Özer Badak

Are complex coronary lesions more frequent in patients with diabetes mellitus

BACKGROUND Coronary atherosclerotic burden is excessive in diabetic patients. Diabetes mellitus (DM) is an independent predictor for both death and myocardial infarction. It is not known whether the prevalence of complex coronary lesions, such as bifurcation and ostial lesions, is different in diabetics from nondiabetics. OBJECTIVE The aim of present study was to investigate the prevalence of these lesions in patients with DM. METHODS One thousand fourteen consecutive patients (mean age 61.3+/-10.7 years) were investigated. Coronary angiograms were examined for bifurcation and ostial lesions using a digital quantitative system. Patients were classified as diabetic (n=281) or nondiabetic (n=733). RESULTS Patient mean age, and rates of hypertension and hyperlipidemia were significantly higher in the diabetic group than in the nondiabetic group (P<0.0001), although smoking was significantly lower (P=0.001). Reasons for coronary angiography and treatment were comparable between the two groups. The prevalence of bifurcation lesions and ostial lesions was significantly greater in the diabetic group than in the nondiabetic group (9.8% versus 4.3% [P=0.001] and 38.4% versus 29.2% [P=0.003] in the diabetic group versus the nondiabetic group). The presence of DM and greater age were found to be independent predictors for bifurcation lesions (OR=2.27 [P=0.004] and OR=1.03 [P=0.01], for DM and age, respectively) and ostial lesions (OR=1.40 [P=0.027] and OR=1.02 [P=0.001], for DM and age, respectively) in multivariate analysis. CONCLUSIONS Complex coronary lesions such as bifurcation and ostial lesions were significantly more common in diabetic patients than in nondiabetic patients. Greater age and the presence of DM were independent predictors for these complex lesions. These results may help to explain the poor prognosis of coronary artery disease among diabetic patients.

Prognostic value of neutrophil-to-lymphocyte ratio in pulmonary arterial hypertension

Objective To evaluate the prognostic value of baseline neutrophil-to-lymphocyte ratio (NLR) in the prediction of long-term mortality in patients with pulmonary arterial hypertension (PAH). Methods This prospective study recorded NLR during initial diagnostic right-sided cardiac catheterization in adult patients with PAH. Demographic, clinical, laboratory and haemodynamic variables were compared by NLR tertile. Univariate and multivariate Cox regression analyses were used to determine whether NLR was independently associated with mortality. Results Adults with PAH (n = 101) were followed-up for mean ± SD 36.8 ± 23.6 months. The number of deaths, New York Heart Association functional capacity (NYHA FC), levels of brain natriuretic peptide (BNP) or C-reactive protein (CRP) and presence of pericardial effusion increased as the NLR tertile increased, but haemoglobin and tricuspid plane annular systolic excursion (TAPSE) decreased. On univariate analysis, high NLR values were associated with mortality, but on multivariate analysis, NLR did not remain an independent predictor of mortality. Baseline NYHA FC, TAPSE, BNP level and pericardial effusion were independent predictors of mortality. Conclusions NLR was correlated with important prognostic markers in PAH such as NYHA FC, BNP and TAPSE. This simple marker may be useful in the assessment of disease severity in patients with PAH.

Dissection of the ascending aorta due to metastatic carcinoma

The association of aortic dissection with a malignancy is a rare finding and previous reports are usually those of primary aortic sarcomas. In this report we present a case with typical ascending aorta dissection associated with metastatic carcinoma originating from the lungs. The metastatic infiltration of the vasovasorum of the aorta by carcinoma cells may have caused aortic dissection by decreasing medial strength and integrity. This is a mechanism of aortic dissection that we have not encountered in previous reports.

Diagnostic accuracy of mean platelet volume in prediction of clopidogrel resistance in patients with acute coronary syndrome.

OBJECTIVE Clopidogrel therapy is the standard of care in patients with acute coronary syndrome (ACS) and stent implantation. However, concern arises because 25% of subjects are nonresponders to clopidogrel. As this nonresponsiveness is associated with increased adverse outcome, detection of these subjects in daily practice is important in order to withhold a more aggressive therapy and closer follow up. In this study we aimed to evaluate the relation between mean platelet volume (MPV) which is an indicator of platelet activation and clopidogrel nonresponsiveness. METHODS The study was planned as a prospective cohort study. A total of 185 patients who had been on clopidogrel therapy for any acute coronary syndrome were enrolled in this study. Clopidogrel responsiveness was analyzed by Multiplate MP-0120 device by using the method of whole blood aggregometry. Blood samples were drawn 3.5 days after clopidogrel loading dose. The amount of ADP induced platelet aggregation was assessed as area under curve (AUC), and a cut-off value of 500, above which the patient is considered as clopidogrel nonresponder, was used. MPV was analyzed from the blood which were sampled at the admission of the patient by using automatic hemocounter. Independent sample t-test, ROC analyses and logistic regression analsis were used in statistical analysis. RESULTS Among the 185 patients analyzed 41 were found to be clopidogrel nonresponder (22.1%). Mean MPV was found to be significantly higher in nonresponders compared to responders (8.7±0.82 fL vs. 8.1±0.83 fL, p<0.001). A cut-off value of 8.3 fL for MPV was detected in prediction of clopidogrel nonresponsiveness with a sensitivity of 76.6% and specificity of 68.3% (OR: 6.4; 95% CI 2.9-14.1, AUC: 0.70, p<0.001). CONCLUSION This study showed that MPV can be used as a predictor of clopidogrel resistance in patients with ACS.

The association of beta-fibrinogen 455 G/A gene polymorphism with left atrial thrombus and severe spontaneous echo contrast in atrial fibrillation.

OBJECTIVE The role of coagulation parameters left atrial thrombus formation in atrial fibrillation has not been investigated before. We aimed to investigate the association between the beta-fibrinogen gene polymorphism or glycoprotein IIIa gene polymorphism and presence of left atrial (LA) thrombus or spontaneous echo contrast (SEC) in patients with atrial fibrillation (AF). METHODS Forty-seven patients with AF, in whom transesophageal echocardiography was performed, were included to this cross-sectional observational study. Patients were divided in two groups; those with LA thrombus (n=24) were assigned to group 1 and those without thrombus in group 2 (n=23). DNA analysis was conducted to determine gene polymorphism in all patients. Mann-Whitney U test or Chi-square tests were used for statistical analysis. RESULTS There were no significant differences between groups regarding to demographic and clinical characteristics. The frequency of beta-fibrinogen 455 G/A polymorphism was higher (37.5%) in group 1 as compared to group 2 (15.1%) but it did not reach statistical difference (p=0.23). When we added patients with severe SEC in the study group (patients with severe SEC and/or thrombus n=27) the difference (44.40%-10%) reached the statistical difference (p=0.01). Glycoprotein IIIa Pl A1/A2 polymorphism was not different between groups with (p=0.82) or without SEC (p=0.73). CONCLUSION In patients with atrial fibrillation, beta-fibrinogen 455 G/A gene polymorphism is associated with the presence of left atrial thrombus and severe SEC. Beta-fibrinogen 455 G/A gene polymorphism may be a promising marker for the prediction of thromboembolism risk in patients with atrial fibrillation.

Using fuzzy logic for morphological classification of IVUS-based plaques in diseased coronary artery in the context of flow-dynamics

Plaque morphology in a diseased coronary artery plays a significant role in the modification of the fluid flow characteristics. The plaque morphology of 42 patients who underwent IVUS (intravascular ultrasound) procedure was quantified by degree of membership in four fuzzy logic sets, which we refer as type I: protruding, type II: ascending, type III: descending, and type IV: diffuse. Of 42 cases, 28% were of type I, 18% type II, 20% type III and 23% type IV, 6% belonged to hybrid types (partial members of multiple types) and the remaining 5% did not fit in any category. The degree of membership is of significance as the inter-class blood flow patterns (those strongly members of the same set) are similar to each other compared to the intra-class behavior, indicating plaque morphology (shape of blockage) is an important metric in addition to the degree of stenosis to represent the flow characteristics in a diseased stenotic coronary artery.

Value of QT dispersion in diagnosis of restenosis after intracoronary stent implantation.

We studied the ECGs of patients with single vessel disease before and after (long term) coronary stent implantation. The interlead variability of the QT interval, known as QT dispersion (QTd), is believed to reflect the regional variations in ventricular repolarization and, thus, may provide an indirect marker of arrhythmogenicity. There are no reliable noninvasive markers of significant restenosis after stent implantation. The effect of coronary revascularization on QTd in patients who underwent coronary stenting has not been investigated extensively. The aim of this study was to evaluate the value of QTd in predicting restenosis after intracoronary stent implantation. QTd with 12 lead surface ECG was measured in 48 patients (21 with restenosis and 27 without restenosis; 33 male; mean age, 58+/-10.8 years) before the procedure and after long-term follow-up (mean, 6.8+/-3.2 months). All patients had coronary angiographic control at the end of the follow-up period. QTd (as the difference between the maximum and minimum QT interval measured from 12 lead ECG) and rate-corrected QT (QTcd) were evaluated at rest. In 27 patients without restenosis, QTd and QTcd decreased from 58+/-14.4 and 62.8+/-20.4 ms to 26.3+/-9.2 and 29.6+/-10.6 ms in the long term follow-up, respectively (P<0.001). However, in 21 patients with restenosis, there was no significant change in QTd and QTcd intervals and they were still increased at the end of the long-term follow-up (P>0.05). In conclusion, increased QT interval dispersion may be an inexpensive and simple marker of restenosis after intracoronary stent implantation.

Rapid retraction of a post-infarction intramyocardial dissecting hematoma.

A 60-year-old male with a recent anterior myocardial infarction (MI) was referred to our hospital for implantable cardioverter defibrillator (ICD) implantation. He was on the 42nd day of MI and clinically stable on admission. Electrocardiography showed right bundle branch block with QS pattern on anterior leads. Transthoracic echocardiographic examination revealed an ejection fraction of 25% with akinesis of the apex and mid-apical segments of anterior and septal walls. In the apical-septal region, a pulsatile cavity with systolic expansion surrounded by a thin endomyocardial border was visualized. Color-Doppler interrogation did not demonstrate any flow within that structure. These findings suggested an intramyocardial dissecting hemorrhage formed after MI. Cardiac magnetic resonance imaging also confirmed an intramyocardial hematoma in the mid-apical anteroseptal region. A conservative approach was assumed as the patient was hemodynamically stable. The planned ICD implantation was postponed due to the high risk of perforation. Subsequently, oral anticoagulant therapy with warfarin was initiated against risk of intracardiac thrombus formation. The existing dual antiplatelet therapy was also continued. One week after hospital discharge, he was rehospitalized due to a very high INR of 6.3. The repeated transthoracic echocardiography revealed an almost complete resolution of the intramyocardial dissecting hematoma and adhesion of the surrounding myocardial layers. Oral anticoagulant therapy was discontinued. Echocardiographic examinations showed no change compared to the last examination during hospitalization. This case illustrates a conservatively managed intramyocardial dissecting hematoma case, in which anticoagulant and antiaggregant therapy yielded a rapid retraction without any complication.

Five Chambered Heart: A Case Report and Brief Review of Literature

We present a patient with chest pain and suspicious findings in electrocardiography and myocardial perfusion scintigraphy for myocardial ischemia. Coronary angiography and then echocardiography and magnetic resonance imaging revealed a dilated left anterior descending coronary artery, which has fistulous communication with a large, separate chamber that occupies the infero-apical interventricular septum. This is a challenging congenital anomaly for a clinician in many aspects, which are discussed in the report.

PP-259 ERGOTAMINE INDUCED TAKOTSUBO CARDIOMYOPATHY

Case: A 53 year old women presented to the outpatient clinic with dyspnea and chest pain. She also complained about burning sensation in both arms. Her medical history included a cardiac surgery for secundum type atrial septal defect 25 years ago and a recent lower respiratory tract infection. She had also neurological diseases such as migreine and restless leg syndrome. Her ECG showed negative T waves in all leads with a mild QT prolongation (QTc =460ms). Laboratory examination showed increased troponin I levels (0.6 ng/ml). Coronary angiography showed normal coronary arteries, but ventriculography was demonstrative for an apical ballooning (Figure 1). Transthoracic echocardiography approved the mid-apical akinesia with basal hyperkinesia (Figure 2). Hence the possible diagnosis was takotsubo cardiomyopathy (TC), the patient was went on serial echocardiographic evaluation. On the 10th day of admission echocardiography showed nearly complete normalization of left ventricular dysfunction (Figure 3). When the patient was further questioned for possible triggers of TC, although there was no emotional or physical stres, a recent history of polymedication including antimigreine drugs and antibiotics was evident. The patient received clarithromycin 1000mg/day for the last 14 days which was prescribed for lower respiratory tract infection. She also received ergotamine tartarate 1.5mg /day for the last 5 days owing to her increased migreine headache. She was already on therapy for restless leg syndrome including pramipexole 0.25mg/day and fluoxetine 20mg/day. When the drugs she used were analyzed, ergotamine toxicity was seen as a possible etiology. Ergotamine, because of its a-adrenergic effects and extensive first pass metabolism via cytochrome p450–3A4 isoenzyme, could possibly cause such a condition in presence of concomitant use of clarithromycin and fluoxetine which were powerful inhibitors of CYP450. The proposed mechanisms of TC; coronary microvasculature vasospasm and catecholamine excess could readily be a consequence of ergotamine toxicity. Ergotamine tartrate and clarithromycin were stopped during the hospital stay. Clinical follow up was uneventful for the next 6 months with totally normal left ventricular functions. TC is a syndrome of transient cardiac dysfunction precipitated by intense emotional or physical stress. Published case reports of TC associated with drug usage consist of sympathomimetic drugs, inotropic agents, thyroid hormone, cocaine and 5 fluorouracil [1]. To the best of our knowledge the peresent case is the first defining an association between ergotamin toxicity and TC.