Clinical Research in Cardiology

https://doi.org/10.1007/s00392-023-02217-0

REVIEW

GOLD COPD DOCUMENT 2023: a brief update for practicing

cardiologists
Alvar Agusti1 · Michael Böhm2 · Bartolomé Celli3 · Gerard J. Criner4 · Ana Garcia‑Alvarez1 · Fernando Martinez5 ·
Don D. Sin6 · Claus F. Vogelmeier7 

Received: 30 June 2022 / Accepted: 25 April 2023

© The Author(s) 2023

Abstract
Many patients seen by cardiologists suffer chronic obstructive pulmonary disease (COPD) in addition to their primary
cardiovascular problem. Yet, quite often COPD has not been diagnosed and, consequently, patients have not been treated
of their pulmonary disease. Recognizing and treating COPD in patients with CVDs is important because optimal treatment
of the COPD carries important benefits on cardiovascular outcomes. The Global Initiative for Chronic Obstructive Lung
Disease (GOLD) publishes an annual report that serves as a clinical guideline for the diagnosis and management of COPD
around the world and has very recently released the 2023 annual report. Here, we provide a summary of the GOLD 2023
recommendations that highlights those aspects of more interest for practicing cardiologists dealing with patients with CVD
who may suffer COPD.

Keywords  Chronic bronchitis · Emphysema · GOLD · Smoking · Tobacco

Introduction been diagnosed and, consequently, patients have not been

treated [1]. Recognizing and treating COPD in patients with
Many patients seen by cardiologists suffer chronic obstruc- CVDs are important because optimal treatment of the COPD
tive pulmonary disease (COPD) in addition to their primary carries important benefits on cardiovascular outcomes [2].
cardiovascular problem [1]. Yet, quite often, COPD has not The Global Initiative for Chronic Obstructive Lung Dis-
ease (GOLD) publishes an annual report that serves as a
clinical guideline for the diagnosis and management of
* Claus F. Vogelmeier COPD around the world and has very recently released the
vogelmei@med.uni-marburg.de 2023 annual report [2]. Here, we provide a summary of the
1
Hospital Clinic, IDIBAPS, University of Barcelona, GOLD 2023 recommendations that highlights those aspects
Barcelona, Spain of more interest for practicing cardiologists dealing with
2
KardiologieAngiologie und Internistische Intensivmedizin, patients with CVD who may suffer COPD [2]. It does not
Universitätsklinikum des SaarlandesKlinik für Innere cover in detail all aspects of COPD. We refer the interested
Medizin III, Saarland University, Homburg/Saar, Germany reader to the full GOLD document, the pocket guide, the
3
Brigham and Women’s Hospital, Harvard Medical School, slide deck, and/or the GOLD App, all freely downloadable
Boston, USA from the GOLD website (www.g​ oldco​ pd.o​ rg). Likewise, we
4
Department of Thoracic Medicine and Surgery at the Lewis acknowledge that other recent, global reviews in COPD may
Katz School of Medicine, Philadelphia, PA, USA also be informative [3].
5
Weill Cornell Medicine, NYPresbyterian Hospital,
New York, NY, USA
6
Centre for Heart Lung Innovation, Department of Medicine Definition and burden
(Division of Respirology), St. Paul’s Hospital, University
of British Columbia, Vancouver, Canada GOLD 2023 now defines COPD as a “heterogeneous lung
7
Department of Medicine, Pulmonary and Critical Care condition characterized by chronic respiratory symptoms
Medicine, Member of the German Center for Lung Research (dyspnea, cough, expectoration, exacerbations) due to
(DZL), University of Marburg, Marburg, Germany

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 Clinical Research in Cardiology

abnormalities of the airways (bronchitis, bronchiolitis) and/ Causes of COPD: beyond tobacco smoking
or alveoli (emphysema) that cause persistent, often progres-
sive, airflow obstruction” [4]. COPD may be punctuated by COPD has been traditionally understood as a self-inflicted
periods of acute worsening of respiratory symptoms, called disease caused by an abnormal inflammatory response
exacerbations (ECOPD), which can be prevented and may elicited by tobacco smoking occurring in older males [11].
require specific treatment and, sometimes, hospitalization Tobacco smoking certainly is a major environmental risk
[5]. In many patients, COPD co-exist with other significant factor for COPD, but it is not the only one since other envi-
concomitant chronic diseases, particularly CVD, such as ronmental exposures, such as biomass fuel, air pollution,
coronary artery disease (CAD) and heart failure (HF), as and occupational particles, can also cause COPD [2]. In fact,
well as diabetes, osteoporosis, cancer, and skeletal muscle between 20 and 40% of COPD patients worldwide are never
dysfunction, among others [2]. smokers [12].
The global prevalence of COPD oscillates around 12% Genetic abnormalities can predispose individuals to
of the general population. COPD currently ranks as the 3rd COPD. The best documented genetic risk factor for COPD
cause of mortality in the world (responsible for 3 million is α1 antitrypsin deficiency (caused by a mutation in the
deaths), just behind CVDs [6]. The incidence of COPD is SERPINA1 gene), although it occurs in a minority (0.12%)
expected to rise over the next 40 years. By 2060, it is esti- of COPD patients, more in Northern Europe [13]. As per
mated that there may be over 5.4 million deaths annually today, almost 100 single-nucleotide polymorphisms have
from COPD [7, 8]. COPD prevalence and mortality are been associated with increased risk of COPD, but their
similar in males and females [9]. COPD has a significant individual effect size is small, so COPD is now considered
economic burden; in the European Union, the total annual a polygenic disease [14].
direct costs of COPD are estimated to be about 38.6 billion Recent research has shown that abnormal lung devel-
Euros [10]. opment before and after birth due to factors like maternal
smoking, prematurity, low birthweight, repeated infections
in infancy, and/or poor nutrition, among others, can lead to
COPD in young adults [15, 16]. Importantly, these young
individuals show a higher prevalence and earlier incidence

Fig. 1  Diagnosis, assessment of
the severity of airflow obstruc-
tion, and proposed ABE clinical
assessment tool for COPD
patients. Reproduced with
permission from Ref. [2]

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Clinical Research in Cardiology

of comorbidities (e.g., CVD and diabetes) and die prema- and more relevant due to increasing availability, reduced
turely [17]. radiation doses, and reduced costs [21]. CT can character-
ize changes in the lungs (such as airway width and walls,
mucus plugs, bronchiectasis, and type, spatial distribution
Diagnosis of COPD and extent of emphysema, interstitial abnormalities, nod-
ules and lymph nodes, and size of the pulmonary arter-
Under-diagnosis of COPD in the general population is ies). Besides, coronary artery calcification, that may be of
huge, in the range of 70–80%, so the vast majority of COPD prognostic relevance in COPD patients [22], osteoporosis
patients in the community are not treated at all [2]. COPD (reduced bone mineral density in the vertebrae), cachexia
should be suspected in any patient who has dyspnea on exer- (diminished area of the pectoralis muscle), and lung tumors
cise, chronic cough or sputum production, and/or a history may also be identified by CT [2].
of exposure to risk factors for the disease (see above), a Besides spirometry, other lung function measurements
constellation of clinical symptoms quite frequent in patients may be informative in some patients. For instance, the meas-
with CVDs, particularly HF. However, spirometry is neces- urement of lung volumes (gas trapping, lung hyperinflation)
sary to establish the diagnosis of COPD by showing persis- by body plethysmography may be relevant to select patients
tent airflow limitation after bronchodilation [2]. The latter for interventional procedures (e.g., endobronchial valve
is identified by a ratio between the volume of gas expired in placement in patients with hyperinflation due to emphy-
the first second (FEV1) and the total volume of gas expired sema). Other functional measurements like the diffusing
(Forced Vital Capacity—FVC) < 0.7 [18] (Fig.  1). The capacity of the lungs for carbon monoxide (DLco) [23],
severity of airflow obstruction is established based on the pulse oximetry, and arterial blood gasses can contribute to
FEV1 value (GOLD grades—Fig. 1). Clinical assessment better characterize the type and therapeutic needs (e.g., oxy-
is based on the presence of symptoms (low vs. high) and gen therapy) of some COPD patients [2]. Finally, objectively
the previous history of ECOPD (≤ 1 moderate ECOPD in measured exercise impairment, assessed by a 6-min walk
the previous year vs. more than that or one severe (hospital- test or other tests, is a powerful indicator of health status
ized) ECOPD). Using these two dimensions, GOLD 2023 impairment and predictor of prognosis, both in patients with
proposes to classify COPD patients in one of three groups COPD and CVDs, and laboratory exercise testing can help
(A, B, or E) (Fig. 1). identify the mechanisms of dyspnea, exercise limitation, and
Mucus hypersecretion, resulting in chronic productive co-existing or alternative comorbid conditions [2].
cough (chronic bronchitis) is not necessarily associated
with airflow limitation; conversely, not all patients with
COPD have mucus hypersecretion [2]. In some patients Primary and secondary prevention
with chronic asthma, a clear distinction from COPD may be
difficult since the two conditions share common traits and The following measures must be considered for primary
clinical expressions. HF can mimic or coexist with COPD. (disease occurrence) and/or secondary (disease progression)
Sometimes it may be difficult to discern whether dyspnea prevention. Smoking avoidance/cessation is the single most
(or poor functional class) is a consequence of COPD and/or important preventive intervention [2]. Counseling delivered
HF, especially in patients with preserved left ventricular sys- by healthcare professionals, even if brief (3 min), improves
tolic function as diastolic dysfunction and COPD frequently quit rates, but nicotine replacement and pharmacotherapy
coexist [19, 20]. reliably increase long-term smoking abstinence rates [2].
Physical examination is rarely diagnostic in COPD except Yet, the following aspects need to be considered in patients
in cases of advanced emphysema where hyper-inflated tho- with CVDs. Nicotine replacement products (nicotine gum,
rax and decreased breath sounds with hyper-resonance inhaler, nasal spray, transdermal patch, sublingual tablet,
may suggest the presence of the disease. Chest X-ray is not or lozenge) reliably increases long-term smoking absti-
helpful to establish a diagnosis in COPD albeit suggestive nence rates [2], but medical contraindications to nicotine
changes include signs of lung hyperinflation (flattened dia- replacement therapy include recent myocardial infarction
phragm and an increase in the volume of the retrosternal or stroke [24, 25]. The contraindication to nicotine replace-
air space), hyper-lucency, and rapid tapering of the vascu- ment therapy soon after acute coronary syndrome remains
lar markings. It may, however, help to exclude alternative unclear [26, 27]. On the other hand, varenicline and bupro-
diagnoses and may give indications for the presence of pion increase long-term quit rates, but should always be
significant respiratory (pulmonary fibrosis, bronchiectasis, used as a component of a supportive intervention program
and pleural diseases), skeletal (e.g., kyphoscoliosis), and rather than as a sole intervention for smoking cessation [2].
cardiac (e.g., cardiomegaly) comorbidities [2]. By contrast, The effectiveness of the antihypertensive drug clonidine for
computed tomography (CT) of the chest is becoming more smoking cessation is limited by side effects [2]. Electronic

13
 Clinical Research in Cardiology

cigarettes (e-cigarettes, vaping) are not recommended as a Initial pharmacologic treatment

smoking cessation aid [2].
Vaccination is key preventive measurement in COPD Pharmacological therapy can reduce COPD symptoms,
[2]: (1) Influenza vaccination can reduce serious illness and reduce the frequency and severity of exacerbations, and
death in COPD patients [2] and can also decrease the risk of improve health status and exercise tolerance [2]. Recent evi-
acute coronary events and other endpoints in patients with dence suggests beneficial effects on rates of lung function
a recent cardiac event [28]; (2) Pneumococcal vaccine with decline and mortality [2]. Here we only discuss the initial
conjugate vaccine (PCV13) or pneumococcal polysaccharide pharmacological treatment of the clinically stable patient
vaccine (PPSV23) is recommended for all patients ≥ 65 years with COPD (Fig. 2) because this likely is the most relevant
of age [2]. The PPSV23 is also recommended for younger aspect for a cardiologist treating patients with CVDs and
COPD patients with significant comorbid conditions COPD. We do not discuss treatment changes during follow-
including chronic heart disease [2]; the CDC recommends up or the treatment of the patient during an ECOPD episode
one dose of a 20-valent pneumococcal conjugate vaccine [2], but we recommend that the practicing cardiologist refers
(PCV20); or one dose of a 15-valent pneumococcal conju- the patient to a pulmonologist if initial treatment does not
gate vaccine followed by PPSV23. We would like to mention improve the health condition of the patient.
that PPSV23 is still recommended in most countries, but the The cornerstone of COPD pharmacologic treatment is
new conjugate vaccines had not been part of the evaluation (in combination with quitting smoking) treatment with one
for these recommendations. However, this will change in the (in patients with few symptoms) or two (most often) inhaled
near future. (3) COVID-19 vaccination (including boosters) long-acting bronchodilators (LABD). If there are safety
is recommended in all patients with COPD [2]; (4) Pertussis concerns for long-acting ß2 agonists (e.g., history of atrial
(whooping cough), tetanus, and diphtheria (Tdap) vaccine is fibrillation) or long-acting anticholinergics (e.g., severe
recommended in those who were not vaccinated in adoles- glaucoma), monotherapy may be considered in patients with
cence; (5) Herpes zoster vaccine to protect against shingles a symptom load that would normally lead to dual therapy.
is recommended in adults with COPD older than 50 years of Short-acting bronchodilators, such as salbutamol (albuterol)
age; and, finally, (6) new respiratory syncytial virus (RSV) or ipratropium, should be used only as a rescue medication.
vaccines are under development. Short-acting β2 agonists are not recommended for regular
chronic use in patients with arterial hypertension or heart
failure. The decision on what is the most appropriate phar-
macologic treatment alternative for a given patient requires

Fig. 2  Recommended initial
pharmacological treatment of
COPD patients. To assess the
level of symptoms, two simple
and validated questionnaires
are recommended: the modified
Medical Research Council
dyspnea scale (mMRC) with
one question [67] or the COPD
Assessment Test™ (CAT) with
eight questions [68]. Abbre-
viations: eos: blood eosinophil
count in cells per microliter.
Reproduced with permission
from Ref. [2]

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Clinical Research in Cardiology

consideration of both the inhaler device to use and the most technique should be checked periodically by the attending
appropriate molecule(s) for the patient. physician or an educated nurse [2].

What inhaler device? Which molecule(s)?

Not all inhaler devices (and the patients to use them) are Pharmacological treatment should be individualized and
equal. There are two main types of portable inhalers (we do guided by the severity of symptoms, risk of exacerbations,
not discuss here the role of nebulizers, which may be con- side effects, comorbidities, drug availability, cost and the
sidered as home treatments in some patients): pressurized patient’s response, preference, and ability to use various
metered dose inhaler (pMDI) and dry powder inhalers (DPI). drug delivery devices.
A pMDI delivers a specific (metered) dose of medication in There are two main pharmacological classes of LABD
the form of a short burst of aerosolized medicine utilizing to use in patients with COPD: the β2 adrenergic agonists
the energy of compressed propellant(s) for the aerosol gener- (LABA) and the muscarinic antagonists (LAMA). LABA
ation. pMDIs can deliver metered drug doses either directly include salmeterol, formoterol, indacaterol, vilanterol, and
(most patients) or via add-on holding chambers (in patients olodaterol. LAMA include tiotropium, aclidinium, umecli-
who are unable to synchronize dose release, inspiration, and dinium, and glycopyrronium. Figure 2 presents the GOLD
breath-hold). Alternatively, DPIs deliver medication to the 2023 ABE quadrants used to guide initial pharmacological
lungs in the form of a dry powder which can be held either in treatment in a patient with COPD. The three groups showed
a capsule for manual loading or in a proprietary form inside (A–E) results from the assessment of the level of symptoms/
the inhaler. Patients with severe airflow limitation may not impairment experienced by the patient (low or high) in the
be able to generate sufficient inspiratory flow to use a DPI horizontal axis and the history of ECOPD experienced in
efficiently; in these patients, pMDI (often via add-on plastic the previous year (low or high), which is the best predic-
chambers) may be the preferred choice. A soft-mist inhaler, tor of future ECOPD episodes [2]. Although there are sev-
which does not use a propellant, is also a potential alterna- eral potential recommendations depending on the assigned
tive. A proper inhalation technique is essential for the proper group, as a rule of thumb, the use of a LAMA/LABA com-
use of both pMDI and DPI (thus for treatment efficiency) bination achieves better results than the single components
and includes, in this order: (1) deep exhalation of thoracic regarding lung function and symptoms irrespective of base-
gas; (2) deep and continuous inspiration (after the actuation line impairment of health status. Therefore, LAMA/LABA
of the device in the case of pMDI with or without cham- combinations may be considered as initial maintenance
ber); and (3) breath holding for several seconds to allow therapy for symptomatic patients with COPD across a broad
proper deposition of the drug in the lungs. Proper inhalation range of symptom severities [29]. These preparations can be

Fig. 3  Proposed clinical Paent with respiratory symptoms not explained by heart disease
strategy for a patient with
respiratory symptoms seen by
a cardiologist not explained Forced spirometry
by heart disease. For further
explanations, see text Normal Airflow obstrucon Other
(FEV1/FVC<0.7) abnormality
• COPD excluded
• Consider other causes of
symptoms (e.g.,
pulmonary hypertension)
and referral to specialist Features of asthma
Features of COPD
(e.g., smoking, emphysema) (e.g., allergies, family history)

LABA-LAMA LABA-ICS Refer the paent for

specialized pulmonary consultaon

Clinical response

Good Poor

• Connue treatment
• Follow-up

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 Clinical Research in Cardiology

prescribed once or twice daily depending on the commercial with increased local and systemic inflammation caused by
product and level of symptoms of the patient, once daily dos- infection, pollution, or other insult to the airways [5]. The
ing better suiting patients with fewer symptoms and twice time frame proposed (< 14 days) aims at differentiating
daily dosing preferred for those who are highly dyspneic. ECOPD from progression of COPD, but many patients
Chronic treatment with LABA–LAMA can be maintained with ECOPD consult much earlier.
in patients with CVDs, even in those treated with β-blockers. ECOPD are the major cause of morbidity and mortality
A second group of drugs is represented by inhaled cor- in patients with COPD and account for 31–68% of COPD
ticosteroids (ICS), of which there are several in the market total care costs; hospitalizations account for most of these
(budesonide, beclomethasone, fluticasone propionate, and costs [34, 35]. Comorbid diseases frequently occurring
fluticasone furoate). In patients with COPD (asthma is dif- in patients with (acute myocardial infarction, congestive
ferent), they should never be administered as a single agent heart failure, cardiac arrhythmias, and pulmonary embo-
or in combination with LABA (LABA–ICS), but rather used lism) can mimic or aggravate the symptoms of ECOPD
in combination with LABA–LAMA (triple therapy), now and contribute to diagnostic confusion [36]. The reverse
available in a single canister, which is preferable to mul- is also true [5]. A patient with HF and worsening dyspnea
tiple canisters [2]. GOLD 2023 recommends considering can actually be misdiagnosed of pulmonary congestion
initial treatment with triple therapy in E patients if their when he/she may suffer ECOPD. Appropriate investiga-
level of circulating eosinophils is higher than 300 cells/μL tions using electrocardiogram, echocardiogram, and bio-
[2] (Fig. 2). Importantly, two recent, large randomized clini- markers, such as N-terminal pro-brain natriuretic peptide
cal trials have shown that triple therapy reduces all-cause (NT-pro-BNP) and troponin or d-dimers, and chest CT
mortality in GOLD E patients [30, 31]. angiography are generally required to exclude acute car-
We recommend that cardiologists become familiar with diac events or pulmonary embolism, respectively, in these
several of the products available, so they become comfort- patients [37]. Treatment of ECOPD requires short-acting
able in initiating therapy in the event of absence of pulmo- bronchodilators for relief of dyspnea, systemic corticos-
nary specialized support at the moment of diagnosis, but teroids, antibiotics if purulent sputum exists (where pos-
whenever in doubt, a consultation with a pulmonary special- sible, sputum culture is recommended) and correction of
ist is advised (Fig. 3). hypoxemia with use of supplemental oxygen [18]. All
these measures can be taken by a cardiologist, but if the
exacerbation is severe, we would recommend referring the
Non‑pharmacological treatments patient to an emergency department where non-invasive
ventilation can be applied to correct hypercapnia and aci-
Non-pharmacological measures are important in COPD. dosis [2]. This therapeutic strategy can be used in patients
Physicians should emphasize the importance of a healthy with CVDs.
environment (avoiding both active and passive smoking,
as well as air pollution, both inside and outside), encour-
age physical activity, and enroll the patient in a pulmonary
rehabilitation program, particularly if the patient suffers Special considerations for cardiologists
from COPD plus a CVD, where the role of rehabilitation dealing with COPD patients
is well established [32, 33]. Vaccine use has been dis-
cussed above. If the patient remains symptomatic despite Arterial hypertension
initial pharmacological and non-pharmacologic treatment,
referral for a specialized assessment and management is Arterial hypertension is the most frequently occurring
encouraged. comorbidity in COPD and may have implications for
prognosis [38, 39]. Diastolic dysfunction as a result of
sub-optimally treated hypertension may be associated with
exercise intolerance and mimic symptoms associated with
What about exacerbations? an acute exacerbation, thereby provoking hospitalization
in COPD [40]. Thus, it is important to control blood pres-
GOLD 2023 has renewed the definition of an exacerbation sure in COPD patients with underlying hypertension [41,
of COPD (ECOPD) following the so-called Rome proposal 42]. Hypertension should be treated according to usual
[5]. Accordingly, an ECOPD is now defined as an event guidelines since there is no evidence that hypertension
characterized by increased dyspnea and/or cough and spu- should be treated differently in the presence of COPD [2].
tum that worsens in < 14 days which may be accompanied
by tachypnea and/or tachycardia and is often associated

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Clinical Research in Cardiology

Heart failure (HF) worsening dyspnea, atrial fibrillation is frequently docu-

mented, and it may be either a trigger or a consequence of
The prevalence of systolic or diastolic HF in COPD an ECOPD episode [61]. The presence of atrial fibrillation
patients ranges from 20 to 70% and its annual incidence should not alter the treatment of COPD. Bronchodilators
between 3 and 4% [40]. Unrecognized HF may mimic or have been previously described as potentially pro-arrhyth-
accompany COPD especially during ECOPD events [43]. mic agents [62, 63]; however, available evidence suggests
Indeed, approximately 40% of COPD patients who are an overall acceptable safety profile for both LABAs and
mechanically ventilated because of hypercapnic respira- LAMAs [18]. Caution is advised, however, when using
tory failure have evidence of left ventricular dysfunction short-acting β2-agonists and theophylline, which may pre-
[44, 45]. Right ventricular function can also be altered in cipitate atrial fibrillation and make control of the ventricular
patients with COPD and can be investigated with to mod- response rate difficult [2]. Generally, theophylline should
ern diagnostic methods [46–49]. Treatment with ß1-recep- be avoided for the treatment of COPD as they do not sig-
tor blockers, such as metoprolol, bisoprolol, and nebivolol nificantly attenuate symptoms or reduce the risk of ECOPD
(typically used in elderly patients), but also the less-prev- [64].
alent ß-blocker carvedilol improves survival in HF and is
recommended in patients with HF who also have COPD.
Selective ß1-receptor blockers should be preferred to treat Peripheral vascular disease
patients with COPD for approved cardiovascular indica-
tions and not for the purpose of preventing exacerbations Peripheral artery disease (PAD) is commonly associated
of COPD [50]. Acute HF should be treated according to with atherosclerotic heart disease and may have significant
usual HF guidelines since there is no evidence to support implications for functional activity as well as quality of life
an alternative management strategy. Non-invasive venti- in patients with COPD [65]. In a large cohort of patients
lation added to conventional therapy improves outcomes with COPD of all degrees of severity, 8.8% were diagnosed
for patients with hypercapnic respiratory failure due to an with PAD that was higher than the prevalence in non-COPD
exacerbation of COPD as well as those with HF and acute controls (1.8%) [65]. COPD patients with PAD reported a
pulmonary edema [51]. worse functional capacity and worse health status compared
to those without PAD.
Ischemic heart disease (IHD)
Surgery in the CVD patient with COPD
Patients with COPD often suffer IHD. Different murine
and clinical studies have shown that systemic inflamma- Patients with CVDs often need surgery and/or percutaneous
tion and oxidative stress are important shared mechanisms interventions. General surgical risk is increased in patients
between COPD and atherosclerosis, thus favoring IHD with COPD. The key risk factors include smoking, poor
[52–54]. During, and for at least 90 days after ECOPD, general health status, age, hypercapnia, obesity, and airflow
there is an increased risk of cardiovascular events (e.g., limitation severity [2]. Common pulmonary postoperative
deaths, myocardial infarction, stroke, unstable angina, complications include lung infections and atelectasis, which
and transient ischemic attack) in patients at a high risk of can lead to acute respiratory failure [2]. To prevent them,
concomitant IHD [55]. Hospitalization for ECOPD has medical COPD treatment should be optimized before sur-
been associated with 90-days mortality of acute myocar- gery. Specialist consultation is advisable. Comorbid condi-
dial infarction, ischemic stroke, and intracranial hemor- tions, particularly in patients with CVD, should be treated
rhage [56]. Patients who demonstrate abnormal cardiac before any major surgical intervention.
troponins during an ECOPD event are at increased risk
of adverse outcomes including short-term (30-days) and
long-term mortality [57, 58]. The treatment of IHD should Conclusions
be according to guidelines irrespective of the presence of
COPD and vice versa. COPD is the elephant in the room for many patients with
CVDs. It is a prevalent, preventable, and treatable condi-
tion, but most often it has not been diagnosed and, hence,
Arrhythmias not treated appropriately [2]. Importantly for cardiology
practice, optimal management of COPD is associated with
Cardiac arrhythmias are common in COPD and vice versa improved cardiovascular outcomes [66]. Yet, such clini-
[59]. Atrial fibrillation is frequent and associated with a cal management requires, to begin with, a high level of
lower ­FEV1 [60]. In COPD patients presenting with severe suspicion and appropriate confirmation of diagnosis by

13
 Clinical Research in Cardiology

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