Cardiopulmonary exercise test (CPET) has been gaining importance as a method of
functional assessment in Brazil and worldwide. In its most frequent
applications, CPET consists in applying a gradually increasing intensity
exercise until exhaustion or until the appearance of limiting symptoms and/or
signs. The following parameters are measured: ventilation; oxygen consumption
(VO2); carbon dioxide production (VCO2); and the other
variables of conventional exercise testing. In addition, in specific situations,
pulse oximetry and flow-volume loops during and after exertion are measured. The
CPET provides joint data analysis that allows complete assessment of the
cardiovascular, respiratory, muscular and metabolic systems during exertion,
being considered gold standard for cardiorespiratory functional
assessment.1-6The CPET allows defining mechanisms related to low functional capacity that can
cause symptoms, such as dyspnea, and correlate them with changes in the
cardiovascular, pulmonary and skeletal muscle systems. Furthermore, it can be
used to provide the prognostic assessment of patients with heart or lung
diseases, and in the preoperative period, in addition to aiding in a more
careful exercise prescription to healthy subjects, athletes and patients with
heart or lung diseases.Similarly to CPET clinical use, its research also increases, with the publication
of several scientific contributions from Brazilian researchers in high-impact
journals.Therefore, this study aimed at providing a comprehensive review on the
applicability of CPET to different clinical situations, in addition to serving
as a practical guide for the interpretation of that test.
HEx reduced office BPs and 24-hour ABPM levels in resistant hypertensive patients. These effects suggest that HEx may be a potential new therapeutic approach in these patients.
Nota: These guidelines are for information purposes and should not replace the clinical judgment of a physician, who must ultimately determine the appropriate treatment for each patient.
MicroRNAs (miRNAs) are a class of non-coding small RNAs representing one of the most exciting areas of modern medical science. miRNAs modulate a large and complex regulatory network of gene expression of the majority of the protein-coding genes. Currently, evidences suggest that miRNAs play a crucial role in the pathogenesis of heart failure. Some miRNAs as miR-1, miR-133 and miR-208a are highly expressed in the heart and strongly associated with the development of cardiac hypertrophy. Recent data indicate that these miRNAs as well as miR-206 change their expression quickly in response to physical activity. The differential regulation of miRNAs in response to exercise suggests a potential value of circulating miRNAs (c-miRNAs) as biomarkers of physiological mediators of the cardiovascular adaptation induced by exercise. Likewise, serum levels of c-miRNAs such as miR-423-5p have been evaluated as potential biomarkers in the diagnosis and prognosis of heart failure. On the other hand, the manipulation of miRNAs levels using techniques such as 'miR mimics' and 'antagomiRs' is becoming evident the enormous potential of miRNAs as promising therapeutic strategies in heart failure.
The obesity paradox has been described in several observational cohorts and meta-analysis. However, evidence of the intentionality of weight loss in all-cause deaths and major cardiovascular events (MACE) in prospective cohorts is unclear. We analysed whether involuntary weight loss is associated with increased cardiovascular events and mortality. In a systematic review, we searched multiple electronic databases for observational studies published up to October 2016. Studies reporting risk estimates for unintentional weight loss compared with stable weight in MACE and mortality were included. Fifteen studies met the selection criteria, with a total of 178,644 participants. For unintentional weight loss, we found adjusted risk ratios (RRs) with confidence intervals (CIs) of 1.38 (95% CI: 1.23, 1.53) and 1.17 (95% CI: 0.98, 1.37) for all-cause mortality and MACE, respectively. Participants with comorbidities, overweight and obese populations, and older adults yielded RRs (95% CI) of 1.49 (1.30, 1.68), 1.11 (1.04, 1.18), and 1.81 (1.59, 2.03), respectively. Unintentional weight loss had a significant impact on all-cause mortality. We found no protective effect of being overweight or obese for unintentional weight loss and MACE.
Background: In patients with heart failure, inflammation has been associated with worse functional capacity, but it is uncertain whether it could affect their response to exercise training. We evaluated whether inflammatory biomarkers are related to differential effect of exercise on the peak oxygen uptake ( _ VO 2 ) among patients with heart failure. Design: Open, parallel group, randomized controlled trial. Methods: Patients with heart failure and ejection fraction 0.4 were randomized into exercise training or control for 12 weeks. Patients were classified according to: 1) inflammatory biomarkers blood levels, defined as 'low' if both interleukin-6 and tumor necrosis factor-alpha blood levels were below median, and 'high' otherwise; and 2) galectin-3 blood levels, which also reflect pro-fibrotic processes. Results: Forty-four participants (50 AE 7 years old, 55% men, 25% ischemic) were allocated to exercise training (n ¼ 28) or control (n ¼ 16). Exercise significantly improved peak _ VO 2 among participants with 'low' inflammatory biomarkers (3.5 AE 0.9 vs. À0.7 AE 1.1 ml/kg per min, p ¼ 0.006), as compared with control, but not among those with 'high' inflammatory biomarkers (0.4 AE 0.6 vs. À0.2 AE 0.7 ml/kg per min, p ¼ 0.54, p for interaction ¼ 0.009). Similarly, exercise improved peak _ VO 2 among participants with below median (2.4 AE 0.8 vs. À0.3 AE 0.9 ml/kg per min, p ¼ 0.032), but not among those with above median galectin-3 blood levels (0.3 AE 0.7 vs. À0.7 AE 1.0 ml/kg per min, p ¼ 0.41, p for interaction ¼ 0.053). Conclusion: In patients with heart failure, levels of biomarkers that reflect pro-inflammatory and pro-fibrotic processes were associated with differential effect of exercise on functional capacity. Further studies should evaluate whether exercise training can improve clinical outcomes in patients with heart failure and low levels of these biomarkers.
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