M. Hakan Tas

Speckle Tracking Echocardiographic Analysis of Left Ventricular Systolic and Diastolic Functions of Young Elite Athletes with Eccentric and Concentric Type of Cardiac Remodeling

In individuals who exercise regularly and for extended periods of time, some structural alterations in the heart, called the athletes heart, develop in time. These alterations vary in type, can be eccentric or concentric, depending on the nature of exercise. Speckle tracking echocardiography (STE) is a novel, angle‐independent method that accurately and reliably measures systolic and diastolic functions of the left ventricle (LV) with considerably lower inter‐operator variability.

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.

Cor triatriatum dexter, atrial septal defects, and pulmonary stenosis-a rare association.

Cor triatriatum dexter (CTD) is an extremely rare congenital anomaly in which the right atrium is divided into 2 chambers by a membrane. The estimated incidence of cor triatriatum has been reported as 0.1% of congenital cardiac malformations. The septation of the right atrium in the setting of CTD is the result of failed resorption of the right valve of the sinus venosus. This results in anterolateral and posteromedial portions of the divided right atrium. CTD can be diagnosed at any age, especially if it is incidentally discovered.

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