4827±1273 mm(-3), p=0.021; monocytes, 512±111 vs 636±192 mm(-3), p=0.001) and EPCs were lower (0.27±0.15% vs 0.17±0.14%, p<0.001; 21±15 vs 13±12 mm(-3), p=0.004) in CAD group than NCA group. When we investigated the collateral growth in patients having ≥90% stenosis in at least one major coronary artery, we found that the patients with good collateral growth had significantly higher EPC (0.22±0.17% vs 0.10±0.05%, p=0.009; 18±15 vs 7±3 mm(-3), p=0.003) in comparison to patients with poor collateral growth. Presence of EPC was associated with reduced risk for coronary artery disease (OR: 0.934, 95%CI: 0.883-0.998, p=0.018) and was an independent predictor for good collateral growth (OR: 1.295, 95%CI: 1.039-1.615, p=0.022). A sum of CD34+KDR-, CD34+KDR+ and CD34-KDR+ cells (192±98 mm(-3)), and a CD34-KDR- cell subpopulation within monocyte gate (514±173 mm(-3)) reached to highest counts in good collateral group among all study population. CONCLUSION: Endothelial progenitor cells can be mobilized from bone marrow to induce the coronary collateral growth in case of myocardial ischemia even in presence of the vascular risk factors and extensive atherosclerosis. This finding may be supportive to investigate the molecules, which can specifically mobilize EPC without inflammatory cells.

Association of matrix metalloproteinase-1, matrix metalloproteinase-9, tissue inhibitor of matrix metalloproteinase-1, and interleukin-6 with epicardial and myocardial perfusion.

OBJECTIVES: Matrix metalloproteinases (MMPs), which are important regulators of extracellular matrix degradation, are known to induce atherosclerotic plaque rupture because of the degradation of collagen fibers in the fibrous cap. We aimed to investigate the possible association between these enzymes and objective coronary angiographic parameters of epicardial or myocardial perfusion. METHODS: A total of 140 patients with acute coronary syndromes or stable angina pectoris, who were advised to undergo coronary angiography, were included. The correlation between the serum levels of MMP-1, MMP-9, tissue inhibitor of matrix metalloproteinase-1, interleukin-6 (IL-6), and Thrombolysis in Myocardial Infarction frame count (TFC), myocardial blush grade, and the magnitude of change in these parameters after percutaneous intervention was investigated in addition to the association between MMPs and the need for revascularization. RESULTS: TFC and corrected TFC scores were found to be higher in patients with higher MMP-1 levels (R: 0.706, P < 0.001; R: 0.867, P < 0.001). The absolute amount of decrease in TFC/corrected TFC after percutaneous intervention in the patients, who were advised to undergo revascularization, was correlated with higher MMP-1 and MMP-9 levels. MMP-1, MMP-9, and IL-6 were negatively correlated with myocardial blush grade although this association was weaker for MMP-9 and IL-6 compared with MMP-1 (R: -0.574, -0.367, and -0.496, P < 0.001). The mean serum levels of MMP-1, MMP-9, and IL-6 were higher in the patients who were advised to undergo revascularization compared with the patients who did not need revascularization. Odds ratios of MMP-1 and IL-6 for predicting revascularization need were calculated as 1.7 (95% confidence interval: 1.4-2.1; P < 0.001) and 6.5 (95% confidence interval: 2.5-16; P < 0.001), respectively. CONCLUSION: Higher levels of serum MMP-1, MMP-9, and IL-6 can be used to predict worse coronary angiographic findings and may be further targets of active investigation for wide use as risk predictors.

Nebivolol therapy improves endothelial function and increases exercise tolerance in patients with cardiac syndrome X.

OBJECTIVE: We sought to determine whether nebivolol affects coronary endothelial function and exercise induced ischemia in patients with cardiac syndrome X (CSX). METHODS: The study protocol undertaken was based on a single-blind randomized controlled prospective study. After a 2-week washout period, 38 patients with cardiac syndrome X were randomized to receive either nebivolol 5 mg daily (n=19) or metoprolol 50 mg daily (n=19) in a single- blind design for 12 weeks. The control group under study was consisted of 16 age- and gender-matched subjects with negative treadmill exercise tests. Plasma endothelial nitric oxide (NOx), L-arginine, and asymmetric dimethylarginine (ADMA) were measured in all patients at baseline and after 12 weeks of treatment. Statistical differences among groups were tested by one-way analysis of variance and unpaired samples t test for parametric; Kruskal-Wallis and Mann-Whitney U tests for non-parametric variables, respectively. A paired samples t test was used to compare continuous variables before and after drug therapy. RESULTS: At baseline, plasma level of NOx, L-arginine, and L-arginine/ADMA ratio were lower (p<0.001 for all) in patients with CSX than in the control patients. Whereas, the plasma ADMA levels were increased in the patient group (p<0.001). After 12 weeks of drug therapy, the patients taking nebivolol had increased levels of plasma NOx , plasma L-arginine, the L-arginine/ADMA ratio and decreased levels of plasma ADMA compared to those of the patients taking metoprolol (p<0.001). In addition, exercise duration to 1-mm ST depression and total exercise duration significantly increased after treatment in the nebivolol group compared to the metoprolol group (p<0.01). In the nebivolol group, Canadian Cardiovascular Society (CCS) angina classification improved by one or more categories in 12 (70%) patients, whereas it deteriorated or remained in the same category in 5 (30%) patients. Meanwhile, in the metoprolol group, the CCS angina classification improved by one or more categories in 7 (41%), whereas it deteriorated or remained in the same category in 10 (59%) patients. CONCLUSION: Circulating endothelial function parameters (plasma ADMA, L-arginine, NOx levels) were impaired in patients with CSX. Nebivolol treatment was associated with better improvements in both circulating endothelial function and exercise stress test parameters than metoprolol. We believe that further studies are needed to evaluate the effects of nebivolol treatment on long-term clinical outcomes in patients with CSX.

The effect of nebivolol treatment on oxidative stress and antioxidant status in patients with cardiac syndrome-X.

BACKGROUND: Free radical-mediated oxidative stress has been implicated in the etiopathogenesis of several disorders. The aim of this study was to elucidate the effect of treatment with nebivolol on the metabolic state of oxidative stress, and antioxidant status markers in patients with cardiac syndrome-X (CSX), additionally, to compare with the effect of metoprolol treatment. METHODS: Thirty patients, 17 female and 13 male, with CSX were enrolled in the study. Nebivolol (5 mg/day) or metoprolol (50 mg/day) was administrated for 12 weeks. Twelve hour fasting blood samples, taken at the initiation and on the third month of therapy, were analyzed for the levels of malondialdehyde (MDA), nitrite+nitrate (NOx), and the activity of myeloperoxidase (MPO), superoxide dismutase (SOD). No patient presented additional risk factors for increased reactive oxygen species levels. RESULTS: Compared with sixteen control participants, patients with CSX had significantly higher activity of MPO and levels of MDA, but significantly lower SOD activity and levels of NOx before treatment. After treatment, MPO activity and MDA levels were significantly reduced; SOD activity and NOx levels were significantly increased with nebivolol but remained unchanged with metoprolol. CONCLUSION: We have shown that patients with CSX who taken nebivolol have lower serum MPO activity, levels of MDA and higher serum SOD activity, NOx levels when compared with metoprolol treatment. Exercise stress test parameters were also ameliorated in patients who had taken nebivolol in contrast to metoprolol. Nebivolol treatment may be a novel treatment strategy in cases with CSX in the future.

Long-term clinical effects of magnetic resonance imaging in patients with coronary artery stent implantation.

OBJECTIVES: We sought to investigate the early and late effects of magnetic resonance imaging (MRI) on stent thrombosis and major adverse coronary events after coronary artery stent (CAS) implantation at a long-term follow-up period. METHODS: Forty-three patients (28 men, mean age 63+/-10 years) who underwent CAS implantation before MRI examination were included. MRI was performed on a 1.5-T MR-system with a phased array multicoil. An average of 1.3 stents per patient were implanted (1-4 stents). More than one MRI was performed for two patients. Patients who underwent MRI within 8 weeks after the procedure were included in the early-term group (17 patients), and those who underwent MRI after 8 weeks were included in the late-term group (26 patients). RESULTS: Mean follow-up period was 36+/-15 months. There was no acute or subacute stent thrombosis. Late stent thrombosis that resulted in acute myocardial infarction was observed in a patient from the early group after an operation for prostate hyperplasia 5 months after MRI, and the patient underwent percutaneous coronary artery angioplasty. De-nova lesion was observed in four patients in the early group and two patients in the late group (P=0.14). In-stent restenosis was recorded in two patients in the early group and three patients in the late group (P=0.98). Composite major adverse cardiac events (acute coronary syndrome, myocardial infarction, death, and cerebrovascular event) were observed in seven of the early-group patients (41%), and in six of the late-group patients (23%) (P=0.20). CONCLUSION: MRI can be safely performed in patients with CAS implantation both in the early and late course, and is not associated with an increased risk of major adverse clinical cardiac events at long-term follow-up.

Coronary vasospastic crisis leading to cardiogenic shock and recurrent ventricular fibrillation in a patient with long-standing asthma.

Acute myocardial infarction in patients with normal coronary arteries is a therapeutic dilemma. Coronary artery vasospasm and thrombosis are the most commonly encountered clinic problems and appear in localized coronary segments. The incidence of cardiovascular disease is increased in asthmatic patients. ß(2)-Adrenergic agonists use is associated with increased cardiovascular events. Although myocardial ischemia during asthma has been described in literature, acute myocardial infarction and ventricular fibrillation with normal coronary arteries in patients with asthma bronchiale is a rare entity. Our patient with long-standing asthma bronchiale presented with cardiogenic shock whose coronary angiography revealed multivessel disease and undergone primary percutaneous coronary intervention. Due to ongoing chest pain and hemodynamic instability; an early bypass surgery was planned. A control angiogram was performed before surgery. After intracoronary nitrate administration all narrowings in coronary vasculature disappeared. Symptom relief and clinical improvement was achieved with nitrate and calcium channel blockers later. After 2 months she was readmitted with cardiac arrest due to recurrent ventricular fibrillation and intracardiac defibrillator implantation was performed.

Heart rate variability and heart rate turbulence in mild-to-moderate aortic stenosis.

AIMS: To study heart rate (HR) variability and HR turbulence parameters in mild-to-moderate aortic stenosis (AS) and to disclose whether any relationship exists between these parameters and echocardiographic findings. METHODS AND RESULTS: Forty-three asymptomatic patients with mild-to-moderate AS (AS group) were studied. Echocardiographic parameters and HR variability and HR turbulence indices obtained over 24 Holter ECG recordings were compared with those of an age and sex matched control population free of cardiovascular disease. Correlation between echocardiographic findings and HR variability and HR turbulence indices was also studied in the AS group. All HR variability parameters except mean RR interval, RMSSD, and pNN50 and one HR turbulence parameter, turbulence onset, were significantly disturbed in the AS group. Echocardiographic findings of diastolic dysfunction had significant correlations with HR variability and HR turbulence parameters in AS patients. CONCLUSION: Symphatovagal imbalance as shown by disturbed HR variability and HR turbulence parameters was demonstrated for the first time in patients with mild-to-moderate AS. This imbalance, which was shown to be correlated with echocardiographic findings of diastolic dysfunction, may lead to arrhythmic complications in this seemingly low-risk patient population.

Assessment of aortic wall stiffness in patients with Familial Mediterranean Fever.

INTRODUCTION: To evaluate aortic wall stiffness and its relation between the aortic stiffness and the left ventricular function in patients with Familial Mediterranean Fever (FMF). METHODS: The study population was composed of 31 patients with FMF in attack-free period (12 men, 19 women; mean age: 36+/-7 years) and 27 healthy subjects (10 men, 17 women; mean age: 34+/-7 years) who had volunteered to participate. Aortic stiffness indices, aortic strain and distensibility, were calculated from the aortic diameters measured by echocardiography and blood pressure obtained by sphygmomanometry. RESULTS: There were significant differences between the control and the patient group in aortic strain (mean (SD), 7.23+/-2.14 versus 4.91+/-1.66%, p=0.01) and distensibility (4.02+/-1.42 versus 2.84+/-1.46, 10(-6)cm(2)dyn(-1), p=0.001). Although there was no correlation between the aortic stiffness parameters and the left ventricular function parameters, there were significant negative correlations between the disease duration and aortic strain index (r=-0.29, p<0.001), and between the disease duration and distensibility (r=-0.32, p<0.001). CONCLUSION: Aortic stiffness measurements were found abnormal in patients with FMF. We have also demonstrated that there were significant correlations between aortic stiffness parameters and disease duration.

The detailed assessment of left and right ventricular functions by tissue Doppler imaging in patients with familial Mediterranean fever.

In the contrary to other rheumatologic disorders, there have been limited numbers of studies investigating the cardiac involvement in patients with familial Mediterranean fever (FMF), although the disease may carry a potential for cardiovascular disorders because of sustained inflammation during its course. In the present study, we used high usefulness tissue Doppler echocardiography for detailed analysis of cardiac changes in FMF patients. The study population included 30 patients with FMF (11 men, 19 women; mean age, 35 +/- 7 years, mean disease duration, 15.4 +/- 7.6 years) and 30 healthy subjects as controls (12 men, 18 women; mean age, 33 +/- 7 years). The diagnosis of FMF was established according to the Tell-Hashomer criteria. Left and right ventricular functions were measured using echocardiography comprising standard two-dimensional, M-mode, and conventional Doppler as well as tissue Doppler imaging. The conventional echocardiographic paratemeters were similar apart from left ventricular relaxation time was longer (107 +/- 25 vs 85 +/- 10 ms, p < 0.001, respectively) in patients with FMF. According to the tissue Doppler measurements, while systolic velocities of both ventricles were not different, diastolic filling velocities of left ventricle including E'(m) (12.6 +/- 3.4 vs 14.7 +/- 3.3 cm/s, p = 0.04), A'(m) (10.1 +/- 2.6 vs 8.6 +/- 2.0 cm/s, p = 0.015), and E'(m)/ A'(m) (1.24 +/- 0.4 vs 1.71 +/- 0.5 cm/s, p = 0.012) values were statistically different between the groups. Left ventricular myocardial performance indices and right ventricular diastolic functions were found similar between two groups. In addition, there were no significant correlations between the disease duration, clinical features, and echocardiographic parameters. In conclusion, we have demonstrated that although systolic functions were comparable in the patients and controls, left ventricular diastolic function indices were impaired in FMF patients by using tissue Doppler analysis.

Effects of scaling and root planing and sub-antimicrobial dose doxycycline on oral and systemic biomarkers of disease in patients with both chronic periodontitis and coronary artery disease.

OBJECTIVES: This study evaluated the effects of scaling and root planing (SRP) +/- sub-antimicrobial dose doxycycline (SDD) on gingival crevicular fluid (GCF) levels of matrix metalloproteinase (MMP) -1, -8, -13 and on serum levels of high-sensitivity C-reactive protein (HsCRP) and lipid fractions in patients with both chronic periodontitis (CP) and coronary artery disease (CAD). MATERIAL AND METHODS: Thirty-six patients were randomly distributed into two groups (Placebo or SDD; 6 weeks) and both received two regimens of SRP. At baseline and 6 weeks, GCF and blood were collected and clinical indices were recorded. MMPs, HsCRP and lipid fractions were assayed. RESULTS: There were statistically significant improvements for all clinical parameters, GCF volumes, GCF MMPs and serum levels of HsCRP, apolipoprotein-A (APO-A), high-density lipoprotein (HDL) and lipoprotein-a between pre- and post-treatment in both groups. Between groups, there were statistically significant greater improvements in pocket depth (PD), gingival index (GI), APO-A and HDL, favouring the group receiving SDD adjunctive to SRP (p < 0.05). CONCLUSION: Greater improvement was detected for PD and GI, and for serum levels of APO-A and HDL cholesterol when using SRP+SDD compared with SRP+placebo in this study. An investigation with larger numbers of patients and a longer duration of drug treatment is needed to confirm these preliminary findings.