ABSTRACT
Troponin I and T as cardiac-specific biomarkers are highly useful tools not only in the diagnosis of acute coronary syndromes but also as independent predictors of several other clinical conditions. High-sensitivity cardiac troponin (hs-cTn) assays allow the detection of considerably low concentrations of cardiac troponin in apparently healthy and asymptomatic individuals, being a candidate tool for cardiovascular risk stratification in the general population. A group of Greek experts summarized the bulk of evidence regarding the use of hs-cTnI as a predictor of cardiovascular events and mortality in apparently healthy individuals and its additive value on top of existing risk stratification methods. This document could serve as a guide for the incorporation of hs-cTnI as an additional risk stratification tool in cardiovascular prevention strategies in apparently healthy individuals.
Subject(s)
Cardiovascular Diseases , Troponin I , Humans , Troponin T , Cardiovascular Diseases/diagnosis , Cardiovascular Diseases/epidemiology , Biomarkers , Risk FactorsABSTRACT
The pivotal role of inflammation in the pathophysiology of heart-failure (HF) development and progression has long been recognized. High blood levels of pro-inflammatory and inflammatory markers are present and associated with adverse outcomes in patients with HF. In addition, there seems to be an interrelation between inflammation and neurohormonal activation, the cornerstone of HF pathophysiology and management. However, clinical trials involving anti-inflammatory agents have shown inconclusive or even contradictory results in improving HF outcomes. In the present review, we try to shed some light on the reciprocal relationship between inflammation and HF in an attempt to identify the central regulating factors, such as inflammatory cells and soluble mediators and the related inflammatory pathways as potential therapeutic targets.
ABSTRACT
BACKGROUND: B-thalassemia carrier state or thalassemia minor confers cardiovascular protection through favorable lipidemic and blood pressure profile. However, its impact on inflammatory status-a common denominator of the above conditions-has not been addressed. METHODS: We investigated a wide range of inflammatory markers [white blood cell (WBC) count, homocysteine, C-reactive protein (CRP), serum amyloid A (SAA), fibrinogen, plasminogen, fibronectin, plasminogen activator inhibitor-1 (PAI-1), and uric acid] in a large cohort of 15â805 newly diagnosed hypertensive patients (8299 men, 7506 women); 626 of them (4.0%) had thalassemia minor. RESULTS: The levels of WBC, homocysteine, CRP, SAA, fibrinogen, and PAI-1 were significantly lower in thalassemia minor patients, but not of plasminogen, fibronectin, and uric acid. In multivariate linear regression analyses, the lower values of WBC (<0.001), CRP (<0.001), homocysteine (<0.001), fibrinogen (<0.001), and PAI-1 (0.008), but not of SAA, were independently associated with thalassemia minor. The interaction between thalassemia minor and body mass index had a significant impact only on WBC and CRP (P for the interaction 0.010 and 0.005, respectively), whereas the interaction between thalassemia minor and sex had a significant impact only on fibrinogen (P for the interaction 0.007). CONCLUSION: Thalassemia minor is followed by a favorable inflammatory profile that may contribute to the overall better cardiovascular health of the carriers.
Subject(s)
Hypertension/blood , Inflammation Mediators/blood , Inflammation/blood , beta-Thalassemia/blood , Aged , Biomarkers/blood , Body Mass Index , C-Reactive Protein/analysis , Female , Fibrinogen/analysis , Health Status , Homocysteine/blood , Humans , Hypertension/diagnosis , Inflammation/diagnosis , Leukocyte Count , Male , Middle Aged , Plasminogen Activator Inhibitor 1/blood , Serum Amyloid A Protein/analysis , beta-Thalassemia/diagnosis , beta-Thalassemia/geneticsSubject(s)
Antigens, CD34/immunology , Electric Stimulation Therapy/methods , Endothelial Progenitor Cells/cytology , Heart Failure/therapy , Stroke Volume/physiology , T-Lymphocytes/immunology , Vascular Endothelial Growth Factor A/blood , Aged , Aged, 80 and over , Female , Heart Failure/blood , Heart Failure/physiopathology , Humans , Lower Extremity , Male , Middle Aged , Treatment OutcomeABSTRACT
Neurohumoral activation is an important feature of heart failure. Recent advances in molecular biology and imaging techniques permitted a better understanding of the central role that hypothalamus plays in the modulation of dysfunctional mechanisms, as well as the occurrence of comorbidities, such as depression, in heart failure patients. This review summarizes the commonly reported neural reflexes and molecular signaling pathways at the level of the hypothalamus along with the dysfunctional mechanisms within the paraventricular nucleus and other areas of the hypothalamus in heart failure and describes some relevant therapeutic implications.
