Profile of hypertension in Turkey: from prevalence to patient awareness and compliance with therapy, and a focus on reasons of increase in hypertension among youths.

Hypertension is one of the most common noncommunicable chronic diseases and is an important risk factor for vascular complications. The prevalence of hypertension is very high worldwide, and it is still increasing in low- and middle-income countries. Although some improvements were reported in high-income countries in recent years, there is still much to do to overcome hypertension and its complications. Identically, hypertension is a severe public health issue in Turkey. Approximately one third of the adult population has got hypertension but almost half is unaware of the disease. Children and youths are also affected by the burden of hypertension. Increased body mass index and obesity frequently accompany hypertension in children and adolescents. Major contributors to the disease burden appears to be consumption of high amounts of dietary sodium, lack of appropriate physical activity, increasing weight and obesity. In the last decades, an improvement at disease awareness has been achieved but blood-pressure control rates are still low in Turkey. Traditional and natural products, including lemon juice and garlic, are very popular among patients with concerns regarding medications' side effects. Patients' adherence to therapy differs between regions and increases in parallel with high education level. Decreasing daily salt intake has been shown to reduce the prevalence of hypertension substantially and to prevent cardiovascular and cerebrovascular deaths in a cost effective manner in projection studies. Finally, improving education of patients, which has positive effects on disease awareness, treatment adherence, and blood-pressure control rates, should be considered.

Comparison of hypertension prevalence and the use of renin-angiotensin-aldosterone system blockers in hospitalized patients with COVID-19 and non-COVID-19 viral pneumonia.

OBJECTIVE: To compare the prevalence of hypertension and pre-existing use of renin-angiotensin-aldosterone system blockers in patients with coronavirus disease (COVID-19) and non-COVID-19 viral pneumonias. METHODS: Real-time polymerase chain reaction confirmed COVID-19 and non-COVID-19 pneumonia patients were retrospectively analyzed. The presence of hypertension, coronary artery disease (CAD), and pre-existing use of angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) were compared between the groups. RESULTS: A total of 103 COVID-19 and 91 non-COVID-19 hospitalized viral pneumonia patients were enrolled. Hypertension and CAD were more common in patients with non-COVID-19 viral pneumonia than in patients with COVID-19 (39.6% vs 22.3%, respectively, p=0.012 and 24.2% vs 4.9%, respectively, p<0.001). In our study, 2.9% and 6.8% of patients with COVID-19 were on ACEIs and ARBs, respectively, whereas 13.2% and 19.8% of patients with non-COVID-19 viral pneumonia were on ACEIs and ARBs, respectively (p=0.009 and p=0.013). Neutrophil-to-lymphocyte ratio (p<0.001) was prominent in patients with non-COVID-19 viral pneumonia compared with patients with COVID-19. CONCLUSION: Our study results indicate that hypertension and CAD are more common among patients with non-COVID-19 viral pneumonia than patients with COVID-19. The prevalence of ACEIs and ARBs use was not higher in patients with COVID-19. Our results support that the use of ACEIs and ARBs do not play a specific role in patients with COVID-19.

Association between renin-angiotensin-aldosterone system inhibitor treatment, neutrophil-lymphocyte ratio, D-Dimer and clinical severity of COVID-19 in hospitalized patients: a multicenter, observational study.

The aim of this study was to investigate the possible relationship between worse clinical outcomes and the use of angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin receptor blockers (ARBs) in hospitalized COVID-19 patients. A total of 247 adult patients (154 males, 93 females; mean age: 51.3 ± 14.2 years) hospitalized for COVID-19 as confirmed by polymerase chain reaction (PCR) were retrospectively reviewed. Demographic and clinical characteristics and laboratory parameters were analyzed using various statistical modeling. Primary outcomes were defined as the need for intensive care unit (ICU), mechanical ventilation, or occurrence of death. Of the patients, 48 were treated in the ICU with a high flow oxygen/noninvasive mechanical ventilation (NIMV, n = 12) or mechanical ventilation (n = 36). Median length of ICU stay was 13 (range, 7-18) days. Mortality was seen in four of the ICU patients. Other patients were followed in the COVID-19 services for a median of 7 days. There was no significant correlation between the primary outcomes and use of ACEIs/ARBs (frequentist OR = 0.82, 95% confidence interval (CI) 0.29-2.34, p = 0.715 and Bayesian posterior median OR = 0.80, 95% CI 0.31-2.02) and presence of hypertension (frequentist OR = 1.23, 95% CI 0.52-2.92, p = 0.631 and Bayesian posterior median OR = 1.25, 95% CI 0.58-2.60). Neutrophil-to-lymphocyte ratio (NLR) and D-dimer levels were strongly associated with primary outcomes. In conclusion, the presence of hypertension and use of ACEIs/ARBs were not significantly associated with poor primary clinical outcomes; however, NLR and D-dimer levels were strong predictors of clinical worsening.

Inflammation and thrombosis in patients with COVID-19: A prothrombotic and inflammatory disease caused by SARS coronavirus-2.

Coronavirus disease 2019 (COVID-19) caused by 'Severe Acute Respiratory Syndrome Coronavirus-2' (SARS-CoV-2) infection emerged in Wuhan, a city of China, and spread to the entire planet in early 2020. The virus enters the respiratory tract cells and other tissues via ACE2 receptors. Approximately 20% of infected subjects develop severe or critical disease. A cytokine storm leads to over inflammation and thrombotic events. The most common clinical presentation in COVID-19 is pneumonia, typically characterized by bilateral, peripheral, and patchy infiltrations in the lungs. However multi-systemic involvement including peripheral thromboembolic skin lesions, central nervous, gastrointestinal, circulatory, and urinary systems are reported. The disease has a higher mortality compared to other viral agents causing pneumonia and unfortunately, no approved specific therapy, nor vaccine has yet been discovered. Several clinical trials are ongoing with hydroxychloroquine, remdesivir, favipiravir, and low molecular weight heparins. This comprehensive review aimed to summarize coagulation abnormalities reported in COVID-19, discuss the thrombosis, and inflammation-driven background of the disease, emphasize the impact of thrombotic and inflammatory processes on the progression and prognosis of COVID-19, and to provide evidence-based therapeutic guidance, especially from antithrombotic and anti-inflammatory perspectives.

Cardiotrophin-1: A new predictor of atrial fibrillation relapses after successful cardioversion.

We aimed to investigate whether or not cardiotrophin-1 (CT-1) can be used as a predictor of sinus rhythm constancy in patients with atrial fibrillation (AF) converted to sinus rhythm. Thirty two patients with AF (48-78 years), without any structural heart disease were enrolled for the study. The control group consisted of 32, age and gender matched healthy persons. Measurements of CT-1 were made after transthoracic and transesophageal echocardiography prior to cardioversion (CV). Relapses of AF were investigated by monthly electrocardiograms (ECGs) and ambulatory ECGs at 1st, 3rd, and 6th month. At the end of 6th month, measurements of CT-1 were repeated. At the beginning patients with AF had increased CT-1 levels when compared to controls (0.94 ± 0.32 pg/mL vs. 0.30 ± 0.12 pg/mL, [p < 0.001]). At the end of follow-up of the 32 patients, 17 (53%) had AF relapse. Age, initial duration of AF, left ventricle diameters, ejection fraction, left atrium appendix flow rates were similar among patients with and without AF relapse. However, basal left atrium diameter (4.24 ± 0.14 cm vs. 4.04 ± 0.22 cm, p = 0.005), pulmonary artery pressure (32.82 ± 5 vs. 28.60 ± 6.23 mmHg, p = 0.004) and CT-1 values (1.08 ± 0.37 vs. 0.82 ± 0.16 pg/mL, p = 0.02) were significantly increased in patients with AF relapse. Furthermore, patients with relapsed AF had higher CT-1 levels at 6th month when compared to those in sinus rhythm (1.00 ± 0.40 vs. 0.71 ± 0.23 pg/mL). We conclude that post-CV, AF relapses are more frequent among patients with increased baseline CT-1 levels, and CT-1 may be a potential predictor of AF relapse.

Monocyte subsets in coronary artery disease and their associations with markers of inflammation and fibrinolysis.

AIMS: The multiple roles of monocytes in atherogenesis, including inflammation, angiogenesis and repair are attributed to the existence of different monocyte sub-populations. Scarce data are available on changes in phenotype and functional status of human monocyte subsets in patients with coronary artery disease (CAD), especially when monocytes are evaluated as three distinct subsets. METHODS AND RESULTS: Surface expression of receptors implicated in inflammation, repair and activation status (intracellular IKKß) of monocyte subsets was assessed by flow cytometry in 53 patients with CAD and compared to 50 age- and sex-matched healthy controls. Monocyte subsets were defined as CD14++CD16-CCR2+ (Mon1), CD14++CD16+CCR2+ (Mon2), and CD14+CD16++CCR2- (Mon3). Plasma levels of inflammatory cytokines (FACSArray) and fibrinolytic factors (ELISA) were measured in CAD. CAD was associated with reduced expression of CD14 on Mon1 (p = 0.02) and Mon3 (p = 0.036), higher expression of IL6 receptor on Mon1 (p = 0.025) and Mon2 (p = 0.015), CXCR4 on Mon1 (p = 0.035) and Mon3 (p = 0.003), and CD34 on all subsets (all p < 0.007). Monocyte CD163 expression correlated negatively with interleukin (IL)-6 levels (p < 0.01 for all subsets). Expression of vascular endothelial growth factor receptor-1 correlated positively with plasminogen activator inhibitor (PAI)-1 antigen levels (r = 0.47, p = 0.006). In vitro, monocyte subsets derived from CAD patients showed significantly altered responses to endotoxin stimulation compared to monocytes from healthy controls. CONCLUSIONS: There is a complex interplay between phenotype and activity of monocytes and plasma cytokines and fibrinolytic factors. These findings support the presence of unique roles for the three human monocyte subsets in atherogenesis and CAD pathogenesis.

Antiplatelet therapy in atherothrombotic cardiovascular diseases for primary and secondary prevention: a focus on old and new antiplatelet agents.

Aspirin has long been the mainstay of primary and secondary prevention against myocardial infarction and ischemic cerebrovascular events. However, the incremental value of aspirin for primary prevention has recently been subject to debate given data from recent large clinical trials, as the net clinical benefit is small. In secondary prevention, aspirin is still strongly recommended. Efforts in obtaining more efficient antiplatelet agents and to reduce cardiovascular morbidity and mortality have led to the development of new adenosine diphosphate (ADP) receptor antagonists, which are superior to clopidogrel. New generation antiplatelet drugs i.e. prasugrel and ticagrelor aim to reduce atherothrombotic events, mortality and stent thrombosis, as well as overcome low- or non-response to clopidogrel. Further agents with antiplatelet properties are being investigated at present. This overview aims to give insights into the rapidly changing field of antiplatelet strategies in cardiovascular diseases.

The nuclear factor--kappa B pathway in atherosclerosis: a potential therapeutic target for atherothrombotic vascular disease.

Nuclear factor kappa B (NFκB) is a transcription factor belonging to 'Rel' family that represents a crucial intracellular signal transduction system involved in several inflammatory diseases including atherosclerosis. Activation of NFκB mediated signal transduction has been established at different stages of atherosclerosis, beginning from plaque formation to its destabilization and rupture. The NFκB pathway is also involved in angiogenic, apoptotic and neoplastic processes. Experimental studies indicate that inhibition of these pathway may reduce inflammatory burden. The development of natural or pharmaceutical, selective and specific inhibitors of NFκB pathway over IκB kinase α or ß, may ultimately prove to be promising anti-atherosclerotic, anti-inflammatory, antiangiogenic and antiapoptotic therapeutic instruments that could potentially reduce inflammation, attenuate atherogenesis and prevent its complications.

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.

The CD40-CD40L system in cardiovascular disease.

The CD40-CD40L system is a pathway which is associated with both prothrombotic and proinflammatory effects. CD40 and its ligand were first discovered on the surface of activated T cells, but its presence on B cells, antigen-presenting cells, mast cells, and finally platelets, is evident. The soluble form of CD40L (sCD40L) is derived mainly from activated platelets and contributes to the pathophysiology of atherosclerosis and atherothrombosis. Indeed, sCD40L has autocrine, paracrine, and endocrine activities, and it enhances platelet activation, aggregation, and platelet-leucocyte conjugation that may lead to atherothrombosis. It has even been suggested that sCD40L may play a pathogenic role in triggering acute coronary syndromes. Conversely, blockade of this pathway with anti-CD40L antibodies may prevent or delay the progression of atherosclerosis. Concentrations of sCD40L also predict risk of future cardiovascular disease in healthy women and clinical outcomes in patients with acute coronary syndromes. However, there are controversial and uncertain points over the application of this biomarker to clinical cardiology. In this review, we provide an overview of potential implications of CD40-CD40L signalling and sCD40L as a biomarker in patients with atherosclerotic vascular diseases.

Dronedarone as a new treatment option for atrial fibrillation patients: pharmacokinetics, pharmacodynamics and clinical practice.

IMPORTANCE OF THE FIELD: Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia, affecting 1 - 2% of the population. Despite several developments in antithrombotic, antiatherosclerotic and device-based cardiac therapies, few noteworthy antiarrhythmic drugs have been developed. AREAS COVERED IN THIS REVIEW: Dronedarone, a modified analogue of amiodarone, has the pharmacological ability of blocking multiple ion channels. This overview summarizes the pharmacokinetic and pharmacodynamic properties of dronedarone, evaluates its potential application to daily clinical cardiology practice according to the evidence provided by clinical trials, and provides a future clinical perspective for the use of this drug. WHAT THE READER WILL GAIN: The readers will gain an understanding of the findings of recent trials performed with dronedarone, which will provide important information for this relatively new antiarrhythmic drug, used for the treatment of atrial fibrillation. TAKE HOME MESSAGE: Dronedarone provides a reasonable efficacy and safety profile. Recent clinical trials indicate that dronedarone may support maintenance of sinus rhythm, decrease hospitalizations and reduce healthcare costs even in AF patients with structural heart disease but without severe or unstable cardiac failure.

The assessment of stroke and bleeding risk in atrial fibrillation: where are we now?

Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia. Patients with AF are at increased risk of thromboembolism and ischemic stroke. Many stroke risk factors, including increasing age, diabetes mellitus, hypertension and congestive heart failure, are themselves associated with the development of AF. The risk of stroke in AF is not homogeneous, and many different risk stratification schemas are available for the evaluation of thromboembolic stroke risk in AF patients. In addition, the risk of bleeding associated with anti-thrombotic therapy also needs to be considered during the anti-thrombotic therapy decision-making process. However, there are few published and validated bleeding risk schema available for AF patients. The availability of user-friendly risk stratification schemas could accurately discriminate patients' risk for stroke and anticoagulant therapy-related bleeding, and improve adherence to guidelines for thromboprophylaxis in AF.

Dronedarone or amiodarone for rhythm control for atrial fibrillation: implications from the DIONYSOS study.

Management of persistent AF involves rhythm or rate control strategies and thromboprophylaxis for cardioembolic events. Although amiodarone appears to be more effective than other current antiarrhythmics for a rhythm control approach in AF patients, many side effects limit its long-term use. Dronedarone is a new antiarrhythmic drug that may offer advantages for rhythm control, given its relative safety (although not in patients with decompensated heart failure), efficacy and tolerability. With regard to the latter, dronedarone has fewer adverse effects and is better tolerated than amiodarone. Nonetheless, in one head-to-head comparison of dronedarone and amiodarone, the latter drug was superior to dronedarone for maintenance of sinus rhythm post cardioversion, but dronedarone was safer and better tolerated, with useful benefit to decrease hospitalizations and thus healthcare costs. This provides clinicians (and patients) with a new option when choosing antiarrhythmic therapy.

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 Pearson's 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.

The role of monocytes in atherosclerotic coronary artery disease.

Inflammation plays a key role in the pathogenesis of atherosclerosis. The more we discover about the molecular pathways involved in atherosclerosis, the more we perceive the importance of monocytes in this process. Circulating monocytes are components of innate immunity, and many pro-inflammatory cytokines and adhesion molecules facilitate their adhesion and migration to the vascular endothelial wall. In addition to the accumulation of lipids and formation of atherogenic 'foam' cells, monocytes may promote atherosclerotic plaque growth by production of inflammatory cytokines, matrix metalloproteinases, and reactive oxidative species. However, the contribution of monocytes to atherogenesis is not only limited to tissue destruction. Monocyte subsets are also involved in intraplaque angiogenesis and tissue reparative processes. The aim of this overview is to discuss the mechanisms of monocyte activation, the pivotal role and importance of activated monocytes in atherosclerotic coronary artery disease, their implication in the development of acute coronary events, and their potential in cardiovascular reparative processes such angiogenesis.

Nebivolol prevents remodeling in a rat myocardial infarction model: an echocardiographic study.

OBJECTIVE: Ventricular remodeling (VR) which develops after myocardial infarction (MI) plays an important role in progressive left ventricular dysfunction. We aimed to investigate the role of nebivolol treatment on VR after a MI in a rat ischemia-reperfusion model. METHODS: Rats were divided into 3 groups of 12 each: sham operated (sham-control), MI-induced (MI-control) and nebivolol treated (MI-nebivolol). Left ventricular (LV) diameters, volumes, and diastolic filling parameters were evaluated by echocardiography. On the 28th day, after recording the systemic and LV pressures and determining the plasma nitric oxide (NO) and peroxynitrite (ONOO-) levels , animals were sacrificed and heart, body and LV weights (HW, BW, LVW) were measured and infarct sizes were determined. Results were evaluated statistically by ANOVA for repeated measurements 3x3 factorial design with post-hoc Bonferroni test. RESULTS: After MI, while VR (an increase in LV diameters and volumes associated with a decrease in EF, FS and posterior wall thickness change (LWPc) was significant in MI-control rats (p<0.05 for; all comparisons) these changes were significantly less in MI-nebivolol group (p=0.08 and p=0.06 for EF and FS respectively). LV end diastolic pressure (LVEDP) was lower (p<0.005) and Delta+/- dp/dt's (p<0.05) were higher in MI-nebivolol group compared to MI-control animals. Although infarct sizes were similar in MI-induced groups (p=0.79); LVW/HW and HW/BW's were significantly greater in the MI-control group compared to sham-control (p<0.01 for all comparisons), these changes were not statistically significant in MI-nebivolol group. The increase in plasma NO and ONOO- levels were also prevented with nebivolol. CONCLUSION: Nebivolol therapy reduced the effects of VR in rats after MI. These beneficial effects were not related to its heart rate and blood pressure reducing effects. Nitric oxide regulatory action of this compound may contribute these beneficial effects on VR developed after MI.

Relationship between left ventricular hypertrophy, hypertensive retinopathy, microalbuminuria and echocardiographic modalities in newly diagnosed hypertensive patients.

Longitudinal myocardial function (LMF) may be impaired while systolic function is still normal. We investigated relationship between LMF and hypertensive organ damage in newly diagnosed stage I hypertensive patients. A total of 57 patient with never treated stage I hypertension and 48 matched healthy control subject were enrolled in the study. Conventional 2-D, Doppler and tissue wave Doppler imaging (TDI) echocardiography were used. LMF was evaluated by the septal and lateral strain (S) and strain rate (SR) measurements. Hypertensive complications were evaluated by the urine microalbumin levels and retinal examination. A multivariate regression analysis was perfomed to assess the relation between the variables. Ejection fraction, mid-wall fractional shortenning, systolic movement rates (TDs) in TDI were similar both in hypertensive and control groups. In patients with left ventricular hypertrophy, septal TDs (7.29 +/- 1.28 vs. 8.06 +/- 1.19 cm, P = 0.03), lateral TDs (8.46 +/- 1.83 vs. 9.87 +/- 2.42 cm, P = 0.01) and lateral S (-13.02 +/- 7.83 vs. -18.86 +/- 8.60%, P = 0.01) values were significantly lower. Septal S (-13.67 +/- 3.52 vs. -19.09 +/- 5.96%, P < 0.01) and SR (-0.83 +/- 0.29 vs. -1.22 +/- 0.28 1/S, P < 0.01) were significantly decreased in hypertensive patients with microalbuminuria. Septal S value was also significantly decreased in patients with retinopathy (-14.76 +/- 5.55 vs. -20.20 +/- 5.44%, P = 0.01). Multivariate analysis showed that only septal and lateral S values were independent factors for the retinopathy and left ventricular hypertrophy, respectively. In hypertensive patients, LMF established by the measurement of S and SR, might be impaired and also related with end organ damage while global circumferential function is preserved.

Impact of genetic polymorphisms on platelet function and aspirin resistance.

Genetic polymorphisms may affect platelets' responses to the antiplatelet therapy. Our aim was to determine the role of genetic polymorphisms on aspirin resistance in patients with coronary heart disease (CHD). A total of 126 consecutive patients (35-85 years old, 32% women) with chronic stable CHD was enrolled in the study. Platelet function assays were realized by the platelet function analyzer (PFA)-100 with collagen and epinephrine (Col/Epi) and collagen and adenosine diphosphate (Col/ADP) cartridges. Aspirin resistance was defined as having a closure time of less than 186 s with Col/Epi cartridges despite regular aspirin therapy. Factor V, prothrombin, factor XIII, beta-fibrinogen, plasminogen activator inhibitor I (PAI-1), glycoprotein IIIa, methylene tetrahydrofolate reductase, ACE and ApoB gene polymorphisms were determined by three consecutive steps: isolation and amplification of DNA and reverse hybridization. We determined that 30 patients (23.8%) had aspirin resistance by the PFA-100. Mean closure time measured with the Col/ADP cartridges was 74 +/- 12 s (51-104 s). Ten of the 30 patients with aspirin resistance were women (33.3%). Genetic polymorphisms were determined in 30 aspirin-resistant and 17 aspirin-sensitive patients. No statistically significant relationship was determined between aspirin resistance and the genetic panel. In our study we did not determine a significant relationship between the aspirin resistance and factor V, prothrombin, factor XIII, beta-fibrinogen, PAI-1, glycoprotein IIIa, methylene tetrahydrofolate reductase, ACE and ApoB gene polymorphisms.