Dexamethasone as Adjuvant Therapy to Moxifloxacin Attenuates Valve Destruction in Experimental Aortic Valve Endocarditis Due to Staphylococcus aureus▿

Although the beneficial effects of dexamethasone have frequently been investigated in various serious-infection settings, insufficient data on valve histology and cardiac function for infective endocarditis are available. The efficacy of moxifloxacin for the treatment of experimental aortic valve endocarditis due to methicillin-susceptible Staphylococcus aureus and the long-term effects of dexamethasone were evaluated in the current study. Sixty-eight rabbits were randomly assigned to four groups: A, B, C, and D. Group A consisted of 18 animals and functioned as a control group. Groups B and C consisted of 11 and 23 subjects, respectively, which received moxifloxacin for 5 days in a human-like pharmacokinetic simulation. Group D consisted of 16 animals that were administered moxifloxacin plus dexamethasone (0.25 mg/kg of body weight twice a day intravenously). The group B animals were sacrificed a day after the completion of treatment, and group C and D animals were sacrificed after 12 days in order to monitor any possible relapse and allow microbiological, histopathological, and echocardiographic evaluation of the long-term effects of glucocorticoids. No differences in survival, sterilization rates, or inflammatory infiltration and calcification of valve tissue were observed among the treated groups. However, the degrees of valve damage and collagenization were significantly worse, the fibroblast content was higher, and fractional shortening of the left ventricle fluctuated significantly in group C compared to group D (all groups, P < 0.05). We concluded that dexamethasone treatment for experimental S. aureus endocarditis attenuates valve destruction and preserves overall cardiac function without impeding the efficacy of moxifloxacin

Dexamethasone as adjuvant therapy to moxifloxacin attenuates valve destruction in experimental aortic valve endocarditis due to Staphylococcus aureus

Although the beneficial effects of dexamethasone have frequently been investigated in various serious-infection settings, insufficient data on valve histology and cardiac function for infective endocarditis are available. The efficacy of moxifloxacin for the treatment of experimental aortic valve endocarditis due to methicillin-susceptible Staphylococcus aureus and the long-term effects of dexamethasone were evaluated in the current study. Sixty-eight rabbits were randomly assigned to four groups: A, B, C, and D. Group A consisted of 18 animals and functioned as a control group. Groups B and C consisted of 11 and 23 subjects, respectively, which received moxifloxacin for 5 days in a human-like pharmacokinetic simulation. Group D consisted of 16 animals that were administered moxiffoxacin plus dexamethasone (0.25 mg;1kg of body weight twice a day intravenously). The group B animals were sacrificed a day after the completion of treatment, and group C and D animals were sacrificed after 12 days in order to monitor any possible relapse and allow microbiological, histopathological, and echocardiographic evaluation of the longterm effects of glucocorticoids. No differences in survival, sterilization rates, or inflammatory infiltration and calcification of valve tissue were observed among the treated groups. However, the degrees of valve damage and collagenization were significantly worse, the fibroblast content was higher, and fractional shortening of the left ventricle fluctuated significantly in group C compared to group D (all groups, P &lt; 0.05). We concluded that dexamethasone treatment for experimental S. aureus endocarditis attenuates valve destruction and preserves overall cardiac function without impeding the efficacy of moxifloxacin

Pharmacodynamic comparison of low-dose ticagrelor to low-dose prasugrel in patients with prior myocardial infarction: the ALTIC-2 study

Given that patients with prior myocardial infarction and features of high ischemic and low bleeding risk may benefit by extending dual antiplatelet therapy beyond 1 year, we aimed of assessing platelet reactivity provided by ticagrelor 60 mg bid versus prasugrel 5 mg od in 20 such patients participating in a randomized, crossover study. The primary end point of platelet reactivity at the end of the two treatment periods (by VerifyNow, in PRU) was significantly lower for ticagrelor (31.9 PRU [95% CI 12.3–51.4]) compared with prasugrel (132.1 PRU [111.9–152.3]) with a least squares mean difference of –100.2 PRU (72.1–128.3, P < .001). This dedicated pharmacodynamic study showed that in post-myocardial infarction patients with high atherothrombotic risk and receiving P2Y12 receptor antagonist beyond 1 year, low-dose ticagrelor results in a significantly lower platelet reactivity compared to low-dose prasugrel

Hypertension‐mediated organ damage regression associates with blood pressure variability improvement three years after successful treatment initiation in essential hypertension

Blood pressure variability (BPV) has been associated with the development, progression, and severity of cardiovascular (CV) organ damage and an increased risk of CV morbidity and mortality. We aimed to explore any association between short‐term BPV reduction and hypertension‐mediated organ damage (HMOD) regression in hypertensive patients 3‐year post‐treatment initiation regarding BP control. 24‐h ambulatory blood pressure monitoring (24 h ABPM) was performed at baseline in 180 newly diagnosed and never‐treated hypertensive patients. We measured 24 h average systolic (24 h SBP) and diastolic BP (24 h DBP) as well as 24 h systolic (sBPV) and diastolic BPV (dBPV). Patients were initially evaluated and 3 years later regarding arterial stiffness (PWV), left ventricular hypertrophy (LVMI), carotid intima‐media thickness (cIMT), 24 h microalbumin levels (MAU), and coronary flow reserve (CFR). Successful BP treatment was defined as 24 h SBP/DBP < 130/80 mm Hg based on 2nd ABPM and subsequently, patients were characterized as controlled (n = 119, age = 53 ± 11 years) or non‐controlled (n = 61, age = 47 ± 11 years) regarding their BP levels. In the whole population and the controlled group, 24 h SBP/DBP, sBPV/dBPV, LVMI, and IMT were decreased. Additionally, LVMI improvement was related with both sBPV (p < .001) and dBPV reduction (r = .18, p = .02 and r = .20, p = .03, respectively). In non‐controlled hypertensives, PWV was increased. In multiple linear regression analysis, sBPV and dBPV reduction predicted LVMI improvement in total population and controlled group independently of initial office SBP, mean BP, and 24 h‐SBP levels. In middle‐aged hypertensive patients, a 3‐year antihypertensive treatment within normal BP limits, confirmed by 24‐h ABPM, leads to CV risk reduction associated with sBPV and dBPV improvement

Peak exercise myocardial deformation indices during cardiopulmonary exercise testing are associated with exercise capacity and ventilatory efficiency in patients with dilated cardiomyopathy

Objective: Little is known about the exercise-induced changes in the multidimensional mechanical properties of the heart. We aimed to evaluate the myocardial deformation indices (MDI) at rest and their response at peak exercise during the same cardiopulmonary exercise testing (CPET) session, investigating their relationship to exercise capacity and ventilatory sufficiency in dilated cardiomyopathy (DCM) patients. Methods: We evaluated left ventricular (LV) function using speckle tracking imaging (STI) at rest and peak exercise during the same CPET session in 57 idiopathic DCM patients in New York Heart Association (NYHA) I–II class [54 ± 12 years, 42 males, ejection fraction (EF) 33 ± 9%]. We measured global longitudinal strain (GLS), longitudinal strain rate at systole (LSRS) and diastole (LSRD), and circumferential strain rate (CircS). Results: Resting GLS, LSRS, and LSRD were impaired compared with the predicted values but were improved at peak exercise (p −1.10 sec−1 (AUC = 0.80, p −13% (AUC = 0.81, p = 0.002) predicted impaired exercise capacity (peak VO2 34). In multiple regression analysis, peak exercise LSRS and GLS were independently related to the peak VO2 (Beta = −0.39, p = 0.003) and VE/VCO2 slope (Beta = 0.35, p = 0.02), respectively. Conclusions: Peak exercise LSRS and GLS in NYHA I–II DCM patients subjected to CPET were associated with aerobic exercise capacity and ventilatory efficiency. Consequently, LSRS and GLS at peak exercise, through their association with CPET-derived CV risk indices, may underline the severity of heart failure and predict future CV events in this DCM population

May We Use Non-Invasive Indices of Aortic Stiffness and Endothelial Glycocalyx as Biomarkers for Idiopathic Pulmonary Artery Hypertension Follow-Up?

Idiopathic pulmonary arterial hypertension (IPAH) initial evaluation and follow-up, a rare and incurable disease if left untreated, is based on a multiparametric approach (functional status of the patient, biomarkers, hemodynamic parameters and imaging evaluation of right heart impairment). Arterial stiffness (AS) and endothelial glycocalyx are indices of systemic circulation. We present the 3-years follow-up of a female IPAH patient. We propose aortic stiffness and endothelial glycocalyx indices as non-invasive markers of either improvement or deterioration of IPAH disease