Hakan Gullu

Impaired left ventricle filling in slow coronary flow phenomenon : An echo-doppler study

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<0.001). In conclusion; the authors detected diastolic filling abnormalities and showed diastolic dysfunction in patients with SCF.

Increased High Sensitive CRP Level and Its Significance in Pathogenesis of Slow Coronary Flow

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.

Effect of slow coronary flow on electrocardiographic parameters reflecting ventricular heterogeneity

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 <0.05). In conclusion, SCF was found to be associated with prolonged QT interval and increased QT dispersion. Ischemia in microvascular level and/or altered autonomic regulation of the heart may be responsible mechanisms.

Isolated large true contractile left ventricular diverticulum mimicking ischemia in an adult patient: a case report

Congenital diverticulum of the ventricle is a rare cardiac abnormality that is characterized by local embryologic development failure of the ventricular muscle. It can be found as an isolated form or associated with other cardiac abnormalities. Clinically, it has been reported that it can lead to heart failure, arrhythmia, or chest pain, although frequently the course is asymptomatic. We present a patient who was referred to our clinic with chest pain due to isolated left ventricular diverticulum mimicking myocardial ischemia.

Contribution of Plasma Lipid Disturbances to Vascular Endothelial Function in Patients With Slow Coronary Flow

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.

Interdialytic weight gain and pulmonary membrane diffusing capacity in patients on hemodialysis

Background: Measurement of pulmonary diffusion capacity for carbon monoxide (DLCO) may be useful for assessing disease affecting the alveolar-capillary bed or the pulmonary vasculature. It was reported that hemodialysis (HD) therapy causes DLCO reduction via decrease of pulmonary capillary blood volume components. The aim of the study was to evaluate the effect of interdialytic weight gain on pulmonary function and especially DLCO. We further determined whether intravascular volume status, assessed by inferior vena cava diameter (IVCD) contributes to DLCO in patients on HD. Methods: Routine pulmonary function testing including forced expiratory volume in 1 second (FEV1), forced vital capacity (FVC), FEV1/FVC, forced mid-expiratory flow rate (FEF25–75), DLCO IVCD index and other echocardiographic parameters were evaluated in 20 patients (mean age 48.6 ± 18.3 years, mean dialysis duration 17.4 ± 19.2 months) on chronic HD, 1 hour after HD and after an interdialytic period (1 hour before HD therapy). Single-breath DLCO measurements were corrected for hemoglobin concentration (cDLCO). Results: Routine pulmonary function tests (spirometry) showed no significant changes in FEV1, FVC and FEF25–75 whereas a statistically significant fall in FEV/FVC was found. At the end of the interdialytic period a statistically significant increase in weight, IVCD index, left ventriculer diastolic diameter (LVDD), and diastolic blood pressure (DBP) were observed (P < 0.05). Using the single-breath DLCO, we found unchanged cDLCO at the end of the interdialytic period. There was no correlation of cDLCO with increases in weight, DBP, IVCD index, LVDD (P > 0.05). Conclusion: The accumulation of body water between dialyses has no significant influence on DLCO.

Effect of paclitaxel administration on P wave duration and dispersion

Abstract.The prototypic taxane paclitaxel, which disrupts tubulin dynamics, has been widely used in the treatment of solid malignancies. However, it has been associated with adverse cardiac effects. Therefore, the effect of the paclitaxel infusion on P wave duration and dispersion (PWD) was investigated. Twelve-lead surface ECG’s were recorded twice from 12 patients with breast, ovarian and non-small-cell lung carcinoma: one just before paclitaxel infusion and the other 1 hour after the end of the infusion. The changes in maximum (Pmax) and minimum P wave duration (Pmin) were measured manually and the difference between the two values was defined as PWD. The mean heart rate, Pmin, did not change after the infusion. However, Pmax, PWD and the average P wave duration significantly increased after infusion (122 ± 5 vs. 125 ± 5 p = 0.001 and 46 ± 7 vs. 53 ± 9 p = 0.03, 97 ± 5 vs. 101 ± 5ms p = 0.02 respectively). We found that paclitaxel infusion increased PWD and this may be a result of the drug’s effect on cardiac autonomic modulation.