Chronic obstructive pulmonary disease (COPD) is a multi-system disorder, resulting in multiple comorbidities and being the fourth common cause of mortality worldwide (1). Cardiovascular disease (CVD) is one of the leading cause of morbidity and mortality in COPD, through manifestations such as ischemic heart disease, heart failure, arrhythmias, stroke and sudden cardiac death (2,3). Moreover, in the last years, a tendency to paradigm shift occured, the chronic respiratory disease itself being defined as a modifiable cardiovascular risk factor (4,5).
This interaction between COPD and cardiovascular disease could be explained either by shared risk factors (aging, smoking, exposure to air pollution and passive smoke, underprescribing of key cardiovascular medication, such as β-blockers) or mechanisms of increased risk that are incompletely understood, beyond the conventional risk factors (4,6).
There is increasing evidence that COPD negatively affect the cardiovascular and autonomic nervous system, leading to sympathovagal imbalance, with increased sympathetic tone, loss of parasympathetic tone and altered baroreceptor sensitivity, which are essential components of cardiovascular risk (7-9). Recurrent episodes of hypoxemia and/or hypercapnea, intrathoracic pressure swings resulting from airway obstruction and hyperinflation, systemic inflammation, oxidative stress, increased respiratory effort and physical inactivity can all be involved in autonomic dysfunction observed in COPD (8-10).
Patients with COPD and functional alterations of cardiac autonomic modulation tend to have an elevated resting heart rate (11-13), reduced heart rate variability (HRV) (14), altered blood pressure variability (BPV) (15), an increase in muscle sympathetic nerve activity (16), reduced baroreflex sensitivity (17) and increased plasma norepinephrine level (9). Other clincal findings related to sympathetic overdrive in COPD could be arterial stiffness, altered PWV and arterial compliance, as well as left ventricular hypertrophy and diastolic dysfunction which may occur through direct effect of tone, modulation of baroreceptor sensitivity or activation of the renin-angiotensin system (4, 18-22).
Hypoxemia, hypercapnia, pulmonary hyperinflation and activity avoidance are involved in developping cardiac autonomic dysfunction but on the other hand, these mechanisms are also responsible for exertional dyspnea and skeletal muscle deconditioning, including respiratory muscle dysfunction, in COPD patients (23,24). Thus develops a vicious spiral of physical deconditioning, impaired quality of life and early development of cardiovascular comorbidities, leading eventually to increased hospitalization and mortality (25).
The “golden standard” in COPD management is pulmonary rehabilitation, based on its main benefits, as resulted from clinical trials: improved exercise capacity and health-related quality of life, reduced symptoms and recovery after hospitalization, decreased anxiety and depression, shortening the number of hospitalizations and days in the hospital (21, 26-28). The impact of cardiovascular comorbidities on clinical outcomes of pulmonary rehabilitation and
vice versa
is only partially investigated and understood. It seems that patients with metabolic and heart diseases might achieve lower degrees of improvement in exercise capacity or quality of life, but conflicting results from clinical trials have been published (29). Moreover, it is still unclear if pulmonary rehabilitation programs address cardiovascular risk factors in COPD patients, but there are encouraging results (30).
Inspiratory muscle training (IMT) is a particular component of pulmonary rehabilitation, arising from the finding that inspiratory muscle dysfunction is an extrapulmonary manifestation of the disease which is often present in COPD patients. Inspiratory muscle weakness is defined as a maximal inspiratory mouth pressure (P
I,max
) of less than 60 cmH
2
O (31) and can be measured with handheld, electronic portable devices, providing automatically processed information on external inspiratory work, power and breathing pattern during loaded breathing tasks in patients with COPD. A recent study concluded that these information are valid estimation of physical units of energy during loaded breathing tasks, enabling healthcare providers to measure P
I,max
, peak inspiratory flow and quantify the load on inspiratory muscles in daily clinical practice (32). Also, it has been developed various pressure threshold loading medical devices, for standardized training, according to current recommendations although there is no established guideline yet (33).
The impact of IMT was extensively studied in recent years. Results from randomised controlled trials in patients with COPD show that IMT as a stand-alone therapy improves strength and endurance of inspiratory muscles, improves symptoms (dyspnea) and exercise capacity (31,34). In a meta-analysis including 32 randomised controlled trials (31), IMT and its effects in patients with COPD were analysed and improved inspiratory muscle strength (+ 13 cmH
2
O; 95% CI 0.54-0.82; p<0.001) and endurance (+ 13 cmH
2
O; 95% CI 0.72-1.25; p<0.001), functional exercise capacity (+ 32 m at 6MWD; 95% CI 0.12-0.44; p<0.001), dyspnea (- 0.9 Borg score; 95% CI -0.66- -0.24; p<0.0001), and quality of life (+3.8 points CRQ; 95% CI 0.09-0.60; p<0.01 ) were found in the training group. A systematic review designed to determine the impact of home-based physiotherapy interventions on breathlessness during activities of daily living (ADL) in severe COPD concluded IMT is a home-based intervention that may improve breathlesness during ADL but there is need for more homogenous research with larger sample size to substantiate the current findings (35).
The value of IMT as an add-on to a general exercise program is still under debate, additional effects of this training on other clinical relevant outcomes than improvement in inspiratory muscle function being insufficiently supported so far (36-39).
IMT was also studied in cardiovascular disease, a recent randomized controlled trial (RCT) showing significantly greater functional improvement in patients with chronic heart failure selected for inspiratory muscle weakness (40), while comparable RCT in patients with COPD are lacking, with a notable exception of one on-going trial designed to examine the effects of adding a high-intensity IMT to a 3-month general exercise training program in patients with COPD and inspiratory muscle weakness. Outcomes will be exercise capacity, inspiratory muscle function, health-related quality of life and participation in daily physical activity (41).
In conclusion, the presence of cardiac autonomic dysfunction has important consequences in COPD assessment and management and prognostic value. We hypothesize that IMT may have beneficial effects on cardiac autonomic dysfunction in COPD patients by improving breathing pattern, respiratory muscle strength, hyperinflation and intrathoracic pressure changes as well as on several functional parameters related to quality of life.
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