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.zaDOI: 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.comDivision of Cardiology, The First People’s Hospital of
Shunde, Guangdong, China
Ying Tan, MD