Clinical Physiology and Functional Imaging最新文献

Tilt table testing (TTT) has been used for decades to study short-term blood pressure (BP) and heart rate regulation during orthostatic challenges. TTT provokes vasovagal reflex in many syncope patients as a background of widespread use. Despite the availability of evidence-based practice syncope guidelines, proper application and interpretation of TTT in the day-to-day care of syncope patients remain challenging. In this review, we offer practical information on what is needed to perform TTT, how results should be interpreted including the Vasovagal Syncope International Study classification, why syncope induction on TTT is necessary in patients with unexplained syncope and on indications for TTT in syncope patient care. The minimum requirements to perform TTT are a tilt table with an appropriate tilt-down time, a continuous beat-to-beat BP monitor with at least three electrocardiogram leads and trained staff. We emphasize that TTT remains a valuable asset that adds to history building but cannot replace it, and highlight the importance of recognition when TTT is abnormal even without syncope. Acknowledgement by the patient/eyewitness of the reproducibility of the induced attack is mandatory in concluding a diagnosis. TTT may be indicated when the initial syncope evaluation does not yield a certain, highly likely, or possible diagnosis, but raises clinical suspicion of (1) reflex syncope, (2) orthostatic hypotension (OH), (3) postural orthostatic tachycardia syndrome or (4) psychogenic pseudosyncope. A therapeutic indication for TTT in the patient with a certain, highly likely or possible diagnosis of reflex syncope, may be to educate patients on prodromes. In patients with reflex syncope with OH TTT can be therapeutic to recognize hypotensive symptoms causing near-syncope to perform physical countermanoeuvres for syncope prevention (biofeedback). Detection of hypotensive susceptibility requiring therapy is of special value.

In sports, physical recovery following exercise-induced fatigue is mediated via the reactivation of the parasympathetic nervous system (PNS). A noninvasive way to quantify the reactivation of the PNS is to assess vagally-mediated heart rate variability (vmHRV), which can then be used as an index of physical recovery. This systematic review and meta-analysis investigated the effects of physical recovery techniques following exercise-induced fatigue on vmHRV, specifically via the root mean square of successive differences (RMSSD). Randomized controlled trials from the databases PubMed, WebOfScience, and SportDiscus were included. Twenty-four studies were part of the systematic review and 17 were included in the meta-analysis. Using physical post-exercise recovery techniques displayed a small to moderate positive effect on RMSSD (k = 22, Hedges' g = 0.40, 95% confidence interval [CI] = 0.20–0.61, p = 0.04) with moderate heterogeneity. In the subgroup analyses, cold water immersion displayed a moderate to large positive effect (g = 0.75, 95% CI: 0.42–1.07) compared with none for other techniques. For exercise type, physical recovery techniques performed after resistance exercise (g = 0.69, 95% CI: 0.48–0.89) demonstrated a larger positive effect than after cardiovascular intermittent (g = 0.52, 95% CI: 0.06–0.97), while physical recovery techniques performed after cardiovascular continuous exercise had no effect. No significant subgroup differences for training status and exercise intensity were observed. Overall, physical post-exercise recovery techniques can accelerate PNS reactivation as indexed by vmHRV, but the effectiveness varies with the technique and exercise type.

To investigate effects of low workload respiratory muscle training (RMT) on respiratory muscle power and lung function in asthmatics, we recruited asthmatic persons who performed a 4-week training programme. The training included 20 daily ex- and inhalations with counter pressure 30% from the individual maximal expiratory pressure (MEP). Lung function was measured before and after the training programme and a follow-up period. The study also included several subjective endpoints for respiratory symptoms. A significant increase in a training group (n = 27) compared with a control group (n = 20) was seen in MEP (+12.4%, vs. +3.5%, p = 0.086), maximal inspiratory pressure (MIP) (+21.1% vs. +0.82%, p = 0.023), slow vital capacity (VC) (+3.7% vs. +1.5%, p = 0.023) and in forced expiratory time (FET, +15.5%, vs. −5.0%, p = 0.022). After being a control for group A, also group B performed similar RMT as group A. In the combined group (A and B, n = 47) MEP (11.3%, p = 0.003), MIP (19.73%, p < 0.001), VC (4.1%, p < 0.001) and FET (14.7%, p < 0.001) increased significantly from the baseline. Changes in other lung function variables were not indicative. On a scale of 1–5, the subjects perceived improvement in reduction of mucus secretion in the airways (median 3, p < 0.001), alleviation of coughing (median 3, p < 0.001) and reduction in dyspnoea (median 3, p < 0.001). As a conclusion, low workload respiratory training of 4 weeks improved respiratory muscle power and increased VC in patients with stable asthma.

Diagnosis and treatment of patients with suspected chronic coronary syndrome (CCS) currently relies on the degree of coronary artery stenosis and its significance for myocardial perfusion. However, myocardial perfusion can be affected by factors other than coronary stenosis. The aim of this study was to investigate to what extent sex, age, diabetes, hypertension and smoking affect quantitative myocardial perfusion, beyond the degree of coronary artery stenosis, in patients with suspected or established CCS. Eighty-six patients [median age 69 (range 46−86) years, 24 females] planned for elective coronary angiography due to suspected or established CCS were included. All patients underwent cardiac ¹³N-NH₃ positron emission tomography to quantify myocardial perfusion at rest and stress. Lowest myocardial perfusion (perfusion_min) at stress and rest and lowest myocardial perfusion reserve (MPR_min) for all vessel territories was used as dependent variables in a linear mixed model. Independent variables were vessel territory, degree of coronary artery stenosis (as a continuous variable of 0%−100% stenosis), sex, age, diabetes, hypertension and smoking habits. Degree of coronary artery stenosis (p < 0.001), male sex (1.8 ± 0.6 vs. 2.3 ± 0.6 mL/min/g, p < 0.001), increasing age (p = 0.025), diabetes (1.6 ± 0.5 vs. 2.0 ± 0.6 mL/min/g, p = 0.023) and smoking (1.9 ± 0.6 vs. 2.1 ± 0.6 mL/min/g, p = 0.052) were independently associated with myocardial perfusion_min at stress. Degree of coronary artery stenosis (p < 0.001), age (p = 0.040), diabetes (1.8 ± 0.6 vs. 2.3 ± 0.7, p = 0.046) and hypertension (2.2 ± 0.7 vs. 2.5 ± 0.6, p = 0.033) were independently associated with MPR_min. Sex, increasing age, diabetes, hypertension and smoking affect myocardial perfusion independent of coronary artery stenosis in patients with suspected or established CCS. Thus, these factors need to be considered when assessing the significance of reduced quantitative myocardial perfusion of patients with suspected or established CCS.