Nese Cam

Effects of drug-eluting stents on systemic inflammatory response in patients with unstable angina pectoris undergoing percutaneous coronary intervention

Inflammatory markers are elevated in acute coronary syndromes, and are also known to play a crucial role in the pathogenesis of neointimal proliferation and stent restenosis. Drug-eluting stents (DESs) have been shown to decrease stent restenosis in different studies. In this study, we aimed to investigate the effect of treatment with DESs on systemic inflammatory response in patients with unstable angina pectoris who underwent percutaneous coronary intervention (PCI). We compared plasma high-sensitivity C-reactive protein (hsCRP), human tumor necrosis factor α (Hu TNF-α), and interleukin 6 (IL-6) levels after DES (dexamethasone-eluting stent [DEXES], and sirolimuseluting stent [SES]) implantation with levels after bare metal stent (BMS) implantation. We performed PCI with a single stent in 90 patients (62 men; 59 ± 9 years of age; n = 30 in the BMS group, n = 30 in the DEXES group, n = 30 in the SES group) who had acute coronary syndrome. Plasma hsCRP, Hu TNF-α, and IL-6 levels were determined before intervention and at 24 h, 48 h, and 1 week after PCI. The results were as follows. Plasma hsCRP levels at 48 h (11.19 ± 4.54, 6.43 ± 1.63 vs 6.23 ± 2.69 mg/l, P = 0.001) after stent implantation were significantly higher in the BMS group than in the DES group; this effect persisted for 7 days (P = 0.001). Plasma Hu TNF-α levels at each time point were higher in the SES group than in the BMS and DEXES groups (P < 0.05). The time course of Hu TNF-α values was similar in all groups. Although IL-6 levels at baseline and at 24 and 48 h showed no statistically significant difference between the study groups, postprocedural values at 7 days were slightly statistically significant in the SES group (P = 0.045). Drug-eluting stents showed significantly lower plasma hsCRP levels after PCI compared with BMSs. This may reflect the potent effects of DESs on acute inflammatory reactions induced by PCI.

An electrocardiographic algorithm for determining the location of pacemaker electrode in patients with right bundle branch block configuration during permanent ventricular pacing

The expected morphology of right ventricular pacing is a left bundle branch block (LBBB) pattern. However, right bundle branch block (RBBB) can also be seen during permanent right ventricular pacing. The aim of this study was to develop an electrocardiographic algorithm to differentiate this benign condition from septal and free wall perforation with subsequent left ventricular pacing. Three hundred consecutive patients who had permanent ventricular or dual-chamber pacemaker implantation between 1999 and 2000 were screened and 25 patients (8.3%) who exhibited RBBB configuration were included in the study. Echocardiograms and chest radiographs were evaluated in order to identify the pacing lead location in this group. The authors formed a study group with their own 25 patients and 22 cases of RBBB with permanent pacemaker from previous publications (total 47 patients). Frontal axis, QRS morphology in lead V1, and the precordial transition point, which is defined as the precordial lead where R wave amplitude is equal to S wave amplitude, were examined. Placement of precordial leads V1 and V2 1 interspace lower than the standard location (Klein maneuver) eliminated the RBBB pattern in 12 patients. RBBB pattern with “true right ventricular pacing” was detected in 24 of the 25 patients, and in 11 of the 22 patients reported in the literature (total 35 patients). Right ventricular pacing was correctly identified in 34 of 35 patients with use of criteria including left superior axis deviation, RS or qR morphology in lead V1, and precor-dial transition at lead V3 with a high sensitivity and specificity. A simple surface electrocardiogram can accurately predict the lead location in patients having RBBB morphology with right ventricular pacing.

The impact of CYP2C9 and VKORC1 genetic polymorphism and patient characteristics upon warfarin dose requirements in an adult Turkish population

In this study, we investigated the contribution of vitamin K epoxide reductase (VKORC1) and cytochrome P450 2C9 (CYP2C9) genotypes, age, and body surface area (BSA) on warfarin dose requirements and in an adult Turkish population. Blood samples were collected from 100 Turkish patients with stable warfarin dose requirements and an international normalized ratio (INR) of the prothrombin time within the therapeutic range. Genetic analyses for CYP2C9 genotypes (*2 and *3 alleles) and VKORC1 −1639 G>A polymorphism were performed and venous INR determined. The mean warfarin daily dose requirement was higher in CYP2C9 homozygous wild-type patients, compared to those with the variant *3 allele (P < 0.05), similar to those with the variant *2 allele (P > 0.05) and highest in patients with the VKORC1 −1639 GG genotype compared to those with the GA genotype and the AA genotype (P < 0.01). The time to therapeutic INR was longer in CYP2C9 homozygous wild-type patients compared with those with the variant *2 and *3 alleles (P < 0.01), and longer in patients with the VKORC1 (position −1639) GG genotype compared with those with the GA genotype and the AA genotype (P < 0.01). The multivariate regression model including the variables of age (R2 = 4.4%), BSA (R2 = 27.4%), CYP2C9 (R2 = 8.1%), and VKORC1 genotype (R2 = 34.1%) produced the best model for estimating warfarin dose (R2 = 60.4%). VKORC1 genotype and CYP2C9 polymorphism affect daily dose requirements and time to therapeutic INR in Turkish patients receiving warfarin for anticoagulation.

Oxidative stress and severity of coronary artery disease in young smokers with acute myocardial infarction.

BACKGROUND Cigarette smoking increases the oxidative stress mediated vascular dysfunction in young adults. We aimed to investigate the relation between the oxidative stress indices and coronary artery disease (CAD) severity in young patients presenting with acute myocardial infarction (AMI). METHODS Young patients (aged 〈 35 years) who were admitted consecutively to our hospital with a diagnosis of AMI were included in the study. Age matched healthy subjects were selected as controls. Oxidative stress indices including lipid hydroperoxide (LOOH), total antioxidant status (TAS), total oxidant status (TOS), oxidative stress index (OSI), paraoxonase (PON) and arylesterase (ARE) activities were measured in serum. CAD severity was assessed by calculating the SYNTAX (Synergy Between Percutaneous Coronary Intervention with Taxus and Cardiac Surgery Study) score. We analyzed the association between the oxidative indices and CAD severity. RESULTS Forty two young patients were admitted to the hospital with AMI (age 32.4 ± 2.6 years; 39 males, 3 females). Current and heavy smoking was commonly observed among the patients (79%). All patients underwent emergency coronary angiography. Twenty-eight healthy subjects were selected as controls. Patients had significantly higher OSI and TOS levels (median, interquartile range) [0.44 (0.26-1.75) vs 0.25 (0.22-0.30), p < 0.001 and 6.0 (4.4-20.8) vs 4.1 (3.7-4.6), p < 0.001], respectively, and lower TAS and LOOH levels [1.6 ± 0.1 vs 1.7 ± 0.1, p = 0.02 and 3.0 ± 0.8 vs 3.6 ± 0.4, p = 0.001], respectively, compared to the control group. CAD severity correlated positively with OSI (r = 0.508, p = 0.001) and TOS levels (r = 0.471, p = 0.002). Subjects with an intermediate to high SYNTAX score (≥ 22) demonstrated significantly higher OSI (median, interquartile range) [0.40 (0.34-1.75) vs 0.34 (0.26-0.68), p = 0.01] and TOS [6.9 (4.4-20.8) vs 5.8 (4.5-11.4), p = 0.01] levels compared to subjects with low SYNTAX score. CONCLUSIONS Oxidative stress is an important contributor to CAD severity among young smokers. Elevated OSI and TOS levels reflect disease severity and vascular damage related to heavy smoking in early onset CAD.

Influence of weight loss on myocardial performance index

Obese patients may have a phase of asymptomatic left ventricular dysfunction. A combined myocardial performance index (MPI) has been demonstrated to be a useful index to estimate left ventricular function and to predict the prognosis of patients with heart failure. The objective of the study was to determine the influence of weight loss on MPI. A total of 18 obese patients (3 men, 15 women, mean age 49.6 ± 5.5 years, body mass index [BMI] >30 kg/m2) were investigated in the study. All patients were treated with a multidisciplinary approach consisting of a hypocaloric diet and orlistat therapy (120 mg three times daily), and all of them underwent two-dimensional and Doppler echocardiographic examination two times before starting the study and after a period of weight loss. Using echo-Doppler methods, ejection fraction, peak velocities of early (E) and late (A) diastolic filling, the E/A ratio, deceleration time (DT), isovolumic contraction time (IVCT), isovolumic relaxation time, ejection time, and MPI were measured. The MPI was obtained by subtraction ejection time from the interval between cessation and onset of the mitral flow. All patients lost at least 10% of their initial body weight, with a mean decrease of 10.8 ± 3.7 kg. This was associated with significant reductions in BMI with a mean decrease 4.5 ± 1.4 kg/m2. Compared with baseline, after weight loss the E/A ratio of 1.01 ± 0.22 before treatment increased to 1.17 ± 0.26 (P = 0.012), left ventricular mass index decreased from 88 ± 23 to 82 ± 19 g/m2 (P = 0.028), IVCT from 71 ± 20 to 53 ± 30 ms (P = 0.004), DT from 233.65 ± 38.14 to 196.72 ± 47.73 s (P = 0.004), and MPI from 0.63 ± 0.13 to 0.50 ± 0.13 (P = 0.0001). Weight loss ameliorates MPI and seems to be a clinically relevant measurement of left ventricular global function, and may prove to be a valuable tool in assessing the risk of developing heart failure.

Anxiety and P Wave Dispersion in a Healthy Young Population

Background: P wave dispersion (P_d), defined as the difference between the maximum (P_max) and the minimum P wave duration (P_min), and P_max are electrocardiographic (ECG) markers that have been used to evaluate the discontinuous propagation of sinus impulses and the prolongation of atrial conduction time. P_d in normal subjects has been reported to be influenced by the autonomic tone, which induces changes in atrial size and the velocity of impulse propagation. However, the association between P_d and anxiety has not been studied in normal subjects. Methods and Results: P_max, P_min and P_d were measured in 726 physically and mentally healthy young male volunteers, aged 21.23 ± 1.25 years (range 20–26). The Spielberger State-Trait Anxiety Inventory (STAI) was scored concomitantly. Blinded intra- and interobserver reproducibility of the P wave duration and P_d measurement were evaluated, and comparison revealed a Pearson correlation coefficient of 0.87 and 0.89 for the P wave duration, and 0.93 and 0.90 for P_d, respectively (p < 0.001). P_max and P_d were significantly correlated with the state anxiety (STAI-1) subscale (r = 0.662, p < 0.001, and r = 0.540, p < 0.001, respectively) and the trait anxiety (STAI-2) subscale (r = 0.583, p < 0.001, and r = 0.479, p < 0.001, respectively). P_min did not show any significant correlation with anxiety. Across 3 variables included in a multiple linear regression analysis, STAI-1 and STAI-2 were the significant independent determinants of P_max and P_d. Beta coefficients indicated that the contribution of STAI-1 to P_max (66.3 and 33.7%) and P_d (65 and 35%) was much greater than that of STAI-2. Conclusions: STAI-1 and STAI-2are associated with an increase in P_max and P_d. The association of P_d resulted from an augmentation of P_max. This is the first study to show the relation between P_max, P_d and anxiety.

Acute migraine attack, angina-like chest pain with documented ST-segment elevation and slow coronary flow

Slow flow of dye in epicardial coronary arteries is not an infrequent finding in patients during routine coronary angiography.The coronary slow flow phenomenon is an angiographic finding characterized by delayed distal vessel opacification in the absence of significant epicardial coronary artery disease. It is speculated that coronary slow flow is a new disease characterized by acute but recurrent perturbations of microvascular function. There are many theories concerning the pathogenesis of migraine.The clinical effectiveness of vasoactive drugs and many investigations on the cerebral blood flow in patients with migraine, strongly support a vascular theory.The relationship between migraine and cardiopathy has not been sufficiently established and controversy exists concerning its favouring role in coronary artery disease.We report a case of an acute migraine attack in a patient who uses triptans (5-HT(1B/1D) receptor agonists). The attack was accompanied by angina-like chest pain with documented ST-segment elevation and slow coronary flow in the absence of any significant obstructive coronary artery disease and no evidence of any major epicardial coronary arterial spasm.

The role of paraoxonase (PON) enzyme in the extent and severity of the coronary artery disease in type-2 diabetic patients

Increased coronary artery disease (CAD) risk is well established in diabetes mellitus (DM). Paraoxonase (PON) enzyme is known to have protective effects on lipid peroxidation. This study aimed to investigate the changes in PON activity levels with duration of DM as well as the role of PON activity in progression of CAD. Eighty-four consecutive diabetic patients (mean age 58 years, 46 men) who underwent coronary angiography for diagnostic purposes were examined. Before the angiography, fasting venous blood samples were taken for PON enzyme activity, thiobarbituric acid reactive substances (TBARS), and routine biochemical parameters. Severity and extent of coronary atherosclerosis were scored numerically using the Gensini scoring system. The population was divided into three groups according to Gensini score: Group 1, mild CAD; Group 2, moderate CAD; Group 3, severe CAD. Group 1 had higher PON levels and shorter DM duration than those of Group 3. Gensini score was significantly correlated with, PON activity (r = −0.361) and apo-AI (r = −0.375). TBARS (r = −0.290) and the duration of DM (r = −0.336) also showed a significant correlation with PON activity levels. Also, multivariate linear regression and Pearson correlation analyses showed that PON activity (P = 0.04), apo-AI levels (P = 0.01), and the duration of DM (P = 0.003) were significantly associated with Gensini score. Paraoxonase activity decreases parallel to DM duration. The lack of protective effect of PON enzyme on lipid peroxidation may be a factor in acceleration of CAD in DM.

Cardiac Troponin I Increase After Successful Percutaneous Coronary Angioplasty: Predictors and Long-Term Prognostic Value:

After successful percutaneous coronary interventions (PCI), elevations of cardiac enzymes are not rare, but it is still not clear whether those elevations are associated with adverse late outcome. The purpose of the study was to investigate the relation between cardiac troponin I (cTn-I) increase after successful percutaneous intervention and late outcome. The study consisted of 100 consecutive patients (mean age 56 ±9.8, 84% male) who had successful elective coronary balloon angioplasty with or without stent implantation. Patients with stable angina (n=54) and unstable angina (n=46) were included in the study. Blood samples for measurement of cTn-I were taken before and immediately after the procedure, and every 6 hours for the first 24 hours. Patients with preprocedural cTn-I elevation were excluded from the study. Postprocedural cTn-I elevation was detected in 34 patients (34%, troponin (+) group) and cTn-I levels were normal in 66 patients (66%, troponin (-) group). Logistic regression analysis showed that intervention in patients with unstable angina, stent implantation following balloon dilation, and maximal inflation pressure were the predictors of cTn-I elevation (p=0.035, p=0.038, and p=0.014, respectively). During the prospective follow-up period for 21 ±7.5 months, the incidence of major cardiac events including recurrent angina, acute myocardial infarction, death, and revascularization were not different in patients with and without cTn-I elevation. Overall, major cardiac events occurred in 9 patients (26%) in the troponin (+) group and in 13 patients (20%) in the troponin (-) group. Kaplan-Meier survival analysis showed that cTn-I elevation was not an important correlate of overall cardiac events (log-rank: 1.66, p=0.19). The authors conclude that postprocedural cTn-I elevation is related to unstable angina, stent implantation following predilation, and inflation pressure, and there is no association with minor myocardial injury occurring after successful percutaneous coronary intervention and late adverse cardiac events.

Effects of anxiety on QT dispersion in healthy young men

Objective — QT dispersion (QTd) is the maximal interlead difference in QT interval on the surface 12-lead electrocardiogram (ECG).An increase in QTd is found in various cardiac diseases and reflects cardiac autonomic imbalance. It has recently been associated with increased anxiety levels, thereby predisposing affected individuals to fatal heart disease. This is the biggest study to assess QTd in anxiety, as a marker of anxiety-induced cardiac dysregulation. Methods and results — QTd and rate-corrected QTd (QTcd) were measured in 726 physically and mentally healthy male volunteers, aged 21.23 ± 1.25 years (range 20-26). The Spielberger State-Trait Anxiety Inventory (STAI) was scored concomitantly. The intra- and inter-observer reproducibilities of QTd were highly correlated (r = 0.92, p < 0.001; r = 0.93, p < 0.001, respectively). QTd and QTcd significantly correlated with the STAI-1 subscale (State Anxiety Scale) (r = 0.529, p < 0.001; r = 0.518, p < 0.001, respectively) and STAI-2 subscale (Trait Anxiety Scale) (r = 0.601, p < 0.001; r = 0.563, p < 0.001, respectively). Conclusions — The State Anxiety Scale and the Trait Anxiety Scale are associated with an increase in QTd. This association may result from sudden and prolonged anxiety and, in turn, a decrease in vagal modulation and/or increase in sympathetic modulation. This is the first study that shows that increased QTd can serve as a state/trait marker. But further large-scale epidemiological studies are needed to determine if increased QTd is a risk factor for sudden cardiac death in patients with anxiety.