Imran Onur

MR imaging features of ventricular noncompaction: Emphasis on distribution and pattern of fibrosis

OBJECTIVE The purpose of this study is to describe morphologic features and delayed contrast-enhancement pattern of the noncompaction of the left ventricle in cardiac magnetic resonance (MR) imaging. METHODS We retrospectively reviewed morphological cardiac MR imaging findings of ventricular noncompaction in 15 patients (eight men, seven women, and ages 6 months to 73 years old, mean 22 year). In 10 patients delayed contrast enhanced images were obtained after the morphological examination. RESULTS In all patients, noncompaction was seen in the apical and midventricular-lateral segment. Basal-septal segment involvement was not determined in any patients. Noncompacted/compacted ratio was 2-4.5 (mean 3). In nine patients, right ventricular involvement was observed in addition to left ventricular noncompaction. Delayed contrast-enhancement was seen in eight out of 10 patients not only involved segments but also normal segments of the heart. CONCLUSION Cardiac MR imaging is a valuable imaging method in patients with suspected ventricular noncompaction by showing increased trabeculations, deep intertrabecular recesses and fibrosis. Fibrosis is a common finding in ventricular noncompaction.

Clinical relevance of aspirin resistance in patients with stable coronary artery disease: a prospective follow-up study (PROSPECTAR).

Aspirin resistance may increase the risk of major adverse cardiac events (MACE) more than threefold in patients with stable coronary artery disease (CAD). This study aimed to determine the prevalence of aspirin resistance in patients with stable CAD, the role of aspirin resistance on outcome in the follow-up, and the effect of clopidogrel therapy in MACE prevention in aspirin-resistant individuals. We detected the prevalence of aspirin resistance in 234 patients with stable CAD. Platelet function was determined by PFA-100 with collagen and/or epinephrine and collagen and/or ADP cartridges. The mean follow-up time was 20.6 ± 6.9 months. The primary endpoints of the study were occurrence of myocardial infarction, unstable angina, stroke and cardiac death. Of patients, 22.2% (n = 52) were aspirin resistant by PFA-100. During follow-up, MACE occurred in eight patients (15.4%) with aspirin resistance and in 20 patients (11.0%) with aspirin-sensitive platelet aggregation (P = 0.269). MACE increased in aspirin-resistant patients after termination of clopidogrel therapy. Eleven patients experienced MACE after cessation of clopidogrel therapy (P < 0.001). The MACE risk in patients with stable CAD having detected aspirin resistance was similar compared with patients having aspirin-sensitive platelet aggregation by PFA-100. The MACE prevalence increased during follow-up, however, just after cessation of clopidogrel therapy.

Serum omentin 1 level is associated with coronary artery disease and its severity in postmenopausal women.

We evaluated whether serum omentin levels are associated with coronary artery disease (CAD) and its severity among postmenopausal women. We enrolled 193 consecutive postmenopausal women who had undergone coronary angiography for suspected stable CAD. The study population was divided into 2 groups based on the results of coronary angiography (CAD group, n = 110 and control group, n = 83). Omentin 1 levels were measured and disease severity was assessed using the SYNTAX score (SS) in the CAD group. Those patients with angiographic CAD had significantly decreased omentin 1 levels, compared to those without CAD (247.5 + 127.4 vs 506 + 246 ng/mL, P < .001). After adjusting for cardiovascular risk factors, a decreased omentin 1 level was found to be an independent predictor of both angiographic CAD and a high SS. Our data indicate that a decreased omentin 1 level is associated with CAD and its severity among postmenopausal women.

The utility of cardiac MRI in diagnosis of infective endocarditis: preliminary results

PURPOSE We aimed to evaluate the utility of cardiac magnetic resonance imaging (MRI) for the diagnosis of infective endocarditis (IE). METHODS Sixteen patients with a preliminary diagnosis of IE (10 women and six men; age range, 4-66 years) were referred for cardiac MRI. MRI sequences were as follows: echo-planar cine true fast imaging with steady-state precession (true-FISP), dark-blood fast spin echo T1-weighted imaging, T2-weighted imaging, dark-blood half-Fourier single shot turbo spin echo (HASTE), and early contrast-enhanced first-pass fast low-angle shot (FLASH). Delayed contrast-enhanced images were obtained using three-dimensional inversion recovery FLASH after 15±5 min. The MRI features were evaluated, including valvular pathologies on cine MRI and contrast enhancement on the walls of the cardiac chambers, major thoracic vasculature, and paravalvular tissue, attributable to endothelial extension of inflammation on contrast-enhanced images. RESULTS Fourteen valvular vegetations were detected in eleven patients on cardiac MRI. It was not possible to depict valvular vegetations in five patients. Vegetations were detected on the aortic valve (n=7), mitral valve (n=3), tricuspid and pulmonary valves (n=1). Delayed contrast enhancement attributable to extension of inflammation was observed on the aortic wall and aortic root (n=11), paravalvular tissue (n=4), mitral valve (n=2), walls of the cardiac chambers (n=6), interventricular septum (n=3), and wall of the pulmonary artery and superior mesenteric artery (n=1). CONCLUSION Valvular vegetation features of IE can be detected by MRI. Moreover, in the absence of vegetations, detection of delayed enhancement representing endothelial inflammation of the cardiovascular structures can contribute to the diagnosis and treatment planning of IE.

Aspirin-resistant platelet aggregation in a cohort of patients with coronary heart disease.

Aspirin resistance could be defined as thrombotic and embolic cardiovascular events despite regular aspirin therapy. The study aimed to determine the profile and prevalence of aspirin resistance in coronary artery disease patients. We evaluated the prevalence of aspirin resistance in a cohort of 505 patients with the diagnosis of coronary artery disease taking 80–300 mg regular aspirin daily. Platelet functions were analyzed by the Platelet Function Analyzer (PFA)-100 with collagen and epinephrine cartridges and collagen and ADP cartridges. A closure time of 186 s or less with the collagen and epinephrine cartridge was defined as aspirin resistance. Of the patients, 118 (23.4%) were aspirin resistant by the PFA-100. Aspirin-resistant patients were more likely to be older than aspirin-sensitive patients (P = 0.024). No statistically significant differences between the aspirin-resistant and aspirin-sensitive individuals were present in gender, major risk factors of coronary artery disease, number and localization of involved coronary vessels, serum lipid levels, and blood counts. According to the high prevalence of coronary heart disease, many people are affected by aspirin resistance, which may play a role in adverse cardiovascular events. Monitoring of platelet function in patients with coronary heart disease may support the optimization of antiplatelet therapy with additional and/or alternative agents.

Effect of Cigarette Smoking on Platelet Aggregation

Background: Cigarette smoking may increase platelet aggregation and cause atherothrombotic cardiovascular events. We aimed to investigate the impact of cigarette smoking on platelet function in patients with ischemic coronary heart disease (CHD).Methods: Twenty patients with ischemic stable CHD under aspirin therapy (300 mg/d), who continue to smoking despite all warnings, and 20 nonsmokers with CHD are enrolled in the study. Platelet function is studied at the morning, before and 15 minutes after the first cigarette, by the Platelet Function Analyzer (PFA)-100, with collagen and epinephrine and collagen and adenosine diphosphate cartridges. Post aspirin platelet hyperactivity is defined as having a closure time (CT) shorter than 186 seconds despite regular aspirin intake. Serial CT measurements are analyzed by paired samples t test.Results: Persistent platelet activity was present in 4 smoker (20%) and 3 nonsmoker (15%) patients at the beginning. Platelet activity measured by the PFA-100 is been increased significantly after cigarette smoking (P = .004). Shorter CTs were determined after smoking in all patients with and without baseline persistent platelet activity, and 4 more participants became aspirin nonresponder (P = .004). No significant differences in demographic, hematological, and biochemical parameters were determined between aspirin responders and nonresponders.Conclusions: We determined that cigarette smoking may increase platelet aggregation in patients with ischemic CHD in an aspirin nonresponsive manner. Our results emphasize the importance of quitting cigarette smoking in patients with CHD.

Coronary flow reserve is impaired in patients with adult growth hormone (GH) deficiency

Objective  Relationship between adult growth hormone deficiency (AGHD) and increased cardiovascular disease risk is very well known in hypopituitary patients treated with conventional hormone replacement therapy other than growth hormone (GH) administration. Endothelial dysfunction, an early and reversible event in pathogenesis of atherosclerosis, is associated with increased vascular smooth muscle tone, arterial stiffening and intima‐media thickness (IMT). Coronary flow reserve (CFR) measurement by transthoracic Doppler echocardiography (TTDE) reflects coronary microvascular and endothelial functions, as a cheaper and an easy screening test. We have used TTDE to evaluate endothelial function and coronary microvascular function in AGHD.

Homocysteine levels in patients with heart failure with preserved ejection fraction.

Objectives: Increased homocysteine (HCY) levels are associated with an increased risk of cardiovascular disease. Plasma HCY is increased in chronic heart failure (CHF) patients, and previous studies suggest that hyperhomocysteinemia causes adverse cardiac remodeling and affects pump function. We aimed to evaluate the HCY levels in patients with diastolic heart failure with preserved left ventricular ejection fraction (LVEF). Methods: We prospectively studied 68 patients (39 females and 29 males) who were hospitalized for symptomatic heart failure, as well as 40 age- and sex-matched healthy subjects who comprised the control group. CHF was diagnosed in all cases based on Framingham diagnostic criteria. CHF with preserved LVEF was defined as cases with CHF with an LVEF of 50% or more. Patients with regional left ventricular wall motion abnormalities, atrial fibrillation, and renal failure were excluded. Results: The mean age was 65.5 ± 9.6 years in the heart failure group and 65.2 ± 9.7 years in the control group. The mean LVEF was 59.8 ± 5.3 in the heart failure group and 61.4 ± 5.2 in the control group. The mean total fasting HCY concentrations were significantly higher in patients with heart failure (16.9 ± 5.27 µmol/l vs. 10.15 ± 3.49 µmol/l, respectively; p < 0.001). Multiple regression analysis indicated that NT-proBNP, hs-CRP, E/A ratio, and HbA1C were independently associated with hyperhomocysteinemia. Conclusions: Our results suggest that hyperhomocysteinemia is prevalent in heart failure with preserved ejection fraction. Larger scale studies are needed to clarify its pathogenic mechanisms and effects on the natural history of heart failure.

Assessment of longitudinal left ventricular systolic function by different echocardiographic modalities in patients with newly diagnosed mild-to-moderate hypertension.

OBJECTIVE Standard echocardiographic methods reflect chamber dynamics and do not provide a direct measure of myocardial fiber shortening. Therefore we evaluated longitudinal left ventricular myocardial function by tissue Doppler echocardiography; strain (S), strain rate (SR), tissue Doppler velocity (TDV) in newly diagnosed mild to moderate hypertensive patients. METHODS Our cross-sectional and observational study population consisted of 57 patients and 48 normotensive control subjects. Patients with obesity, diabetes mellitus, regional wall motion abnormality, secondary hypertension and a history or clinical evidence of cardiovascular disease, arrhythmias or conduction abnormalities were excluded from the study. Ejection fraction, endocardial fractional shortening (eFS), meridional end-systolic stress (mESS), stress-adjusted eFS (observed /predicted eFS) were measured by M-mode echocardiography. Relationship between the left ventricular mass index and mESS was assessed by Pearsons linear regression model. RESULTS Hypertensive patients had significantly decreased longitudinal myocardial function compared to control subjects determined by septal (-1.25+/-0.30 vs. -1.02+/-0.33, p<0.001) and lateral (-1.20+/-0.28 vs. 1.02+/-0.41, p<0.01) SR (1/s) measurements. However, there was no significant correlation between the mESS and strain-strain rate measurements in both normal and hypertensive subjects. CONCLUSIONS Early impairment in longitudinal left ventricular systolic function can be expected despite normal endocardial left ventricular function indicated by M-mode echocardiography in patients with newly diagnosed and never treated mild to moderate hypertension.

Galectin-3 correlates with arrhythmogenic right ventricular cardiomyopathy and predicts the risk of ventricular ­arrhythmias in patients with implantable defibrillators

Background Arrhythmogenic right ventricular dysplasia (ARVD) is a heritable disorder characterized by fibro-fatty replacement of right ventricular myocytes, increased risk of ventricular arrhythmias, and sudden cardiac death. Galectin-3 (GAL3) is known to play an important role in a number of fibrotic conditions, including cardiac fibrosis. Many studies have focused on the association between GAL3 levels and cardiac fibrosis in heart failure. However, the role of GAL3 in the pathogenesis of ARVD and ventricular arrhythmias has not yet been evaluated thoroughly. The aim of this study was to explore GAL3 levels in patients with ARVD and its association with ventricular arrhythmias. Methods Twenty-nine patients with ARVD and 24 controls were included. All patients with ARVD had an implantable cardiac defibrillator (ICD) for primary or secondary prevention. Ventricular arrhythmia history was obtained from a chart review and ICD data interrogation. Galectin-3 levels were measured using an enzyme-linked immunosorbent assay. Results Patients with ARVD had higher plasma GAL3 levels (16.9 ± 2.6 ng/mL vs 11.3 ± 1.8 ng/mL, P < 0.001) than the control group. Ten patients had sustained or non-sustained ventricular arrhythmias during follow-up. In the multivariable analysis, left ventricular disease involvement (HR: 1.05; 95% CI: [1.01-1.12]; P = 0.03); functional capacity >2 (HR: 1.21; 95% CI: [1.13-1.31]; P < 0.005); and GAL3 levels (HR: 1.05; 95% CI: [1.00-1.11]; P = 0.01) independently predicted VT/VF. Conclusion We demonstrated that serum GAL3 was significantly elevated in patients with ARVD. Also, serum GAL 3 levels could be regarded as a candidate biomarker in the diagnosis of ARVD which needs to be tested in larger prospective studies. In addition, GAL3 levels were higher in patients with VT/VF as compared with those without VT/VF.