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.

Influences of genetic variants in interleukin-15 gene and serum interleukin-15 levels on coronary heart disease.

Interleukin-15 (IL-15) is a potent proinflammatory cytokine that is now considered a key component of atherosclerosis. Proinflammatory gene polymorphisms lead to variations in the production and level of the proteins. In light of these findings, we hypothesized that variations in the gene coding for IL-15 influence the risk of coronary heart disease (CHD) by modulating the IL-15 levels. To test this hypothesis, we examined 5 single nucleotide polymorphisms (SNPs) in IL-15 gene and IL-15 levels in 102 patients with acute coronary syndrome (ACS), 102 patients with chronic ischemic stable CHD and 162 healthy control subjects. This study is the first report showing the influences of IL-15 gene variants and IL-15 levels on CHD. The five single nucleotide polymorphisms (SNPs) within the IL-15 gene, G367A, C267T, A14035T, C13687A, and A10504G were carried out by polymerase chain reaction/restriction fragment length polymorphism (PCR/RFLP). Serum IL-15 levels were significantly higher in both acute and chronic patients than in controls. Genetic variants of IL-15 gene and IL-15 levels were associated with CHD. In conclusion, our study supports the hypothesis that genetic variation in IL-15 gene and IL-15 levels influence the risk of CHD. Further studies are needed to confirm our hypothesis.

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.

Association of genetic variants in Methylenetetrahydrofolate Reductase and Paraoxonase-1 genes with homocysteine, folate and vitamin B12 in coronary artery disease.

BACKGROUND: The aim of the present study was to investigate the association between genetic variants in metylenetetrahydrofolate reductase (MTHFR) and Paraoxonase-1 (PON1) 55/192 genes and total homocysteine (tHcy), folate, B12 vitamin, and PON1 levels in patients with coronary artery disease (CAD). METHODS: The study included 235 patients with CAD and 268 healthy control subjects. RESULTS: LL and LM genotypes and L allele of PON1 55 were over-represented in patients. In contrast, MM genotype and M allele were more frequent in controls. QQ genotype and Q allele of PON1 192 and CT genotype of MTHFR were significantly diminished and QR genotype and R allele were significantly elevated in CAD patients compared with controls. The plasma tHcy were elevated but B12 levels were diminished in patients. PON1 55 and 192 genetic variants were significantly associated with PON1 activity, triglyceride, total cholesterol, tHcy and, high-density lipoprotein-cholesterol and low-density lipoprotein-cholesterol in patients, respectively. CONCLUSION: Genetic variants of PON1 55/192 and MTHFR were associated with CAD.

Atrial and ventricular arryhthmogenic potential in Turner Syndrome.

BACKGROUND: P-wave dispersion (Pd), corrected P-wave dispersion (Pdc), QT-wave dispersion (QTd), and corrected QT-wave dispersion (QTdc) parameters were not assessed in Turner Syndrome (TS) before. The aim of this study is to investigate the cardiac arrhythmogenic potential in patients with TS. METHODS: Thirty-one patients with TS and 30 healthy women were enrolled in the study. For this purpose 12-lead electrocardiogram (ECG) and 24-hour ambulatory ECG recordings were performed. RESULTS: Pd, Pdc, QTd, and QTdc were significantly higher in patients with TS. On 24-hour ambulatory ECG recording, the mean heart rate (HR) was higher, while the mean of all RR intervals between normal beats (MeanNN), the standard deviation of all the RR intervals (SDNN), the square root of the mean of the squared differences of two consecutive RR intervals (rMSSD), and the percentage of the beats with consecutive RR interval difference more than 50 milliseconds (pNN50) were lower in TS. CONCLUSION: There were significant increases in Pd, Pdc, QTd, and QTdc in patients with TS and they may be features of the disease. The frequency of supraventricular arrhythmias was increased. There also was a significant deterioration of sympathetic and parasympathetic components of autonomic function as assessed by heart rate variability (HRV) in Turner patients.

Metastatic Ewing's sarcoma involving the right ventricle.

Cardiac metastasis of Ewing's sarcoma is rare. A 22-year-old woman was admitted with complaints of palpitation and fatigue on exertion. She had a seven-year history of radical right tibial resection for Ewing's sarcoma and was also receiving chemotherapy for lung metastasis of Ewing's sarcoma. Both transthoracic and transesophageal echocardiography demonstrated a single, large (3x3.5 cm) inhomogeneous mass located in the free wall of the right ventricle. To differentiate the mass from a massive thrombus, contrast-enhanced magnetic resonance imaging was performed. The mass showed partial contrast enhancement, suggesting a malignant metastatic mass. Surgical resection was not considered due to accompanying lung metastasis and potentially poor outcome of the operation.

[The relationship between aspirin resistance and endothelial dysfunction in patients with stable coronary artery disease]. / Kararli koroner arter hastaliginda aspirin direnci ile endotel disfonksiyonu arasindaki iliski.

OBJECTIVES: Endothelial dysfunction may enhance platelet aggregation despite regular aspirin therapy. We investigated the relationship between aspirin-resistant platelet aggregation and endothelial dysfunction in patients with stable coronary artery disease. STUDY DESIGN: The study included 98 patients (60 males, 38 females; mean age 62+/-8 years) receiving medical treatment for stable coronary artery disease. Platelet function assays were performed with the Platelet Function Analyzer (PFA)-100 with collagen and epinephrine (Col/Epi) and collagen and adenosine diphosphate cartridges. Aspirin resistance was defined as a closure time of less than 186 seconds with Col/Epi cartridges despite regular aspirin therapy. Endothelial function was assessed via measurement of flow-mediated dilatation by brachial artery ultrasonography. RESULTS: Twenty patients (20.4%) were found to be aspirin-resistant by the PFA-100. There were no significant differences between patients with and without aspirin resistance with respect to the mean aspirin dose administered and other medications. The mean basal diameter of the brachial artery was 4.11 mm and the mean flow-mediated dilatation (percentage change from basal diameter) was 4.7% in patients with aspirin resistance. The corresponding figures were 4.14 mm and 5.3% in the absence of aspirin resistance (p>0.05). CONCLUSION: In our study, endothelial dysfunction was found in all the patients with stable coronary artery disease, without any association of its presence and severity with aspirin resistance.

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.

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.

The role of platelet glycoprotein IIIa polymorphism in the high prevalence of in vitro aspirin resistance in patients with intracoronary stent restenosis.

OBJECTIVES: The aim of our study was to determine the relation between platelet glycoprotein IIIa (Pl A ) polymorphism and aspirin resistance in patients with intracoronary stent restenosis. BACKGROUND: Clinically, aspirin resistance is defined as having thrombotic and embolic cardiovascular events despite regular aspirin therapy. Platelet glycoprotein IIIa polymorphism is said to be a possible mechanism of aspirin resistance. METHODS: We studied the prevalence of aspirin resistance in 204 previously intracoronary stent-implanted patients with stable coronary artery disease. In 102 of these patients, intracoronary stent restenosis was present. Platelet functions were analyzed in a platelet function analyzer (PFA-100, Dade Behring, Germany) with collagen and/or epinephrine (Col/Epi) and collagen and/or adenosine diphosphate cartridges. Closure time <186 seconds was defined as aspirin resistance with Col/Epi cartridges of PFA-100. The Pl A polymorphisms of 43 aspirin-resistant and 51 aspirin-sensitive subjects were determined with polymerase chain reaction and restriction fragments length polymorphism. RESULTS: A total of 31.3% (n = 32) of patients with intracoronary stent restenosis and 10.7% (n = 11) of patients with patent intracoronary stents were resistant to aspirin by PFA-100. The Pl A1,A1 allele of glycoprotein IIIa was present in 36 subjects (83.7.%) and the Pl A1,A2 allele was present in 7 subjects (16.2.%) in the aspirin-resistant patients group. The Pl A1,A1 allele of glycoprotein IIIa was present in 37 subjects (72.5%) and the Pl A1,A2 allele was present in 14 subjects (27.5%) in the aspirin-sensitive patients group ( P = .195). CONCLUSION: Our results suggest that platelets of patients with intracoronary stent restenosis with or without Pl A2 heterozygosity of glycoprotein IIIa are more likely to be resistant to low-dose aspirin therapy.

Non-invasive evaluation of endothelial function in hypertensive elderly patients.

Impaired endothelium-dependent vasomotion is a diffuse disease process resulting in abnormal regulation of blood vessel tone and loss of several atheroprotective effects of the normal endothelium. The aim of the present study was to investigate the effects of aging and hypertension on endothelial function. Sixty-six geriatric subjects with ages over 60 (48 hypertensive and 18 healthy) and 40 middle-aged subjects (16 hypertensive and 24 healthy) were included in the study. Systemic vascular endothelial function was evaluated through measuring brachial arterial vasodilation, a physiologic answer to reactive hyperemia occured with increased blood flow in the vessel after transient ischemia (flow-mediated dilation, FMD%), and with carotid artery intima-media thickness (IMT) measurement, using high-resolution ultrasonography. Endothelial independent vasodilation was also measured after administration of sublingual isosorbide dinitrate (isosorbide dinitrate mediated dilation, IDNMD%). FMD% was significantly decreased in elderly and/or hypertensive (HT) patients (geriatric HT: 9.5 +/- 4.7%, geriatric non-HT: 12.7 +/- 5.5%, middle-aged HT: 12.9 +/- 4.3% and middle-aged non-HT: 18.9 +/- 8.1%) (geriatric HT versus geriatric non-HT (P = 0.02), geriatric HT versus middle-aged HT (P = 0.01), geriatric non-HT versus middle-aged non-HT (P = 0.008)). Both FMD% and IDNMD% were inversely correlated with age, baseline vessel diameter and carotid artery intima-media thickness. FMD% was also inversely correlated with diastolic blood pressure. No correlation was found between FMD% and systolic blood pressure, serum cholesterol and triglyceride levels. Endothelium dependent (EDD) and independent dilatation of large arteries decreased with aging even in the healthy elderly, and FMD further declined in HT elderly patients, indicating that age and hypertension independently impair endothelial function. Positive correlations with age and hypertension, and significant inverse correlation with FMD, makes carotid artery IMT a possible indicator of endothelial function.

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.

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 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.