Objectives: The aim of this study was to evaluate atrial electromechanical delay measured by tissue Doppler imaging (TDI) and left atrial (LA) mechanical functions in patients with rheumatoid arthritis (RA).
Study design: The study included 68 patients (53 females, 15 males; mean age 43.7 years) with RA. Using TDI, atrial electromechanical coupling (PA) was measured from the lateral mitral annulus (PA lateral), septal mitral annulus (PA septum), and right ventricular tricuspid annulus (PA tricuspid). Left atrial volumes (maximal, minimal, and pre-systolic) were measured by the method of discs in the apical four-chamber view and were indexed to body surface area. Mechanical function parameters of the LA were calculated. The results were compared with those of 41 age- and gender-matched healthy volunteers (32 females, 9 males; mean age 41.9 years).
Results: Patients with RA had significantly prolonged PA lateral, PA septum, and intra- (PA septum-PA tricuspid) and interatrial (PA lateral-PA tricuspid) electromechanical delays compared to controls (p<0.0001, p=0.05, p<0.0001, and p<0.0001, respectively). Left atrial volumes were similar in the two groups (p>0.05). Left atrial passive emptying fraction was significantly decreased, LA active emptying volume and active emptying fraction were increased in RA patients (p=0.05, p=0.01, and p<0.0001; respectively). Interatrial electromechanical delay was correlated with systolic blood pressure (r=0.20, p=0.04), left ventricular mass index (r=0.22, p=0.02), C-reactive protein (CRP) (r=0.27, p=0.005), and LA active emptying fraction (r=0.29, p=0.002). In linear regression analysis, LA active emptying fraction and CRP were independent variables of interatrial electromechanical delay (β=0.28, p=0.002 and β=0.25, p=0.006, respectively).
Conclusion: Prolonged electromechanical delays and impaired LA mechanical functions may be an early manifestation of subclinical cardiac involvement in RA patients.

Objectives: Both metabolic syndrome (MetS) and nondipping status (insufficient reduction in nocturnal blood pressure) have been linked with target organ damage. We evaluated the effect of nondipping status on target organ damage in subjects with MetS.
Study design: Eighty-two patients diagnosed as having MetS were divided into two groups according to the findings of 24-hour ambulatory blood pressure monitoring as dipper (n=35, 19 women, 16 men; mean age 48.4±6.4 years) and nondipper (n=47, 35 women, 12 men; mean age 50.4±4.7 years). Cardiac damage was assessed by conventional and tissue Doppler echocardiography, and renal damage by 24-hour urinary albumin excretion.
Results: The two groups were similar with regard to age, body mass index, presence of diabetes, smoking, clinical and 24-hour, daytime and nighttime blood pressures, plasma lipid profile, distribution of and the mean total number of MetS criteria. The ratio of early (Em) to late (Am) left ventricular peak diastolic myocardial velocities (Em/Am) was significantly lower in nondippers (p=0.016). Nondippers also had higher values of left ventricular mass index, myocardial performance index, and 24-hour urinary albumin excretion, but these differences did not reach a significant level (p=0.110, p=0.099, p=0.093, respectively). Multivariate regression analysis showed increasing age and nondipping status as independent factors associated with decreased Em/Am ratio (β=-0.25, p=0.020 and β=-0.22, p=0.042, respectively).
Conclusion: In subjects with MetS, nondipping status may be associated with both cardiac and renal damage independent of other components of MetS. Since the degree of diastolic dysfunction is more marked than that of albuminuria in nondippers, it may be extrapolated that the extent of cardiac damage surpasses renal damage in these subjects.

Objectives: Aspirin is recommended for primary prevention in patients with metabolic syndrome (MetS). In this study, we evaluated aspirin resistance in MetS patients.
Study design: The study included 32 patients (23 males, 9 females; mean age 60.7±11.4 years) with the diagnosis of MetS, according to the criteria of the International Diabetes Federation. Aspirin resistance was determined by the PFA-100 analysis (Platelet Function Analyzer). The results were compared with a control group of 30 patients (16 males, 14 females; mean age 61.6±7.3 years) without MetS. All the patients were taking aspirin at the time of the PFA-100 analysis.
Results: Overall, 21 patients (33.9%) were aspirin nonresponders. The prevalence of aspirin resistance was 46.9% in the MetS group, and 20% in the control group. The difference between the two groups was statistically significant (p=0.033). Compared to aspirin responders, fasting blood glucose level was higher (102.0±14.6 mg/ dl vs. 95.3±9.9 mg/dl; p=0.036) and waist circumference tended to be greater in nonresponders (97.4±14.1 cm vs. 89.7±15.0 cm; p=0.053). Multivariate logistic regression analysis showed that MetS (OR 0.28, 95% CI 0.09- 0.88; p=0.029), fasting blood glucose (OR 0.95, 95% CI 0.91-0.99; p=0.045), uric acid (OR 0.46, 95% CI 0.28- 0.76; p=0.002), gamma-glutamyl transferase (OR 1.04, 95% CI 1.00-1.08; p=0.043), high-sensitivity C-reactive protein (OR 1.07, 95% CI 1.01-1.12; p=0.015) levels and platelet count (OR 0.99, 95% CI 0.98-0.99; p=0.034) significantly affected aspirin resistance. Conclusion: Our results show that a significant proportion of MetS patients will not benefit from aspirin use due to high aspirin resistance.

Objectives: It has been shown that serum uric acid (SUA) constitutes an important independent risk factor for cardiovascular disease. We investigated SUA levels in patients with coronary artery ectasia (CAE).
Study design: Serum uric acid levels were measured in three groups of patients who underwent coronary angiography. One group consisted of 97 consecutive patients (69 males, 28 females; mean age 58.1±9.5 years) with isolated CAE, another group included 104 patients (79 males, 25 females; mean age 58.4±8.8 years) with coronary artery disease (CAD), and finally 90 subjects (66 males, 24 females; mean age 57.6±10.1 years) with normal coronary arteries comprised the control group. Coronary artery ectasia was defined as a luminal dilatation of at least 1.5 times of the adjacent normal coronary segments, without any stenotic lesions. In addition, patients with CAE were assessed in four groups of severity and extension.
Results: The three groups were similar with respect to age, sex, body mass index, and the frequencies of hypertension, diabetes mellitus, and smoking (p>0.05). The mean SUA level did not differ significantly between the CAE and CAD groups (6.6±1.9 mg/dl and 6.3±1.9 mg/dl, respectively; p=0.184); however, compared with the control group (5.4±1.8 mg/dl), SUA levels were significantly higher in both groups (p<0.001). A significant correlation was found between the SUA level and the presence of isolated CAE (r=0.625; p<0.001). Multivariate logistic regression analysis showed an independent relationship between isolated CAE and SUA (OR 1.896; 95% CI 1.1048-1.5014; p<0.001). Serum uric acid levels did not differ significantly among the four subgroups of CAE severity.
Conclusion: Our study is the first to demonstrate significantly increased SUA levels in patients with isolated CAE. Our results support relevant data suggesting an association between endothelial function and the SUA level.

Objectives: Paraoxonase (PON1) is a high-density lipoprotein (HDL)-associated esterase that hydrolyses lipoperoxides. PON1 serves as a protective factor against oxidative modification of LDL, suggesting that it may play an important role in the prevention of atherosclerotic process. Research has focused on two polymorphisms: leucine (L allele) to methionine (M allele) substitution at codon 55, and glutamine (A allele) to arginine (B allele) substitution at codon 192.
Study design: We examined amino acid changes at codon 55 and 192 in the PON1 gene by polymerase chain reaction and using restriction enzymes in 120 patients (92 men, 28 women; mean age 48.2±4.3 years) with premature coronary artery disease (CAD) and in 102 healthy subjects (80 men, 22 women; mean age 46.8±5.2 years) with no history of CAD and a normal electrocardiogram.
Results: Distribution of genotypes in the patient and control groups at codon 55 were 6.7% and 4.9% for MM, 46.7% and 29.4% for LM, 46.7% and 65.7% for LL, respectively. The frequency of genotypes at codon 192 were as follows: 4.2% and 2% for RR, 40% and 35.3% for QR, and 55.8% and 62.8% for QQ, respectively. While the frequency of PON1 55M allele was higher in the CAD group (0.3 vs. 0.2), PON1 192R allele frequency did not differ (0.2). There was a significant relationship between the PON1 M/L55 polymorphism and CAD (p=0.017), whereas the R/Q192 polymorphism was not associated with CAD (p=0.445).
Conclusion: These data suggest that the PON1 M/L55 polymorphism shows a significant relationship with CAD and the Q/R192 polymorphism is not a major risk factor causing susceptibility to CAD in our population.

We present asymptomatic right atrial myxoma in a patient with breast ductal adenocarcinoma. A 58-year-old female was referred to our clinic for the evaluation of the potential cardiotoxic side effects of anthracycline-based chemotherapy. She had a 10-month history of modified radical mastectomy for ductal adenocarcinoma of the breast, followed by adjuvant chemotherapy. To evaluate potential side effects of anthracycline-based regimen, transthoracic echocardiography was performed, which showed a highly mobile, cystic, and heterogenous mass, 20x25 mm in size, located in the right atrium. Transesophageal echocardiography confirmed the highly mobile mass originating from the inferior vena cava and extending to the right atrium. Surgery was planned. Upon exposure, the tumor had a broad base, with attachment to the lower dorsal free wall, interatrial septum of the right atrial cavity, and upper border of the inferior vena cava. The tumor was completely excised and histopathologic diagnosis was myxoma. Localization of right atrial myxoma at the junction of the inferior vena cava and right atrium is a rare condition, and its coexistence with breast carcinoma has only been reported once.

We report on the use of multidetector computed tomography (MDCT) in the diagnosis of prosthetic heart valve thrombosis and a giant left atrial (LA) thrombus extending into the LA appendage (LAA), in comparison with findings of transesophageal echocardiography (TEE). A 52-year-old woman with an eight-year history of mechanical mitral valve (MMV) replacement presented with progressive dyspnea. The electrocardiogram (ECG) showed atrial fibrillation. Transesophageal echocardiography showed severely increased MMV gradients and decreased MMV area. Two thrombi were identified on the atrial aspect of the MMV, one restricting the motion of the lateral leaflet, and the other localized on the septal side of the valve ring. Two other thrombi were also visualized, one in the LA and the other in the LAA, measuring 4.3x1.3 cm and 2.1x1 cm, respectively. ECG-gated 64-slice contrast-enhanced MDCT depicted a thrombus, involving both atrial and ventricular aspects of the MMV, and also a giant thrombus, 8.3x2.4 cm in size, in the LA extending into the LAA. The patient underwent redo-mitral valve replacement, LA thrombectomy, and LAA ligation, and was discharged uneventfully. The size and localization of thrombi in the LA and on the explant MMV matched to the findings of MDCT. In this case, MDCT was superior to TEE in showing the precise nature of both MMV thrombosis and the integrated thrombus involving the LA and LAA.

Reel syndrome is a rare form of Twiddler’s syndrome and is characterized by rotation of permanent pacemaker on its transverse axis and rolling of the electrode around the generator. An 83-year-old man with severely impaired mental status, agitation, and uncontrolled movement of extremities underwent pacemaker implantation for symptomatic atrial fibrillation. The pacemaker generator was fixed to the pectoral fascia with nonabsorbable ligatures. On the next day, failure to capture the ventricle was noted. Fluoroscopic examination showed coiling of the electrode around the generator. During urgent intervention, the ligature of the generator was observed to be released from the pectoral fascia. The pacemaker lead was not damaged; therefore, the same lead was re-implanted, connected to the generator, and carefully fixed to the pectoral fascia. The patient showed rapid clinical improvement together with his mental status. No abnormality was detected during three months of follow-up. Patients with impaired consciousness, children, and older persons require a close follow-up because of their propensity to this serious and life-threatening complication.

Bicuspid aortic valve is one of the most common congenital heart valve disorders. We present the development of acute myocardial infarction (AMI) in an 18-year-old male patient with unrecognized bicuspid aortic valve and moderate aortic regurgitation. He presented with chest pain. The electrocardiogram showed ST-segment elevation in leads V2 to V6. Creatine kinase-MB level was elevated to 97 U/l and troponin I was very high (45,000 ng/ml). The diagnosis was made as anterior wall AMI. Following treatment with intravenous rt-PA, ST-segment elevation completely returned to normal. Transthoracic echocardiography showed a bicuspid aortic valve, moderate aortic regurgitation, and apical wall hypokinesia; left ventricular global systolic function was normal. The patient had no risk factors for coronary atherosclerosis, nor a history of substance addiction or a family history of coronary artery disease. Protein C, protein S and homocysteine levels were normal. He refused any further intervention. Two weeks after discharge, he presented again with chest pain. Electrocardiography, cardiac markers, and coronary arteriography were normal. He was discharged on appropriate medical treatment. The presented case is the first report of AMI in a patient with bicuspid aortic valve

We present a 36-year-old male patient with a previous diagnosis (22 years) of Eisenmenger’s syndrome, who had a giant proximal pulmonary artery aneurysm complicated by massive thrombus formation. The patient had been experiencing paroxysmal atrial fibrillation attacks for the past month. His functional capacity was of New York Heart Association class III. Chest radiography showed aneurysmal dilatation in the left pulmonary artery. The patient was assessed by transthoracic echocardiography and multislice computed tomography. There was mild narrowing in the thick and calcified pulmonary valve (peak systolic gradient 35 mmHg) and moderate regurgitation. The mean pulmonary artery pressure was estimated at 50 mmHg. The diameters of the main, left, and right pulmonary arteries were 6.5 cm, 10 cm, and 3.7 cm, respectively. There was a massive thrombus in the aneurysmal left pulmonary artery. The patient was referred to the cardiovascular surgery department for pulmonary artery reconstruction and cardiopulmonary transplantation. In addition, medical treatment was instituted with warfarin for thrombus and paroxysmal atrial fibrillation, metoprolol for atrial fibrillation, and bosentan for pulmonary hypertension. The patient’s functional capacity showed improvement after the first month of medical treatment and no complications were seen within a year follow-up.

Capsaicin is the active component of chili peppers, which has been shown to possess several beneficial effects. Currently, the best-known medical use of capsaicin is as a topical painkiller. Drug-induced myocardial infarction is not a common phenomenon and the underlying mechanism has been related with coronary spasm in the majority of cases. We present a 29-year-old man who experienced coronary vasospasm and acute myocardial infarction (AMI) which were possibly induced by the use of a topical capsaicin patch to relieve lumbago. He presented with chest pain of one hour onset. The electrocardiogram showed ST-segment elevation in the leads II, III, and aVF, consistent with inferior wall AMI. Echocardiography confirmed inferior hypokinesia. Urgent coronary angiography showed normal right and left coronary arteries. Since he had no cardiac risk factors for coronary artery disease, nor a history of recent emotional or physical stress, or ingestion of any illicit substance, the vasospasm and subsequent AMI was attributed to the use of the capsaicin patch for six days. Upon institution of appropriate treatment and removal of the patch, no new anginal attacks or ischemic episodes were seen within a follow-up of one month. This is the first case report of AMI induced by the use of a topical capsaicin patch.

It is well-known that statin therapy results in significant reductions in cardiovascular morbidity and mortality in patients with hyperlipidemia and coronary heart disease. Findings of observational studies on lipids and heart failure demonstrate that statins prevent the development of heart failure and decrease heart failure-related mortality and hospitalization. It is not clear, however, whether these beneficial effects result from their lipid-lowering actions or pleiotropic actions. Besides, some of the effects of statins (e.g. decreasing coenzyme Q and selenoprotein levels) may lead to adverse consequences. Two studies yielded significant information on the efficacy and safety of statins in patients with heart failure: the CORONA study included patients with ischemic heart failure and the GISSI-HF study included patients with heart failure of any cause. In both studies, 10 mg rosuvastatin reduced blood cholesterol and inflammatory parameters without any effect on mortality. In addition, rosuvastatin caused a decrease in the rate of hospitalization in the CORONA study. Both of these studies are important to demonstrate that rosuvastatin might be safe in patients with heart failure.