76 research outputs found

    Practical solutions for hypertensive patients with dyslipidemia

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    Arterial hypertension and dyslipidemia often coexist and constitute major risk factors of ischemic heart disease. Aggressive treatment of both comorbidities is of paramount importance to decrease global risk. Low adherence is a determinant of poor risk factor control and increases adverse cardiovascular outcomes. Regarding treatment of hypertension, combination therapy is superior in achieving target BP values compared to up-titrating monotherapy and it is recommended in hypertension guidelines. The combined use of drugs in a single pill formulation increases adherence and reduces cardiovascular risk. Our review of the literature indicates that triple therapy with an angiotensin converting enzyme inhibitor, a calcium channel blocker and a statin is associated with a significant reduction in major cardiovascular events. This is attributed to synergy at the vascular, and is translated into efficacy at the clinical level. (C) 2017 Association for Research into Arterial Structure and Physiology. Published by Elsevier B.V. All rights reserved

    Effect of coffee and caffeine on aortic stiffness

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    Background: Caffeine has an unfavourable acute effect on aortic stiffness and wavereflections; however, whether there is a differential effect on arterial stiffness betweencaffeine alone and caffeine in conjunction with coffee has not been investigated. Aim ofthis study was to compare the acute effect of caffeine given alone and coffee on arterialstiffness and the influence of habitual coffee consumption on this effect. We also soughtto examine the effect of chronic coffee consumption on arterial stiffness and whetherthere is a differential mid-term change in aortic elastic properties and wave reflectionsafter a 2-week daily coffee and caffeine administration.Methods: Acute effect. The acute effect of coffee and caffeine was studied in 24 healthyvolunteers (11 habitual-13 nonhabitual coffee consumers) on four separate occasionsreceiving: a) triple coffee espresso, b) triple decaffeinated coffee espresso, c) 240 mg ofcaffeine alone (amount contained in a triple espresso) and d) placebo. Chronic effect.Aortic stiffness and wave reflections were evaluated in 228 healthy individualscategorized by reported daily coffee consumption. Furthermore, the effect of a 2-weeklong, daily coffee and caffeine consumption in the same dosage form was examined in12 healthy volunteers (mid-term effect). Results: Acute effect: In both habitual andnonhabitual coffee consumers, caffeinated coffee significantly increased carotid-femoral pulse wave velocity (PWV) and augmentation index (AIx) compared to decaffeinatedcoffee. In both groups caffeinated coffee and caffeine alone, significantly increased PWVand AIx, however, in nonhabitual drinkers, caffeinated coffee compared to caffeine led toa more potent effect. The effect of caffeinated and decaffeinated coffee was morepronounced in nonhabitual compared to habitual drinkers, whereas both groupsdemonstrated similar changes with caffeine. Population study: A linear relation betweencoffee consumption and PWV and AIx was observed (P for trend 450 mL/d). Mid-term effect: CarotidfemoralPWV and AIx did not significantly change with either 2-week long, daily coffeeor decaffeinated coffee consumption while the mid-term effect of daily caffeine intakesignificantly increased PWV and AIx (by 0.52 m/sec and 4.5 %, respectively at the end ofthe treatment period, P450 mL/ημέρα) παρουσίασαν 13%υψηλότερη τιμή της ΚΜΤΣΚ και 2πλάσια τιμή του 0Ε (P<0.01). Η ΚΜΤΣΚ και ο 0Ε δεμεταβλήθηκαν σημαντικά μετά από 2 εβδομάδες καθημερινής χορήγησης καφέ με ή χωρίς καφεΐνη ενώ αντίθετα, η καφεΐνη με τη μορφή δισκίου αύξησε σημαντικά τηνΚΜΤΣΚ (κατά 0.52 m/sec) και το 0Ε (κατά 4.5%) (P<0.05) μετά τις 2 εβδομάδεςκαθημερινής λήψης. Συμπεράσματα: Η χορήγηση καφέ (με ή χωρίς καφεΐνη) στα άτομαπου δεν καταναλώνουν καφέ σε καθημερινή βάση αυξάνει σε μεγαλύτερο βαθμό τουςδείκτες αρτηριακής σκληρίας και ανακλώμενων κυμάτων σε σχέση με τα άτομα πουπροσλαμβάνουν συστηματικά καφέ. Ενώ στην οξεία χορήγηση η παρουσία καφεΐνηςστον καφέ συνοδεύεται από μεγαλύτερη μεταβολή της αρτηριακής σκληρίας σε σχέση μετην απουσία της, στη μακροχρόνια χορήγηση δε υπάρχουν διαφορές μεταξύ των δύοαυτών τύπων καφέ. Αντίθετα, η μακροχρόνια χορήγηση καφεΐνης μεταβάλλει σημαντικάτους δείκτες αρτηριακής σκληρίας και ανακλώμενων τόσο οξέως όσο και μακροχρόνια.Τέλος, τα άτομα που προσλαμβάνουν μεγάλες ποσότητες καφέ παρουσιάζουν μειωμένηελαστικότητα στην αορτή και ενίσχυση των ανακλώμενων κυμάτων. Τα παραπάνωευρήματα είναι ιδιαίτερα σημαντικά και υποδηλώνουν τον προστατευτικό ρόλο πουδιαδραματίζουν άλλα συστατικά που βρίσκονται στον καφέ

    Pharmacologic Therapy for Erectile Dysfunction and its Interaction With the Cardiovascular System

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    Phosphodiesterase (PDE) enzymes are widely distributed throughout the body, having numerous effects and functions. The PDE type 5 (PDE5) inhibitors are widely used to treat erectile dysfunction (ED). Recent, intense preclinical and clinical research with PDE5 inhibitors has shed light on new mechanisms and has revealed a number of pleiotropic effects on the cardiovascular (CV) system. To date, PDE5 inhibition has been shown to be effective for the treatment of idiopathic pulmonary arterial hypertension, and both sildenafil and tadalafil are approved for this indication. However, current or future PDE5 inhibitors have the potential of becoming clinically useful in a variety of CV conditions such as heart failure, coronary artery disease, and hypertension. The present review discusses recent findings regarding pharmacologic treatment of ED and its interaction with the CV system and highlights current and future clinical applications beyond ED

    Biomarkers, erectile dysfunction, and cardiovascular risk prediction: the latest of an evolving concept

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    A number of circulating and imaging biomarkers are robustly associated with cardiovascular (CV) risk. The overall expectation from a biomarker in the erectile dysfunction (ED) setting is to enhance the optimal management of a man with this disorder but no clinical atherosclerosis. Evidence demonstrating that these biomarkers enhance risk prediction for individuals with ED is at this stage still limited for most of them. A better identification of the subsets of the ED population that require further risk stratification, as well as the initiation of randomized trials that will formally test the ability of biomarkers to predict CV risk, could make biomarker-guided prevention an attainable goal
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