Left ventricular dysfunction in chronic
obstructive pulmonary disease
Saha B Kr1, Sarkar D.2, Sarkar L.3
Bandyopadhyay R.4
1Dr. Bikram Kr Saha,
Assistant Professor. NBMC, Darjeelingat present at Malda Medical College. 2Dr.
Debasis Sarkar, Assistant Professor, Malda MCH, 3Dr. Liton Sarkar, Assistant
Professor, RG Kar Medical College, 4Dr. Ramtanu Bandyopadhyay, Professor,
Malda MCH,West Bengal, India.
Corresponding Author: Dr. Debasis Sarkar, Assistant
Professor, Malda Medical College, Malda WB, India. Email:dr.debasis99bmc@yahoo.in
Abstract
Introduction: The
prevalence of LV dysfunction is probably high in COPD patients because this
condition shares common risk factors.The diagnosis of left heart failure is difficultin
the early phases of COPD and also during exacerbation due to similarities in
signs and symptoms. Bio-markers like hsCRP is found to be elevated in stable
phase as well as in exacerbation of COPD. Objectives:
To assess LV Dysfunction(Systolic and Diastolic) and to correlate Age,
Symptoms, Duration and stage of illness, CRP with LV Dysfunction. Methods: Total 100 patients of which 50
were age and sex matched controls not having COPD complying with Inclusion and
Exclusion Criteria. After taking history and clinical examination they were
evaluated for COPD and Left ventricular Dysfunction using PFT and
Echocardiogram. Results: Out of 50
patients, 37 patients (74%) had Diastolic dysfunction, of them 2 patients hadSystolic
dysfunction also. 13 patients were normal.In the control group only 4 had
Diastolic Dysfuncion.CRP was high in 35% (70%) of patients. In the higher age
group of 50-60 years Diastolic dysfunction was significant. In patients of GOLD
stage IV 5 out of 5 patients (100%) whereas in GOLD stage I and II it was in 1
case (16.66%) and21 case (80.76%) respectively. While comparing with the
control group incidence of LV dysfunction parameters and CRP is more in case
group. Conclusion: There is
increased incidence ofLV Diastolic dysfunction and also with advanced GOLD
stage.CRP also correlates well LVDD. Therefore it is pertinent to explore LVDD
in all patients with acute exacerbation of COPD and advanced disease stage.
Keywords: COPD, Left Ventricular Dysfunction, Diastolic Dysfunction.
Author Corrected: 26th October 2018 Accepted for Publication: 30th October 2018
Introduction
Chronic Obstructive Pulmonary Disease (COPD) is a major cause of Chronic
Morbidity and Mortality worldwide. It is the fifth leading cause of death worldwide
[1]. Acute exacerbation of COPD (AECOPD) accounts for large amounts of the
Morbidity and Mortality attributed to COPD [2]. AECOPD refers to the
exaggeration of COPD symptoms: aggravation of dyspnoea, an increase in
expectoration volume, and a change in the appearance of sputum which becomes purulent
[3].Although dominated by bacterial or viral infection, etiologies of AECOPD
remain unrecognised in as much as one third of these patients [4].Added to
this, acute left ventricular (LV) dysfunction is suspected as a cause of
exacerbation in many such patients. Nevertheless in many of these situations LV
dysfunction might be associated without being the cause of the exacerbation.
Yet a diagnosis of LV dysfunction in patients with dyspnoea is challenging to
the emergency department physicians, because bed side clinical assessment has a
poor performance record and cardiac function test with enough accuracy to
diagnose (in particular echo-cardiography) are not always possible because they
are unavailable or difficult to interpret[5].The prevalence of LV dysfunction is
probably high in COPD patients because this condition shares many risk factors
with coronary disease: age, male predominance, cigarette smoking and so on [6].
The diagnosis of left heart failure is fraught difficult notably in the early
phases of COPD and also duringexacerbation due to similarities in signs and
symptoms.Importantly co-existence of COPD and heart failure is plausible in
view of overlap of risk factors: notably smoking.Echocardiography is essential
for establishing the diagnosis of heart failure. Accessibility to this
diagnostic facility however is limited for primary care patients and
echocardiography is not a part of the standard investigational protocol of
pulmonologists.It seems therefore plausible that a considerable proportion of
patients with a diagnosis of COPD have concomitant heart failure which remains
unrecognized by primary care physicians or pulmonologists. In addition, due to
similarities in symptoms some COPD patients may be misclassified and in fact
have heart failure. Earlier studies suggested that the use of pulmonary
medication often coincides with unrecognized heart failure [7,8]. The
prevalence of heart failure can be as high as 20% – 30% in those COPD patients
who are referred for acute exacerbation. [9,10]. However information is lacking
on the prevalence of left heart dysfunction as a cause of left heart failure in
the much larger population of patients with stable COPD. Development of right
ventricular hypertrophy and eventual right heart failure is also quite common
in patients of COPD. However, some disturbance in left ventricular function has
been observed by several workers among such patients. The present study is
undertaken with a view to determine the degree of disturbance in left
ventricular function if any, among patients of COPD. Bio-markers like hsCRP is
found to be elevated in stable phase COPD patients and Brain Natriuretic
Peptide (BNP) and amino terminal Pro-brain Natriuretic Peptide have been shown
to perform well in distinguishing between dyspnea of cardiac origin and dyspnoea
of pulmonary causes in patients attending emergency department[11-16].However
extrapolation of these results to the specific context of AECOPD is not
straight forward because BNP secretion might be secondary to left ventricular
stress or right ventricular stress. [17,18].
In this study we have also tried to find out the prevalence of raised
CRP in those patients of COPD with LV dysfunction. Traditional texts and review
articles suggest that dyspnoea due to COPD can be readily distinguished from
LVF by clinical, radiographic and spirometric abnormalities. COPD may obscure
clinical signs of LVD, both disorders may produce paroxysmal nocturnal dyspnoea,
orthopnoea and cough. Radiographic and clinical findings of pulmonary
congestion and cardiomegaly may be obscured by large barrel chest and
hyper-inflated lungs of patient with emphysema. Evidence of airway obstruction
and a bronchodilator response on pulmonary function test is found not only in COPD,
but also in acute congestive failure [19-21]. Hence in this present study we
tried to show the prevalence of LVD co-existent with COPD in the absence of
factors known to produce LVD.
Objectives
1.To assess LV Dysfunction(Systolic and Diastolic).
2.To correlate Age, Symptoms, Duration and stage of illness, CRP with LV
Dysfunction.
Methods
a) Study Type: Cross-sectional
Analytical Study.
b) Sample Size: 100
patients with Left ventricular Dysfunction were enrolled.
c) Sampling Technique:
Consecutive Non-probability sampling technique used.
d) Inclusion Criteria:Any
patient with COPD between 50 – 65yrs. The upper age limit is 65 yrs since above
that; sizeable number of otherwise normal persons can develop diastolic
dysfunction.
e)Exclusion Criteria: Acute
myocardial infarction within 6 weeks, Severe congestive cardiac failure, Hypertension,
Diabetes, Valvular Heart Diseases, Known patient of Cardiomyopathy.
f) Procedure:
After taking approval from Hospital ethical Committee, written informed consent
were taken from patients. 50 patients with COPD admitted in Medicine Indoor and
50 age and sex matchedpatients not having COPD were enrolled in this study. A
detailed history followed by clinical examination were documented as per
proforma. PFT, Chest X-ray, ECG, Echocardiogram to document Systolic and
Diastolic Dysfunction and CRP in blood examination were done. Transthorasic
Echocardiogram was done wherever necessary. Echocardiographic analysis
The echocardiograph device was an Envisor C
model (Philips Medical Systems, Andover, Massachusetts, USA) equipped with a
2.0–4.0 MHz probe capable of capturing second harmonic, tissue, pulsed,
continuous and color Doppler traces, as well as one- and two-dimensional mode
images. With participants positioned in left lateral decubitus and monitored
using an electrocardiographic lead, the followingEchocardiographic cuts were
performed: short parasternal axis to measure ventricles, aorta and left atrium
and apical two, four and five chambers to evaluate cavities and systolic and
diastolic functions of ventricles. All of the measurements were performed in
accordance with the American Society of Echocardiography/ European Association
of Echocardiography recommendations. An average of three measurements was calculated
for each variable.
The left ventricular (LV) mass (LVM) was
calculated according to the following formula: LVM =
0.8×{1.04×[(LVDD+IVSDT+PWDT)3-LVDD3]}+0.6, where LVDD, IVS and PWDT represent
the LV diastolic diameter, interventricular septum and posterior wall
thickness, respectively. The left ventricular systolic function was evaluated
by measuring the ejection fraction (EF) according to the Teichholz method. The
LV diastolic function was evaluated by measuring the early (E wave) and late (A
wave) diastolic mitral inflow velocities, their ratio, the E wave deceleration
time (EDT) and the isovolumic relaxation time (IVRT).
Results
Table 1: Diastolic dysfunction in cases vs controls
Total no of patients |
No of patients having Diastolic dysfunction |
percentage |
|||
50 (cases) |
37 |
74% |
|||
50 (controls) |
04 |
8% |
|||
CRP |
|||||
|
No
of patients |
Percentage |
|||
>0.60 |
35 |
70% |
|||
<0.60 |
15 |
30% |
|||
GOLD
Stage & Diastolic dysfunction |
|||||
|
N0
of patient |
DD |
Percentage |
||
1 |
6 |
1 |
16.66% |
||
2A |
26 |
21 |
80.76% |
||
3 |
13 |
10 |
76.92% |
||
4 |
5 |
5 |
100% |
||
CRP
&Diastolic dysfunction |
|||||
|
N0
of patient |
DD |
Percentage |
||
>.60 |
35 |
34 |
97.14% |
||
<.60 |
15 |
3 |
20% |
||
CRP
in cases and controls |
|||||
Cases (Mean+/-SD) |
Controls (Mean+/-SD) |
P Value |
|||
0.699+/-0.184 |
0.414+/-0.063 |
<0.001 |
|||
In our study, we found thatDiastolic
dysfunction is a significant occurrence in the case arm
than among control arm.CRP is also
significantly raised in COPD patients (p value<0.001) and in patients having
raised CRP have diastolic dysfunction too (p value 0.0000 i.e<0.05).Comparing
the presence of diastolic dysfunction in early stage i.e. 1 and in advanced
stage i.e. 4 we find that the association between stage 4 disease and diastolic
dysfunction is significant (P = 0.0057 i.e. < 0.05).
Table
2: Various parameters of LV Functions in cases vs controls
Indices
of LVD |
Cases(Mean+/-SD) |
Controls(Mean+/-SD) |
P
Value |
E/A |
0.964+/-0.257 |
1.218+/-0.135 |
<0.001 |
DT |
242+/-14.424 |
230.44+/-8.836 |
<0.001 |
IVRT |
94.2+/-9.029 |
80.88+/-7.862 |
<0.001 |
EF |
60%+/-0.062 |
60%+/-0.029 |
>0.001 |
We find that each parameter of DD (E/A, DT, IVRT) to be abnormal in the
case group we find that each parameter of DD is significant (P < 0.001) in
the case group, whereas parameter of SD (EF) is not significant (P > 0.001).
Discussion
In the present study we have found presence of LVD in COPD patients and
have found that majority of them have Diastolic dysfunction and that it is a
significant occurrence (p < 0.001) in them. In our study, also we got
diastolic dysfunction in the control group; however comparing two groups we
found DD is more prevalent in patients with COPD.
In our study we found dyspnoea to be the predominant symptom. Although
some studies indicate a weak relationship between the symptoms of dyspneoa and
indicators of disease severity (FEV, LVEF)[22-24], there also exist some other
studies which indicate that no relationship is evident between them [22,25,26].
We too did not find any significant association between this predominant
symptom of dyspneoa and DD (p > 0.05).
Funk GCet
alreported that the maximal atrial filling velocity was increased and the early
filling velocity was decreased in patients with COPD compared to control subjects
[27].The early flow velocity peak/late flow velocity peak (E/A) ratiomarkedly
decreased in patients with COPD compared to control subjects (0.79 + 0.035 vs
1.38 + 0.069, respectively; p < 0.0001), indicating the presence of left
ventricular diastolic dysfunction. The atrial contribution to total left
diastolic filling was increased in patients with COPD. This was also observed
in COPD patients with normal PAP, as ascertained using a right heart catheter.
The atrial contribution to total left diastolic filling was further increased
in COPD patients with higher PAP. PAP correlated with the E/A ratio (r = -0.85;
p < 0.0001).
In our study also, early flow velocity peak/late flow velocity peak
(E/A) ratio was markedly decreased in patients with COPD compared to control
subjects (cases 0.964 +0.257 vs. controls 1.218 +0.135 respectively; p <
0.001) and the values of DT and IVRT were increased in them compared to control
subjects (cases 242 + 14.424 vs. controls 230.44 +8.836 and cases 94.2 + 9.029
vs. controls 80.88 + 7.862respectively; p < 0.001)
In our study too we founda trial contribution to total left diastolic
filling was further increased in COPD patients with higher PAP as we saw the
occurrence ofP Pulmonale, an ECG marker of pulmonary hypertension to be
significant in the cases having DD (p<.05)
Suchoń Eet
alreported in COPD patients LV diastolic function is significantly impaired and
its magnitude is related with increase in pulmonary artery pressure, while
systolic LV function is well preserved [28]. In our subset of patients we
observe that there is increase prevalence of DD but only in two patients we got
systolic dysfunction (SD) which is not significant statistically. As we have
excluded patients with known myocardial infarction, ischaemic heart disease,
dilated cardiomiopathy, so cause of SD in these two patients cannot be
confirmed. To find out hidden ischaemic heart disease or myocardial disease,
cardiac catheterization, coronary angiography or myocardial biopsy were
necessary but these procedures were out of our reach.
Regarding patients who have echo proved DD, we found DD is more
prevalent in the higher age group, however since age related myocardial changes
occur in normal person’s without COPD, and age related increased occurrence
were reported in the case arm also.
DD is more prevalent in our study in patients whose duration of symptoms
was more than 5 years. This observation is significant (p < 0.05) among the
cases. DD is found to be more prevalent in those who presented with predominant
dyspnoea. However statistical analysis fails to show any significant
association between symptom nature and DD (p > 0.05).
Another salient feature in our study is that significant occurrence of
DD in the advanced stage of COPD i.e. GOLD STAGE IV than in early stage of the
disease i.e. GOLD STAGE I, probably higher presence of pulmonary hypertension
and right ventricular strain by the virtue of inter ventricular dependence
accounts for this observation.
In our study we found raised CRP, is a significant occurrence among DD
patients in the case arm. However, though traditional studies depict hsCRP to
be raised in COPD patients due to scarcity of resources we used ordinary CRP as
an alternative. Raised CRP in the COPD patients in our study is not solely due
to chest infection in these patients since initially they were all stabilized
with nebulization and antibiotics; they represent an inflammatory nature of the
disease itself and a plausible cause of their significant association with DD
may be the contribution of this inflammatory process in atherogenesis thereby
giving rise to microvascular ischemia to the cardiac muscle.
Kirsten Jörgensenet al reported LV
in patients with severe emphysema is hypovolemic,and operates on a steeper
portion of the LV function curve,while indices of systolic function are not
significantly impaired compared to non-emphysematous controls.
A. K. Poddar et al [29]. Reported
parameters of LVD like MRCF, EF, FS were depressed in the subset of patients of
COPD with Corpulmonale and overt right heart failure while in patients of COPD
with Corpulmonale only the parameters of LVD were intact. However, our
finding is that diastolic dysfunction is present in majority of
patients of COPD without any features of overt failure i.e in stable phase
COPD.
Conclusion
Left ventricular diastolic dysfunction is significantly present in COPD
patients more in those with Older age, Long symptom duration ,Advanced stage of
disease,Pulmonary hypertension and Raised CRP level.
Facts regarding raised CRP level: It is nothing new to know that, COPD
is a systemic and inflammatory disease. Like any other inflammatory disease, CRP
is also raised in our study. The inflammation is giving rise to atherogenesis
and microvascular ischaemia leading to diastolic dysfunction. This data only reinforces
the current knowledge of association between raised CRP, inflammation and
microangiopathy.
Funding: Nil. Conflict of Interest: None initiated. Permission from IRB: Yes.
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How to cite this article?
Saha B Kr, Sarkar D, Sarkar L, Bandyopadhyay R. Left ventricular dysfunction in chronic obstructive pulmonary disease. Int J Med Res Rev 2018; 6(07):385-390. doi:10.17511/ijmrr.2018.i07.08.