Is smog innocuous? Air pollution and cardiovascular disease

Abstract

Air pollution is a significant environmental and health hazard. Earlier studies had examined the adverse health effects associated with short- and long-term exposure to particulate matter on respiratory disease. However, later studies demonstrated that was actually cardiovascular disease that accounted for majority of mortality. Furthermore, it was not gaseous pollutants like oxides of nitrate, sulfur, carbon mono-oxide or ozone but the particulate matter or PM, of fine or coarse size (PM2.5 and PM10) which was linearly associated with mortality; PM2.5 with long term and PM10 with short term. Several cardiovascular diseases are associated with pollution; acute myocardial infarction, heart failure, cardiac arrhythmias, atherosclerosis and cardiac arrest. The ideal way to address this problem is by adhering to stringent environmental standards of pollutants but some individual steps like choosing to stay indoors (on high pollution days), reducing outdoor air permeation to inside, purifying indoor air using air filters, and also limiting outdoor physical activity near source of air pollution can help. Nutritional anti-oxidants like statins or Mediterranean diet, and aspirin have not been associated with reduced risk but specific nutritional agents like broccoli, cabbage, cauliflower or brussels sprouts, fish oil supplement may help. Use of face-mask has been controversial but may be useful if particulate matter load is higher.

Full text

Editorial
Is smog innocuous? Air pollution and cardiovascular disease
ARTICLE INFO
Keywords:
Air pollution
Particulate matter
Cardiovascular risk
ABSTRACT
Air pollution is a significant environmental and health hazard. Earlier studies had examined the adverse
health effects associated with short- and long-term exposure to particulate matter on respiratory disease.
However, later studies demonstrated that it was actually cardiovascular disease that accounted for
majority of mortality. Furthermore, it was not gaseous pollutants like oxides of nitrate, sulfur, carbon
mono-oxide or ozone but the particulate matter or PM, of fine or coarse size (PM
2.5
and PM
10
) which was
linearly associated with mortality; PM
2.5
with long term and PM
10
with short term. Several
cardiovascular diseases are associated with pollution; acute myocardial infarction, heart failure, cardiac
arrhythmias, atherosclerosis and cardiac arrest. The ideal way to address this problem is by adhering to
stringent environmental standards of pollutants but some individual steps like choosing to stay indoors
(on high pollution days), reducing outdoor air permeation to inside, purifying indoor air using air filters,
and also limiting outdoor physical activity near source of air pollution can help. Nutritional anti-oxidants
like statins or Mediterranean diet, and aspirin have not been associated with reduced risk but specific
nutritional agents like broccoli, cabbage, cauliflower or brussels sprouts, fish oil supplement may help.
Use of face-mask has been controversial but may be useful if particulate matter load is higher.
© 2017 Published by Elsevier B.V., a division of Reed Elsevier India, Pvt. Ltd on behalf of Cardiological
Society of India. This is an open access article under the CC BY-NC-ND license (http://creativecommons.
org/licenses/by-nc-nd/4.0/).
1. Great smog of London
Great smog of 1952 also known as Big Smoke was an episode of
severe air-pollution that affected London in December 1952. It was
really a collection of airborne particles, arising mostly from the use
of coal, culminating in a thick layer of smog over the city, lasting 5
days (from 5–9 December 1952) and then dispersing as quickly as it
came. As London was accustomed to heavy fogs, at the time it
happened, there was no panic; it just seemed a denser and a longer
standing fog, The only problem seemed to be such a low visibility
that driving became impossible, all public transport ceased,
ambulance service stopped functioning and all outdoor sporting
events were called off. The fog even seeped indoors, resulting in the
cancellation/abandonment of concerts and movies, since stage
could not be viewed from the seats. Since that time there are
several myths associated with air pollution (Table 1). However, the
health aspects became apparent only after few weeks when
medical statistics revealed that the smog had killed 4000 people.
1
As a matter of fact mortality remained elevated for months. The
cause was attributed mostly to pulmonary system; asthma,
respiratory tract infections: influenza, bronchopneumonia and
purulent bronchitis but all this remained speculative because of
faulty records. However, it was only more than 4 decades later that
Harvard Six Cities study, with a large prospective cohort, for the
first time convincingly demonstrated a definite relation between
long term environmental pollution exposure and adverse health
outcome. In over 8000 adults with 14–16 years of exposure,
mortality rate was 26% higher in city with most pollution versus
that with least pollution. Interestingly, this study made another
surprising observation, it was not respiratory but rather cardio-
vascular (CVS) deaths which accounted for single largest cause of
mortality, nearly half of all mortality (646 out of 1401).
Furthermore, the risk for lung cancer and overall cardio-pulmo-
nary mortality was increased by a similar ratio (but numerically
numbers were higher for CVS).
2
The largest study to date, ACS
Cancer Prevention II study enrolling nearly 500,000 individuals
over a 16 year period also revealed that each 10 mg/m
3
increase in
fine particulate matter (PM)contributed to increase in all cause,
cardiopulmonary and lung cancer mortality of 4%, 6% and 8%,
respectively.
3
Other hospital based studies also suggested specific
association between air pollution and acute cardiac events.
4,5
Peter
and co-workers provided the first evidence of association between
air pollution and acute myocardial infarction (AMI).
6
It was Hoch
and co-workers who found that it was exposure to traffic-related
pollutants which were more co-relative with mortality than back-
ground level of pollutants within the city. Living near a major road
was most strongly co-related tomortality in this study.
7
Among the
specific CVS causes, 10 mg/m
3
increase in fine particulate matter
contributed to 12% increased risk of CVS mortality, 18% increased
risk of coronary artery disease (CAD) and 13% risk of cardiac
arrhythmia, heart failure and cardiac arrest.
8
The short-term risks
with acute exposure may even be higher. The NMMAPS study
http://dx.doi.org/10.1016/j.ihj.2017.07.016
0019-4832/©2017 Published by Elsevier B.V., a division of Reed Elsevier India, Pvt. Ltd on behalf of CardiologicalSociety of India. This is an open access article under the CC BY-
NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
Indian Heart Journal 69 (2017) 425–429
Contents lists available at ScienceDirect
Indian Heart Journal
journal homepage: www.elsevier.com/locate/ihj

conducted in 50 million individuals spread over 20 largest cities of
US revealed that 10 mg/m
3
increase in coarser PM contributed to
21% increase in all-cause mortality and 31% increase in cardiopul-
monary mortality.
9
Air Pollution and Health: a European Approach
(APHEA-2) study conducted in another 43 million individuals in 29
European cities revealed an even more robust association between
short term exposure and health effects. For each 10 mg/m
3
increase
in coarse PM, daily mortality increased by 0.6% and CVS mortality
by 0.7%.
10
Furthermore, this study went on to show that this
increased mortality was not due to mere harvesting (temporal
displacement of mortality or advancement of mortality by a few
days) because after a lag period of 40 days this increase in CVS
mortality was even more pronounced - actually more than doubled
(1.97%).
11
Again even with short term exposure, direct association
has been found with CAD, arrhythmia and heart failure, an
increased rates of hospitalization: 0.8% increase for heart failure
and 0.7% increase for CAD. In addition increased risk for AMI,
implantable cardioverter defibrillator (ICD) discharges myocardial
ischemia on stress testing, elevated systolic blood pressure and
ischemic stroke have also been demonstrated.
12
In the developing
world Beijing, China issued a first “red alert”when air pollution
surpassed a level of 200 parts per million of fine particulates
(referred to as PM
2.5
) for at least three days on a four-tier index that
catalogs air pollutants. The Great Smog of Delhi marked the worst
period of bad air quality in New Delhi and adjoining areas in the
National Capital Territory of India (between 1 and 9 November
2016). The pollution was reputed to be even worse than the London
smog.
2. Mechanism of cardio-toxicity of air pollutants
Currently, combustion of fossil fuel, whether in industrial
applications and power plants or exhaust from motor vehicles
(airplanes, cars, trucks, or ships) account for the majority of
pollution at least in developed countries. The emissions include
gases; nitric oxide (NO), nitrogen dioxide (NO
2
), carbon monoxide
(CO) or sulfur dioxide (SO
2
), PM (both solid and liquid) like carbon
black, organic carbon, even transition metals and volatile and
semi-volatile organic compounds such as benzene, toluene,
xylene, and aromatic hydrocarbons. However, as far as health
hazards are concerned, while several gaseous pollutants, SO
2
,
nitrogen oxides, CO, Ozone (O
3
) have been implicated to some
extent, it is the PM which is the major culprit and has been co-
related to total and CVS mortality. Particulate matter is of two
types; fine PM –with particle median aerodynamic diameter
<2.5 mm called PM
2.5
and coarse PM –with particle median
aerodynamic diameter <10 mm called PM
10
. Short-term mortality
is co-relative of PM
10
while long term mortality is related to
exposure to PM
2.5
. Particulate matter can be directly toxic to
circulatory system (soluble components of PM
2.5
can cross
respiratory epithelium into systemic blood stream) but more
commonly affects the CVS indirectly. It may incite pulmonary and
systemic oxidative stress, resulting into inflammation. The
circulatory inflammation (even without significant lung toxicity)
may serve as the initiator of a whole cascade of events culminating
in alterations in blood rheology and pro-thrombotic effects
(increased fibrinogen, enhanced platelet aggregation), alteration
in cardiac autonomic system (blunting of cardiac parasympathetic
system) leading to rhythm disturbances, endothelial dysfunction
leading to vascular spasms and plaque disturbance in short-term
and atherosclerosis in long term. The PM
10
could readily penetrate
and deposit in the extra-thoracic and trachea-bronchial tree, while
PM
2.5
can reach the small airways and alveoli. Generally, PM
2.5
are
derived from combustion sources including vehicular exhaust and
constitute fine particles like nitrates and sulfates while PM
10
are
derived from natural sources (forest fires, bio-aerosol –endo-
toxins, fungal spores, pollen, windblown soil), and occupational
exposure (grinding, smelting, etc.). Recently a third type of
particles have also been described, the ultra-fine particles (UFP)
(<0.1mm). They can penetrate deeper into the lungs and even
directly enter the bloodstream. They arise from emissions of
factory chimneys (smoke stacks) or exhaust from trucks (tail
pipes), quickly coalesce together, absorb water, organic material
and other gases to grow large to reach a particle size in the range of
PM
2.5
. Sulfur dioxides is derived from sulfur containing fuels like
diesel, power plants, mining processes and kerosene space heaters
but also from forest fires. It can cause toxicity by forming
particulate sulfates. Diesel exhaust particles are known to increase
interleukin-8 and thus provoke inflammatory cascade. Increased
SO
2
levels increase fibrinogen levels. Nitrogen oxides are derived
primarily from combustion of fossil fuel including vehicular
exhaust and industrial processes. The major problem associated
with nitrates is that they can readily form particulate nitrates.
Ozone is the predominant component of photo-chemical smog. It
can be sourced to vehicular exhaust and industrial processes, acted
upon by UV radiation (nitrogen oxides and reactive hydro-
carbons). It can induce direct oxidation of both pulmonary and
systemic vasculature, resulting in inflammation. It is also known to
provoke arterial vasoconstriction. Carbon monoxide derived by
incomplete combustion of carbon based fuel; vehicular exhaust,
coal combustion, residential wood burning and tobacco smoking
acts as a direct toxicant. Both nitrogen oxides and CO are known to
impair ICD discharges.
12
3. Types of studies
There are three types of studies on air pollution
1. Time series or case-crossover studies which are hospital based
and evaluate end-points such as daily total mortality, CVS
mortality or hospital admissions.
2. Panel studies with repeated measures of clinical endpoints such
myocardial revascularization or arrhythmias documented by
ECGs, Holter monitors and ICD or even potential markers of
arrhythmic risk including changes in myocardial repolarization
and altered heart rate variability (HRV).
3. Prospective follow-up studies of cohort of subjects.
The largest body of evidence comes from hospital based studies
which provide a statistical link between air pollution and end-
points on a short term basis. On the other hand prospective follow-
up studies are useful to determine temporal link of associations
and determine long term risks. Panel studies are useful to identify
link with individual components like arrhythmias.
Table 1
Myths associated with air pollution.
Myth Reality
Fog/smog is innocuous Smog has a definite adverse health effects
Health effects of air pollution are related to respiratory system Majority of deaths related to pollutants are due to cardiovascular causes
Gaseous pollutants are major causes of health effects Particulate matter in the air are most strongly related to health effects
The health effects are instantaneous Health effects are both instantaneous and some occur after a lag period
426 Editorial / Indian Heart Journal 69 (2017) 425–429

4. Definition of pollution
In general, contamination of air by smoke and harmful gases
such as oxides of carbon, sulfur and nitrogen may be considered as
air pollution. Objectively, the standards for ambient air quality for
PM have been given buy US EPA. In general daily levels of up to
150 mg/m
3
of PM
10
and 65 mg/m
3
of PM
2.5
is acceptable. On annual
basis, 30 mg/m
3
of PM
10
and 15 mg/m
3
of PM
2.5
is considered
acceptable (Table 2). Anything above this value may be considered
as air pollution and it is recommended that the daily levels should
not exceed these values >35 times/year.
5. Effect on cardiovascular system
5.1. Acute myocardial infarction
The mechanism of AMI occurrence with air pollution has been
well elucidated. Both short term exposure to PM
10
and PM
2.5
can
induce systemic oxidation, inflammation, elevation of serum
fibrinogen contributing to increased platelet reactivity as well
endothelial dysfunction and plaque instability. In a large study
based on Medicare records PM
10
was associated with triggering of
AMI.
13
Likewise, Peter and co-workers revealed the association of
PM
2.5
with transient risk of AMI at two temporal periods (2 h and 1
day) after exposure.
6
Recently Argacha and co-workers analyzing
Belgian STEMI registry demonstrated that PM
2.5
and NO
2
exposure
incrementally increased the risk of ST elevated AMI (STEMI).
Interestingly, the risk related to PM appeared greater in the elderly,
while younger patients appeared to be more susceptible to NO
2
exposure.
14
In a even more recent study, Zuin and co-workers
found a direct correlation between the number patients treated
with primary percutaneous coronary interventions for STEMI and
the NO
2
,PM
10
and O
3
air concentration levels of the same day.
15
In
another recent inter-city study from China, air pollutants like PM
10
,
SO
2
,NO
2
, CO were associated with a 0.8%, 2.0%, 2.2%, and 1.1%
increase in AMI admissions, respectively on 2nd day after exposure
while O
3
showed a positive association on day 4, 1.3%.
16
6. Heart failure
The link of air pollution and heart failure is less certain. The
mechanistic basis of acute de-compensation in patients with heart
failure involve demand supply mismatch; increasing demand by
increased heart rate, blood pressure, and filling pressures and
reduced supply due to reduced contractility as also increased
myocardial injury. Exposure to PM
2.5
has been associated with
increased systemic blood pressure (BP) and vasoconstriction and
pulmonary vasoconstriction leading to increased pulmonary and
right ventricular diastolic filling pressures. Onset of arrhythmias or
STEMI can also precipitate acute de-compensation. On long term
basis exposure to PM may contribute to adverse ventricular re-
modeling and a worsening of myocardial fibrosis. Cumulatively,
these factors could have synergistic detrimental effects on cardiac
function.
17
In a meta-analysis of pollution and heart failure studies,
Shah and co-workers revealed that heart failure hospitalization or
death were associated with elevations in CO (3.52%/1 ppm), SO
2
(2.36%/10 parts per billion), and NO
2
(1.70% per 10 parts per billion;
1.25–2.16), but not O
3
(0.46%/10 parts per billion) concentrations.
Increases in these pollutants were also associated with heart
failure hospitalization or death (PM
2.5
–2.12%/10mg/m
3
;PM
10
–
1.63%/10 mg/m
3
), stronger association seen on the day of exposure,
with more persistent effects for PM
2.5
.
17
7. Arrhythmias
Environmental pollution can affect cardiac electrophysiology in
many ways. Many of these mechanisms have been elucidated based
on ICD studies. In a first of such studies, 100 patients from a US city
had 223 ICD discharges for ventricular arrhythmias during the
exposure.In this study associations were found with NO
2
(increased
defibrillator therapy) and for CO, black carbon, fine particles, NO
(increased frequency of discharge).
18
In another cohort of patients
followed for >3 years, linear association was found between PM
2.5
,
O
3
and cardiac arrhythmias.
19
However, the data regarding the co-
relation of environmentalpollution and risk of arrhythmiashas been
inconsistent. A US study and a study conducted in a German and
Swedish town showed some correlation between pollutants and
arrhythmia; In Swedish and German study2-h morning PM
10
values
were found associated with ventricular arrhythmias.
20,21
In some
other studies such as one conducted in Vancouver, a relatively clean
metro area and a large study conducted in city of Atlanta, US there
was little evidence for any air pollutant triggering arrhythmias
(except coarse particles –PM
10–2.5
in Atlanta study).
22,23
Another
study conducted in Sao Paulo evaluated the occurrence of
arrhythmias requiring presentation to emergency department co-
relating with environmental pollution. They found that several
arrhythmias; sinus tachycardia, atrial fibrillation (AF) and flutter,
supraventricular tachycardias, ventricular tachycardia and fibrilla-
tionwere positivelyassociated with increasesin CO, NO
2
and PM
10
.
24
Evaluatingthe lag intervalsbetween the airpollution and the onsetof
arrhythmias they foundthat the effects were acuteand limited to the
day of exposure. Furthermore, while other pollutants have a
threshold effect, PM
10
had a linear association. Several mechanisms
havebeen proposed for theseeffects; alteration in cardiacautonomic
system activity (cardiac sympathetic: parasympathetic mismatch),
repolarization abnormalities and worsening myocardial ischemic
sensitivity. Inthe Boston ICD study therewas a significantassociation
between atrial fibrillation but also probable association with fine
particles, NO
2
, and carbon black.
19
Another study revealed an
increased risk of supraventricular arrhythmias for 5-day mean of
PM
2.5
, sulfate and O
3
.
25
In a German Holter study, elevated PM and
NO
2
concentration increased the risk for supraventricular runs and
ventricular runs which correlated with last 1–3 days of air
pollution.
26
Several studies have evaluated correlation between daily
variations in environmental pollution and HRV –a marker of
parasympathetic input to the heart. Most studies (except in young)
reveal association of PM levels with reduction in HRV and thus may
explain predisposition to tachy-arrhythmias, sometimes even
fatal.
12,27,28
Besides PM, sulfates, nitrates and even O
3
may also
reduce HRV.
29
8. Predisposition of risk to air pollution
There is evidence that not all are affected equally by
environmental pollution. The most important predisposition is
with pre-existing cardiovascular disease, but also Stransferase M1
deletion (which reduces defense to oxidative stress due to
glutathione), diabetes and impaired glucose tolerance, smokers,
age and those with COPD.
30
9. Cardiac arrest
In a study conducted on >5000 individuals in Rome, both PM
and CO on the day of exposure predicted sudden cardiac arrest
Table 2
Current US EPA National Ambient Air Quality Standards for PM.
Time period PM
10
,
m
g/m
3
PM
2.5
,
m
g/m
3
Daily 150 65
Annual 50 15
Editorial / Indian Heart Journal 69 (2017) 425–429 427

(SCD).
31
Elderly (>65 years of age), hypertensives and those with
chronic pulmonary disease were predisposed to SCD. In a study
performed in Indianapolis, increased PM
2.5
was predictive of
witnessed cardiac arrests although no similar association was
found in another study performed in US.
32,33
10. Congenital heart disease
Congenital heart disease has long back been found associated
with medications, radiation, infections. An American study found a
dose response relationship of CO with ventricular septal defects.
Also O
3
levels were found co-relative of valvular, aortic, and truncal
defects although no co-relation could be found with PM or other
pollutants.
34
11. Atherosclerosis
While several mechanisms have been proposed linking
environmental pollution with atherosclerosis and indeed some
early studies suggesting a link of pollution with atherosclerosis a
recent meta-analysis evaluating four cross-sectional European
studies found no significant co-relation between carotid intima
medial thickness (a marker of atherosclerosis), at least with eight
commonly known markers of residential pollution like PM
2.5
,
traffic load within 100 m of home, and traffic intensity at the
nearest road.
35–38
12. Can the effects of pollution be reversed?
12.1. Community efforts
The individual health risk of environmental pollution may be
small, at best it mayqualify as a minor risk factorfor CAD but the risk
to thewhole community may be enormousas also likely benefitifthe
pollution is reduced. World Health Organization has postulated that
nearly 8 million disabilities and 800,000 deaths occurper year only
related to PM exposure.
39
In the city of London 1 in 50 AMI may be
sparked off as a consequence of environmental pollution.
The only way to control this situation is to formulate stringent
air control policy (particularly for PM) and ensure strict compli-
ance.
40
Indeed US EPA, UK air quality strategy and the EU Ambient
Air Quality Directive has been formulated. Unfortunately even in
the most developed countries these criteria may not be met for, e.g.
in sate of California air-quality monitoring systems are presently
not meeting this standard in 60% of cases.
41
On the other hand
there is evidence that if these norms are adhered to there would be
a reduction in >40 thousand hospital admissions and >20,000
deaths in US alone.
42
12.2. Individual efforts
While regulatory measures to reduce emissions at their sources
are effective and desirable there is some evidence that an
individual action can also help to reduce exposure and personal
risk. Awareness of air pollution levels is the key to initiating
individual action. It can be achieved by putting in place public air
quality alert systems which give appropriate alarms. Individual
risk arising from air pollution can be curtailed by choosing to stay
indoors, reducing outdoor air permeation to inside, purifying
indoor air using air filters, and also limiting physical activity,
especially outdoor activity near source of air pollution at least on
the days of higher pollution.
43
The risk of air pollution is highest in
patients with pre-existing chronic cardiovascular or pulmonary
disease, elderly and the children. On the other hand efforts to avoid
exposure should be carefully balanced against negative conse-
quences of reduced physical activity. There is limited evidence that
the ill-effects of environmental pollution can be mitigated by some
therapeutic agents like antioxidant or antithrombotic agents.
Statins and aspirin while useful in primary prevention of CAD
require validation of their role in air pollution. Diet based
interventions have been slightly more favorable. Mediterranean
diet was postulated to have beneficial effects in ameliorating
adverse effects of pollution, however, multiple randomized
controlled trials (RCTs) of vitamin supplements and antioxidants
(in Mediterranean and other beneficial diets) have not demon-
strated any benefit; rather in some RCTs they have proven
harmful.
44
Specific food based antioxidants such as sulforaphanes
which are organic compounds found in cruciferous vegetables
such as broccoli, cabbage, cauliflower, brussel sprouts, kale etc.,
may have some potential.
45
Foods rich in nitrates such as beet-root
may exhibit a beneficial effect on blood pressure but there is no
data to suggest that this may impact upon ill-effects of
environmental pollution.
46
Fish oil supplementation by its
multitude of effects; on blood lipids as also HRV might be useful.
47
12.3. Use of respirators
Limited evidence suggests that the use of respirators may be
effective in some circumstances.
43
Wearing inexpensive respira-
tors (facemasks) to reduce exposure to air pollutants can be one of
the options in highly polluted areas. Its efficacy depends on the
type of pollutant, type of filter/adsorbent material, respirator type
and conditions of use. While useful to curtail PM, its efficacy with
gaseous pollutants remains controversial (dependant on absorbent
used and pollutant gas). An effective respirator is expected to
reduce the concentration of the pollutant within the face-piece to
10% outside. Some evidence suggests that the use of negative
pressure generating air-purifiers may reduce cardiovascular risks
from exposure to urban PM.
48,49
On the other hand, physiological
effects may confound CVS effects (elevated heart rate and
variations in BP) that might be attributed to reductions in exposure
to PM. Thus benefit with this type of respirator depends on the
degree and type of pollution, efficacy of device and its possible
physiological effects.
50
Finally, some other adverse effects are also
reported with the use of these devices; higher face temperature at
rest and exercise, feeling of anxiety and claustrophobia, incom-
plete fit with dense facial hair as well as social issues with
communication (with a mask wearing individual)
43
(Table 3).
13. Conclusions
Air pollution has adverse effects on health, particularly CVS. It
can precipitate AMI, heart failure, arrhythmia and even cardiac
arrest. Air pollution with particulate matter (both fine and coarse)
has been correlated to both CVS and total mortality. While
intervention at societal level is most effective some personal steps
can be taken to reduce its risk.
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Table 3
Tips to reduce health risk in individuals exposed to air pollution.
During high pollution days stay indoors, avoid physical exertion in an outdoor
activity located near the source of pollution
Reduce outdoor air permeation to inside
Purifying indoor air using air filters
Some foods rich in sulphorane based antioxidants like broccoli, cabbage,
cauliflower, brussels sprouts
Fish oil supplementation
Use of respirators –face mask
428 Editorial / Indian Heart Journal 69 (2017) 425–429

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Sundeep Mishra
Cardiology, AIIMS, New Delhi, IndiaE-mail address:
drsundeepmishraihj@gmail.com (S. Mishra).
Editorial / Indian Heart Journal 69 (2017) 425–429 429