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CARDIOVASCULAR JOURNAL OF AFRICA • Volume 26, No 3, May/June 2015

AFRICA

e1

Case Report

ST-elevation myocardial infarction following systemic

inflammatory response syndrome

Ying Tan, Yan Tu, Di Tian, Chen Li, Jian-Kai Zhong, Zhi-Gang Guo

Abstract

Systemic inflammatory response syndrome (SIRS) compli-

cated with ST-elevation myocardial infarction has rarely

been reported, and the precise mechanisms of myocardial

injury remain unclear. Here, we present a case involving a

45-year-old man who developed SIRS secondary to diabetes-

induced infection, and who ultimately developed ST-elevation

myocardial infarction with acute heart failure, fulminant

diabetes, acute liver dysfunction, acute kidney dysfunction

and rhabdomyolysis. The patient eventually recovered due

to early detection, correct diagnosis and powerful treatment.

Clinicians should be aware of this new type of myocardial

infarction, which is induced by inflammatory injury, but is not

due to a primary coronary event such as plaque erosion and/

or rupture, fissuring or dissection.

Keywords:

systemic inflammatory response syndrome,

ST-elevation myocardial infarction

Submitted 28/1/14, accepted 27/11/14

Cardiovasc J Afr

2015;

26

: e1–e3

www.cvja.co.za

DOI: 10.5830/CVJA-2014-071

Systemic inflammatory response syndrome (SIRS) results from

a variety of severe clinical insults, such as infection, pancreatitis,

trauma, surgery or other critical illness, and its diagnosis

1

includes the presence of at least two of the following: (1)

heart rate

>

90 beats/min; (2) respiratory rate

>

20 breaths/

min or carbon dioxide pressure (PaCO

2

)

<

32 mmHg; (3) body

temperature

>

38°C or

<

36°C; or (4) leukocyte count

>

12

×

10

9

cells/l or

<

4

×

10

9

cells/l.

Although the exact mechanisms of SIRS are unclear, in

general, many scholars believe that SIRS is a clinical process that

is characterised by generalised inflammatory hyper-reactivity

caused by various severe clinical insults triggered by infectious

factors and non-infectious host stimulatory agents. Extensive

capillary leakage and mesenchymal oedema caused by various

inflammatory mediators and cytokines lead to reduced blood

perfusion of vital organs, microcirculatory disturbances, shock,

and organ function decline or failure, ultimately resulting in

multiple organ dysfunction syndrome (MODS) and multiple

organ failure (MOF). When SIRS progresses to MODS and

MOF, the mortality rate increases to a range of 30–80%,

depending on the number of failed organs.

2

Cardiovascular complications of SIRS include shock,

pericardial effusion, and even non-specific ST–T changes in

the electrocardiogram (ECG) that mimic acute myocardial

infarction. However, ST-elevation myocardial infarction

(STEMI) complicated by SIRS has rarely been reported, and

most of the reported cases could not be classified as true

myocardial infarction, according to cardiac enzyme levels and

echocardiographic or angiographic findings.

A literature review performed with PubMed, using the

keywords ‘systemic inflammatory response syndrome (SIRS)’

and ‘ST-elevation acute myocardial infarction (STEMI)’,

identified few reports in the English language literature between

1990 and 2013. In contrast to our case, two published reports by

Samimi-Fard

et al

.

3

and van Diepen

et al

.

4

found that patients

with STEMI may present with SIRS after primary percutaneous

coronary intervention (PPCI). Conversely, our case showed that

SIRS may cause STEMI, which is an extraordinary finding,

given the absence of relevant coronary stenosis.

Here, we report a case of SIRS-related myocardial infarction

involving a 45-year-old man who developed SIRS secondary to

diabetes-induced infection, followed by ST-elevation myocardial

infarction with acute heart failure, fulminant diabetes, acute

liver dysfunction, acute kidney dysfunction and rhabdomyolysis.

Awareness of this type of myocardial infarction is critical to

enable prompt diagnosis and treatment in similar cases.

Case report

A 45-year-old man with a history of diabetes was admitted with

cough, polyuria and polydipsia of one week’s duration. The

patient had no medical history of hypertension and myocardial

infarction. Upon physical examination, the patient was found

to have a body temperature of 38.2°C, a respiratory rate of 23

breaths/min, a pulse rate of 106 beats/min and a systolic/diastolic

Division of Cardiology, Nanfang Hospital, Southern

Medical University, Guangzhou, Guangdong, China

Ying Tan, MD

Yan Tu, MD

Di Tian, MD

Chen Li, MD

Jian-Kai Zhong, MD

Zhi-Gang Guo, MD,

guozhigang126@126.com

Division of Cardiology, The First People’s Hospital of

Shunde, Guangdong, China

Ying Tan, MD