Ziya Simsek

Evaluation of left ventricular function with strain/strain rate imaging in patients with rheumatic mitral stenosis

OBJECTIVE The most important sequel of acute rheumatic fever is mitral stenosis in long-term. The aim of the study is to determine left ventricular (LV) functions by tissue Doppler imaging (TDI) and strain/strain rate echocardiography (SE/SRE) in mitral stenosis patients who had no clinical signs of heart failure. METHODS Our study was designed as cross-sectional study. The study population consisted of 32 patients with isolated mitral stenosis and mitral valve area = 2.0 cm(2) (Group 1) and 25 healthy control subjects (Group 2). In addition to standard echocardiographic methods, TDI and SE/SRE were performed to assess LV functions in all participants. Students t-test was used to compare continuous variables. Fisher- exact test was used to compare categorical variables. RESULTS Systolic myocardial velocity (Sm) were significantly lower in Group 1 than in Group 2 (6.0+/-1.4 cm/sec vs 7.9+/-1.8 cm/sec, p=0.001) also, early diastolic myocardial velocity (Em) were significantly lower in Group 1 than in Group 2 (4.4+/-1.5 cm/sec vs 10.8+/-2.1 cm/sec, p=0.001). But there was no significant difference in late diastolic myocardial velocity (Am) between two groups. Peak systolic strain and strain rate of septal wall in Group 1 were significantly lower than Group 2 (p=0.001 for both). Besides, peak systolic strain and strain rate of lateral wall in Group 1 were significantly lower than in Group 2 (p=0.001 for both). CONCLUSION Although, global ejection fraction was normal and there were no symptoms of heart failure clinically in the patients with mitral stenosis, LV dysfunction demonstrated that using by echocardiography. TDI and strain/strain rate imaging to be new echocardiographic methods may be used reliably for detection LV function in early stage of mitral stenosis.

Quantitative assessment of the left atrial myocardial deformation in patients with chronic mitral regurgitation by strain and strain rate imaging: an observational study

OBJECTIVE We evaluated regional left atrial (LA) myocardial deformations by strain (S) and strain rate (SR) imaging during LA pump, reservoir, and conduit phases in patients with chronic rheumatic mitral regurgitation (MR). METHODS This cross-sectional observational study included 42 patients with moderate-to-severe MR who had normal left ventricular (LV) function, and 36 healthy control subjects. Conventional echocardiographic data were used to calculate LV and LA dimensions, volumes and functional indices (LA ejection fraction, LA active and passive emptying fraction). Longitudinal S/SR indices of the mid and superior segments of LA walls were measured during the three LA phases. Student t-test, Mann-Whitney U test, Chi-square test and Bland-Altman analysis were used for statistical analysis. RESULTS LV systolic functions were similar in the patient and control groups. LV diameters, LA diameters and LA volumes were greater in the patient group compared with the control group (p<0.05, p<0.001, and p<0.001). LA ejection fraction and LA active emptying fraction values were lower in the patient group than in the control group (56 ± 7 vs. 63 ± 5%, 33 ± 9 vs. 40 ± 4%, p<0.05 for both). During the three LA phases, longitudinal S/SR values were significantly lower in all the segments in the patient group compared with the control group (p<0.001 for S, p<0.001 and p<0.05 for SR). CONCLUSION Regional LA longitudinal myocardial deformations are observed to be impaired during all the mechanical phases in patients with moderate-to-severe MR. Volume overload, remodeling and rheumatic effects may be responsible for the LA myocardial dysfunction in these patients.

Uric acid levels and atrial fibrillation.

We read the article entitled ‘‘Serum uric acid levels are associated with atrial fibrillation in patients with ischemic heart failure’’ by Tekin et al with interest. They evaluated the association between serum uric acid (SUA) and atrial fibrillation (AF) in patients with chronic heart failure (HF). Patients with AF had significantly higher SUA levels, and this was independently associated with AF in patients with ischemic HF. We have some comments about this study. Both AF and HF share common risk factors and frequently coexist. Hypertension is a well-known risk factor for AF. In the Tekin et al study, the number of patients with hypertension in the AF group was low. In addition, there are data to support an association between inflammation and AF. C-reactive protein and fibrinogen are rapid, reliable, and noninvasive tests. The study would be stronger if Tekin et al measured these markers and carried out a correlation analysis between SUA and AF with these markers in their study. Tekin et al did not explain how they defined and measured the SUA levels. Although left atrium (LA) size seems to reflect left ventricular diastolic dysfunction, they could also assess other specific indexes of ventricular diastolic function. Furthermore, they did not provide data on the body mass index (BMI) that is related to the LA size. Uric acid is often elevated in patients with HF. Gotsman et al found that younger age, male gender, diabetes, BMI, urea, reduced glomerular filtration rate, treatment with furosemide, thiazide, spironolactone, b-blocker, and angiotensin-converting enzyme inhibitor/angiotensin receptor blocker were predictive of an increased SUA level. Tekin et al did not define the standard medical treatment. Because many drugs can affect SUA levels, it would be useful if the authors provided data about the usage of drug classes other than diuretics. Also, there is no information about the usage of statins in patients with hyperlipidemia, and they did not denote any distinction between the groups for acute or chronic HF.

Can Left Atrial Strain and Strain Rate Imaging Be Used to Assess Left Atrial Appendage Function

Background: The aim of this study was to evaluate the efficiency of left atrial strain (S) and strain rate (SR) imaging in assessing left atrial appendage (LAA) function. Methods: We studied 78 consecutive patients (35 females and 43 males; mean age 38 ± 15 years) referred for transesophageal echocardiography (TEE). LAA late emptying velocity (LAA-EV) was calculated. Real-time color Doppler myocardial velocity imaging (MVI) data were recorded from the LAA by TEE and the lateral wall of the left atrium (LA) by transthoracic echocardiography. Longitudinal S and SR were measured in the mid portion of the lateral LA wall and lateral LAA wall during the contractile period. LAA late systolic velocity (LSV) and LA-LSV were obtained from Doppler analysis. Results: A significant positive correlation was detected between LAA-EV and MVI parameters (for LAA-S, r = 0.88, p < 0.001; for LAA-SR, r = 0.84, p < 0.001; for LAA-LSV, r = 0.83, p < 0.001; for LA-S, r = 0.84, p < 0.001; for LA-SR, r = 0.79, p < 0.001, and for LA-LSV, r = 0.70, p < 0.001). In addition, a significant positive correlation was detected between LAA-S and LA-S (r = 0.85, p < 0.001). Conclusion: We suggest that LA-S and LA-SR imaging is a beneficial method to evaluate LAA functions noninvasively.

A rare case of isolated complete congenital sternal cleft

A 20-year-old male soldier presented to our clinic with complaints of dyspnea on exertion, pain and clash at the upper part of the sternum while he was carrying a heavy object for 4 years. His past medical history was unremarkable. He was non-smoker and working at furniture store. There were no intermarriage and inherited diseases in his family. On his physical examination, vital signs were in normal limits. On respiratory system examination, a wide gap at the upper part of the sternum was observed. Pulsations of the heart could easily be seen through the sternal abnormality. Bulging was seen clearly between sternal parts throughout the defect while patient was coughing. There was no abnormal lung and heart sounds on auscultation. Abdominal raphe was present between umbilicus and lower part of the sternum (Fig.1, Video 1. See corresponding video/movie images at www.anakarder.com). Other system examinations were unremarkable. Laboratory examinations were within the normal limits. Chest X-ray and thorax computed tomography (CT) showed complete fusion defect with a 4 cm in diameter of upper 2/3 and lesser than 1 cm in diameter of lower 1/3 of the sternal part of anterior chest wall (Fig. 2). Pulmonary function test was in normal limits. Echocardiography, abdominal ultrasonography and cranial CT did not reveal any coexisting abnormalities. Patient was diagnosed as an ‘isolated complete congenital sternal cleft’ and was referred to a superior center for surgical repair of the defect. Ersin Günay, Ziya Şimşek*, Gökhan Güneren**, Fatih Çelikyay*** From Clinics of Chest Diseases, *Cardiology, **Thoracic Surgery and ***Department of Radiology, Girne Military Hospital, Girne, Turkish Republic of Northern Cyprus

Impact of insulin resistance on contrast induced nephropathy in patients undergoing percutaneous coronary intervention

Contrast-induced nephropathy (CIN) is a common complication following percutaneous coronary intervention (PCI). Contrast-induced nephropathy after emergency PCI in subjects with insulin resistance (IR) has not been studied before. In this prospective study we determined the relation between IR on CIN, among those undergoing PCI due to acute coronary syndrome. One hundred twenty four consecutive acute coronary syndrome patients with diabetes (N = 44), insulin resistance (N = 38) and normal glycemic metabolism (N = 42) were included in the study. They were all treated with PCI. Pre- and post procedural creatinines were measured and independent predictors of CIN were analyzed. IR was defined as a HOMA level (HOMA-IR = Serum Glucose (mg/dL) X Plasma Insulin (micro unit/mL) / 405 >2.5. Patients with IR or diabetes had significantly higher levels of creatinine after procedure, serum cholesterol, glucose, contrast volume, hospital stay and HOMA. Female gender, frequency of CIN and multivessel disease were also higher in these patients. On the other hand they had significantly lower ejection fraction. Logistic regression analysis showed that HOMA was the single independent risk factor for CIN in patients with acute coronary syndrome treated with PCI. Insulin resistance is an independent risk factor for CIN in patients with acute coronary syndrome treated with PCI. It carries a similar risk with diabetes and proper prophylaxis should be performed.

Can statins alter coronary plaque morphology assessed by intravascular ultrasound

We read with interest the article by Hikita et al entitled ‘‘Impact of Statin Use Before the Onset of Acute Myocardial Infarction on Coronary Plaque Morphology of the Culprit Lesion.’’ They evaluated the impact of statin treatment before the onset of acute myocardial infarction (AMI) on coronary plaque morphology at culprit lesions by using intravascular ultrasound virtual histology (IVUS-VH) before percutaneous coronary intervention (PCI). They concluded that statin use before the onset of AMI might have effects on coronary plaque morphology of the AMI culprit lesion with less necrotic core and greater fibrous and fibrofatty component. Statin therapy, especially intensive doses, is associated with a decreased plaque size, lipid content, and thickness of the fibrous cap. Statins have pleiotropic effects that are independent of lipid-lowering effects. The pleiotropic effects of statins (anti-inflammatory and antithrombotic properties) are often greater with high doses of statins, and there may be individual differences among various statins. A study comparing 8 months of pitavastatin (4 mg daily) with pravastatin (20 mg daily) showed that pitavastatin induced a reduction in fibrous and fibrofatty tissue, but an increase in necrotic core while on pravastatin showed no effects on fibrous tissue and the necrotic core but a decrease in fibrofatty tissue. In the Hikita et al study, the statin doses are low and there is no information about the patients’ medication other than statins and whether there was statin loading before PCI. It would be useful if the authors provided information about the treatment duration of statins. Hikita et al evaluated the impact of statin treatment on coronary plaque morphology only at culprit lesions; it would be useful if they also evaluated nonculprit lesions. A 3-vessel gray-scale IVUS study showed that at least 1 plaque rupture was found somewhere other than at the culprit lesions in 79% of the patients with AMI. The results of the Providing Regional Observation to Study Predictors of Events in Coronary Tree (PROSPECT) trial provided data about the natural history of vulnerable plaques observed by gray-scale IVUS and IVUSVH. In this study, 697 patients with acute coronary syndrome underwent 3-vessel coronary angiography and IVUS study after PCI. At follow-up, recurrent clinical events were equally attributable to the culprit and nonculprit lesions. There have also been some concerns raised about the IVUS-VH because of its poor correlation with necrotic core in a porcine model. Although our goal must be the identification of vulnerable plaques before they rupture, assessment of ruptured plaques provides information regarding plaque vulnerability. Therefore, caution must be taken when drawing conclusions from studies using different IVUS approaches.

Mean Platelet Volume and Acute Coronary Syndrome

We read the article entitled ‘‘The Relationship Between Mean Platelet Volume and Atherosclerosis in Young Patients With ST Elevation Myocardial Infarction’’ by Ozkan et al with interest. The authors concluded that a high mean platelet volume (MPV) can be an independent predictor of acute myocardial infarction (AMI). They also suggested that MPV can be added to the new risk factors for AMI. Patients with nonalcoholic fatty liver disease is associated with higher MPV compared with control individuals. Nadar et al found that among patients with hypertension, regular aspirin treatment was associated with increased MPV. Lifestyle modification, antihypertensive, lipid-lowering, and diet therapies can also affect the MPV. Ozkan et al did not define the MPV reference value. Also, the MPV values of EDTA samples are at least 9% higher than those of citrated samples. There are conflicting results about the effect of aspirin on MPV. Contrary to what has been assumed, aspirin has no effect on platelet size. Therefore, we wonder why Ozkan et al excluded treatment with aspirin in their study. It would be useful if they provide data about the management of patients and draw blood samples in the second and final hospital days. In the Ozkan et al’s study, the patients might be categorized into tertiles according to the admission, MPV value, and platelet count. Bigalke et al reported that low platelet counts were associated with higher expression of glycoprotein VI and elevated inflammatory markers in the acute coronary syndrome. Azab et al found that the MPV/platelet count ratio was superior to MPV alone in predicting long-term mortality after non-STsegment elevation myocardial infarction. Therefore, the use of MPV/platelet ratio might be a reasonable approach. The cross-interaction between platelets and leukocytes has been reported. Ozkan et al could also assess this relationship in their study. We think that it is difficult to attribute risk to a particular MPV value. In a review, Gasparyan et al illustrated that while high-grade inflammatory disorders (eg, active rheumatoid arthritis and ulcerative colitis) were associated with numerous small platelets, low-grade inflammatory disorders (eg, psoriasis and Behcet’s disease) were associated with a large MPV. The diagnostic value of MPV and other platelet indices in thrombotic diseases requires further studies. References

The relationship between neutrophil-to-lymphocyte ratio and coronary artery disease.

applied as a good cardiac biomarker. However, there are many concerns of this biochemical test. First, as it is widely discussed, this biomarker is considered a non specific marker (3). Its increase level can be due to many causes and if there is no good ruling out of other concomitant disease, the application as cardiac marker can lead to misinterpretation. Second, the standardization of the technique is very important. At least, the consensus to develop the international laboratory procedure guideline and reference range setting is needed. Bojesen et al. (4) found that “plasma YKL-40 increases with age within and across healthy individuals from the general population ” and concluded for the necessity of “age-stratified or age-adjusted reference levels”

Assesment of Myocardial Ischemia by Combination of Tissue Synchronisation Imaging and Dobutamine Stress Echocardiography

Background and Objectives Dobutamine stress echocardiography (DSE) is an important non-invasive imaging method for evaluating ischemia. However, wall motion interpretation can be impaired by the experience level of the interpreter and the subjectivity of the visual assessment. In our study we aimed to combine DSE and tissue syncronisation imaging to increase sensitivity for detecting ischemia. Subjects and Methods 50 patients with indications for DSE were included in the study. In 25 patients we found DSE positive for ischemia and in the other 25 patients we found it to be negative. The negative group was accepted as the control group. There was no significant difference in terms of risk factors and echocardiographic parameters between the two groups, except for wall motion scores. In both groups, left ventricular dyssychrony was accepted as the difference between time to peak systolic velocity (Ts) in the reciprocal four couple of non-apical segments at rest and during peak stress. Timings were corrected for heart rate. We compared the differences of the dyssynchronisation value at rest and during peak stress to determine the distinctions within the groups and between the groups of DSE positive and negative patients. Results We found that stress and ischemia did not create any significant difference over the left intraventricular dyssynchrony with DSE, although at the segmenter level it prolonged the time to peak systolic velocity (p<0.05). These alterations did not show any significant difference between positive and negative DSE groups. Conclusion As a result, this segmenter dyssynchrony and the time to peak systolic velocity, which is corrected for heart rate, did not enhance any new value over DSE for detecting ischemia.