Millions of individuals have used illicit anabolic-androgenic steroids (AAS), but the long-term cardiovascular associations of these drugs remain incompletely understood.
Using a cross-sectional ...cohort design, we recruited 140 experienced male weightlifters 34 to 54 years of age, comprising 86 men reporting ≥2 years of cumulative lifetime AAS use and 54 nonusing men. Using transthoracic echocardiography and coronary computed tomography angiography, we assessed 3 primary outcome measures: left ventricular (LV) systolic function (left ventricular ejection fraction), LV diastolic function (early relaxation velocity), and coronary atherosclerosis (coronary artery plaque volume).
Compared with nonusers, AAS users demonstrated relatively reduced LV systolic function (mean±SD left ventricular ejection fraction = 52±11% versus 63±8%;
<0.001) and diastolic function (early relaxation velocity = 9.3±2.4 cm/second versus 11.1±2.0 cm/second;
<0.001). Users currently taking AAS at the time of evaluation (N=58) showed significantly reduced LV systolic (left ventricular ejection fraction = 49±10% versus 58±10%;
<0.001) and diastolic function (early relaxation velocity = 8.9±2.4 cm/second versus 10.1±2.4 cm/second;
=0.035) compared with users currently off-drug (N=28). In addition, AAS users demonstrated higher coronary artery plaque volume than nonusers (median interquartile range 3 0, 174 mL
versus 0 0, 69 mL
;
=0.012). Lifetime AAS dose was strongly associated with coronary atherosclerotic burden (increase 95% confidence interval in rank of plaque volume for each 10-year increase in cumulative duration of AAS use: 0.60 SD units 0.16-1.03 SD units;
=0.008).
Long-term AAS use appears to be associated with myocardial dysfunction and accelerated coronary atherosclerosis. These forms of AAS-associated adverse cardiovascular phenotypes may represent a previously underrecognized public-health problem.
Non‐technical summary MicroRNA (miRNA) molecules are essential intracellular mediators of numerous biological processes including angiogenesis, inflammation, and mitochondrial metabolism. Recently, ...it has been shown that miRNAs are secreted into the bloodstream and that circulating miRNAs (c‐miRNAs) may serve important endocrine functions. This study examined plasma profiles of specific c‐miRNAs in healthy competitive athletes at rest and during exhaustive exercise testing, before and after a 90 day period of exercise training. In this setting, we observed four distinct patterns of c‐miRNA response to exercise: (1) c‐miRNAs up‐regulated by acute exhaustive exercise before and after sustained exercise training, (2) c‐miRNAs responsive to acute exhaustive exercise before but not after sustained exercise training, (3) c‐miRNAs responsive only to sustained exercise training, and (4) non‐responsive c‐miRNAs. These findings set the stage for further work aimed at defining the role of c‐miRNAs as fitness biomarkers and physiological mediators of exercise‐induced cardiovascular adaptation.
MicroRNAs (miRNAs) are intracellular mediators of essential biological functions. Recently, plasma‐based ‘circulating’ miRNAs (c‐miRNAs) have been shown to control cellular processes, but the c‐miRNA response to human exercise remains unknown. We sought to determine whether c‐miRNAs are dynamically regulated in response to acute exhaustive cycling exercise and sustained rowing exercise training using a longitudinal, repeated measures study design. Specifically, c‐miRNAs involved in angiogenesis (miR‐20a, miR‐210, miR‐221, miR‐222, miR‐328), inflammation (miR‐21, miR‐146a), skeletal and cardiac muscle contractility (miR‐21, miR‐133a), and hypoxia/ischaemia adaptation (miR‐21, miR‐146a, and miR‐210) were measured at rest and immediately following acute exhaustive cycling exercise in competitive male rowers (n= 10, age = 19.1 ± 0.6 years) before and after a 90 day period of rowing training. Distinct patterns of c‐miRNA response to exercise were observed and adhered to four major profiles: (1) c‐miRNA up‐regulated by acute exercise before and after sustained training (miR‐146a and miR‐222), (2) c‐miRNA responsive to acute exercise before but not after sustained training (miR‐21 and miR‐221), (3) c‐miRNA responsive only to sustained training (miR‐20a), and (4) non‐responsive c‐miRNA (miR‐133a, miR‐210, miR‐328). Linear correlations were observed between peak exercise levels of miR‐146a and (r= 0.63, P= 0.003) and between changes in resting miR‐20a and changes in (pre‐training vs. post‐training, r= 0.73; P= 0.02). Although future work is required, these results suggest the potential value of c‐miRNAs as exercise biomarkers and their possible roles as physiological mediators of exercise‐induced cardiovascular adaptation.
Echocardiography in the Time of COVID-19 Picard, Michael H; Weiner, Rory B
Journal of the American Society of Echocardiography,
06/2020, Letnik:
33, Številka:
6
Journal Article
Current clinical practice guidelines for managing Coronary Artery Disease (CAD) account for general cardiovascular risk factors. However, they do not present a framework that considers personalized ...patient-specific characteristics. Using the electronic health records of 21,460 patients, we created data-driven models for personalized CAD management that significantly improve health outcomes relative to the standard of care. We develop binary classifiers to detect whether a patient will experience an adverse event due to CAD within a 10-year time frame. Combining the patients’ medical history and clinical examination results, we achieve 81.5% AUC. For each treatment, we also create a series of regression models that are based on different supervised machine learning algorithms. We are able to estimate with average
R
2
= 0.801 the outcome of interest; the time from diagnosis to a potential adverse event (TAE). Leveraging combinations of these models, we present ML4CAD, a novel personalized prescriptive algorithm. Considering the recommendations of multiple predictive models at once, the goal of ML4CAD is to identify for every patient the therapy with the best expected TAE using a voting mechanism. We evaluate its performance by measuring the prescription effectiveness and robustness under alternative ground truths. We show that our methodology improves the expected TAE upon the current baseline by 24.11%, increasing it from 4.56 to 5.66 years. The algorithm performs particularly well for the male (24.3% improvement) and Hispanic (58.41% improvement) subpopulations. Finally, we create an interactive interface, providing physicians with an intuitive, accurate, readily implementable, and effective tool.
The anatomy of the adult human left ventricle (LV) is the result of its complex interaction with its environment. From the fetal to the neonatal to the adult form, the human LV undergoes an ...anatomical transformation that finally results in the most complex of the four cardiac chambers. In its adult form, the human LV consists of two muscular helixes that surround the midventricular circumferential layer of muscle fibers. Contraction of these endocardial and epicardial helixes results in a twisting motion that is thought to minimize the transmural stress of the LV muscle. In the healthy myocardium, the LV twist response to stimuli that alter preload, afterload, or contractility has been described and is deemed relatively consistent and predictable. Conversely, the LV twist response in patient populations appears to be a little more variable and less predictable, yet it has revealed important insight into the effect of cardiovascular disease on LV mechanical function. This review discusses important methodological aspects of assessing LV twist and evaluates the LV twist responses to the main physiological and pathophysiological states. It is concluded that correct assessment of LV twist mechanics holds significant potential to advance our understanding of LV function in human health and cardiovascular disease.
Exercise capacity as measured by peak oxygen uptake (Vo2) is similarly impaired in patients with heart failure with preserved ejection fraction (HFpEF) and heart failure with reduced ejection ...fraction (HFrEF). However, characterization of how each component of Vo2 changes in response to incremental exercise in HFpEF versus HFrEF has not been previously defined. We hypothesized that abnormally low peripheral o2 extraction (arterio-mixed venous o2 content difference, C(a-v)o2) during exercise significantly contributes to impaired exercise capacity in HFpEF.
We performed maximum incremental cardiopulmonary exercise testing with invasive hemodynamic monitoring on 104 patients with symptomatic NYHA II to IV heart failure (HFpEF, n=48, peak Vo2=13.9±0.5 mL kg(-1) min(-1), mean±SEM, and HFrEF, n=56, peak Vo2=12.1±0.5 mL kg(-1) min(-1)) and 24 control subjects (peak Vo2 27.0±1.7 mL kg(-1) min(-1)). Peak exercise C(a-v)o2 was lower in HFpEF compared with HFrEF (11.5±0.27 versus 13.5±0.34 mL/dL, respectively, P<0.0001), despite no differences in age, hemoglobin level, peak respiratory exchange ratio, Cao2, or cardiac filling pressures. Peak C(a-v)o2 and peak heart rate emerged as the leading predictors of peak Vo2 in HFpEF. Impaired peripheral o2 extraction was the predominant limiting factor to exercise capacity in 40% of patients with HFpEF and was closely related to elevated systemic blood pressure during exercise (r=0.49, P=0.0005).
In the first study to directly measure C(a-v)o2 throughout exercise in HFpEF, HFrEF, and normals, we found that peak C(a-v)o2 was a major determinant of exercise capacity in HFpEF. The important functional limitation imposed by impaired o2 extraction may reflect intrinsic abnormalities in skeletal muscle or peripheral microvascular function, and represents a potential target for therapeutic intervention.
Objectives The aim of this study was to evaluate whether chronic heart failure (HF) therapy guided by concentrations of amino-terminal pro–B-type natriuretic peptide (NT-proBNP) is superior to ...standard of care (SOC) management. Background It is unclear whether standard HF treatment plus a goal of reducing NT-proBNP concentrations improves outcomes compared with standard management alone. Methods In a prospective single-center trial, 151 subjects with HF due to left ventricular (LV) systolic dysfunction were randomized to receive either standard HF care plus a goal to reduce NT-proBNP concentrations ≤1,000 pg/ml or SOC management. The primary endpoint was total cardiovascular events between groups compared using generalized estimating equations. Secondary endpoints included effects of NT-proBNP–guided care on patient quality of life as well as cardiac structure and function, assessed with echocardiography. Results Through a mean follow-up period of 10 ± 3 months, a significant reduction in the primary endpoint of total cardiovascular events was seen in the NT-proBNP arm compared with SOC (58 events vs. 100 events, p = 0.009; logistic odds for events 0.44, p = 0.02); Kaplan-Meier curves demonstrated significant differences in time to first event, favoring NT-proBNP–guided care (p = 0.03). No age interaction was found, with elderly patients benefitting similarly from NT-proBNP–guided care as younger subjects. Compared with SOC, NT-proBNP–guided patients had greater improvements in quality of life, demonstrated greater relative improvements in LV ejection fraction, and had more significant improvements in both LV end-systolic and -diastolic volume indexes. Conclusions In patients with HF due to LV systolic dysfunction, NT-proBNP–guided therapy was superior to SOC, with reduced event rates, improved quality of life, and favorable effects on cardiac remodeling. (Use of NT-proBNP Testing to Guide Heart Failure Therapy in the Outpatient Setting; NCT00351390 )
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