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Previous studies have suggested that microvascular abnormalities cause slow coronary flow (SCF). The role of inflammation has not been investigated, to date. The purpose of this study was to determine the role of inflammation in pathogenesis of SCF. The study included 32 patients with angiographically proven SCF (mean age 49 ±9 years) (group I) and 30 subjects with normal coronary flow (mean age 48 ±8 years) (group II). Blood samples were collected for high sensitive CRP (hs-CRP) measurements. Thrombolysis in myocardial infarction frame count (TFC) was compared in both groups. Distribution of sex, age, body mass index (BMI), arterial blood pressure, and ejection fraction were similar in the 2 groups. TFC was significantly higher in group I than in group II for each artery including left anterior descending coronary artery (LAD), left circumflex artery (Cx), and right coronary artery (RCA) (38.9 ±6.6 vs 22.1 ±1.8 frames, p = 0.0001; 39.6 ±4.9 vs 22.3 ±1.8 frames, p = 0.001 ; 39.0 ±3.8 vs 22.0 ±1.8 frames, p = 0.001, respectively). In group I, serum hs-CRP concentration was significantly higher than that of group II (0.6 ±0.58 vs 0.24 ±0.1 mg/dL p = 0.03). Correlation analysis showed a positive correlation between hs-CRP level and TFC for each artery (for CTFCLAD, r = 0.36 p = 0.004; for TFCCx, r = 0.42 p = 0.003; and for TFCRCA, r = 0.42, p = 0.0001 respectively). Increased hs-CRP level suggests that inflammation may be associated with pathogenesis of SCF or at least in part contributes to its pathogenesis. Increased hs-CRP level may also be an early marker of impaired coronary blood flow.

QT interval dispersion reflects regional variations in ventricular repolarization and cardiac electrical instability. Previous studies have showed that QT interval dispersion changes during episodes of myocardial ischemia. Slow coronary flow (SCF) in epicardial coronary arteries is a rare and unique angiographic finding. Whether this pattern of flow is associated with electrocardiographic abnormalities is unknown. Therefore, this study was designed to investigate whether SCF results in electrocardiographic (ECG) changes compared to normal coronary flow. For this aim 24 patients with angiographically proven SCF who had no obstructive coronary lesion (group I) and 25 patients without coronary artery disease (group II) were included in the study. Both groups underwent a routine standard 12-lead surface electrocardiogram recorded at 50 mm/s during rest. QT dispersion (QTd), corrected QT (QTc), and corrected QT dispersion (QTcd) were calculated. Distributions of sex, age, body mass index (BMI), and cardiac risk factors were similar in the 2 groups. Mean heart rate was similar in the 2 groups (74 ±8 vs 77 ± 7 p > 0.05). Mean QRS interval durations were similar in the groups (92 ±7 vs 90 ±6 ms p > 0.005). In group I, QTd, QTcd, and QTc, were significantly higher than in group II (QTd: 73 ±14 vs 40 ±14; QTcd: 71 ±15 vs 42 ±9; QTc: 414 ±14 vs 388 ±13, respectively p

Slow coronary flow (SCF) in a normal-appearing coronary angiogram is a well-recognized clinical entity, but its etiopathogenesis remains unclear. The aim of the study was to evaluate echocardiographic features in patients with SCF. Thirty-four patients with angiographically proven SCF (group I) and 25 patients with normal coronary flow (group II) were enrolled in the study. The diagnosis of SCF was made with use of the “TIMI frame count (TFC)” method. All patients underwent complete transthoracic echocardiographic examination (M-mode, 2-dimensional [2-D], and Doppler parameters such as color, continuous, pulsed wave). There were no significant differences with respect to systolic parameters between the 2 groups; in spite of these, group I showed impaired left ventricular diastolic patterns compared to group II. Group I patients had higher peak late diastolic filling velocities due to enhanced atrial systole (A), lower peak (E/A) diastolic filling velocity ratios, and longer isovolumetric relaxation times compared with group II, and these were statistically significant (p

Atherosclerosis is a diffuse process that involves vessel structures. In recent years, the relation of noninvasive parameters such as intima-media thickening (IMT), arterial distensibility (AD), and stiffness index (SI) to cardiovascular diseases has been researched. However, we have not found any study that has included all these parameters. The aim of this study is to examine the relation between the presence of coronary artery disease (CAD) and its risk factors to AD, SI, and IMT, which are the noninvasive predictors of atherosclerotic process in the carotid artery. Included in the study were 180 patients who were diagnosed as having CAD by coronary angiography (those with at least ≥ 30% stenosis in the coronary arteries) and, as a control group, 53 persons who had normal appearing coronary angiographies. IMT, AD, and SI values of all the patients in the study were measured by echo-Doppler imaging (AD formula = 2 × (AoS-AoD)/PP × AoD, SI formula = (SBP/DBP)/([AoS - AoD]/AoD). Significantly increased IMT (0.82 ±0.1, 0.57 ±0.1, p < 0.05), decreased AD (0.25 ±0.9, 0.37 ±0.1, p < 0.05), and increased SI (13 ±4, 8 ±3, p < 0.05) values were detected in the CAD group compared to the control group. A significant correlation was found between IMT and presence of diabetes mellitus (DM), systolic blood pressure, total cholesterol, and presence of plaque in carotids, and age. In the coronary artery disease group there was a significant correlation between AD and age, systolic blood pressure, and HDL cholesterol levels, while there was no significant correlation with plaque development. A significant correlation was also found between stiffness index and systolic blood pressure and age; however, there was no relation between number of involved vessels and IMT, AD, and SI. We found sensitivity, specificity, and positive predictive and negative predictive values for CAD diagnosis to be 70%, 75%, 77%, and 66%, respectively. In CAD cases, according to data in this study, IMT and SI increased while AD decreased, and this was detected by carotid artery Doppler ultrasonography. Therefore, it was concluded that these cheaper, noninvasive, and easily available parameters could be used in early diagnosis of CAD.

Overweight/obesity is a complex multifactorial chronic disorder, and the American Heart Association (AHA) has recently classified as a modifiable risk factor for coronary heart disease (CAD). This study (1) evaluates the association between CAD in a patient population mostly overweight (MOP) and conventional and novel coronary risk factors by using univariate and multivariate logistic regression analysis and (2) seeks to find the best model by comparing univariate and multivariate logistic regression analysis algorithms, which were systematically applied to risk factors by using Hosmer-Lemeshow statistic test. In univariate analysis, there were significant associations between CAD in MOP and conventional and novel risk factors. However, the model's sensitivity, specificity, and accuracy levels were weak. In multivariate analysis, although some risk factors were not found as predictors of coronary artery disease, the model showed good fit to data and had high sensitivity, specificity, and accuracy levels. This was also confirmed by using the Hosmer-Lemeshow goodness of fit test, more specifically.

The authors evaluated the effects of beta blockers (metoprolol) and calcium channel blockers (diltiazem) in patients having mild to moderate mitral stenosis (MS) with sinus rhythm. Eighty patients with a complaint of dyspnea with diagnosed MS were included in this study. Patients were randomized into metoprolol and diltiazem groups. The first group received oral diltiazem treatment for 3 months following an IV dose of 25 mg diltiazem. The second group received oral metoprolol for 3 months following an IV dose of 5 mg metoprolol. All patients performed a treadmill exercise test at the beginning of and after 3 months of treatment. Transthoracic echocardiographic studies were also performed following the IV drug administration and after 3 months of treatment. In addition, oxygen uptakes of patients were measured before and after the stress and after 3 months of treatment. Decreases in peak gradient (PG) and mean transmitral gradient (MG) were observed in the metoprolol group after IV and oral metoprolol treatment. A prolongation of exercise time in treadmill exercise test (TET) and a decrease in the maximum heart rate after oral metoprolol treatment were noted. Eighteen patients in the metoprolol group had benefited symptomatically from this treatment and complaints of dyspnea were alleviated, whereas no symptomatic relief was seen in the diltiazem group. No significant prolongation was observed in effort times (p>0.05) of the diltiazem group. Transmitral gradients measured via echocardiographic examination did not change (p>0.05). With respect to oxygen uptake rates, a statistically significant decrease was determined in the metoprolol group, whereas no difference was found in diltiazem group. The authors conclude that metoprolol may be useful in patients with MS and can provide symptomatic relief. They did not observe any beneficial effect of diltiazem in these patients.

The previous studies relating to the effect of the Valsalva maneuver on P wave do not provide detailed information. In those studies, the parameters related to P wave duration during the release phase of the Valsalva maneuver were evaluated. The authors evaluated P wave amplitude as well as P wave duration during the strain phase of the Valsalva maneuver. Thirty- seven normal subjects and 36 patients with paroxysmal atrial fibrillation (PAF) were included in the study. Twelve-lead surface electrocardiography (ECG) was obtained from all the patients before and during the strain phase of the Valsalva maneuver. The authors evaluated the para meters related to both P wave duration and P wave amplitude. The highest P wave voltage was expressed as the P wave amplitude maximum (P amp max), the lowest P wave voltage as the P wave amplitude minimum (P amp min), and the P wave amplitude dispersion (P amp dispersion) as "the P amp max — the P amp min." Also, the maximum P wave duration was expressed as the P maximum (P max), the minimum P wave duration as the P minimum (P min), and the P wave dispersion as "the maximum P wave duration (P max) — the minimum P wave duration (P min)." All these parameters were measured before and during the strain phase of the Valsalva maneuver. P max, P dispersion, P amp max, and P amp dispersion were higher in patients with PAF compared to those of normal subjects before the Valsalva maneuver. In normal subjects, P max, P wave dispersion, P amp max, and P amp dispersion values were significantly higher in the strain phase of the Valsalva maneuver than before (p

Behçet’s disease (BD) is a multisystemic disorder characterized by endothelial dysfunction. However, the relationship between oxidative stress and endothelial function has not been clearly shown. We investigated the relationship between oxidative stress markers and endothelial function in patients with BD. Patients with BD (n = 40) having active disease and sex- and age-matched 40 controls were included. Endothelial function was assessed by flow-mediated dilatation (FMD) technique. Serum gamma-glutamyltransferase (GGT) and high-sensitive C-reactive protein levels (hsCRP) were measured in all participants. Brachial artery FMD was significantly lower in patients with BD than in controls. Gamma-glutamyltransferase and hsCRP levels were higher in patients with BD than in controls. Also, GGT and hsCRP levels were inversely correlated with endothelial function. Oxidative stress markers are elevated in patients with BD having active disease. This may be one of the reasons behind the vasculitis in active BD.

The aim of this study is to evaluate the effect of type 2 diabetes mellitus on epicardial coronary flow velocity assessed by the thrombolysis in myocardial infarction frame count. The thrombolysis in myocardial infarction frame count was measured in 272 coronary arteries from 101 patients with type 2 diabetes mellitus and in 271 coronary arteries from 104 age- and gender-matched patients without type 2 diabetes mellitus referred for coronary angiography. The thrombolysis in myocardial infarction frame count was measured only in normal arteries or in arteries without significant lesion. By both univariate and multivariate analysis, the thrombolysis in myocardial infarction frame count was not related with either type 2 diabetes mellitus or the duration and glycated hemoglobin levels in the patients with type 2 diabetes mellitus. The thrombolysis in myocardial infarction frame count was significantly associated with body surface area, heart rate, and proximal coronary artery diameter. Type 2 diabetes mellitus did not affect epicardial coronary flow velocity assessed by the thrombolysis in myocardial infarction frame count.

Previous studies have suggested that microcirculatory abnormalities cause slow coronary flow (SCF). However, the underlying mechanism of this phenomenon has not yet been well documented. Therefore, the aim of this study was to determine the role of plasma lipid disturbances in pathogenesis of slow coronary flow (SCF). Forty patients with SCF (group I) and 37 subjects with normal coronary arteries (group II) were included in the study. In each subject plasma lipid concentrations (total cholesterol [TC], low-density lipoprotein cholesterol [LDL-C], high-density lipoprotein cholesterol [HDL-C], and triglyceride [TG]) and brachial artery flow-mediated dilatation (FMD) and nitroglycerin (NTG)-induced dilatation were measured. Total cholesterol level was found to be similar in the 2 groups. In group I, HDL-C level was lower than in group II (34 ±3 vs 40 ±4 mg/dL, p=0.0001). In group I, TG level was higher than in group II (213 ±29 vs 198 ±24 mg/dL p=0.002). In group I, FMD was smaller than that of group II (3.48 ±3.1% vs 10.4 ±5.6%, p=0.0001). The percent NTG-induced dilatation was not different between the groups (15.5 ±5.3% vs 17.3 ±6.9%, p=0.27). On regression analysis; there was a significant relationship between percent of FMD and HDL-C ( r =0.65, p=0.0001). When the 2 groups were analyzed separately, HDL-C was still related to percent of FMD in both groups ( r =0.47 p=0.002 and r =0.45 p=0.005, respectively). Multivariate regression analysis showed that only plasma HDL-C was independently related to FMD (F=7.5 p=0.0001). In patients with SCF, reduced flow-mediated dilatation was detected and was found to be associated with plasma lipid disturbances, principally low HDL and high TG levels.

Coexisting coronary artery disease (CAD) is an important cause of morbidity and mortality in patients with peripheral arterial disease (PAD). Clinical evaluation and noninvasive tests have some important limitations for the detection of CAD in patients with PAD. The purpose of this study was to investigate whether urinary albumin excretion (UAE) was a sign of atherosclerotic involvement of coronary arteries in patients with PAD. Our study consisted of 65 consecutive patients (56 men, 9 women, mean age; 59.7 ±7.9 years) with PAD who underwent coronary angiography. Urinary albumin excretion was measured in 24-hour urine samples by immunoprecipitation technique. PAD was defined as the presence of ≥50% stenotic lesions in at least 1 of the iliac, femoral, popliteal, tibialis anterior, tibialis posterior, or peroneal arteries. CAD was defined as ≥25% diameter stenosis in at least 1 coronary artery. Patients without any coronary lesions were accepted as having normal coronaries. Age, sex, distributions of coronary risk factors, and UAE rates were compared between patients with and without CAD. Mean UAE was 17.9 ±15.6 mg/day in the total population. Thirty-seven percent of patients had CAD, and 63% had no coronary lesion. UAE rates were 22.33 ±18.74 and 15.32 ±13.01 mg/day in patients with CAD and those with normal coronary arteries, respectively (p=0.021). Microalbuminuria was detected in 25% in patients with CAD and 12% in those without coronary artery lesions (p=0.184). The difference was not statistically significant. The distributions of other risk factors and sex were not different between the 2 groups. These data suggest that in patients with PAD, urinary albumin excretion rates may be used to determine those with a high probability of CAD. Further studies are required to decide whether this noninvasive testing is appropriate in detecting high-risk patients.

This study was designed to examine the effect of left bundle branch block (LBBB) on systolic and diastolic function of the left ventricle (LV) in patients with heart failure and in normal subjects. Thirty-six patients with heart failure and LBBB (group I), 36 patients with heart failure with normal conduction (group II), and 41 subjects with isolated LBBB (group III) were compared. Coronary angiography was performed and LV end diastolic pressure was calculated. Echocardiography was performed on all patients. LV ejection fraction and mean rate of circum ferential shortening were calculated. The following Doppler parameters were evaluated: peak rapid filling velocity (E wave), peak atrial filling velocity (A wave), E- and A-wave integrals, E- wave acceleration time and deceleration time (EDT) and rates (EAR and EDR), the E/A ratio and its integral, and diastolic flow time (DT). The ejection time, isovolumetric relaxation time (IRT), and preejection period were measured using the aortic and mitral flow. LV end diastolic pressure was calculated as 28 ±4 mm Hg, 22 ±5 mm Hg, and 15 ±3 mm Hg in groups I, II, and III, respectively. Although the systolic function parameters in group III patients were different, the diastolic function parameters of group II were found to be quite similar to those of group III patients. Comparison of group I patients with group II patients showed that there was a similarity between LV systolic function parameters while the diastolic function parameters were different (E/A, p = 0.004; EAR, p

Gemfibrozil-statin combination therapy is a well-known risk factor for myopathy and rhabdomyolysis. Cerivastatin is a currently available statin with dual elimination; it is therefore expected to cause less drug-drug interaction. This case is the second reported case with severe rhabdomyolysis caused by cerivastatin-gemfibrozil combination. Moreover, in this case, the rhabdomyolysis was more severe and caused severe renal failure and death. The authors discuss how these drugs cause rhabdomyolysis and how rhabdomyolysis can cause renal failure.