Objectives: Valvular heart diseases (VHD) occur frequently in Turkey. However, epidemiological studies of VHD have not been completed until now. The aim of this study is to identify the VHD type, clinical, laboratory characteristics, and treatment methods among VHD patients in Turkey. Study design: The study was conducted prospectively between June 2009 and June 2011 at 42 centers, and included patients with native VHDs, infective endocarditis, and/or previous valve interventions. Results: All medical data from 1300 patients were recorded. Mean age was 57±18 years and the female/male ratio was 1.5. VHD was native in 84% of patients, 15% had previous interventions, and 1% had infective endocarditis. Among the native VHDs, mitral regurgitation was the most frequent lesion (43%), followed by multiple VHDs (32%). Degenerative etiology (86%) was more frequent in aortic VHD, and rheumatic origin was the main cause in all VHDs. While the prevalence of aortic stenosis increased with age, mitral stenosis decreased with patient age. The most frequent symptom was shortness of breath (73%). Clinical and echocardiographic examinations (54%) were mostly used as diagnostic techniques for determining treatment course. Percutaneous mitral balloon valvuloplasty (PMBV) was performed in 76% of the patients with mitral stenosis and mechanical prosthetic valve replacement was performed in 74% of the patients with other lesions. Conclusion: This study showed that the main cause of VHD is rheumatic fever. Mitral regurgitation and multiple valvular lesions are the most frequent VHDs in Turkey. PMBV and mechanical prosthetic valve replacement are the preferred treatment methods for VHD.

Objectives: Obstructive sleep apnea syndrome (OSAS) is associated with increased cardiovascular morbidity and mortality. Platelet activation and aggregation are central processes in the pathophysiology of atherothrombosis. Mean platelet volume (MPV), a determinant of platelet activation, is a newly-emerging risk factor for atherothrombosis. Therefore, we have investigated the possible association between OSAS and MPV. Study design: We selected 30 mild, 32 moderate, and 31 severe OSAS patients and 31 healthy control subjects matched for age, sex, and body mass index. MPV was measured using an automated blood cell counter. Results: The MPV levels were significantly higher in the severe OSA group than in the control group (8.6±1.1 vs. 7.8±0.7 fl, p=0.03). There were no significant differences in respect to MPV between controls and patients with mild and moderate OSA (7.8±0.7 vs. 8.3±1.2 fl, p=0.2; 7.8±0.7 vs. 8.4±1.3 fl, p=0.08) and between patients with mild, moderate, and severe OSA (8.3±1.2 vs. 8.4±1.3 vs. 8.6±1.1 fl, p=0.9). Significant correlations were seen between MPV and apneahypopnea index (r=0.347, p≤0.001), minimal oxygen saturation (r=-0.224, p=0.03), and the percentage of recording time spent at a oxygen saturation less than 90% (r=0.240, p=0.02). Conclusion: Our results suggest that OSAS patients tend to have relatively increased platelet activation andatherothrombotic risk.

Objectives: The iso-osmolar contrast agent iodixanol may be associated with fewer contrast-induced acute kidney injuries when compared with low-osmolar contrast agents. The aim of this study is to compare iodixanol and iopamidol in patients with acute coronary syndrome (ACS) who are currently undergoing coronary angiography. Study design: Two hundred and seventy five consecutive patients who presented to a tertiary cardiovascular center with acute non-ST elevation myocardial infarction and underwent coronary angiography as a part of an early invasive strategy were included in the study (mean age 58±11 years, 79% male). Study participants were administered either iodixanol (n=45) or iopamidol (n=230) and the groups were compared for the highest creatinine levels, the absolute and percent change in creatinine levels, and for the development of contrast induced nephropathy within 72 hours of the procedure. Results: Baseline demographic and clinical characteristics of the patients were similar between the two groups. There were no differences in the preprocedural serum creatinine (iopamidol 1.10±0.54 mg/dl, iodixanol 1.09±0.24 mg/dl, p=0.680), glomerular filtration rate (iopamidol 89±35 ml/dk/1.73 m2, iodixanol 89±26 ml/dk/1.73 m2, p=0.934), or contrast volume used during the procedure (iopamidol 180±80 ml vs. iodixanol 166±73 ml, p=0.226) between the groups. The absolute change in serum creatinine after the procedure (iopamidol 0.136±0.346 mg/dl, iodixanol 0.072±0.070 mg/dl, p=0.118) and the percent change in serum creatinine after the procedure (iopamidol 12.1±29.6%, iodixanol 6.8±6.9%, p=0.075) were not statistically significant between the two groups. Contrast induced nephropathy developed 10% (95% confidence interval [CI] 6–14%) in iopamidol group whereas it was 2.2% (95% CI -2-7%) in iodixanol group (p=0.144). Conclusion: Iodixanol was not superior to iopamidol regarding contrast induced acute kidney injury after coronary angiography in an unselected general patient population with ACS.

Objectives: Pregnancy associated cardiovascular changes may result in a significant hemodynamic burden and can lead to morbidity and even mortality in women with cardiac disease. The present study aimed to evaluate clinical and echocardiographic follow-up in pregnant patients with valvular heart disease (VHD). Study design: The medical records of pregnant patients diagnosed with VHD from January 2004 to January 2011 were screened. Demographic characteristics including history of cardiac intervention performed during pregnancy, pulmonary edema, and maternal and fetal mortality, and cesarean section (C/S) history were collected from the hospital database and clinical records of the cardiology and obstetrics departments. The echocardiographic examination was carried out at presentation, 3rd trimester, and 1 month after delivery. The outcomes evaluated were cardiac intervention, pulmonary edema, and both fetal and maternal mortality during pregnancy and C/S. Results: We evaluated the outcomes of 884 pregnant patients with VHD. Adverse clinical outcomes including death, pulmonary edema, and valvular interventions were frequent among patients with severe VHD, whereas no adverse clinical outcome was observed in patients with mild-moderate VHD (n=49, 5.5% vs. n=0, 0%, p<0.001). In patients with severe VHD, clinical outcomes were frequent among patients with valve stenosis, but lower among patients with regurgitation [death 4 (0.45%) vs. 0 (0%); pulmonary edema (15 (1.7%) vs. 13 (1.5%); valvular intervention 11 (1.2%) vs. 6 (0.7%); respectively). Conclusion: Valvular heart disease is associated with fetal/ maternal morbidity and mortality. Pregnant with severe VHD constitute a high-risk group in which life-threatening complications are likely to occur in the course of pregnancy.

Objectives: Familial Mediterranean fever (FMF) is an autosomal recessive disorder and the most frequent periodic syndrome characterized by recurrent attacks of polyserositis. Heart-type fatty acid-binding protein (h-FABP) is an intracellular molecule engaged in the transport of fatty acids through the myocardial cytoplasm and a rapid marker of myocardial injury. FMF is an autoinflammatory disease characterized by ongoing inflammatory activity. Inflammation also plays an important role in the development and progression of atherosclerosis in some rheumatic diseases. We aimed to investigate markers of atherosclerosis in patients with FMF by the measurement of serum h-FABP and malondialdehyde levels (MDA).
Study design: Forty consecutive patients with FMF and twenty healthy volunteers were selected to participate in the study. The diagnosis of FMF was based on Tel-Hashomer criteria. Serum h-FABP and MDA levels were determined to examine the association.
Results: The mean h-FABP level in FMF patients was significantly higher than the normal population (4.89±0.83 vs. 3.06±2.13 ng/ml, p<0.01). The mean platelet volume was significantly higher in FMF patients than in the normal group (8.87±0.99 vs. 8.22±0.45 fl, p=0.04). Serum MDA levels were the same between the groups (1.08±0.66 vs. 1.08 ± 0.33 nmol/ ml, p=0.99). h-FABP and MDA levels were the same in FMF patients with an acute attack and during an attack free period.
Conclusion: Our results show that h-FABP increases in patients with FMF. Higher h-FABP levels may lead to increased atherosclerotic propensity in FMF, independent of the oxidative stress status of these patients.

Objectives: The aim of this study was to assess the relationship between mean platelet volume (MPV) and the presence and extent of coronary artery disease (CAD) in patients who underwent coronary angiography for stable chest pain.
Study design: A total of 540 patients (350 male, 190 female; mean age: 59.6±11.4 years) were consecutively included in the study. The patients were divided into four groups according to the presence and extent of their CAD as follows: Group 1 - patients with no significant CAD, group 2 - one vessel disease, group 3 - two vessel diseases, and group 4 - three vessel disease. Also, the Gensini score of each coronary angiogram was calculated.
Results: There were 159 patients in group 1, 169 in group 2, 110 in group 3, and 102 in group 4. As expected, we found significant differences among the groups regarding mean age and other coronary risk factors including gender, hypertension, diabetes mellitus, hyperlipidemia, smoking, and family history of ischemic heart disease. However, there were no significant differences among the groups regarding platelet counts and MPV values (8.5±0.1 fl, 8.5±1.2 fl, 8.6±0.9 fl and 8.6±0.9 fl, MPV values of groups 1-4, respectively). Although the Gensini score was found to be significantly correlated with age, plasma uric acid level, white blood cell count, hemoglobin level, fasting blood glucose, and high density lipoprotein level, no significant association was detected between MPV and Gensini score values.
Conclusion: This study is one of the largest studies assessing the relationship between MPV and the extent of coronary atherosclerosis in patients with stable CAD to date. However, we found no association between MPV and the presence and extent of coronary atherosclerosis.

A 23-year-old male who had a VDDR pacemaker implanted seven years ago due to sick sinus syndrome and recurrent syncope episodes was admitted with symptoms of dyspnea, fever, and tachycardia, which were present for a few days. He was suspected to be suffering from pneumonia and underwent computed tomography scanning of the thorax, which revealed widespread infiltration in the lung parenchyma and pulmonary emboli. Transthoracic echocardiography revealed an extremely mobile echogenic structure in the right atrium, which was determined to be the free portion of a ruptured pacemaker lead. There was an overlying thrombus and/or vegetation-like organized soft tissue within the right ventricle around the lead component. In this article, the rupture of a permanent pacemaker lead, which complicated the course of infective endocarditis associated with pulmonary embolism and pneumonia is reported. We hypothesize that the underlying mechanism for the rupture is soft tissue entrapment within the right ventricle. Unfortunately, this rare and life-threatening situation led to the death of our patient after the surgical removal of the device and its components.

Bardet-Biedl Syndrome (BBS) is a rare autosomal recessive disorder with multiple morphological abnormalities. Clinical diagnosis is based on the presence of central obesity, polydactyly, rod-cone dystrophy, varying degrees of learning disability, hypogonadism (in men) and renal abnormalities. Cardiac involvement is a rare condition. We present a 28-year-old male with complaints of progressive dyspnea and palpitation diagnosed as BBS and subaortic discrete membrane. Careful echocardiographic evaluation of patients with BBS, such as in this case report, may allow us to discover novel cardiac abnormalities in this patient population.

An aneurysm of the sinus of Valsalva (SVA) may rupture into the cardiac cavities and cause abnormal connections between these cavities and the aorta. The right atrium and/or right ventricle are the cavities into which the SVA is most commonly observed to rupture. A 30-year-old patient presented to our cardiology clinic with the complaint of dyspnea. His physical examination revealed a thrill localized in the 5th intercostal space on the right edge of the sternum and systolicdiastolic murmur beginning from the aortic focus and spreading to the neck and back along the right edge of the sternum. The echocardiographic and invasive examinations revealed two defects leading to a passage from the right sinus Valsalva to the right ventricle. While the left-to-right shunt ratio was calculated as 3.8, the anatomic locations and dimensions of the defects were found to be eligible for percutaneous closure. Using the Amplatzer Duct Occluder I device, the defects were closed in two sessions. Although the classical treatment method of ruptured SVA is surgical repair, percutaneous closure devices may be used as a reliable alternative method in suitable patients.

Pacemaker (PM)-related thrombosis is an infrequent complication of pacing. We present the case of a 58-year-old man with heart failure and atrial fibrillation who had recurrent episodes of PM lead thrombosis while undergoing anticoagulation therapy. The patient was admitted to the hospital with complaints of dyspnea and palpitation. Echocardiography revealed normal right ventricular dimensions and an enlarged left ventricle with poor contractility and an ejection fraction of 20%. Transesophageal echocardiography demonstrated a large, mobile thrombus in the right atrium that was attached to the PM lead. The patient was successfully treated with a thrombolytic agent. Genetic tests revealed that the patient was a heterozygous carrier of the methylenetetrahydrofolate reductase (MTHFR) gene mutation.

Coronary perforation is a rare complication of percutaneous coronary intervention. A 60-year-old male patient with a diagnosis of hepatocellular carcinoma was admitted to our hospital with crescendo anginal attacks. Coronary angiogram revealed significant stenosis in distal left main coronary artery (LMCA). After implanting a 4.0×18 mm coronary stent from LMCA to left anterior descending artery (LAD), coronary angiography showed a perforation in the proximal part of the LAD and a plaque shift to the osteum of circumflex artery (Cx), causing 60% stenosis. Rupture was sealed by implantation of a polytetrafluoroethylene (PTFE) coated stent in proximal LAD. Due to ongoing chest pain and electrocardiographic ischemic changes, a 3.5×18 mm coronary stent was implanted in Cx. Unfortunately, another perforation occurred in Cx. The PTFE coated stent was not flexible enough to advance from the former LMCA to LAD stent to the Cx artery, and another 3.5×18 mm coronary stent was deployed in Cx artery successfully. Although control angiography showed complete sealing of the rupture, echocardiography showed a large pericardial effusion compressing the right side of the heart. Autotransfusion was done to stabilize the hemodynamic status. One-week later, coronary angiography did not show any contrast agent extravasation. In this case, we present double coronary perforations of the LAD and Cx arteries, and successful treatment with both covered and conventional stents and autotransfusion.

Hypertrophic cardiomyopathy (HCM) is characterized by heterogeneous clinical expression. Cardiac transplantation continues to be the gold standard for the treatment of end-stage cardiac diseases refractory to medical therapy. We presented a 27-year-old female patient with HCM who underwent successful cardiac resynchronization therapy after cardiac transplantation. Our patient had an indication for standard pacing. However, previous reports have shown that right ventricular apical pacing might lead to adverse clinical outcomes in patients with heart failure. We have discussed cardiac resynchronization therapy after heart transplantation in patients with standard pacing indications.

Neurocardiogenic syncope is known to be associated with autonomic nervous system dysfunction, although the mechanism has not been entirely elucidated. In this study, we sought to highlight the pathogenic role of the autonomic nervous system in neurocardiogenic syncope and to review the associated co-morbidities known to have a dysautonomic basis. Herein we discuss migraine, orthostatic hypotension, postural orthostatic tachycardia syndrome, endothelial dysfunction, chronic fatigue syndrome, and carotid sinus hypersensitivity with a focus on the pathogenic role of the autonomic nervous system and any consecutive clinical implications. Other conditions, such as pre-syncopal heart rate acceleration and/or instability and pre-syncopal breathing instability, which occur during a tilt test, are discussed in the same perspective.

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This letter to the editor was written in order to underline some methodological problems that we thought to be present in the article entitled "Assesment of Left Ventricular Volume and Functions by Real-time three-dimensional echocardiography in patients with compansated and decompansated heart failure".