6. Biteker M. A new classication of Kounis syndrome.

Int J
Cardiol. 2010 Dec 3;145:553.
Muhammed Karadeniz
Ahmet Akyel*
_
Ibrahim Etem C elik
Tayyar Cankurt
Veysel O

zgu r Bars
Sani Namk Murat
Ankara Education and Research Hospital,
Department of Cardiology,
Ankara, Turkey
*Corresponding author. Tel.: 90 5424817759.
E-mail address: akyelahmet@gmail.com (A. Akyel)
Relationship of high-sensitive C-reactive protein with
cardiovascular risk factors, clinical presentation and
angiographic prole in patients with acute coronary
syndrome: An Indian perspective
Dear Editor
We would like to report our research ndings about hs CRP
and its correlation with conventional risk factors and angio-
graphic severity of CAD among patients of acute coronary
syndromes.
1. Introduction
Worldwide, atherosclerotic cardiovascular disease (CVD)
including coronary artery disease (CAD) is estimated to be the
leading cause of death and loss of disability-adjusted life
years. Unfortunately, while the incidence and prevalence of
CVD is now declining in the developed countries, it continues
to increase exponentially in the developing nations. Reddy
reported that from 1970 to 2015, mortality from CVD was
projected to almost double in the developing countries while it
was projected to decline during the same period in the
developed nations.
1
The Global Burden of Diseases (GBD)
study reported the estimated mortality from CAD in India to
be roughly 1.6 million in the year 2000.
2
Several modiable and non-modiable risk factors have
been identied to cause CVD. The major modiable risk fac-
tors include hypertension (HTN), diabetes (DM), smoking and
hyperlipidemia and whereas non-modiable risk factors
include age, gender and family history of premature CAD.
However, not all coronary events can be predicted by these
risk factors. In particular, nearly half of all myocardial
infarctions or stroke occurs among individuals without
hyperlipidemia. Consequently, alternate risk assessment
approaches are being explored to facilitate early and accurate
identication of individuals at risk of having CVD. Since
atherosclerosis is an inammatory process, several markers
of inammation have been evaluated for this purpose. Among
them, high-sensitive C-reactive protein (hs-CRP) has emerged
as the most important CV risk marker. More than a simple
marker of inammation, hs-CRP may inuence vascular vul-
nerability directly through several mechanisms including,
enhanced expression of adhesive molecules, reduced nitric
oxide, increased expression of endothelial PAI-1 and altered
LDL uptake by macrophages. A scientic statement issued by
Centre for Disease Control (CDC) and American Heart Asso-
ciation (AHA) has mentioned hs-CRP as the only inammatory
marker that can be used for risk prediction both for primary
and secondary prevention of cardiovascular events.
3
How-
ever, very limited information is available about the rela-
tionship between various CV risk factors and hs-CRP levels
and the signicance of elevated hs-CRP in Indian patients,
who as compared to the western populations have vast dif-
ferences in CVD epidemiology. Therefore, this study was
sought to assess the relationship between the levels of hs-CRP
and clinical prole, CV risk factors and the coronary angio-
graphic ndings in Indian patients presenting with acute
coronary syndrome (ACS).
2. Material and methods
This cross-sectional study was conducted at a tertiary care
center in North India. All consecutive patients who presented
with ACS over a period of two years and who consented to be
included in the study were enrolled. The study eligibility of
every participant was determined by the principal author, a
Consultant inCardiology, who was also responsible for the nal
adjudication of the diagnosis of ACS. The study protocol was
approved by the Intuitional Research and Ethical Committee.
2.1. Inclusion criteria
As mentioned above, all consecutive patients with ACS
including unstable angina (UA), non-ST elevation myocardial
infarction (NSTEMI) and ST elevation myocardial infarction
(STEMI) were enrolled in to the study. UA was diagnosed if the
patient had at least one of the following- angina chest dis-
comfort at rest lasting for 20 min, recent onset (less than one
month) angina of sufcient severity or exertional angina with
a crescendo pattern, along with either ST segment
i nd i a n he a r t j o ur na l 6 5 ( 2 0 1 3 ) 3 5 7 e3 6 7 359
depression 0.5 mm or T inversion 0.3 mV in any two
contiguous leads. If the patient also had elevated Troponin T
as a marker of myocyte necrosis, he was labeled to have suf-
fered NSTEMI. However, for the diagnosis of STEMI, the
patients needed to have symptoms consistent with acute
myocardial infarction (AMI) [chest discomfort with or without
radiation to arm(s)/jaw/back/epigastrium, weakness, diapho-
resis, nausea, light headedness] of greater than 30 min dura-
tion, with ECG changes of STEMI i.e. ST elevation of at least
0.1 mV in 2 contiguous precordial leads or 2 limb leads or new/
presumably new left bundle branch block.
2.2. Exclusion criteria
All patients with recent or ongoing infection or fever, chronic
inammatory disorders e.g. rheumatoid arthritis, systemic
lupus erythematosus etc or any other condition which could
have affected hs-CRP levels were excluded from the study.
2.3. Clinical evaluation and investigations
Once enrolled into the study, all patients underwent detailed
clinical assessment, biochemical investigations and coronary
angiography. Clinical evaluation included detailed history
regarding the presenting symptoms, presence or absence of
various conventional CV risk factors, socioeconomic status
(SES) of the patients, followed by general physical and car-
diovascular system examination including height, weight, cal-
culation of body-mass index (BMI), waist-to-hip ratio (WHR)
measurement and blood pressure (BP) measurement. BMI was
calculated as weight (in kg)/height
2
(in meters). The patients
with BMI > 30 kg/m
2
were considered obese. Waist and hip
circumferences were measuredinthestandingposition, usinga
non-stretchable standard tape measure. The waist circum-
ference was measured at the narrowest point between the
costal marginand iliac crest and hip circumferences at the level
of thewidest diameter aroundthe buttocks. Central obesitywas
dened as the WHR > 0.9 for males and >0.8 for females.
All patients also underwent a complete dental examina-
tion by a trained dentist to look for denitive evidence of
periodontitis. The examination consisted of determination of
suppuration index, plaque index (PI), gingival index (GI),
pocket depth (PKT), bleeding index (BI), attachment loss
measurements (AL), and tooth mobility. Missing and decid-
uous teeth were also recorded.
4,5
The biochemical investigations included routine blood
investigation such as hemoglobin level, white blood cell count,
blood urea, serum creatinine, serum electrolytes levels, fasting
blood glucose (FBG) estimation, fasting lipid prole and hs-CRP
measurement. Fasting lipid prole was performed using com-
mercial kits from Boehringer Mannheim. Low-density lip-
oprotein (LDL) cholesterol was calculated by using the
Friedewald equation: LDL cholesterol total cholesterol e
[(Triglycerides/5) high-density lipoprotein (HDL) cholesterol].
The hs-CRP estimation was done at the time of pre-
sentation and the analysis was done by turbidimetry immu-
noassay using QUANTA Reagent kit (latex) manufactured by
Tulip corporation, USA. Values of 1 mg/l, 1e3 mg/l
and >3 mg/l were labeled as low risk, intermediate risk and
high risk, respectively.
The selective coronary angiography was performed in all
patients who consented for the same (71.8%of all). The timing
of coronary angiography was determined in accordance with
the accepted treatment protocols for the patients with ACS.
Images in multiple views were obtained by standard techni-
que to access both the extent and severity of disease. Sig-
nicant CAD was dened as at least 70% reduction in the
diameter of major epicardial coronary arteries i.e. left anterior
descending (LAD), left circumex (LCx) or right coronary
artery (RCA) and their branches; or 50% luminal narrowing of
the left main coronary artery (LMCA). Patients were classied
as having single-vessel disease (SVD), double-vessel disease
(DVD) or triple vessel disease (TVD) accordingly. Presence of
signicant CAD in LMCA was classied as DVD.
2.3.1. Criteria for CV risk factors, metabolic syndrome (MS)
and SES
For the purpose of the present study, DM was dened as
deranged FBG level 126 mg/dl or a patient who was
already on treatment for diabetes. HTN was dened as 2 or
more BP readings of >140 mmHg systolic BP or >90 mmHg
diastolic BP, or a patient who was already on anti-
hypertensive medication. Smoking was dened as the reg-
ular smoking of tobacco in any form currently or within the
last 1 year. A positive family history of premature CAD was
dened as the presence of documented CAD in a rst-degree
relative before 55 years of age in males and before 65 years
of age in females. Dyslipidemia was dened by presence of
any one of the following: LDL cholesterol > 130 mg/dl,
TG 150 mg/dl or HDL cholesterol <40 mg/dl in men and
<50 mg/dl in women.
The MS was dened using the National Cholesterol Edu-
cation Program- Adult Treatment Panel III criteria as presence
of 3 of the following vascular risk factors e waist circum-
ference > 102 cm in men or > 88 cm in women, fasting
triglycerides 150 mg/dl, HDL-cholesterol < 40 mg/dl in men
or <50 mg/dl in women, BP 130/85 mmHg or use of blood
pressure medication, and FBG 110 mg/dl.
6
For determination of SES of the patients, modied
Kuppuswamys scale
7
was used which included education
(maximum 7 points), profession (maximum 10 points) and
income (maximum 12 points). The patients were categorized
in to lower, middle and upper SES if the total points were 10,
11e25 or >25, respectively.
2.4. Statistical analysis
The data was analyzed using Statistical Package for Social
Sciences (SPSS) Version 15.0. Values were expressed as mean
(standard deviation) or as percentages. Comparisons
between the groups were done using students unpaired t test
or chi-square test wherever appropriate. A p < 0.05 was con-
sidered statistically signicant.
3. Results
We studied 337 subjects including 287 (85.2%) males and 50
(14.8%) females. The mean age of the subjects was
58.32 11.24.
i nd i a n he a r t j o ur na l 6 5 ( 2 0 1 3 ) 3 5 7 e3 6 7 360
Overall, 69 (20.5%), 68 (20.2%) and 200 (59.3%) patients had
hs-CRP levels <1 mg/l, 1e3 mg/l and >3 mg/l,
respectively. Table 1 shows relationship of hs-CRP levels with
the gender and Table 2 shows the relationship between hs-
CRP levels and the SES. The female patients had higher lev-
els of hs-CRP with 76% having values >3 mg/l as compared to
only 56.5% male patients (p 0.02). A total of 104 patients
(30.9%) belonged to lower SES, 207 (61.4%) to middle SES and 26
(7.7%) to upper SES. The prevalence of high hs-CRP (>3 mg/l)
was signicantly higher in the lower SES (78.8%) as compared
to the upper SES (46.2%, p < 0.05).
Table 3 shows values of hs-CRP according to the different
CV risk factors. The smokers were found to have signicantly
higher proportion of patients with higher CRP (55.3% with
>3 mg/l as compared to 18.8% with <1 mg/l, p 0.03 for
comparison with non-smokers). Similarly, the patients with
MS, central obesity and periodontitis were also found to have
greater prevalence of elevated hs-CRP levels. In contrast, no
statistically signicant association was seen between hs-CRP
levels and HTN, DM and dyslipidemia.
Overall, 52 patients had presented with premature CAD
(age of onset <45 years). Among them, the majority (80.8%)
had high hs-CRP levels with only few (3.8%) having hs-CRP
levels within the normal limits (<1 mg/l, p 0.001).
Figs. 1 and 2 depict relationship between hs-CRP levels and
the type of ACS and the angiographic extent of CAD, respec-
tively. Nearly two-thirds of the patients with STEMI had hs-
CRP levels above 3 mg/l as compared to only half with UA/
NSTEMI (p value < 0.001). Similarly, majority of the patients
with SVD had hs-CRP levels <1 mg/l whereas most of the
patients with TVD had elevated (>3 mg/l) hs-CRP levels (p
< 0.001).
4. Discussion
Epidemiological studies have revealed that the prevalence of
CVD in India is increasing along with the prevalence of con-
ventional risk factors for CVD. Present health transition from
predominance of infections to the preponderance of car-
diovascular disorders, such as HTN, DM and CVD is now
responsible for 53% of all deaths in India. Indians have one of
the highest rates of heart disease in the world and the disease
also tends to be more aggressive and manifests at a younger
age. Consequently, prevention of CVD has become one of the
most important public health challenges of our times. Several
modiable and non-modiable factors such as HT, DM,
smoking etc are recognized as major risk factors for CVD and
aggressive correction of these play vital role in CVD pre-
vention. However, not all adverse CV events can be predicted
or explained by these conventional risk factors, which limits
our ability to accurately identify the individuals who are at
high risk of developing CVD. Therefore, a host of alternate
risk assessment approaches such as imaging of subclinical
atherosclerosis, detection of vascular inammation etc are
being evaluated to overcome this limitation and to provide
more accurate risk estimates in any given individual.
Numerous studies have provided the evidence that
inammation plays a central role in the occurrence of
CVD.
8e10
Accordingly, several mediators of the inammatory
response, including acute-phase proteins, cytokines and cel-
lular adhesion molecules have been evaluated as potential
indicators of the risk of a rst acute atherothrombotic event,
as well as of recurrent complications after initial pre-
sentation.
11
As the prototypical acute-phase reactant, hs-CRP
has been the focus of much of the clinical investigation.
12
Various epidemiological studies have demonstrated that hs-
CRP is a strong predictor of future cardiovascular even-
ts.
13e15
The relationship between baseline hs-CRP and future
Table 1 e Levels of hs-CRP in relation to gender prole of
the patients.
Gender hs-CRP categories p
<1 mg/l
n 69
>1e3 mg/l
n 68
>3 mg/l
n 200
Females n 50 4 (8) 8 (16) 38 (76) 0.02
Males n 287 65 (22.6) 60 (20.9) 162 (56.5)
Values in parentheses represent proportion of the population
belonging to the particular gender.
Table 2 e Levels of hs-CRP in relation to the
socioeconomic status of the patients.
Risk
factor
Hs-CRP categories c
2
p
<1 mg/l
n 69
>1e3 mg/l
n 68
>3 mg/l
n 200
Lower SE
Class,
n 104
6 (5.8) 16 (15.4) 82 (78.8) 27.237 <0.001
Middle SE
Class,
n 207
57 (27.5) 44 (21.3) 106 (51.2) 19.368 <0.001
Upper SE
Class,
n 26
6 (23.1) 8 (30.8) 12 (46.2) 2.486 0.289
Values in parentheses represent proportion of the population in the
particular socioeconomic class.
Table 3 e Levels of hs-CRP in relation to various
cardiovascular risk factors.
Risk factor hs-CRP categories p
<1 mg/l
n 69
>1e3 mg/l
n 68
>3 mg/l
n 200
Smoker, n 170 32 (18.8) 44 (25.9) 94 (55.3) 0.031
Metabolic syndrome,
n 62
4 (6.5) 10 (16.1) 48 (77.4) 0.002
Central obesity, n 114 24 (21.1) 14 (12.3) 76 (66.7) 0.032
Periodontitis, n 102 10 (9.8) 16 (15.7) 76 (74.5) <0.001
Hypertension, n 136 30 (22.1) 22 (16.2) 84 (61.8) 0.315
Diabetes, n 102 26 (25.5) 14 (13.7) 62 (60.8) 0.088
Dyslipidemia, n 195 33 (16.9) 36 (18.5) 126 (64.6) 0.058
Premature CAD, n 52 2 (3.8) 8 (15.4) 42 (80.8) 0.001
Values in parentheses represent proportion of the population with
the particular risk factor.
i nd i a n he a r t j o ur na l 6 5 ( 2 0 1 3 ) 3 5 7 e3 6 7 361
CV events in most cases has been proven independent of the
major traditional risk factors evaluated in daily clinical prac-
tice. In terms of clinical application, hs-CRP seems to be a
stronger predictor of CV events than LDL cholesterol, and it
adds prognostic information at all levels of calculated Fra-
mingham risk and at all levels of MS. Using widely available
high sensitivity assays, hs-CRP levels of 1, 1 to 3, >3 mg/l
correspond to low, moderate and high risk groups for future
CV events. An added advantage of hs-CRP is that its levels
have been shown to be stable with little or no diurnal varia-
tion,
16
making hs-CRP the most commonly used and best
standardized inammatory marker of CV and metabolic dis-
orders.
17
Unfortunately, very limited information is available
about hs-CRP levels and their relationship with CV risk factors
or incident CVD in Indian studies. Our study therefore pro-
vides important insights in to this aspect which is eminently
pertinent to day-to-day clinical practice.
In our study, women were found to have higher hs-CRP
levels as compared to men. This is consistent with the pre-
vious population studies that have shown that the levels of
hs-CRP are usually higher in women in healthy populations.
18
Whether this information implies the need to have gender-
specic cut-off values of hs-CRP for prediction of CV risk
needs to be evaluated in large-scale outcome studies.
19
For many decades and across multiple nations, differences
in SES have been consistently associated with variations in
CVD and mortality rates. Low SES is associated with an
increased risk of CAD with greater morbidity and mortality.
20
However, the mechanisms by which low SES leads to adverse
cardiovascular outcomes are not very well known. Previous
studies have shown that the patients belonging to low SES
tend to have higher CRP levels, suggesting a link between
inammation and increased risk of CVD in these individuals.
Lubbock et al
21
in their study showed that after adjustment for
traditional cardiovascular risk factors and potential con-
founding variables, lower income and education remained
associated with higher CRP levels. Similarly, Sethi et al
22
also
found that signicantly higher number of patients with high
hs-CRP (>3 mg/l) were from low SES. In our study, we too
found that the patients from low SES had signicantly higher
prevalence of elevated hs-CRP levels as compared to those
from upper SES.
In our study, higher hs-CRP levels were also found to be
associated with smoking, MS and central obesity. These
ndings were consistent with several previous studies show-
ing similar results.
23e29
It has been shown that the hs-CRP
levels are not only elevated in patients with MS but may also
predict the development of MS.
30
During the last two decades, there has been an increasing
interest in the impact of oral health on atherosclerosis and
subsequent CVD. The advent of the inammation paradigmin
coronary pathogenesis stimulated research in chronic infec-
tions caused by a variety of micro-organisms e such as
Chlamydia pneumoniae, Helicobacter pylori, and cytomega-
lovirus e as well as dental pathogens. Several epidemiological
studies investigating the relation between infections e
including dental infections e and various clinical manifes-
tations of atherosclerotic vascular disease have been pub-
lished suggesting periodontal disease as a risk factor for CVD.
Results of our study documented higher hs-CRP levels of
>3 mg/l being signicantly associated with periodontitis. It
was seen that amongst patients with high hs-CRP (>3 mg/l),
the incidence of periodontitis was 38% whereas in low hs-CRP
(<1 mg/l) it was only 14.5%, which were in accordance with
data shown by Slade et al,
31
Glurich et al
32
and Noack et al.
33
Similarly Joshipura et al
34
have published cross-sectional
data from the prospective male health professionals follow-
up study, where self-reported periodontal disease was ana-
lyzed in a sample of 468 men with respect to a variety of
biomarkers of CAD. Their results showed, in part, that perio-
dontal disease was associated with higher levels of CRP,
thereby supporting the hypothesis that periodontal disease
might also be causally linked with CAD.
However, in our study we did not nd signicant associa-
tion between elevated hs-CRP levels and HTN, DM or dyslipi-
demia. These ndings were quite unexpected and contrary to
the previous literature on this subject.
35e41
It is possible that
the concomitant lifestyle modication and antidiabetic and
lipid-lowering agents in some of these patients might have
confounded this relationship.
42e47
In addition, genetic factors
0
10
20
30
40
50
60
70
<1mg% 1-3mg% >3mg%
19.9
17.2
62.9
22.9
28.9
48.2
STEMI UA/NSTEMI
Fig. 1 e Levels of hs-CRP in relation to the type of ACS
(p <0.001 for comparison between STEMI and
UA/NSTEMI).
0
10
20
30
40
50
60
70
80
<1mg% 1-3mg% >3mg%
78.1
40.9
20.9
15.6
50
37.3
6.3
9.1
41.8
SVD DVD TVD
Fig. 2 e Levels of hs-CRP in relation to the angiographic
extent of CAD (p <0.001 for comparison).
i nd i a n he a r t j o ur na l 6 5 ( 2 0 1 3 ) 3 5 7 e3 6 7 362
may also have contributed to the lack of association between
hs-CRP levels and HTN, DM and dyslipidemia. CRP levels are a
complex phenotype with both genetic and environmental
determinants. Recent work has highlighted the impact of
genetic variants on CRP levels.
48
Baseline levels of CRP show a
clear heritability of approximately 40% in studies of families
49
whereas Brull et al
50
have shown a genetic determinant in
both baseline levels and response to stimulation, which may
involve separate mechanisms. Moreover, genetic variants on
the CRP locus and other loci may inuence the effect of dietary
and lifestyle factors on hs-CRP levels and may contribute to
inter- individual variability of plasma hs-CRP concentrations.
In addition, these genetic variants have been shown to affect
even the CRP response to pharmacological agents such as
fenobrate.
51
Unfortunately, due to logistic reasons, we could
not evaluate the impact of these measures on the relationship
between hs-CRP and HTN, DM and dyslipidemia.
In present study, elevated hs-CRP levels were signicantly
more commoninpatients withpremature CADas comparedto
the older patients. Similar results were observed in a study
where hs-CRP levels were increasedsignicantly (p <0.0001) in
patients of premature CAD as compared to controls and hs-
CRP levels were in high risk range in all the young patients.
52
The patients withSTEMI are knownto have higher peak hs-
CRP levels as compared to those with UA/NSTEMI.
53
Moreover,
a study by Brunetti et al
54
reported that plasma CRP concen-
trations showed a different release curve with Q-wave AMI in
comparison with non Q-wave AMI and patients with UA. The
higher increase in CRP levels during Q-wave MI than in non Q-
wave MI seems to be linked to the extension of myocardial
damage, rather than to the pre-existing inammation. Similar
results were obtained in the present study also.
In our study, we found signicant correlation between the
extent of CAD and hs-CRP levels, similar to several previous
studies.
54,55
Nyandak et al
55
observed a signicant correlation
betweenthe hs-CRP levels and the extent of CADas well as the
angiographic stenosis score. A study from Zairis and col-
leagues also reported that hs-CRP concentration correlated
with the stenosis complexity in patients with acute coronary
syndrome.
56
These ndings suggest that higher hs-CRP level
also reect increased disease burden apart from being just an
indicator of the presence of ACS. It further corroborates the
belief that inammation is not only an important trigger
mechanism of ACS related to plaque rupture, but also a pro-
moter of chronic atherosclerosis.
5. Limitations
Our study had several limitations that merit attention. As
discussed above, due to logistic reasons, we could not assess
the impact of ongoing pharmacological and non-
pharmacological measures on hs-CRP levels. However, high
prevalence of elevated hs-CRP levels along with a signicant
association with the angiographic extent of CAD found in our
study suggests that the ongoing therapies, if at all, did not
materially affect the overall pattern of hs-CRP levels in these
patients. Another important limitation of our study was that
we measured hs-CRP levels in patients with ACS whereas the
prognostic value of hs-CRP for CV risk prediction has been
established largely in patients with stable CAD or those with
CAD. Nevertheless, the ndings of the present study have
helped demonstrate important associations between hs-CRP
levels and the different aspects of CAD (CV risk factors, type
of ACS, angiographic extent of CAD, etc) in Indian patients
which had been lacking thus far.
6. Conclusions
The present study, for the rst-time, demonstrated that in
Indian patients presenting with ACS, the hs-CRP levels cor-
relate with several CV risk factors such as smoking, MS, obe-
sity etc, lower SES, clinical evidence of periodontitis, the type
of ACS and the angiographic severity of CAD. We also found
that the hs-CRP levels were higher in women as compared to
men implying a need to have different gender-specic cut-off
values for hs-CRP for prediction of CV risk. However, we did
not nd any signicant association between hs-CRP levels and
HTN, DM and dyslipidemia which needs to be explored in
future, larger studies.
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Sharad Gupta
Consultant Cardiologist, Max Super Specialty Hospital,
Bathinda, Punjab, India
Vitull K. Gupta*
Assistant Professor, Department of Medicine,
Adesh Institute of Medical Sciences and Research, 5042,
Am Wali Gali, Bathinda 151001, Punjab, India
Rupika Gupta
Consultant Pathologist, Lal Path Labs, Bathinda,
Punjab, India
Sonia Arora
Consultant Diet and Nutrition, Kishori Ram Hospital and Diabetes
Care Centre, Kishori Ram Road, Basant Vihar, Bathinda,
Punjab, India
Varun Gupta
MBBS Final Student, Adesh Institute of Medical Sciences and
Research, Bathinda, Punjab, India
*Corresponding author. Tel.: 91 9417020903 (mobile),
Tel.: 91 01642253903 (residence).
E-mail address: vitullgupta2000@yahoo.com
Recent spurt of coronary disease among relatively young
cardiologists in India
Dear Sir,
Very recently Mumbais cardiology community was shocked
to hear about the sudden and tragic death of one of its young,
bright and budding cardiologists who died of sudden cardiac
arrest. Such an unfortunate episode is a strong stimulus to the
press, lay public and the medical profession to do some soul
searching and ask a question e why?
One could ignore such an episode as a one off case.
However in cases as these, a scientic thought process is
bound to creep in to argue if there indeed was some sort of
epidemiological or logical pattern.
Members of the cardiology community, whether past or
present, have been the targets of extreme degrees of stress
while attending to critically ill patients at odd hours. Is pre-
mature CAD leading to acute coronary syndromes a new
phenomenon? Were the cardiologists belonging to the earlier
generations affected by ACS as frequently as the present ones
and that too prematurely?
Some how or the other it seems there is a subtle pattern in
the process. There has been a tragic and sudden spurt in the
occurrence of ACS amongst the new generation cardiology
community in the city.
The purpose of this communication is neither meant to
infringe on the private life of any individual nor to share the
information regarding the personal health of any one whose
history I might have known. These are merely general
observations of the four generations of cardiology commun-
ity of Mumbai city. Any conclusions that one might infer
from this writing are purely observational and personal. They
cannot be substantiated by statistical analysis, since the
numbers are far and few. They may even appear to be too
elementary and would certainly attract debate. However I
thought, I owe it to my fellow cardiologists to share some of
these observations:
1. Four generations of cardiology community
of Mumbai.
Cardiology as a specialty began to shape up sometimes in the
late 50s.
One could identify four distinct generations of cardiolo-
gists in the city.
I had the opportunity to closely observe my seniors in the
rst and second generation, work with my peers in the third
generation, and train several of the fourth generation
cardiologists.
The rst three generations comprised of 30 odd cardiolo-
gists. They pioneered the specialty in various medical colleges
and private hospitals. While the earliest ones were primarily
clinical cardiologists, several of the later ones in the sub-
sequent 2nd and 3rd generations were responsible for setting
up cardiac catheterization and angiography laboratories. It
was due to their untiring efforts that invasive and interven-
tional cardiology came into existence not only in the city but
all over the country. In addition to routine cardiac catheter-
ization and coronary angiography, they were responsible for
pioneering infant and newborn cardiac catheterization and
further established coronary angioplasty and primary angio-
plasty programs.
All or some of them might have had silent or minimally
symptomatic CAD. Considering 55e60 years as the average
Indian life span during that era, as far as we know, all of them
had fruitful and successful life beyond the sixth decade. None
i nd i a n he a r t j o ur na l 6 5 ( 2 0 1 3 ) 3 5 7 e3 6 7 365