A new biomarker that predicts ventricular arrhythmia in patients with ischemic dilated cardiomyopathy: Galectin-3.

INTRODUCTION: Ventricular arrhythmias are caused by scar tissue in patients with ischemic dilated cardiomyopathy. The gold standard imaging technique for detecting scar tissue is magnetic resonance imaging (MRI). However, MRI is not feasible for use as a screening test, and also cannot be used in patients who have received an implantable cardioverter-defibrillator (ICD). In this study, we aimed to assess the association between levels of galectin-3 (Gal-3), which is known to be secreted by scar tissue, and the history of ventricular arrhythmias in patients with ischemic dilated cardiomyopathy who received an ICD. METHODS: Nineteen healthy controls and 32 patients who had previously undergone VVI-ICD implantation due to ischemic dilated cardiomyopathy were enrolled in the study. Patients were divided into three groups: the first group including patients who had received no ICD therapies, the second including patients with arrhythmia requiring therapies with no arrhythmia storm, and the third including patients who had arrhythmia storm. We assessed the association between Gal-3 levels and the history of ventricular arrhythmias in these patients. RESULTS: Gal-3 levels were significantly higher in the patient groups than in the control group (p<0.01). Gal-3 levels of patients with arrhythmias requiring ICD therapies were significantly higher than in patients with ICD not requiring therapies (p=0.02). They were also higher in patients with a history of arrhythmia storm than in patients without shocks (p=0.05). Receiver operating curve analysis showed with 84% sensitivity and 75% specificity that Gal-3 levels over 7 ng/ml indicated ventricular arrhythmia that required therapies. CONCLUSION: Gal-3 may be used to further improve risk stratification in patients with ischemic cardiomyopathy who are more prone to developing life-threatening arrhythmias.

Impairment of right ventricular longitudinal strain associated with severity of pneumonia in patients recovered from COVID-19.

Myocardial injury caused by COVID-19 was reported in hospitalized patients previously. But the information about cardiac consequences of COVID-19 after recovery is limited. The aim of the study was comprehensive echocardiography assessment of right ventricular (RV) in patients recovered from COVID-19. This is a prospective, single-center study. After recovery from COVID-19, echocardiography was performed in consecutive 79 patients that attended follow-up visits from July 15 to November 30, 2020. According to the recovery at home vs hospital, patients were divided into two groups: home recovery (n = 43) and hospital recovery (n = 36). Comparisons were made with age, sex and risk factor-matched control group (n = 41). In addition to conventional echocardiography parameters, RV global longitudinal strain (RV-GLS) and RV free wall strain (RV-FWS) were determined using 2D speckle-tracking echocardiography (2D STE). Of the 79 patients recovered from COVID-19, 43 (55%) recovered at home, while 36 (45%) required hospitalization. The median follow-up duration was 133  ±  35 (87-184) days. In patients recovered from hospital, RV-GLS and RV-FWS were impaired compared to control group (RV-GLS: -17.3  ±  6.8 vs. -20.4  ±  4.9, respectively [p = 0.042]; RV-FWS: -19.0  ±  8.2 vs. -23.4  ±  6.2, respectively [p = 0.022]). In subgroup analysis, RV-FWS was impaired in patients severe pneumonia (n = 11) compared to mild-moderate pneumonia (n = 28), without pneumonia (n = 40) and control groups (-15.8  ±  7.6 vs. -21.6  ±  7.6 vs. -20.8  ±  7.7 vs. -23.4  ±  6.2, respectively, [p = 0.001 for each]) and RV-GLS was impaired compared to control group (-15.2  ±  6.9 vs. -20.4  ±  4; respectively, [p = 0.013]). A significant correlation was detected between serum CRP level at hospital admission and both RV-GLS and RV-FWS (r = 0.285, p = 0.006; r = 0.294, p = 0.004, respectively). Age (OR 0.948, p = 0.010), male gender (OR 0.289, p = 0.009), pneumonia on CT (OR 0.019, p = 0.004), and need of steroid in treatment (OR 17.424, p = 0.038) were identifed as independent predictors of impaired RV-FWS (> -18) via multivariate analysis. We demonstrated subclinic dysfunction of RV by 2D-STE in hospitalized patients in relation to the severity of pneumonia after recovery from COVID-19. 2D-STE supplies additional information above standard measures of RV in this cohort and can be used in the follow-up of these patients.

Wide QRS Complex and Lateral ST-T Segment Abnormality Are Associated With Worse Clinical Outcomes in COVID-19 Patients.

BACKGROUND: The information on electrocardiographic features of patients with coronavirus disease 2019 (COVID-19) is limited. Our aim was to determine if baseline electrocardiographic features of hospitalized COVID-19 patients are associated with markers of myocardial injury and clinical outcomes. METHODS: In this retrospective, single center cohort study, we included 223 hospitalized patients with laboratory-confirmed COVID-19. Clinical, electrocardiographic and laboratory data were collected and analyzed. Primary composite endpoint of mortality, need for invasive mechanical ventilation, or admission to the intensive care unit was assessed. RESULTS: Forty patients (17.9%) reached the primary composite endpoint. Patients with the primary composite endpoint were more likely to have wide QRS complex (>120 ms) and lateral ST-T segment abnormality. The multivariable Cox regression showed increasing odds of the primary composite endpoint associated with acute respiratory distress syndrome (odds ratio 7.76, 95% CI 2.67-22.59; p < 0.001), acute cardiac injury (odds ratio 3.14, 95% CI 1.26-7.99; p = 0.016), high flow oxygen therapy (odds ratio 2.43, 95% CI 1.05-5.62; p = 0.037) and QRS duration longer than >120 ms (odds ratio 3.62, 95% CI 1.39-9.380; p = 0.008) Patients with a wide QRS complex (>120 ms) had significantly higher median level of troponin T and pro-BNP than those without it. Patients with abnormality of lateral ST-T segment had significantly higher median level of troponin T and pro-BNP than patients without. CONCLUSIONS: The presence of QRS duration longer than 120 ms and lateral ST-T segment abnormality were associated with worse clinical outcomes and higher levels of myocardial injury biomarkers.

Silent myocardial dysfunction in vitamin D deficiency.

INTRODUCTION: Vitamin D (VD) deficiency is a common disease that occurs in all stages of life. A growing number of studies call attention to the relationship between VD deficiency and cardiovascular disease. The aim of this study was to investigate the effect of VD on subclinical left ventricular (LV) function in diabetic and non-diabetic patients with no significant coronary artery disease. MATERIAL AND METHODS: We recruited 140 patients (80 diabetics and 60 non-diabetics) with symptoms of stable ischemic heart disease who underwent coronary angiography and who had no significant coronary artery disease in our clinic. The 25(OH)D3 levels were measured and patients who had 25-(OH)D3 levels below 20 ng/dl were defined as the VD deficient group. In addition to conventional echocardiographic parameters, tissue Doppler echocardiography was used for LV diastolic functions and 2D speckle tracking strain echocardiography (2D STE) for evaluating the longitudinal deformation indices of the LV myocardium. RESULTS: In all groups, LV global longitudinal strain (GLS) was significantly impaired in patients with VD deficiency (p < 0.001) compared to patients without VD deficiency. LV global longitudinal strain rate (GLSR) was significantly impaired in patients with VD deficiency (p = 0.003). The GLS was negatively associated with 25-(OH)D3 in the VD deficiency group (r = -0.52623, p < 0.001). Conversely, GLS was positively associated with 25-(OH)D3 levels in the normal VD group (r = 0.28, p = 0.048). CONCLUSIONS: VD deficiency is associated with impaired myocardial GLS. The present study demonstrated that VD deficiency may be the cause of subclinical myocardial dysfunction in patients with or without diabetes mellitus and no history of significant coronary artery disease.

Predictors of left ventricle ejection fraction and early in-hospital mortality in patients with ST-segment elevation myocardial infarction: Single-center data from a tertiary referral university hospital in Istanbul.

BACKGROUND: Little is known about the management and mortality rates of ST-segment elevation myocardial infarction patients in developing countries. In this study, to expose independent predictors of early (24 h) in-hospital mortality and ejection fraction, we report our experience with 362 ST-segment elevation myocardial infarction patients admitted to the Istanbul Medical Faculty, Istanbul University, a tertiary referral university hospital, and treated with primary percutaneous intervention. METHODS: This is a retrospective study that enrolled all patients (362) admitted with ST-segment elevation myocardial infarction to Department of Cardiology, Istanbul Medical Faculty, Istanbul University, between January 2015 and December 2016. The clinical characteristics of patients were collected retrospectively from medical chart review. Collected data were analyzed using IBM SPSS Statistics (version 21). RESULTS: In the forward stepwise logistic regression analysis, target vessel diameter (p = 0.001), systolic blood pressure (p < 0.001), and troponin T levels (p = 0.007) were independent predictors for early in-hospital mortality, while target vessel diameter (p = 0.03), troponin T level (p < 0.001), heart rate (p = 0.001), and chest pain (p = 0.001) duration were the independent predictors for ejection fraction of 50% and above. CONCLUSION: Our study is one of the few studies to investigate the predictors of early in-hospital mortality among patients hospitalized with ST-segment elevation myocardial infarction in a tertiary referral university hospital in a developing country. The identified predictors for mortality (including left ventricle ejection fraction and troponin T levels), left ventricle ejection fraction (including troponin T level, chest pain duration), and heart rate are consistent with what has been described in large registries in the United States and Europe.

Predictive value of global and territorial longitudinal strain imaging in detecting significant coronary artery disease in patients with myocardial infarction without persistent ST-segment elevation.

INTRODUCTION: Two-dimensional (2D) speckle-tracking echocardiographic (STE) imaging is frequently performed in the assessment of cardiovascular diseases. We aim to investigate the role of the global and territorial longitudinal strain (GLS and TLS) values assessed via 2D STE imaging to detect significant coronary artery disease (CAD) in non-ST-segment elevation myocardial infarction (NSTEMI) patients without wall-motion abnormalities. METHODS: This study enrolled 150 patients with the diagnosis of NSTEMI. Patients who had typical chest pain with unstable angina characteristics within the last 24 hours were 18-80 years of age and had a typical rise and/or fall of cardiac biomarkers were included. Myocardial functions were assessed via myocardial deformation analyses of 2D STE images. RESULTS: The mean age of the CAD group was 52.91 ± 9.11, vs 50.31 ± 8.32 in the control group. In the CAD group, 56 patients were male (65%), whereas 21 were male (60%) in control group. GLS and TLS assessments demonstrated a statistically significant difference between CAD and control groups, with GLS values of -16.27 ± 1.91 and -18.74 ± 1.93 (P < 0.001), TLS-LAD values of -15.67 ± 1.83 and -18.54 ± 1.97 (P < 0.001), TLS-RCA values of -17.04 ± 1.81 and -19.20 ± 1.86 (P < 0.001), and TLS-Cx values of -17.40 ± 2.08 and -18.34 ± 2.18 (P = 0.028), respectively. Correlation analyses revealed that as high-sensitivity troponin (hsTnT) values increased, GLS decreased significantly, and further, an increase in severity of CAD resulted in decreased TLS-LAD, -CX and -RCA (TLS-LAD: P < 0.001, r = -0.743; TLS-CX: P < 0.001, r = -0.449; TLS-RCA: P < 0.001, r = -0.737). Multivariate analyses indicated that GLS and GRACE ACS risk scores are independent predictors of CAD in patients with NSTEMI (GLS: OR = 0.514, P < 0.001; GRACE score: OR = 0.938, P = 0.007). CONCLUSIONS: Global longitudinal strain (GLS) assessed with 2D STE is a promising, easy to perform and quick imaging method to predict CAD in patients with NSTEMI.

Galectin-3: A Novel Biomarker Predicts Sudden Cardiac Death in Hypertrophic Cardiomyopathy.

BACKGROUND: Hypertrophic cardiomyopathy is a primary cardiac disease characterized by left ventricular hypertrophy, myocyte hypertrophy and irregularities and interstitial fibrosis in the absence of any cardiac or systemic diseases and may lead to sudden cardiac death (SCD). Galectin-3 is a ß-galactoside-binding lectin that has been associated with cardiac fibrosis and inflammation. In this study, we aimed to investigate the relationship between serum galectin-3 levels and the criteria for 5-year sudden death risk, recently defined in the European Society of Cardiology guidelines (2014), in patients with hypertrophic cardiomyopathy. MATERIALS AND METHODS: A total of 52 hypertrophic cardiomyopathy patients were enrolled in the study. Patients were questioned for sudden death risk predictors as outlined in the 2014 European Society of Cardiology guideline. A standardized clinical evaluation was carried out on the basis of previously described prognostic variables to calculate the 5-year risk of SCD. Blood samples were taken from all patients to measure serum galectin-3 levels. A statistical significance level of P < 0.05 was accepted in all tests. RESULTS: We found that there was a significant correlation between the estimated 5-year risk of SCD and serum levels of galectin-3. CONCLUSIONS: Galectin-3 may be an inexpensive and easily accessible parameter to predict arrhythmia risk. In addition, it can be used to determine antiarrhythmic prophylaxis as a predictor of an arrhythmia storm in implantable cardioverter defibrillator-implanted patients who are not available for magnetic resonance imaging.

Glycoprotein Ibα Kozak polymorphism in patients presenting with early-onset acute coronary syndrome.

INTRODUCTION: Glycoprotein Ibα (GPIbα) receptor is the chief molecule responsible for initial platelet adhesion to the subendothelium. A thymidine to cytosine single nucleotide substitution at position -5 from the ATG start codon characterizes the Kozak sequence polymorphism. The Kozak sequence polymorphism may increase the surface expression of GPIbα and contribute to thrombogenesis. We evaluated the allele frequencies of GPIbα Kozak sequence polymorphism in the Turkish population and examined the relationship between GPIbα Kozak sequence polymorphism and early-onset acute coronary syndrome (ACS). MATERIAL AND METHODS: This study enrolled 200 patients (122 male, 78 female, mean age: 39 ±5 years) and 200 healthy control subjects (110 male, 90 female, 41 ±4 years). The patient group was composed of patients admitted to our coronary care unit with early-onset ACS and patients who attended to our cardiology outpatient clinic after hospital discharge with a diagnosis of early-onset ACS. RESULTS: Kozak polymorphism frequencies in patients and control subjects did not differ significantly (23% versus 22.5%, p = 0.812, respectively). In patients who presented with non-ST elevation myocardial infarction (NSTEMI), the frequency of GPIbα Kozak polymorphism was borderline significantly higher when compared with patients who presented with ST elevation myocardial infarction (STEMI) (35% vs. 20%, p = 0.05, respectively). Allele frequencies of T and C were calculated to be 0.873 and 0.128. CONCLUSIONS: Although the frequency of GPIbα Kozak polymorphism did not differ significantly in early-onset ACS patients versus control subjects, Kozak polymorphism frequency was borderline significantly higher in patients who presented with NSTEMI when compared to patients with STEMI.

Endocan: a novel biomarker associated with well-developed coronary collateral circulation in patients with stable angina and chronic total occlusion.

Angiogenesis and arteriogenesis have a crucial role in the formation of coronary collateral vessels. It has been shown that endocan and vascular cell adhesion molecule-1 (VCAM-1) are potential angiogenetic factors. We investigated the relationship between serum endocan levels and grade of coronary collaterals, and also the correlation of endocan levels with serum VCAM-1 levels. Patients with stable angina and at least one total coronary occlusion at invasive coronary angiography were included in our study. Collateral degree was graded according to Rentrop and Cohen's classification. Patients who had grade 0 or 1 collateral vessels were included in the poorly-developed collateral group, and those with grade 2 or 3 coronary collateral vessels were included in the well-developed collateral group. Serum endocan and VCAM-1 levels were significantly higher in the well-developed collateral group (436.6 ± 213.3 ng/mL vs. 216.1 ± 78.5 ng/mL, p < .001; 11.02 ± 6.58 ng/mL vs. 6.78 ± 1.14 ng/mL, p < .001, respectively). In a logistic regression analysis, only serum endocan level remained as an independent predictor for good collateral development. In the ROC curve analysis, 282 ng/mL endocan level had an a 82 % sensitivity and 86 % specificity for prediction of the well-developed collateral group. Higher endocan level was related to better coronary collateral development. In the event that these results are confirmed in further studies, endocan may be considered as an anti-ischemic treatment strategy in order to improve collateral development.

Doppler-derived strain imaging detects left ventricular systolic dysfunction in children with Turner syndrome.

OBJECTIVES: Children with Turner syndrome (TS) are at increased risk of cardiovascular disease (CVD), but associations with subclinical CVD are not well-characterized. The purpose of this study was to assess myocardial function using strain imaging (SI) by echocardiography in children with TS and without known CVD. METHODS: The study included 48 children with TS aged 4-16 years and 20 healthy control children. Children with TS were excluded if they had a cardiac malformation, a decreased left ventricular (LV) systolic function, or any chronic disease. Each child had an echocardiographic examination with conventional echocardiography and one-dimensional longitudinal strain (1DST) echocardiography. RESULTS: Septal and lateral systolic strain (S) and strain rate (SR) values, which are indicative of longitudinal myocardial function, were significantly decreased in TS patients. However, LV ejection fraction (LVEF) and LV fractional shortening (LVFS) was not significantly different between groups. LV mass index (LVMi), interventricular septum (IVS) thickness, LV posterior wall (LVPW) thickness, and left atrial (LA) diameter index were significantly higher in TS children compared to controls. Peak transmitral flow velocity in late diastole (peak A) was significantly higher, whereas peak transmitral flow velocity in early diastole (peak E), deceleration time (DT), and the ratio of early to late diastolic filling were significantly lower, in TS patients. CONCLUSION: Reduced LV systolic S and SR in children with TS may indicate early myocardial dysfunction before any detectable change in LVEF.

Effect of carvedilol on silent anthracycline-induced cardiotoxicity assessed by strain imaging: A prospective randomized controlled study with six-month follow-up.

BACKGROUND: The use of antracycline (ANT) in breast cancer has been associated with adverse cardiac events. Two-dimensional (2D) strain imaging (SI) can provide a more sensitive measure of altered left ventricular (LV) systolic function. We aimed to evaluate the preventive effect of carvedilol administration assessed by SI in a patient with breast cancer treated with ANT. METHODS: Patients receiving ANT were randomly assigned to the carvedilol- or placebo-receiving group. Each received an echocardiographic examination with conventional 2D echocardiography, pulsed tissue Doppler, and 2D SI prior to and 6 months post ANT treatment. RESULTS: During the 6-month follow-up period there were no patient deaths or interrupted chemotherapy treatments due to doxorubicin-induced cardiotoxicity. Both left ventricular ejection fraction (LVEF) and fractional shortening (FS) were within normal limits for all patients before and after ANT therapy. EF, FS and LV dimensions were measured using M-mode echocardiography and found to be similar in both groups before and after ANT therapy. The mean EF, FS, and LV echocardiograph baseline and control dimensions were similar in both groups after 6 months. Though baseline SI parameters were similar between the groups, there was a significant decrease in LV basal septal and basal lateral peak systolic strain in the control group compared to the carvedilol group. CONCLUSIONS: These results indicate that carvedilol has a protective effect against the cardiotoxicity induced by ANT.

Impact of vitamin D insufficiency on the epicardial coronary flow velocity and endothelial function.

OBJECTIVE: Increasing evidence suggests a relationship between vitamin D (VD) insufficiency and cardiovascular disease. The present study evaluated the effect of VD insufficiency on epicardial coronary flow rate, subclinical atherosclerosis, and endothelial function. METHODS: The present study was cross-sectional and observational. We enrolled 222 consecutive patients who had undergone coronary angiography for suspected ischemic heart disease and were found to have normal or near-normal coronary arteries. Thereafter, 25(OH)D3 levels were measured and the coronary flow rate was assessed using the thrombolysis in myocardial infarction frame count. Slow coronary flow (SCF) was defined as a thrombolysis in myocardial infarction frame count greater than 27/frame. Endothelial function was assessed by brachial artery flow-mediated dilatation. Carotid intima-media thickness, an indicator of subclinical atherosclerosis, was measured using B-mode ultrasonography. RESULTS: The mean level of 25(OH)D3 was 31.8 ng/ml, and 47% (n=106) of the patients had insufficient 25(OH)D levels (<30 ng/ml). Baseline characteristics were similar between VD-insufficient and VD-sufficient groups. The incidence of SCF was significantly higher in the VD-insufficient group than in patients with sufficient VD (relative risk=3.5, 95% confidence interval=1.1-10.5, P=0.01). After adjusting for cardiovascular disease risk factors, VD insufficiency was independently associated with SCF. The linear regression analysis showed that VD insufficiency was correlated independently with % flow-mediated dilatation (ß=0.424, P<0.001) and carotid intima-media thickness (ß=0.43, P<0.001). CONCLUSION: A strong association was found between VD insufficiency and the SCF phenomenon. In addition, VD insufficiency was associated with endothelial dysfunction and subclinical atherosclerosis. We believe that further studies are required to clarify the role of VD in patients with SCF.

Does aspirin use prevent acute coronary syndrome in patients with pneumonia: multicenter prospective randomized trial.

OBJECTIVES: The aim of this study was to test the hypothesis that aspirin would reduce the risk for acute coronary syndromes (ACSs) in patients with pneumonia. BACKGROUNDS: Pooled data suggest that pneumonia may trigger an ACS as a result of inflammatory reactions and the prothrombotic changes in patients with pneumonia. Hypothetically considering its antiaggregating and anti-inflammatory effects, aspirin might also be beneficial for the primary prevention of ACS in patients with pneumonia. METHODS: One hundred and eighty-five patients with pneumonia who had more than one risk factor for cardiovascular disease were randomized to an aspirin group (n=91) or a control group (n=94). The patients in the aspirin group received 300 mg of aspirin daily for 1 month. ECGs were recorded on admission and 48 h and 30 days after admission to assess silent ischemia. The level of high-sensitivity cardiac troponin T was measured on admission and 48 h after admission. The primary endpoint was the development of ACS within 1 month. The secondary endpoints included cardiovascular death and death from any cause within 1 month. RESULTS: The χ-test showed that the rates of ACS at 1 month were 1.1% (n=1) in the aspirin group and 10.6% (n=10) in the control group (relative risk, 0.103; 95% confidence interval 0.005-0.746; P=0.015). Aspirin therapy was associated with a 9% absolute reduction in the risk for ACS. There was no significant decrease in the risk of death from any cause (P=0.151), but the aspirin group had a decreased risk of cardiovascular death (risk reduction: 0.04, P=0.044). CONCLUSION: This randomized open-label study shows that acetyl salicylic acid is beneficial in the reduction of ACS and cardiovascular mortality among patients with pneumonia.

Intracoronary autologous bone marrow-derived mononuclear cell transplantation improves coronary collateral vessel formation and recruitment capacity in patients with ischemic cardiomyopathy: a combined hemodynamic and scintigraphic approach.

This study investigated the effects of intracoronary autologous bone marrow-derived mononuclear cell (BMC) transplantation on coronary microcirculation. Fifteen patients with ischemic cardiomyopathy were treated by intracoronary infusion of BMCs via the patent infarct-related artery. The thermodilution-derived coronary flow reserve, index of microvascular resistance, pressure-derived collateral flow index, and coronary wedge pressure were measured at baseline and at 6 months. Successive balloon inflations during BMC transplantation were performed to observe the recruitment in pressure-derived collateral flow index and coronary wedge pressure, and the percentage changes between baseline and 6 months were calculated. The mean (SD) coronary flow reserve increased from 1.3 (0.4) to 2.1 (0.5), and the mean (SD) index of microvascular resistance decreased from 44.9 (24.4) to 21.2 (14.1) (P = .001 for both). The mean (SD) improvement in pressure-derived collateral flow index (from 0.14 [0.05] to 0.22 [0.08]) was also statistically significant (P = .001). Similarly, the percentage improvements in pressure-derived collateral flow index and coronary wedge pressure were statistically significant (P = .01 for both). The percentage improvement in perfusion assessed by single-photon emission computed tomography strongly correlated with the percentage changes in pressure-derived collateral flow index (r = 0.88, P = .001) and coronary wedge pressure (r = 0.69, P = .01). These results demonstrate for the first time (to our knowledge) that intracoronary autologous BMC transplantation improves coronary collateral vessel formation and recruitment capacity in human subjects.

Early detection of right ventricular systolic dysfunction by using myocardial acceleration during isovolumic contraction in patients with mitral stenosis.

AIM: The aim of the study was to determine if the tissue Doppler imaging (TDI)-derived myocardial acceleration during isovolumic contraction (IVA) of tricuspid lateral annulus could be used in early detection of RV systolic dysfunction in patients with mitral stenosis (MS), before the clinical signs of systemic venous congestion occur. METHODS: One hundred and twelve patients with rheumatic MS without relevant regurgitation and 60 control subjects were enrolled in the study. Conventional echocardiographic parameters (mitral valve area, transmitral diastolic gradients, pulmonary artery pressure, RV fractional shortening, pulmonary flow acceleration time, tricuspid annular plane systolic excursion) and TDI-derived systolic velocities of tricuspid annulus (isovolumic myocardial acceleration: IVA, peak myocardial velocity during isovolumic contraction: IVV, peak systolic velocity during ejection period: Sa and RV Tei index) were recorded from all patients. RESULTS: TDI-derived IVA, IVV, Sa and Tei index were found to be significantly decreased in patients with MS. IVA was the only parameter which had a significant negative correlation with the traditional echocardiographic parameters and RV Tei index in patients with MS. Additionally, in subgroup analyses, IVA was significantly lower in patients with severe degree of MS. CONCLUSION: TDI-derived right ventricular IVA may be used as an adjunctive, reliable, noninvasive parameter for the early detection of right ventricular systolic dysfunction in patients with MS but without signs of systemic venous congestion.

The trivest in overreaching syndrome: cardiac fatigue, muscular weakness, and vascular dysfunction.

Although the underlying mechanisms responsible for cardiac dysfunction after prolonged exercise remains to be elucidated, it has reported cardiac deterioration following exhaustive exercise in the absence of underlying cardiovascular diseases, which has been attributed to cardiac fatigue. The objective of this study was to evaluate cardiac functions, exercise capacity, and flow-mediated dilatation in overreaching syndrome. We studied 13 male marathon runners who took part in a marathon. Cardiopulmonary exercise testing, transthoracic echocardiography and endothelium-dependent vasodilatation of the brachial artery were performed at before- and after-race. Peak oxygen consumption, left ventricular tissue Doppler imaging parameters and flow-mediated dilatation were decreased after-race values compared with before-race values. Overreaching syndrome could arise involves a physio-pathological trivest, cardio-vasculo-muscular axis, which include three vicious cycles.

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.

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.

The association of P-selectin glycoprotein ligand-1 VNTR polymorphisms with coronary stent restenosis.

BACKGROUND: P-selectin and P-selectin glycoprotein ligand-1 (PSGL-1) regulate the initial interactions between leukocytes, activated platelets and endothelial cells. Recently, a variable number of tandem repeats (VNTR) polymorphism in PSGL-1 gene affecting the length of the extracellular domain of PSGL-1 and the distance of the P-selectin binding site to the cell surface has been described. There are limited numbers of studies reporting PSGL-1 polymorphism might affect the inflammatory response and thrombosis. We explored the association between PSGL-1 VNTR polymorphisms (especially AB genotype that has the most deformed configuration of the binding site) and the development of coronary stent restenosis and stent thrombosis in patients with coronary artery disease (CAD). MATERIALS AND METHODS: Eighty-seven patients with in-stent restenosis and 93 patients with patent coronary stents were included into the study. The distributions of age, gender, hypertension, diabetes, smoking, total cholesterol and triglyceride levels were similar between the groups. Genomic DNAs were obtained by standard methods from whole blood samples. Specific primers were used to amplify PSGL-1 gene by polymerase chain reaction (PCR). RESULTS: Three alleles and 5 different genotypes were detected. In the in-stent restenosis group; allele frequencies were 79.5% for A allele, 18.1% for B allele and 2.4% for C allele and in the patent stent group; allele frequencies were 79.3% for A allele, 20.1% for B allele and 0.6% for C allele. The allele frequencies were similar between the in-stent restenosis group and patent stent group (P = 0.97 for A allele, P = 0.73 for B allele and P = 0.19 for C allele). Genotype distributions were also similar between the groups. There were not any significant associations between PSGL-1 AB genotype and stent restenosis (31.3% vs. 27.2%, P = 0.54), repetitive stent restenosis (33.3% vs. 28.8%, P = 0.82) or in-stent thrombosis (44.4% vs. 28.2%, P = 0.37). In neither male patients nor female patients, there was any significant association between AB genotype and restenosis (32.2% vs. 24.3% P = 0.31 and 29.2% vs. 38.9% P = 0.51, respectively). However, among patients with a family history of early CAD, significantly higher percentage of AB genotype was found in those with stent restenosis (41.4% vs. 18.8%, P = 0.03). CONCLUSIONS: No significant association was found between PSGL-1 VNTR polymorphisms and in-stent restenosis. However, in patients with a family history of early CAD presence of PSGL-1 AB genotype might increase the risk of in-stent restenosis.