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Pubblicazioni recenti - cardiac failure
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Subclinical cardiac stiffness is associated with arterial stiffness in healthy young nulligravid women: Potential links to preeclampsia.
Pregnancy Hypertens2019 Sep;18():49-54. doi: S2210-7789(19)30349-6.
Cooper Kylie M, Barrett Trace, McBride Carole A, Badger Gary J, Steiner Johannes, LeWinter Martin M, Bernstein Ira M,
Abstract
OBJECTIVES:
Preeclampsia is an independent risk factor for subsequent cardiovascular disease and diastolic dysfunction and has been linked to arterial stiffness. We hypothesized that arterial stiffness would be associated with echocardiographic markers of diastolic dysfunction in healthy nulligravid women.
STUDY DESIGN:
31 healthy nulligravid women underwent assessment of peripheral arterial stiffness via aorto-femoral pulse wave velocity, popliteal distensibility and ? stiffness measures as well as hemodynamic response to volume challenge. 22 underwent cardiac assessment via conventional and stress echocardiography with a focus on diastolic function utilizing tissue/pulse wave Doppler imaging and 3D speckle tracking. Bivariate associations between variables were evaluated using correlation coefficients (Pearson r) and Student's t-tests.
RESULTS:
No participants had echocardiographic values meeting criteria for overt diastolic dysfunction. Baseline global circumferential strain was significantly correlated with distensibility and ? stiffness (n?=?18, r?=?-0.61, p?=?0.007, n?=?18, r?=?0.56, p?=?0.01). Peak deceleration time was correlated with ?stiffness (n?=?9; r?=?0.80, p?=?0.01). Pulse wave velocity was not significantly correlated with cardiac measures (p?>?0.05). Family history of a first or second degree relative with myocardial infarction or hypertension was associated with decreased popliteal artery distensibility (p?=?0.02 and p?=?0.03, respectively).
CONCLUSIONS:
In healthy nulligravid women there is evidence that markers of decreased left ventricular relaxation are associated with increased peripheral vascular stiffness as is a family history of myocardial infarction or hypertension. These findings raise the possibility that the diastolic dysfunction and arterial stiffness observed in the setting of preeclampsia are driven by underlying properties present prior to pregnancy and contribute to lifetime cardiovascular risk.
Copyright © 2019 International Society for the Study of Hypertension in Pregnancy. Published by Elsevier B.V. All rights reserved.
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Interrupting providers with clinical decision support to improve care for heart failure.
Int J Med Inform2019 Sep;131():103956. doi: S1386-5056(19)30462-9.
Blecker Saul, Austrian Jonathan S, Horwitz Leora I, Kuperman Gilad, Shelley Donna, Ferrauiola Meg, Katz Stuart D,
Abstract
BACKGROUND:
Evidence-based therapy for heart failure remains underutilized at hospital discharge, particularly for patients with heart failure who are hospitalized for another cause. We developed clinical decision support (CDS) to recommend an angiotensin converting enzyme (ACE) inhibitor during hospitalization to promote its continuation at discharge. The CDS was designed to be implemented in both interruptive and non-interruptive versions.
OBJECTIVES:
To compare the effectiveness and implementation of interruptive and non-interruptive versions of a CDS to improve care for heart failure.
METHODS:
Hospitalizations of patients with reduced ejection fraction were pseudo-randomized to deliver interruptive or non-interruptive CDS alerts to providers based on even or odd medical record number. We compared discharge utilization of an ACE inhibitor or angiotensin receptor blocker (ARB) for these two implementation approaches. We also assessed adoption and implementation fidelity of the CDS.
RESULTS:
Of 958 hospitalizations, interruptive alert hospitalizations had higher rates of discharge utilization of ACE inhibitors or ARBs than non-interruptive alert hospitalizations (79.6% vs. 74.2%, p?=?0.05). Utilization was higher for interruptive alert versus non-interruptive alert hospitalizations which were principally for causes other than heart failure (79.8% vs. 73.4%; p?=?0.05) but no difference was observed among hospitalizations with a principal heart failure diagnosis (85.9% vs.81.7%; p?=?0.49). As compared to non-interruptive hospitalizations, interruptive alert hospitalizations were more likely to have had: an alert with any response (40.6% vs. 13.1%, p?
CONCLUSIONS:
A CDS implemented as an interruptive alert was associated with improved quality of care for heart failure. Whether the potential benefits of CDS in improving cardiovascular care were worth the high burden of interruptive alerts deserves further consideration. CLINICALTRIALS.
GOV IDENTIFIER:
NCT02858674.
Copyright © 2019 Elsevier B.V. All rights reserved.
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Commentary on "Indicators of Impending Pig Kidney and Heart Xenograft Failure: Relevance to Clinical Organ Xenotransplantation" (Int J Surg 2019;Aug 21. pii: S1743-9191(19)30215-8. https://doi.org/10.1016/j.ijsu.2019.08.024. [Epub ahead of print]).
Int J Surg -
Identification of inhibitors of the RGS homology domain of GRK2 by docking-based virtual screening.
Life Sci2019 Sep;():116872. doi: S0024-3205(19)30799-4.
Echeverría Emiliana, Rueda Ana Julia Velez, Cabrera Maia, Juritz Ezequiel, Burghi Valeria, Fabián Lucas, Davio Carlos, Menna Pablo Lorenzano, Fernández Natalia Cristina,
Abstract
AIMS:
G protein-coupled receptor (GPCR) kinases (GRKs) are mainly involved in the desensitization of GPCRs. Among them, GRK2 has been described to be upregulated in many pathological conditions and its crucial role in cardiac hypertrophy, hypertension, and heart failure promoted the search for pharmacological inhibitors of its activity. There have been several reports of potent and selective inhibitors of GRK2, most of them directed to the kinase domain of the protein. However, the homologous to the regulator of G protein signaling (RH) domain of GRK2 has also been shown to regulate GPCRs signaling. Herein, we searched for potential inhibitors of receptor desensitization mediated by RH domain of GRK2.
MATERIALS AND METHODS:
We performed a docking-based virtual screening utilizing the crystal structure of GRK2 to search for potential inhibitors of the interaction between GRK2 and G?q protein. To evaluate the biological activity of compounds we measured, calcium response of histamine H1 receptor (H1R) using Fura-2AM dye and H1R internalization by saturation binding experiments in A549 cells. GRK2(45-178)GFP translocation was determined in HeLa cells through confocal fluorescence imaging.
KEY FINDINGS:
We identified inhibitors of GRK2 able to reduce the RH mediated desensitization of the histamine H1 receptor and GRK2 translocation to plasma membrane. Also candidates presented adequate lipophilia and cytotoxicity profile.
SIGNIFICANCE:
We obtained compounds with the ability of reducing RH mediated actions of GRK2 that can be useful as a starting point in the development of novel drug candidates aimed to treat pathologies were GRK2 plays a key role.
Copyright © 2019. Published by Elsevier Inc.
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The homozygous variant c.245G>A/p.G82D in PNPLA2 is associated with arrhythmogenic cardiomyopathy phenotypic manifestations.
Clin Genet2019 Sep;():. doi: 10.1111/cge.13642.
Rao Man, Guo Guang-Ran, Li Meng-Meng, Chen Shi, Chen Kai, Chen Xiao, Song Jiang-Ping, Hu Sheng-Shou,
Abstract
Arrhythmogenic cardiomyopathy (ACM) is a familial cardiomyopathy featured by fibro-fatty replacement of cardiomyocytes. Responsible genetic factors are not discernible in approximately one third of ACM probands. To investigate this further, we performed whole genome sequencing (WGS) in 14 mutation-negative ACM probands who underwent cardiac transplantation, and we identified one ACM proband with a rare homozygous missense variant in PNPLA2 (c.245G>A, p.G82D), a rate-limiting enzyme that hydrolyzes triglycerides into fatty-acids and diacylglycerol. Bioinformatic analysis suggested that this missense variant may lead to loss-of-function and therefore impair lipid catabolism. Genetic screening in this proband's family also inferred that the homozygous variant co-segregated with disease. To validate the pathogenicity of this variant and confirm its association with ACM, we established a knock-in mouse model carrying the orthologous human homozygous PNPLA2 variant. Interestingly, mice with the homozygous variant presented with arrhythmias and significant cardiac dysfunction at 12-weeks, whereas heterozygous mice were not affected. Moreover, those homozygous mice suffered sudden death and/or heart failure by age of 14-weeks. Pathological examination showed that extensive lipogenesis in cardiomyocytes and cardiac fibrosis were prominent in the myocardium. Herein, our data demonstrated that the homozygous missense variant PNPLA2 (c.245G>A, p.G82D) associated with a recessive form of ACM. This article is protected by copyright. All rights reserved.
This article is protected by copyright. All rights reserved.
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The impact of thoracic paravertebral block over post-operatory evolution in open lobectomy.
Ann Ital Chir2019 Sep;8():. doi: S0003469X19030641.
Popovici Bogdan I, Matei Dana, Iacoban Laura, Simion Ioana, Man Milena, Al Hajjar Nadim, Mois Emil, Popovici Cornelia, Chira Romeo, Iancu Cornel,
Abstract
AIM:
The thoracic paravertebral block (PVB), a technique of post-thoracotomy analgesia of similar effectiveness as continuous epidural analgesia (CEA) but with a better safety profile, is underutilized in current practice. This study compares the outcome of post-lobectomy patients in relation to the analgesic method used: parenteral analgesia (PA) vs. PVB + PA, and provides justification for the routine use of PVB in all patients where CEA is contraindicated.
METHODS:
We randomized 213 consecutive patients undergoing open lobectomy to benefit from two different protocols of postoperative analgesia: PA vs. PVB +PA. We compared the frequency of cardiac hemodynamic, respiratory, pleural or surgical-related complications.
RESULTS:
After lobectomy, the PVB patients (72/213) were found to have a significantly lower frequency of congestive heart failure (7.1%vs.0.0%)(p=0.049), ischemic cardiomyopathy (10.6%vs.0.0%)(p=0.010), pulmonary atelectasis (35%vs.1.1%)(p<0.001), residual pleural space (29.8%vs.15.3%)(p=0.032) and residual intrapleural blood clots (14.9%vs.1.4%)(p=0.005). Other postoperative complications, Intensive Care stay, total hospital stay and mortality rate were less frequent in the PVB group but without reaching statistical significance.
CONCLUSION:
The use of SPVB is associated with significant less postoperative complications than PA only. This study suggests that the SPVB might be the ideal choice in post-thoracotomy pain management when CEA cannot be used.
KEY WORDS:
Open lobectomy, Post-lobectomy, Thoracic paravertebral block.
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Correction to: Type 2 Diabetes Mellitus and Heart Failure: A Scientific Statement From the American Heart Association and the Heart Failure Society of America.
Circulation -
Adenosine Kinase Inhibition Augments Conducted Vasodilation and Prevents Left Ventricle Diastolic Dysfunction in Heart Failure With Preserved Ejection Fraction.
Circ Heart Fail2019 Aug;12(8):e005762. doi: 10.1161/CIRCHEARTFAILURE.118.005762.
Davila Alec, Tian Yanna, Czikora Istvan, Li Jie, Su Huabo, Huo Yuqing, Patel Vijay, Robinson Vincent, Kapuku Gaston, Weintraub Neal, Bagi Zsolt,
Abstract
BACKGROUND:
Heart failure with preserved ejection fraction (HFpEF) is often manifested as impaired cardiovascular reserve. We sought to determine if conducted vasodilation, which coordinates microvascular resistance longitudinally to match tissue metabolic demand, becomes compromised in HFpEF. We hypothesized that the metabolic vasodilator adenosine facilitates and that inhibition of ADK (adenosine kinase) augments conducted vasodilation for a more efficient myocardial perfusion and improved left ventricle (LV) diastolic function in HFpEF.
METHODS AND RESULTS:
We assessed conducted vasodilation in obese ZSF1 rats that develop LV diastolic dysfunction and is used to model human HFpEF. Additionally, conducted vasodilation was measured in arterioles isolated from the right atrial appendages of patients with HFpEF. We found a markedly reduced conducted vasodilation both in obese ZSF1 rats and in patients with HFpEF. Impaired conducted vasodilation was accompanied by increased vascular ADK expression. Isolated rat and human arterioles incubated with adenosine (10 nmol/L) or ADK inhibitor ABT-702 (0.1 µmol/L) both displayed augmented conducted vasodilation. Treatment of obese ZSF1 rats with ABT-702 (1.5 mg/kg, IP for 8 weeks) prevented LV diastolic dysfunction, and in a crossover design augmented conducted vasodilation and improved LV diastolic function. ABT-702 treated obese ZSF1 rats exhibited reduced expression of myocardial carbonic anhydrase 9 and collagen, surrogate markers of myocardial hypoxia.
CONCLUSIONS:
Upregulation of vascular ADK mitigates adenosine-facilitated conducted vasodilation in obese ZSF1 rats and in patients with HFpEF. We propose that pharmacological inhibition of ADK could be beneficial for therapeutic augmentation of conducted vasodilation, thereby improving tissue perfusion and LV diastolic function in HFpEF.
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Long-Term Effect of Ultrathin-Strut Versus Thin-Strut Drug-Eluting Stents in Patients With Small Vessel Coronary Artery Disease Undergoing Percutaneous Coronary Intervention: A Subgroup Analysis of the BIOSCIENCE Randomized Trial.
Circ Cardiovasc Interv2019 Aug;12(8):e008024. doi: 10.1161/CIRCINTERVENTIONS.119.008024.
Iglesias Juan F, Heg Dik, Roffi Marco, Tüller David, Noble Stéphane, Muller Olivier, Moarof Igal, Cook Stéphane, Weilenmann Daniel, Kaiser Christoph, Cuculi Florim, Häner Jonas, Jüni Peter, Windecker Stephan, Pilgrim Thomas,
Abstract
BACKGROUND:
Randomized trials evaluating the Orsiro biodegradable polymer sirolimus-eluting stent (BP-SES; 60 and 80 ?m strut thickness for stent diameters ?3 and >3 mm, respectively) did not stratify according to vessel size and failed to specify the impact of ultrathin-strut thickness on long-term clinical outcomes compared with durable polymer everolimus-eluting stents (DP-EES). We sought to assess the long-term effect of ultrathin-strut (60 ?m) BP-SES versus thin-strut (81 ?m) DP-EES on long-term outcomes in patients undergoing percutaneous coronary revascularization for small vessel disease.
METHODS:
In a subgroup analysis of the randomized, multicenter, noninferiority BIOSCIENCE trial, patients with stable coronary artery disease or acute coronary syndrome randomly assigned to treatment with BP-SES or DP-EES were stratified according to vessel size (?3 mm versus >3 mm) as a surrogate to compare patients treated with ultrathin-strut versus thin-strut drug-eluting stent. The primary end point was target lesion failure, a composite of cardiac death, target vessel myocardial infarction, and clinically indicated target lesion revascularization, within 5 years.
RESULTS:
Among 2109 patients, 1234 (59%) were treated for small vessel disease. At 5 years, target lesion failure occurred in 124 patients (cumulative incidence, 22.3%) treated with ultrathin-strut BP-SES and 109 patients (18.3%) treated with thin-strut DP-EES (rate ratio, 1.22; 95% CI, 0.94-1.58; =0.13). Cumulative incidences of cardiac death, target vessel myocardial infarction, and clinically indicated target lesion revascularization and definite stent thrombosis at 5 years were similar in patients treated with ultrathin-strut BP-SES and thin-strut DP-EES. After adjustment for potential confounders, there was no significant interaction between vessel size and treatment effect of BP-SES versus DP-EES.
CONCLUSIONS:
We found no significant difference in clinical outcomes throughout 5 years between patients with small vessel disease treated with ultrathin-strut BP-SES versus thin-strut DP-EES.
CLINICAL TRIAL REGISTRATION:
URL: https://www.clinicaltrials.gov. Unique identifier: NCT01443104.
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Arterial Remodeling and Dysfunction in the ZSF1 Rat Model of Heart Failure With Preserved Ejection Fraction.
Circ Heart Fail2019 Jul;12(7):e005596. doi: 10.1161/CIRCHEARTFAILURE.118.005596.
Leite Sara, Cerqueira Rui J, Ibarrola Jaime, Fontoura Dulce, Fernández-Celis Amaya, Zannad Faiez, Falcăo-Pires Inęs, Paulus Walter J, Leite-Moreira Adelino F, Rossignol Patrick, López-Andrés Natalia, Lourenço André P,
Abstract
BACKGROUND:
The interplay between the stiffened heart and vessels has long been viewed as a core mechanism in heart failure with preserved ejection fraction, but the incremental vascular molecular remodeling mechanisms from systemic arterial hypertension to heart failure with preserved ejection fraction remain poorly investigated. Our aim was to characterize central arterial remodeling and dysfunction in ZSF1 obese rats and to compare it with hypertensive ZSF1 lean and healthy Wistar-Kyoto controls.
METHODS AND RESULTS:
Twenty-week-old male ZSF1 obese (n=9), lean (n=9), and Wistar-Kyoto rats (n=9) underwent left ventricular pressure-volume loop evaluation and synchronous acquisition of ascending aortic flow and pressure. Aortic rings underwent functional evaluation, histology, and molecular biology studies. Although mean arterial pressure, characteristic aortic impedance, and reactivity to phenylephrine were similarly increased in hypertensive ZSF1 lean and obese, only ZSF1 obese showed impaired relaxation and upward-shifted end-diastolic pressure-volume relationships despite preserved systolic function indexes, denoting heart failure with preserved ejection fraction. ZSF1 obese phenotype further showed decreased aortic compliance, increased wave reflection, and impaired direct NO donor and endothelial-mediated vasodilation which were accompanied on structural and molecular grounds by aortic media thickening, higher collagen content and collagen/elastin ratio, increased fibronectin and ?-5 integrin protein expression and upregulated TGF (transforming growth factor)-? and CTGF (connective tissue growth factor) levels.
CONCLUSIONS:
Functional, molecular, and structural disturbances of central vessels and their potentially underlying pathways were newly characterized in experimental heart failure with preserved ejection fraction rendering the ZSF1 obese rat model suitable for preclinical testing.
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Effect of Baseline Left Ventricular Ejection Fraction on 2-Year Outcomes After Transcatheter Aortic Valve Replacement: Analysis of the PARTNER 2 Trials.
Circ Heart Fail2019 Aug;12(8):e005809. doi: 10.1161/CIRCHEARTFAILURE.118.005809.
Furer Ariel, Chen Shmuel, Redfors Bjorn, Elmariah Sammy, Pibarot Philippe, Herrmann Howard C, Hahn Rebecca T, Kodali Susheel, Thourani Vinod H, Douglas Pamela S, Alu Maria C, Fearon William F, Passeri Jonathan, Malaisrie S Chris, Crowley Aaron, McAndrew Thomas, Genereux Philippe, Ben-Yehuda Ori, Leon Martin B, Burkhoff Daniel,
Abstract
BACKGROUND:
Impaired left ventricular function is associated with worse prognosis among patients with aortic stenosis treated medically or with surgical aortic valve replacement. It is unclear whether reduced left ventricular ejection fraction (LVEF) is an independent predictor of adverse outcomes after transcatheter aortic valve replacement.
METHODS AND RESULTS:
Patients who underwent transcatheter aortic valve replacement in the PARTNER 2 trials (Placement of Aortic Transcatheter Valves) and registries were stratified according to presence of reduced LVEF (<50%) at baseline, and 2-year risk of cardiovascular mortality was compared using Kaplan-Meier methods and multivariable Cox proportional hazards regression. Of 2991 patients, 839 (28%) had reduced LVEF. These patients were younger, more often males, and were more likely to have comorbidities, such as coronary disease, diabetes mellitus, and renal insufficiency. Compared with patients with normal LVEF, patients with low LVEF had higher crude rates of 2-year cardiovascular mortality (19.8% versus 12.0%, <0.0001) and all-cause mortality (27.4% versus 19.2%, <0.0001). Mean aortic valve gradient was not associated with clinical outcomes other than heart failure hospitalizations (hazard ratio [HR], 0.99; CI, 0.99-1.00; =0.03). After multivariable adjustment, patients with reduced versus normal LVEF had significantly higher adjusted risk of cardiovascular death (adjusted HR, 1.42, 95% CI, 1.11-1.81; =0.005), but not all-cause death (adjusted HR, 1.20; 95% CI, 0.99-1.47; =0.07). When LVEF was treated as continuous variable, it was associated with increased 2-year risk of both cardiovascular mortality (adjusted HR per 10% decrease in LVEF, 1.16; 95% CI, 1.07-1.27; =0.0006) and all-cause mortality (adjusted HR, 1.09; 95% CI, 1.01-1.16; =0.02).
CONCLUSIONS:
In this patient-level pooled analysis of PARTNER 2 patients who underwent transcatheter aortic valve replacement, baseline LVEF was an independent predictor of 2-year cardiovascular mortality.
CLINICAL TRIAL REGISTRATION:
URL: https://www.clinicaltrials.gov. Unique identifiers: NCT01314313, NCT02184442, NCT03222128, and NCT02184441.
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Heart Rate and Heart Failure With Preserved Ejection Fraction: Time to Slow ?-Blocker Use?
Circ Heart Fail2019 Aug;12(8):e006213. doi: 10.1161/CIRCHEARTFAILURE.119.006213.
Meyer Markus, LeWinter Martin M,
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GDMT for heart failure and the clinician's conundrum.
Clin Cardiol2019 Sep;():. doi: 10.1002/clc.23268.
Samarendra Padmaraj,
Abstract
Therapeutic advances in management of CHF have decreased mortality and have impacted progression in patients with mild to moderate heart failure. Aggressive campaigns by cardiology societies aimed at increasing implementation of these measures in routine practices have almost generalized the treatment of heart failure irrespective of individual variations of clinical status of patients and stages of heart failure. This explains why morbidity compression and quality of life improvement have not been realized fully particularly in patients with advanced disease. To examine whether GDMT for CHF is backed by unambiguous evidence of clinical efficacy for its global implementation in every patient at all stages of the syndrome. ACC/AHA, ESC Guidelines for CHF, and their updates were reviewed. Clinical trial cited in the guideline documents and other pertaining published literatures were analyzed. FINDINGS: Many of the recommended GDMT for CHF lack unequivocal evidence of clinical efficacy in patients with diverge etiology of heart failure and concomitant comorbid conditions Some of the recommendations which are useful in early stages, lack evidence of efficacy in more advanced stages of heart failure. Application of results of research trials in patients beyond their inclusion and exclusion criteria, appears mere extrapolation, Clinicians are faced with the conundrum of implementing the recommendations without indubitable evidence of their efficacy in every patient of their practice. CONCLUSION: A reappraisal of Guidelines is needed to address outstanding questions pertaining to the efficacy of recommendations and plug the knowledge gaps without assumption and extrapolation of results of RCTs beyond their inclusion and exclusion criteria.
© 2019 The Author. Clinical Cardiology published by Wiley Periodicals, Inc.
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Change in Physical Activity and Cardiac Structure over 10 Years: The Multi-Ethnic Study of Atherosclerosis.
Med Sci Sports Exerc2019 Oct;51(10):2033-2040. doi: 10.1249/MSS.0000000000002027.
Florido Roberta, Zhao D I, Ndumele Chiadi E, Bluemke David A, Heckbert Susan R, Allison Matthew A, Ambale-Venkatesh Bharath, Liu Chia-Ying, Lima Joao, Michos Erin D,
Abstract
INTRODUCTION:
Physical activity (PA) is inversely associated with risk of heart failure and cardiovascular disease (CVD), whereas increased left ventricular (LV) mass and mass to volume (m:v) ratio are unfavorable CVD risk factors. We assessed whether changes in leisure time PA were associated with longitudinal changes in cardiac structure in a community-based population.
METHODS:
We included 2779 Multi-Ethnic Study of Atherosclerosis participants, free of baseline CVD, who had available data on PA and cardiac magnetic resonance imaging at examinations 1 (2000-2002) and 5 (2010-2012). Physical activity was measured by a Typical Week PA Survey and converted to MET-minutes per week of moderate+vigorous activity. We used linear mixed effect models to estimate the associations of baseline and change in PA with baseline and change in cardiac structure, adjusting for CVD risk factors and body size.
RESULTS:
At baseline, the mean age was 59 yr, 53% were women, and 58% of nonwhite race/ethnicity. During average 10-yr follow-up, and after accounting for baseline PA levels, the highest quintiles of PA increase were significantly associated with increases in LV mass (2.3 g; 95% confidence interval [CI], 0.4-4.2), LV end-diastolic volume (4.7 mL; 95% CI, 2.4-7.0), and stroke volume (3.3 mL; 95% CI, 1.6-5.1), but lower M:V ratio (-2.9; 95% CI, -5.0 to -0.8) compared with the lowest quintiles. Increasing exercise PA was associated with increases in LV diameter and reductions in M:V ratio, whereas occupational PA was associated with increases in m:v ratio. Increasing PA over 10 yr was also associated with greater risk of eccentric dilated LV hypertrophy at examination 5.
CONCLUSIONS:
After accounting for baseline PA, greater positive changes in leisure-time PA levels were associated with a more eccentric-type of LV remodeling pattern over 10 yr. The clinical implications of such findings remain to be determined.
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Continuation of Newly Initiated Midodrine Therapy: Appropriate in Patients With Heart Failure?
Crit Care Med2019 Oct;47(10):e845. doi: 10.1097/CCM.0000000000003914.
Reed Brent N, Gale Stormi E, Ramani Gautam,
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Prevention and Management of Supine Hypertension in Patients With Orthostatic Hypotension.
Am J Ther2019 Sep;():. doi: 10.1097/MJT.0000000000001054.
Moroi Morgan K, Ruzieh Mohammed, Ahmed Aamir, Kanjwal Shaffi, Kanjwal Khalil,
Abstract
BACKGROUND:
Orthostatic hypotension (OH) is a potentially debilitating condition caused by dysfunction of the autonomic nervous system, which is essential for the physiologic response to orthostatic posture. In addition to OH, autonomic dysfunction may also be associated with the development of concurrent supine hypertension (SH).
AREAS OF UNCERTAINTY:
This paradoxical effect speaks to the complexity of the pathogenesis of autonomic disease and greatly complicates management of these patients. Clinicians are faced with a dilemma because aggressive treatment of orthostatic intolerance can worsen supine hypertension and attempts to control supine hypertension can worsen orthostatic intolerance.
DATA SOURCES:
Systematic review of the published literature.
PREVENTION OF SUPINE HYPERTENSION:
Patients should aim to avoid known stressors, perform physical maneuvers (eg, slowly getting up from bed, sleeping with head of bed elevated), manage underlying related conditions (eg, diabetes mellitus), and exercise.
MANAGEMENT OF SUPINE HYPERTENSION:
With failure of conservative management, patients may advance to pharmacologic therapy. It is important to understand the underlying suspected etiology of the syndrome of supine hypertension and OH (SH-OH) to select promising pharmacologic agents. This article reviews medical treatment options to work toward achieving a better quality of life for patients afflicted with this disease. Although clonidine and beta-blockers can be used to treat hypertension without causing significant hypotension, midodrine, pyridostigmine, and droxidopa may be helpful in preventing OH.
CONCLUSION:
The etiology and severity of autonomic dysfunction vary widely between patients, suggesting a need for an individualized treatment approach. Achieving perfect blood pressure control is not a realistic goal. Rather, treatment should be aimed at improving the patient's quality of life and decreasing their risk of injury and organ damage.
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Dapagliflozin Effects on Biomarkers, Symptoms, and Functional Status in Patients With Heart Failure With Reduced Ejection Fraction: The DEFINE-HF Trial.
Circulation2019 Sep;():. doi: 10.1161/CIRCULATIONAHA.119.042929.
Nassif Michael E, Windsor Sheryl, Tang Fengming, Khariton Yevgeniy, Husain Mansoor, Inzucchi Silvio E, McGuire Darren, Pitt Bertram, Scirica Benjamin M, Austin Bethany, Drazner Mark, Fong Michael, Givertz Michael M, Gordon Robert, Jermyn Rita, Katz Stuart, Lamba Sumant, Lanfear David, LaRue Shane, Lindenfeld JoAnn, Malone Michael, Margulies Kenneth B, Mentz Robert, Mutharasan R Kannan, Pursley Michael, Umpierrez Guillermo, Kosiborod Mikhail, ,
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Double missense mutations in cardiac myosin-binding protein C and myopalladin genes: A case report with diffuse coronary disease, complete atrioventricular block, and progression to dilated cardiomyopathy.
Ann Noninvasive Electrocardiol2019 Sep;():e12687. doi: 10.1111/anec.12687.
Mastroianno Sandra, Palumbo Pietro, Castellana Stefano, Leone Maria Pia, Massaro Raimondo, Potenza Domenico Rosario, Mazza Tommaso, Russo Aldo, Castori Marco, Carella Massimo, Di Stolfo Giuseppe,
Abstract
Cardiomyopathies caused by double gene mutations are rare but conferred a remarkably increased risk of end-stage progression, arrhythmias, and poor outcome. Compound genetic mutations leading to complex phenotype in the setting of cardiomyopathies represent an important challenge in clinical practice, and genetic tests allow risk stratification and personalized clinical management of patients. We report a case of a 50-year-old woman with congestive heart failure characterized by dilated cardiomyopathy, diffuse coronary disease, complete atrioventricular block, and missense mutations in cardiac myosin-binding protein C (MYBPC3) and myopalladin (MYPN). We discuss the plausible role of genetic profile in phenotype determination.
© 2019 Wiley Periodicals, Inc.
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Increased Clinical and Economic Burden Associated With Peripheral Intravenous Catheter-Related Complications: Analysis of a US Hospital Discharge Database.
Inquiry;56():46958019875562. doi: 10.1177/0046958019875562.
Lim Sangtaeck, Gangoli Gaurav, Adams Erica, Hyde Robert, Broder Michael S, Chang Eunice, Reddy Sheila R, Tarbox Marian H, Bentley Tanya, Ovington Liza, Danker Walt,
Abstract
The burden of complications associated with peripheral intravenous use is underevaluated, in part, due to the broad use, inconsistent coding, and lack of mandatory reporting of these devices. This study aimed to analyze the clinical and economic impact of peripheral intravenous-related complications on hospitalized patients. This analysis of Premier Perspective Database US hospital discharge records included admissions occurring between July 1, 2013 and June 30, 2015 for pneumonia, chronic obstructive pulmonary disease, myocardial infarction, congestive heart failure, chronic kidney disease, diabetes with complications, and major trauma (hip, spinal, cranial fractures). Admissions were assumed to include a peripheral intravenous. Admissions involving surgery, dialysis, or central venous lines were excluded. Multivariable analyses compared inpatient length of stay, cost, admission to intensive care unit, and discharge status of patients with versus without peripheral intravenous-related complications (bloodstream infection, cellulitis, thrombophlebitis, other infection, or extravasation). Models were conducted separately for congestive heart failure, chronic obstructive pulmonary disease, diabetes with complications, and overall (all 7 diagnoses) and adjusted for demographics, comorbidities, and hospital characteristics. We identified 588?375 qualifying admissions: mean (SD), age 66.1 (20.6) years; 52.4% female; and 95.2% urgent/emergent admissions. Overall, 1.76% of patients (n = 10?354) had peripheral intravenous-related complications. In adjusted analyses between patients with versus without peripheral intravenous complications, the mean (95% confidence interval) inpatient length of stay was 5.9 (5.8-6.0) days versus 3.9 (3.9-3.9) days; mean hospitalization cost was $10?895 ($10?738-$11?052) versus $7009 ($6988-$7031). Patients with complications were less likely to be discharged home versus those without (62.4% [58.6%-66.1%] vs 77.6% [74.6%-80.5%]) and were more likely to have died (3.6% [2.9%-4.2%] vs 0.7% [0.6%-0.9%]). Models restricted to single admitting diagnosis were consistent with overall results. Patients with peripheral intravenous-related complications have longer length of stay, higher costs, and greater risk of death than patients without such complications; this is true across diagnosis groups of interest. Future research should focus on reducing these complications to improve clinical and economic outcomes.
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Sarcopenia: A Time for Action. An SCWD Position Paper.
J Cachexia Sarcopenia Muscle2019 Sep;():. doi: 10.1002/jcsm.12483.
Bauer Juergen, Morley John E, Schols Annemie M W J, Ferrucci Luigi, Cruz-Jentoft Alfonso J, Dent Elsa, Baracos Vickie E, Crawford Jeffrey A, Doehner Wolfram, Heymsfield Steven B, Jatoi Aminah, Kalantar-Zadeh Kamyar, Lainscak Mitja, Landi Francesco, Laviano Alessandro, Mancuso Michelangelo, Muscaritoli Maurizio, Prado Carla M, Strasser Florian, von Haehling Stephan, Coats Andrew J S, Anker Stefan D,
Abstract
The term sarcopenia was introduced in 1988. The original definition was a "muscle loss" of the appendicular muscle mass in the older people as measured by dual energy x-ray absorptiometry (DXA). In 2010, the definition was altered to be low muscle mass together with low muscle function and this was agreed upon as reported in a number of consensus papers. The Society of Sarcopenia, Cachexia and Wasting Disorders supports the recommendations of more recent consensus conferences, i.e. that rapid screening, such as with the SARC-F questionnaire, should be utilized with a formal diagnosis being made by measuring grip strength or chair stand together with DXA estimation of appendicular muscle mass (indexed for height2). Assessments of the utility of ultrasound and creatine dilution techniques are ongoing. Use of ultrasound may not be easily reproducible. Primary sarcopenia is aging associated (mediated) loss of muscle mass. Secondary sarcopenia (or disease-related sarcopenia) has predominantly focused on loss of muscle mass without the emphasis on muscle function. Diseases that can cause muscle wasting (i.e. secondary sarcopenia) include malignant cancer, COPD, heart failure, and renal failure and others. Management of sarcopenia should consist of resistance exercise in combination with a protein intake of 1 to 1.5 g/kg/day. There is insufficient evidence that vitamin D and anabolic steroids are beneficial. These recommendations apply to both primary (age-related) sarcopenia and secondary (disease related) sarcopenia. Secondary sarcopenia also needs appropriate treatment of the underlying disease. It is important that primary care health professionals become aware of and make the diagnosis of age-related and disease-related sarcopenia. It is important to address the risk factors for sarcopenia, particularly low physical activity and sedentary behavior in the general population, using a life-long approach. There is a need for more clinical research into the appropriate measurement for muscle mass and the management of sarcopenia. Accordingly, this position statement provides recommendations on the management of sarcopenia and how to progress the knowledge and recognition of sarcopenia.
© 2019 The Authors. Journal of Cachexia, Sarcopenia and Muscle published by John Wiley & Sons Ltd on behalf of the Society on Sarcopenia, Cachexia and Wasting Disorders.
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