Journal of The Association of Physicians of India Vol.

63 November 2015

67

Acute Myocardial Infarction in Nephrotic Syndrome

Kavita Krishna1, Shirish Hiremath2, Sachin Lakade3, Sudarshan Davakhar4

Abstract
A 28 year old male, known case of nephrotic syndrome since 12 years, hypertensive
presented with acute myocardial infarction (AMI) and accelerated hypertension.
Coronary angiography revealed 100% thrombotic occlusion of mid left anterior
descending artery, treated with thrombus aspiration and intracoronary tirofiban
and nitroglycerine. He was stabilized within 24 hours. The pathogenesis of AMI
in nephrotic syndrome has been discussed with this case report.

Introduction

cute myocardial infarction (AMI)

in young adults can be broadly
classified into 2 groups those with
angiographically normal arteries and
those with coronary artery disease
of varying aetiology; there could be
significant overlap between the two
groups. The former may be due to
coronary artery thrombosis, embolism,
spasm or a combination of these.
Coronary thrombosis can be seen
in hypercoagulable states such as
antiphospholipid syndrome, nephrotic
syndrome (NS), protein C, S and factor
XII deficiencies, etc. The pathology in
the abnormal coronary arteries in the
young include significant accelerated
atherosclerosis, spontaneous dissection,
aneurysm, ectasia and anomalous
origin of coronary artery. In autopsy
studies the incidence of advanced
atheroma in young adults is reported
to be 2% and 20% in males aged 15-19
years and 30-34 years respectively. In
females it was 0% and 8 % respectively
in the same age groups. 1

pathogenesis of AMI in NS has been

discussed.

Case Report
A 28 year old male presented to the
emergency department with severe
retrosternal chest pain radiating to
left arm and sweating since 4 hours.
AT t h e a g e o f 1 6 y e a r s , h e h a d
developed puffiness of face, underwent
investigations. As per the old records
available, there was no hematuria,
proteinuria was 1.5 g/day; ASO, ANA/
anti-dsDNA were negative and IgA
levels were 104 mg/dL, which were
normal for that age. Thyroid function
tests were within normal limits. As
per kidney biopsy he was diagnosed
to have NS mesangioproliferative
glomerulonephritis. He was treated

We report the case of a 28 year

o l d m a l e w i t h N S s i n c e 1 2 ye a r s ,
h y p e r t e n s i ve p r e s e n t e d w i t h A M I
requiring emergency percutaneous
c o r o n a r y i n t e r ve n t i o n ( P C I ) . T h e
Fig. 2: Coronary angiogram showing
100% occlusion of mid left
anterior descending (LAD). LAD:
Left anterior descending artery;
LCx: Left circumflex artery

Fig.1: ECG shows acute anterior wall ST

elevated myocardial infarction

with oral prednisolone 1 mg/kg; there

was reduction in proteinuria to 0.5 g/
day. Dose of prednisolone was reduced
to 10/mg/day and azathioprine was
a d d e d . O ve r t h e n e s t 3 ye a r s , h e
was also put on antihypertensives
namely, losartan, atenolol and
frusemide. However, he had omitted
all medications on his own 1 year ago.
There was no family history of ischemic
heart disease.
On admission he was pale, had
a pulse 84/min, blood pressure of
240/130 mm Hg, puffy face and pedal
edema; chest was clear, fundus showed
changes of hypertensive retinopathy.
ECG was suggestive of acute anterior
wall ST elevated myocardial infarction
(Figure 1). Two-D echocardiography
showed left ventricular hypertrophy,
apical and septal hypokinesia, LVEF
of 45%. Intravenous metoprolol
and nitroprusside infusion was
administered. But the blood pressure
remained persistently high, so he was
unsuitable for intravenous thrombolysis
and was taken up for PCI. Coronary
angiography (CAG) revealed 100%
occlusion of mid left anterior descending
(LAD), Thromobolysis In Myocardial
Infarction (TIMI) grade I flow, 50%
stenosis of proximal circumflex and
a mild plaque in distal right coronary
artery (Figure 2). Thrombus aspiration
was done from LAD with thrombus
a s p i r a t i o n c a t h e t e r ( 6 F D i ve r C ) .
Thrombus quantity was excessive.
Intracoronary tirofiban, nitroglycerine
and nitroprusside were administered.
At the end of the procedure, TIMI grade
III flow was established with TIMI
myocardial perfusion grade (TMPG)
III perfusion (Figure 3). Intravenous
tirofiban and unfractionated heparin
was continued for 24 hours. Patient
soon stabilized. After 24 hours, he was
haemodyanamically stable and had
no chest pain. ECG showed decrease
in ST elevation and echocardiography

1
Professor of Medicine, 4Senior Resident, Department of Medicine, Bharati Vidyapeeth University Medical College and Bharati
Hospital (BVUMC and BH), Pune, Maharashtra; 2Consultant Cardiologist, Director Cardiac Cath Lab, 3Consultant Cardiologist,
Department of Cardiology, Ruby Hall Clinic, Pune, Maharashtra
Received; 15.12.2012; Revised: 05.12.2014; Accepted: 08.12.2014

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Journal of The Association of Physicians of India Vol. 63 November 2015

Fig. 3: Post PTCA, LAD showing TIMI

grade III flow; LAD (left anterior
descending artery), LCx (left
circumflex artery)

showed only moderated left ventricular

dysfunction.
His laboratory parameters revealed
Hb 10.4 g%, platelet count of 4.8
lakhs/cmm; hyperlipidemia with
serum cholesterol of 410 mg/dl and
triglycerides of 280 mg/dl; blood urea 94
mg/dl and creatinine of 3.5 mg/dl. There
was severe proteinuria 4.5 g/24 hours
and hypoalbuminemia (serum albumin
of 1.9 g/dl). Plasma concentration of
fibrinogen was elevated (564 mg/dl)
and antithrombin III levels significantly
reduced (<50%). He was discharged on
antihypertensives, antiplatelets and
statins. He is following up with the
nephrologist for immunosuppressive
therapy.

Discussion
Pr oteinuria associat ed wit h NS
results in the loss of low molecular
weight proteins which in turn alters
the concentration and activity of
coagulation factors. Due to increased
excretion, factors IX, XI and XII are
reduced. As the liver tries to compensate
for the hypoalbuminemic state, there is
increased synthesis of factors II, VII,
VIII, X, XIII and fibrinogen resulting
in their increased blood levels. There
is also evidence of decreased levels
of antithrombin III, a coagulation
inhibitor, reduced fibrinolytic activity
with hypertriglyceridemia which often

occurs in NS. The extent of alteration

in levels of all the proteins mentioned
above correlate with the degree of
hypoalbuminemia. A serum albumin
of <25 g/L is a significant risk factor
f o r c o m b i n e d a r t e r i a l a n d ve n o u s
thrombosis in NS. 1 A rise in plasma
fibrinogen is also due to increased
hepatic synthesis proportional to
the urinary protein loss. Protein C
and protein S deficiency have also
been implicated.2 Other factors
contributing to hypercoagulable state
are a thrombocytosis and increased
platelet adhesiveness and aggregation
(that correlates with serum cholesterol
concentrations). All these abnormalities
can cause coronary thrombosis without
atherosclerotic plaque rupture.1
Besides this, patients with long lasting
N S a n d e ve n m i l d p r o p e n s i t y f o r
hyperlipidemia may be at increased
r i s k f o r i s c h a e m i c c a r d i o va s c u l a r
events. 3 Patients with hyperlipidemia
and proteinuria >3.5 g/day predisposes
(nephrotic hyperlipedemia), as in our
patient, predisposes thes patients to
accelerated atherosclerosis and may
be another contributing factor in AMI.
Thromboembolic episodes in
NS remain one of the most serious
complications in patients with NS.
The most frequent site of thrombosis
is the venous system, particularly
the renal vein, incidence reported as
2-62.5%. It is seen predominantly in
adults. Arterial thrombosis in NS is
uncommon, incidence about 3%; is
seen mainly in children and rarely
reported. The first report on ischaemic
heart disease complicating NS was
published in 1969 by Berlyne and
Mallick, who described the occurrence
of AMI in four patients with NS due to
glomerulonephritis. 2
In cases of ACS with ST elevation,
like our patient, it has been reported
that intracoronary administration of
tirofiban followed by intravenous
infusion with an improved TIMI flow
and TMPG, and reduced thrombus
scores following primary PCI. It does

not increase the risk of bleeding or

platelet reduction. Also intracoronary
tirofiban may improve left ventricular
function through its beneficial effects on
coronary flow and myocardial perfusion
soon after successful PCI. 4 Compared
to systemic pharmacotherapy,
highly localized administration of
intracoronary pharmacotherapy is
associated with several hundred
fold increase in the microcirculation.
Benefits of intracoronary tirofiban and
mechanical clot aspiration are being
evaluated with respect to improvement
in myocardial perfusion and other
surrogate outcomes.
We have presented this case to
highlight the association of AMI with
NS in the young; aetiology being nonatherogenic pathology like coronary
thrombosis. Prompt management and
vigilance with intracoronary / invasive
pharmacotherapy plays a crucial role
and improve the outcome remarkably.
There are a couple of reports by Indian
authors but they have been published
in international journals. 5,6 To the best
of our knowledge there is no recent
similar case reports published in Indian
journal.

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Osula S, Bell GM, Hornung RS. Acute Myocardial infarction

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Meyer T, Schulze F, Grone H, Kreuzer H. Simultaneous

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3.

Hopp L, Gilboa N, Kurland G, Weichler N, Orchard TJ.

Acute myocardial infarction in a young boy with nephritic
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Wu T, Zhao Q, Huang W, et al. Effect of intracoronary

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Sivarajappa P. Acute myocardial infarction in young below
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