Capecitabine-induced coronary artery vasospasm in a patient who previously experienced a similar episode with fluorouracil therapy.

Capecitabine is a chemotherapeutic agent used in the treatment of metastatic colon cancer and metastatic breast cancer. It is metabolized into fluorouracil (5-FU) in the liver; hence, its mechanism of action is similar to that of 5-FU. Cardiac toxicity, although rarely seen, may be of concern in some patients. Although multiple hypotheses have been proposed for the mechanism of cardiotoxicity, coronary vasospasm is the most commonly accepted one, as patients usually present with chest pain resembling acute myocardial infarction. Electrocardiography may demonstrate ST-segment elevation, and cardiac biomarkers may be elevated. Cardiotoxicity with 5-FU has been reported widely. Capecitabine has been shown to be much less cardiotoxic compared to 5-FU, with only a handful of cases reporting cardiotoxicity with capecitabine. There are no cases reporting cardiotoxicity with both 5-FU and capecitabine in the same patient. In this case report, we present a patient with adverse cardiac effect with capecitabine whose previous 5-FU therapy was stopped due to cardiotoxicity.

New insights into the mechanisms of diastolic dysfunction in patients with type 2 diabetes.

BACKGROUND: Little is known about the role of advanced glycation end products (AGEs) and their receptor (RAGE) in diabetic cardiovascular complications. Therefore, we aimed to evaluate the association of serum soluble RAGE (sRAGE) levels and left ventricular (LV) diastolic dysfunction in patients with type 2 diabetes. METHODS: Our study consisted of 40 patients with type 2 diabetes and 40 age- and sex-matched healthy control group. Subjects with age ≥ 50 years old and any cardiovascular risk factors or conditions were excluded from the study. Serum sRAGE levels determined by enzyme-linked immunosorbent assay and LV diastolic dysfunction were evaluated according to current American Society of Echocardiography guidelines. RESULTS: Baseline characteristics were similar between groups except body mass index, waist-hip ratio, and fasting glucose levels. Serum sRAGE level was significantly lower in diabetic group compared with control group (676 ± 128 vs. 1044 ± 344, p < 0.05). Diastolic dysfunction was observed in 50% of diabetic patients (40% grade I and 10% grade II). Correlation analysis showed that serum sRAGE was negatively correlated with duration of diabetes, septal E'/A', lateral E'/A', and average E/E'. In multivariate regression analysis, serum sRAGE level was strongly associated with diastolic dysfunction in patients with type 2 diabetes. CONCLUSION: Our study showed that serum sRAGE level was significantly lower in type 2 diabetic patients aged < 50 years old. Also, sRAGE has negative correlation with the duration of diabetes and it was significantly associated with the presence of diastolic dysfunction in type 2 diabetes.

Hypoplastic left anterior descending artery associated with a single coronary artery.

Coronary artery anomalies are rarely seen in patients undergoing coronary arteriography. Single coronary artery anomaly is a rare subgroup. Hypoplastic coronary artery is a rare entity which refers to congenital underdevelopment of one or more main branches of the coronary arteries. The combination of these is extremely rare. Herein, we present a 64-year-old female case with a single coronary artery classified as type R-III with hypoplastic left anterior descending artery.

Novel cardiovascular risk factors and cardiac event predictors in female inactive systemic lupus erythematosus patients.

Systemic lupus erythematosus (SLE) is associated with severe and premature cardiovascular disease, which cannot be explained by traditional risk factors alone. This study aims to investigate novel cardiovascular risk factors and cardiac event predictors in inactive SLE female patients who do not have any major cardiovascular risk factors. Twenty-five inactive (SLE disease activity index score <4) SLE female patients and 22 healthy control women were studied. SLE patients with a history of diabetes mellitus, hypertension, hyperlipidemia, smoking, or coronary artery disease (CAD) were excluded. Venous blood samples were analyzed for lipid subfractions and novel cardiovascular risk factors such as lipoprotein (a), homocysteine, fibrinogen, high-sensitivity C-reactive protein (hs-CRP), and serum amyloid A (SAA) levels. Endothelial dysfunction was assessed by flow-mediated dilatation (FMD) from the brachial artery at baseline and during reactive hyperemia. SLE patients and controls were similar in terms of age (40+/-10 years vs 38+/-10 years, p = NS). No significant difference was found between the groups regarding family history of premature CAD, blood pressure, body mass index, lipoprotein (a), homocysteine, fibrinogen, SAA, apoprotein A-1 and B levels. Compared with the controls, SLE patients had higher levels of hs-CRP [median (range): 1.82 (0.02-0.98) vs 0.68 (0.02-0.35), p=0.04]. FMD was lower in SLE patients than controls (7.1+/-2.1 vs 11.4+/-1.2%, p<0.001). Increased levels of hs-CRP and decreased FMD were found in inactive SLE patients. Increased hs-CRP levels may reflect ongoing low-grade inflammation that could be a cause of impaired FMD in SLE patients. These findings suggest that SLE patients without traditional major cardiovascular risk factors may have increased risk of cardiovascular disease and future cardiac events.

QT interval dispersion changes according to the vessel involved during percutaneous coronary angioplasty.

Increased QT dispersion (QTd) is a noninvasive marker of an electrophysiologic abnormality associated with high mortality in coronary artery disease. The purposes of this study were to measure changes in QTd and ST-segment changes immediately before, during and after intracoronary balloon inflation and to determine whether the coronary artery vessel involved and/or the duration of inflation affect(s) QTd. A total of 45 patients (32 men, 13 women, mean age 58 +/- 11 years) who were referred for elective percutaneous transluminal coronary angioplasty were included. The mean QT interval dispersions for all patients before the inflation, during the balloon inflation at 60 sec and after the balloon deflation at 5 min were 68 +/- 13 ms, 82 +/- 16 ms and 71 +/- 13 ms, respectively. There was no significant difference between baseline and 5 min after deflation. The increase in QTd during the balloon inflation was significant (p<0.01). There was no significant QTd change in patients with left circumflex artery (Cx) lesions during inflation and after deflation compared with baseline. The differences were statistically significant only in patients with left anterior descending (LAD) lesions and right coronary artery (RCA) lesions at 60 sec during balloon inflation (p=0.001 vs. p=0.04). Acute reversible myocardial ischemia induced by balloon inflation causes an increase in QTd limited to the LAD and RCA vessels. Therefore, when using QTd as a marker of myocardial repolarization abnormality due to acute reversible ischemia, the involved coronary artery vessel must be taken into account.

Plasma soluble osteopontin concentrations are increased in patients with rheumatic mitral stenosis and associated with the severity of mitral valve calcium.

Although the severity of valvular calcification is an important prognostic indicator, the cellular mechanisms of the calcification process are unknown. Osteopontin modulates inflammation and biomineralization, and increased osteopontin expression has been demonstrated in calcified degenerative or rheumatic cardiac valves. The present study evaluated soluble plasma osteopontin in 32 patients with echocardiographically determined rheumatic mitral stenosis and compared the results to those of a control group of 22 healthy patients. Patients were evaluated with routine echocardiographic techniques, Wilkins scoring, and 2-dimensional echocardiographic calcium scoring. Patients with rheumatic involvement other than in the mitral valve were excluded. Plasma osteopontin and high-sensitivity C-reactive protein levels in patients with mitral stenosis were significantly higher those of the control group (p = 0.006 and p = 0.0001, respectively). A significant correlation was found between plasma osteopontin levels and the severity of mitral valve calcification (p = 0.003) and also between high-sensitivity C-reactive protein levels and Wilkins score (p = 0.009). There was a stepwise and statistically significant increase in soluble plasma osteopontin levels in association with the severity of mitral valve calcification. In conclusion, increased osteopontin levels were correlated with the severity of mitral valve calcification in patients with rheumatic mitral stenosis, suggesting an important role of osteopontin in the modulation of valvular calcification. Elevated levels of high-sensitivity C-reactive protein concentrations suggest the presence of ongoing inflammation in those patients.

Plasma osteopontin levels are elevated in non-ST-segment elevation acute coronary syndromes.

BACKGROUND: The regions of ruptured atherosclerotic plaques have numerous macrophages. Osteopontin that modulates macrophage function has been shown in atherosclerotic plaques. We aimed to study the plasma levels of osteopontin in patients with unstable angina or non-ST-seg ment elevation myocardial infarction (NSTEMI) and the rela tionship between osteopontin and the extent of the coronary artery disease (CAD). METHODS: We studied 65 patients with unstable angina or NSTEMI, 25 patients with stable angina and 18 patients as the control group. The extent of coronary artery stenosis was determined by the number of vessels with >50% stenosis. Plasma osteopontin concentrations were measured from the blood samples that were drawn immediately after admission to the emergency department in unstable angina/NSTEMI patients and before the coronary angiograph in the stable angina and control groups. RESULTS: The plasma osteopontin concentration was (495 118 ng/ml) significantly higher in the patients with unstable angina/NSTEMI compared to the stable angina group (319 106 ng/ml) and control group (125+/-54 ng/ml) (p=0.0001 The plasma osteopontin levels were lower in the patients with stable angina pectoris who had one-vessel disease compared to those with two-vessel disease (p=0.01). How ever, in the unstable angina/NSTEMI group, the plasma osteopontin levels were statistically not different among the patients with one-vessel, and two-vessel and three-vessel disease (p=NS). There was no correlation between the plasma osteopontin levels and the extent of coronary stenosis. CONCLUSIONS: The plasma osteopontin levels are elevatedin patients with unstable angina/NSTEMI, but there appears to be no correlation with the extent of CAD. These results ma suggest that osteopontin may have a role in the pathobiology of ACS.

Right ventricular outflow tract thrombus in a case of Behcet's disease.

Behcet's disease is known as a chronic systemic vasculitic syndrome, the hallmark of which is recurrent oral aphthous and genital ulcerations and uveitis. Vascular involvement, mainly thrombosis, reportedly affects as many as one-third of patients. Cardiac involvement, however, is very rare. We present in this report a young female patient developing right ventricular thrombus while being treated medically.

Impaired fibrinolytic capacity in rheumatic mitral stenosis with or without atrial fibrillation and nonrheumatic atrial fibrillation.

Chronic atrial fibrillation (AF) has often been associated with systemic embolization, and patients with mitral stenosis (MS) have the highest thromboembolic risk. Increased risk of thromboembolism could be in part due to impaired fibrinolytic function. Global fibrinolytic capacity (GFC) is an innovative technique for evaluating the entire fibrinolytic system. The aim of our study was to evaluate fibrinolytic activity in patients with rheumatic and nonrheumatic chronic AE To investigate fibrinolytic activity, we assessed GFC in peripheral blood samples of 32 patients with nonrheumatic AF (14 women; mean age, 56 +/- 1 years), 30 patients with rheumatic MS and AF (23 women; mean age, 35 +/- 9 years), and 32 patients with rheumatic MS and sinus rhythm (24 women; mean age, 36 +/- 8 years). The control group comprised 30 healthy adult subjects in normal sinus rhythm. Patients with chronic AF (rheumatic and nonrheumatic) had lower GFC than did the controls (P = .0001). The rheumatic AF group also showed decreased levels of GFC compared with the nonrheumatic AF group, with the rheumatic MS and sinus rhythm group, and with controls (P = .03, P = .02, P = .0001, respectively). GFC was lower in patients with rheumatic MS and sinus rhythm than in controls (P = .003). Although there were correlations between GFC and mitral valve area, transmitral mean gradient, left atrial diameter, and mitral calcification in patients with rheumatic MS, multivariate analysis showed only transmitral gradient as an independent factor affecting GFC. Patients with AF have decreased GFC, a finding that suggests the presence of a hypofibrinolytic state. Fibrinolytic dysfunction was more pronounced in rheumatic MS patients with AF than in those with nonrheumatic AF. Moreover, patients with rheumatic MS and sinus rhythm had decreased global fibrinolytic activity. Hypofibrinolysis documented by decreased GFC can be one of the important causes of increased risk of embolism in patients with AF and rheumatic MS.

Treatment of mild-to-moderate hypertension with calcium channel blockers: a multicentre comparison of once-daily nifedipine GITS with once-daily amlodipine.

BACKGROUND: Hypertension is one of the most important causes of cardiovascular disease, and treatment of hypertension leads to a significant reduction in cardiovascular mortality and morbidity. Although calcium channel blockers are regarded as an important part of the therapeutic armamentarium against cardiovascular diseases, and are among the most frequently prescribed antihypertensive medications, concern has been aroused about these drugs, particularly the short-acting dihydropyrldine derivatives. However, the value of nifedipine GITS(Adalat-Crono), the long-acting dihydropyrldine, is in need of being re-established. OBJECTIVE: To compare the effectiveness, safety and tolerability of once-daily nifedipine and amlodipine treatment in patients with mild-to-moderate essential hypertension. DESIGN: Randomised multicentre trial with an open comparison of treatments for 12 weeks, with a preceding placebo run-in period of 2 weeks (patients on beta-blockers at the time of enrollment entered a mandatory 2-week wash-out period before being allowed In the placebo run-in period;this wash-out period was one week for patients using any antihypertensive medication other than beta-blockers). SETTING: Nine centres (all university hospitals) in Turkey. PATIENTS: 155 patients with essential hypertension(diastolic blood pressure 95-109 mmHg). INTERVENTIONS: Initial treatment (step 1) consisted of 30 mg nifedipine GlTS (n = 76; (Adalat-Crono tablets), or 5 mg amlodipine (n = 79; Norvasct5-mg tablets), either administered once daily, as a morning dose, or f the blood pressure was not below 140/90 mmHg, or the reduction In diastolic blood pressure was lower than 10 mmHg after a treatment period of 6 weeks, the dose was increased (Step 2) to 60 mg once daily in the nifedipine group, or 10 mg once daily in the amlodipine group. MAIN EFFICACY PARAMETER: Diastolic blood pressure at trough after 12 weeks of active compound therapy adjusted to baseline. RESULTS: After 12 weeks of treatment, the mean diastolic blood pressure was 83.1 and 81.9 mmHg,in the nifedipine and amlodipine groups, respectively (p = 0.436). The mean decrease in systolic blood pressure (28.5 +/- 11.9 and 28.2 +/- 11.2 mmHg in the nifadipine and amlodipine groups, respectively) and the mean decrease in diastolic blood pressure (16.4A +/- 7.0 and 17.5 +/- 6.9 mmHg in the nifedipine and amlodipine groups, respectively), as well as the responder rates (88.1%and 92.1%, in the nifediplne and amlodipine groups, respectively) were comparable at the end of the study. No significant differences between groups were detected In the efficacy parameters assessed in this study. Both drugs were well tolerated. The overall incidence of adverse events was 7.9% in the nifadipine group and 10.1% In the amlodipine group. However, more patients discontinued treatment prematurely in the amlodipine group (13 patients; 19.7%), than in the nifedipine group (four patients; 5.6%). CONCLUSIONS: The results of this study demonstrated that once-daily nifedipine in GITS formation and amlodipine are comparably safe and effective treatment options in patients with mild-to-moderate essential hypertension.

Effects of short-term atorvastatin treatment on global fibrinolytic capacity, and sL-selectin and sFas levels in hyperlipidemic patients with coronary artery disease.

BACKGROUND: The beneficial effects of HMG-CoA reductase inhibitors (statins) in patients with coronary artery disease (CAD) appear to be attributable not only to their lipid-lowering properties, but also to their therapeutic effects on the coagulation system, and anti-inflammatory effect. Furthermore, statins mitigate the apoptosis of vascular smooth muscle cells (VSMC) and macrophages in atherosclerotic plaques. HYPOTHESIS: The purpose of this study was to evaluate the effects of short-term atorvastatin treatment on the fibrinolytic system and systemic inflammatory status, and on apoptosis in hyperlipidemic patients with CAD. METHODS: The study population consisted of 36 hyperlipidemic patients (14 women and 22 men, mean age 53+/-9 years) with stable CAD, untreated with lipid-lowering medications. Serum lipoproteins, fibrinogen levels, sFas and sL-selectin, and global fibrinolytic capacity (GFC) were measured at baseline and after 12 weeks of treatment with atorvastatin, 10 mg/day. RESULTS: Atorvastatin treatment decreased serum low-density lipoprotein (-39%, P=0.0001), total cholesterol (-32%, P=0.0001), and triglycerides (-22%, P=0.0001), and increased high-density lipoprotein (+13%, P=0.0001) at 12 weeks compared to baseline. These effects were associated with a decrease in plasma fibrinogen from 331+/-73 to 298+/-58 mg/dl (P=0.0001), and sL-selectin levels from 666+/-201 to 584+/-162 ng/ml (P=0.0001). sFas levels and GFC increased from 3754+/-1264 to 4873+/-1835 pg/ml and from 3.5+/-2.4 to 5.6+/-2.9 microg/ml, respectively (both P=0.0001). CONCLUSIONS: These results suggest that lipid lowering with atorvastatin therapy significantly increases GFC, decreases fibrinogen levels, and causes leukocyte deactivation. Our findings also suggest that atorvastatin treatment mitigates apoptosis of VSMC in the atherosclerotic plaque. These effects of atorvastatin may, in part, explain the early decrease in cardiovascular events observed in clinical trials of statins.

Angiotensin-converting enzyme genotype predicts valve damage in acute rheumatic fever.

BACKGROUND AND AIM OF THE STUDY: The genetic basis for host susceptibility to subsequent valve damage and scarring is not well defined in patients with a history of acute rheumatic fever (ARF). A high angiotensin-converting enzyme (ACE) activity has been demonstrated in valve tissue; hence, the study aim was to determine whether the ACE-DD genotype was a predisposing factor to heart valve damage after ARF attack. METHODS: A total of 165 patients diagnosed previously (16 +/- 5 years ago) with ARF was evaluated. Diagnoses were conducted according to Jones' criteria, and all received similar treatment and remain on regular penicillin prophylaxis. The ACE genotype was determined using polymerase chain reaction methods. RESULTS: Echocardiography showed that 39 patients (11 males, 28 females; mean age 25 +/- 6 years) had completely normal valves, and 126 patients (38 males, 88 females; mean age 21 +/- 6 years) had valve disease. The mitral valve was involved in 93% of patients (stenosis 86%, regurgitation 69%), and the aortic valve in 50% (stenosis 19%, regurgitation 48%). The ACE-DD genotype is associated with a significantly greater risk of valve involvement (risk ratio 2.7, 95% CI 1.15-6.5, p = 0.02). The distribution of genotypes was similar between aortic and mitral valve involvement. CONCLUSION: In patients with acute rheumatic fever the ACE-DD genotype is associated with an increased risk of subsequent heart valve damage.

Detection of patients with hypertrophic cardiomyopathy at risk for paroxysmal atrial fibrillation during sinus rhythm by P-wave dispersion.

BACKGROUND: Paroxysmal atrial fibrillation (PAF) in hypertrophic cardiomyopathy (HCM) is associated with poor prognosis. Previous studies have shown good correlation between P-wave dispersion (Pd) and occurrence of PAF. However, Pd in patients with HCM for predicting PAF has not been studied. HYPOTHESIS: The aim of the study was to determine whether Pd could identify patients with HCM who are likely to suffer from PAF. METHODS: Twenty-two patients with HCM with a history of PAF (Group 1) and 26 patients with HCM without a history of PAF (Group 2) were studied. Maximum (Pmax) and minimum (Pmin) P-wave durations, as well as P-wave dispersion (Pd = Pmax - Pmin) were calculated from 12-lead surface electrocardiograms (ECG). RESULTS: P-wave dispersion was significantly different between the groups (Group 1: 55 +/- 6 ms vs. Group 2: 37 +/- 8 ms; p<0.001), while Pmax (Group 1: 134 +/- 11 ms vs. Group 2: 128 +/- 13 ms; p = 0.06) and Pmin (Group 1: 78 +/- 9 ms vs. Group 2: 81 +/- 7 ms; p = 0.07) was not significantly different. Patients with a history of PAF had higher left atrial diameter than the patients without PAF (Group 1: 52 +/- 8 mm vs. Group 2: 48 +/- 10 mm; p = 0.02). A cut-off value of 46 ms for Pd had a sensitivity of 76% and a specificity of 82% in discriminating between patients with and without PAF. CONCLUSION: This study suggests that P-wave dispersion could identify patients with HCM who are likely to develop PAF.

Diminished global fibrinolytic capacity in patients with mitral valve prolapse is associated with transient ischemic attacks.

Although mitral valve prolapse (MVP) has shown to be associated with thromboembolic complications, the cause of thromboembolic events in those patients is still unknown. The purpose of this study was to evaluate the fibrinolytic activity in MVP patients. The study included 35 consecutive patients (25 women, mean age 25+/-11 years) with echocardiographically documented MVP and 25 age- and sex-matched subjects as a control group. Four of MVP patients have a history of transient ischemic attack (TIA). Global fibrinolytic capacity (GFC), a new technique that examines the effectiveness of the entire fibrinolytic system, was measured. Global fibrinolytic capacity was found to be nonsignificantly increased in MVP patients (3.14+/-1.42 microg/mL) compared to those in control subjects (2.36+/-1.33 microg/mL) (p>0.05). However, in four of these MVP patients who had a history of transient ischemic attack, the GFC level was significantly lower than in patients who have no history of transient ischemic attack (1.67+/-0.6 microg/mL vs 3.27+/-1.46 (microg/mL, p=0.003). Furthermore, the GFC levels of these four patients were less than those of controls (p=0.04). These results showed that global fibrinolytic activity was similar in MVP patients without a history of TIA and control subjects. However, MVP patients with a history of TIA had significantly decreased global fibrinolytic activity compared to controls and as well as MVP patients without a history of TIA.

Prevalence of coronary artery disease before valvular surgery in patients with rheumatic valvular disease.

BACKGROUND: Although many patients with valvular heart disease have concomitant coronary artery disease (CAD), there are limited data on the association between rheumatic valvular disease (RVD) and CAD. In this study, we aimed to investigate the prevalence of CAD in a group of patients with RVD and undergoing coronary angiography before valvular surgery. METHODS: In this retrospective analysis, we enrolled a total of 1075 patients (658 women, 61.2%; mean age: 53.2 ± 9.9 years) who underwent coronary angiography for the evaluation of CAD before valvular surgery between January 2003 and May 2010. RESULTS: The overall prevalence of significant CAD was 11.1%. Patients with significant CAD were older than patients without significant CAD (55.16 ± 10.4 vs. 51.45 ± 9.1; P<0.001). In addition, hypertension, smoking, diabetes mellitus, and dyslipidemia were more prevalent among patients with significant CAD (P<0.05). After adjustment for several risk factors, only aortic stenosis remained the predictor of significant CAD (odds ratio: 1.66; 95% confidence interval: 1.26-2.19; P<0.001). However, aortic regurgitation was inversely associated with the presence of CAD (odds ratio: 0.56; 95% confidence interval: 0.21-1.01; P<0.001). CONCLUSION: The overall prevalence of CAD in our population with RVD was low. Rheumatic aortic stenosis is associated with an increased prevalence of CAD, whereas the prevalence of CAD is lower in those patients with aortic regurgitation.

Diagnostic accuracy and clinical utility of echocardiographic indices for detecting left ventricular diastolic dysfunction in patients with coronary artery disease and normal ejection fraction.

OBJECTIVE: The aim of present study was to assess the clinical utility and diagnostic accuracy of diastolic dysfunction criteria that were recommended in current American Society of Echocardiography and European Association of Echocardiography recommendations for prediction of increased LVEDP (>16 mmHg) in patients with coronary artery disease and normal EF. METHODS: Forty-five consecutive patients (mean age=61.5±10.3 years) referred for cardiac catheterization were enrolled in this prospective study. All patients underwent transthoracic echocardiography and tissue Doppler imaging within 24 hours before cardiac catheterization. Patients were divided into 2 groups according to left ventricular end diastolic pressure (LVEDP) (LVEDP>16 mmHg, n=23; LVEDP≤16 mmHg, n=22). Receiver operating characteristics curve analyses were performed and sensitivity, specificity, positive predictive value and negative predictive value were calculated for indices to detect high LVEDP. RESULTS: Among the indices, left atrial volume index (LAVI) ≥34 ml/m2 (sensitivity=60.0% and specificity=90.0%) and ratio of transmitral to septal annular velocities during early filling (septal E/e' ratio) ≥15 (sensitivity=30.4% and specificity=95.5%) had more reasonable sensitivity and specificity. Receiver operating characteristics curve analysis revealed that best predictors of high LVEDP were septal E/e' [area under curve (AUC)=0.694, standard error (SE)=0.66, p=0.01] and LAVI (AUC=0.669, SE=0.63, p=0.045]. There were statistically significant correlations between LVEDP and septal E/e' (r=0.541, p=0.001) and LAVI (r=0.461, p=0.002). A proposed algorithm consisting LAVI ≥34 ml/m2 and septal E/e' >8 could determine diastolic dysfunction with a 95.6% sensitivity and 54.5% specificity. CONCLUSION: Septal E/e' (≥15) and LAVI (≥ 34 ml/m2) were the better predictors of the increased LVEDP than the other echocardiographic parameters. There were statistically significant moderate positive correlations of LVEDP with septal E/ e' and LAVI. Combination of LAVI and septal E/e' is useful to detect diastolic dysfunction.

[Mean systolic annular velocity and strain score index: new and non-invasive parameters for the evaluation of acute myocardial infarction patients]. / Ortalama sistolik anüler velosite ve strain skor indeksi: akut miyokart enfarktüsü hastalarinin degerlendirilmesinde yeni ve invazif olmayan parametreler.

OBJECTIVE: To evaluate the diagnostic value of mean annular velocity (MAV) and strain score index (SSI) for determination of the left ventricular systolic dysfunction in patients with first acute myocardial infarction (AMI). METHODS: Seventy-one patients (55 male, mean age: 59+/-12 years) with first acute ST-elevation myocardial infarction and 30 healthy subjects were included in this cross-sectional and observational study. Echocardiography with tissue Doppler and strain analysis was performed during initial hospital admission. Peak systolic myocardial velocities were recorded from 4 different sites on the mitral annulus. A MAV value was calculated and the peak systolic strain values of 12 segments were measured and a mean SSI was calculated. ROC curve analysis was used in order to determine cut-off values for MAV and SSI. RESULTS: The patients with AMI had a significantly reduced MAV compared with healthy subjects (5.52+/-1.78 cm/s vs 9.80+/-1.13 cm/s, p<0.001). In ROC analysis, a cut-off value of 8.41 cm/s (AUC 0.915, 95%CI 0.887-0.952, p<0.001) for MAV differentiated AMI patients from controls with 97.2% sensitivity and 93.3% specificity. The patients with AMI have also decreased SSI (11.23+/-2.83 vs 19.11+/-2.05, p<0.001). A cut-off value of 15.35% differentiated AMI patients from controls with 94.4% sensitivity and 100% specificity (ROC AUC 0.945, 95%CI 0.901-0.972, p<0.001). There was a good correlation between left ventricular EF and MAV (r=0.73, p<0.001) and SSI (r=0.66, p<0.001). CONCLUSION: The patients with first myocardial infarction have decreased mean systolic annular velocity and mean systolic strain score index.

Multiple coronary artery aneurysm formation one year and four years after sirolimus-eluting coronary stent implantation.

A 61 years old male patient having the complaint of angina pectoris underwent coronary angiography that revealed critical luminal stenosis at left anterior descending artery (LAD) and diagonal branch. Percutaneous transluminal coronary angioplasty was performed and sirolimus eluting stents (CYPHER; Johnson & Johnson--Cordis) 2.75 x 10 mm and 2.75 x 10 mm were deployed respectively. One year after the procedure coronary angiography revealed coronary artery aneurysm (CAA) formation in diagonal branch and mild ectasia in LAD stent area. Last coronary angiography four years and three months after initial intervention showed multiple CAA at diagonal branch and LAD. This case report is an example of late formation of CAA by sirolimus-coated coronary stent.

[The early predictors of ventricular remodeling after myocardial infarction: the role of tumor necrosis factor-alpha]. / Akut miyokard infarktüsü sonrasi ventriküler yeniden biçimlenme erken belirleyicileri: Tümör nekrozis faktör-alfa'nin rolü.

OBJECTIVE: Ventricular remodeling (VR) is a pathologic process characterized by progressive ventricular dilatation occurring after acute myocardial infarction (MI) leading to left ventricular systolic dysfunction. The purpose of the study was to evaluate the efficacy of plasma tumor necrosis factor alpha (TNF-alpha) levels to predict the left VR. METHODS: This prospective observational cohort study included 72 consecutive patients with newly diagnosed MI with age ranging between 38-87 years (mean 59 +/- 12 years). Control group was consisted of 30 patients with no additional systemic disease and normal coronary arteriograms. Transthoracic echocardiography was performed to all patients and controls both in the beginning of the study and in the 6th follow-up. A coronary arteriography was also performed to all patients. Patients with an increment in the diastolic volume index more than 20% in the follow-up compared with basal values included in the VR subgroup. The patient subgroup with VR consisted of 19 patients. Statistical analyses were performed using ANOVA and Kruskal Wallis tests for comparison of variables between groups. Logistic regression and ROC analyses were used for evaluation of accuracy of TNF-alpha in prediction of VR. RESULTS: There were no significant differences between groups according to demographic characters. The basal plasma levels of TNF-alpha were higher in the patient subgroup with VR as compared with patients without VR and controls (14.59 +/- 4.28 pg/ml vs 7.30 +/- 4.48 pg/ml, and 1.64 +/- 1.49 pg/ml, p< 0.001). In logistic regression analysis only TNF-alpha predicted the VR (OR-1.356, 95% CI 1.117-1.647). Plasma TNF-alpha levels with a cut-off > or = 10.33 pg/ml were found to have 89.5% sensitivity and 79.3% specificity to predict the development of VR. CONCLUSION: These results demonstrate the increment of plasma TNF-alpha levels in the acute phase of MI and the close relationship between the TNF-alpha levels and VR in the patients with first MI.