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

AFRICA

e3

have demonstrated that maintenance of normoglycaemia with

intensive insulin therapy may reduce morbidity and mortality

rates in critically ill patients.

9,10

The case reported here represents true myocardial infarction,

based on the changes in cardiac enzyme levels, as well as

echocardiographic and ECG findings. To our knowledge, this is

the first reported case of SIRS-induced myocardial infarction.

Different from previous reports, there was no relevant coronary

stenosis in this case, as shown by the coronary angiography and

IVUS (Fig. 2).

A new clinical classification of myocardial infarction was

proposed in the 2007 ESC/ACCF/AHA/WHF consensus

conference,

11

and clinically various types of myocardial

infarction were classified by pathogenesis, as described in

Table 1. In the present case, the myocardial infarction should

be classified as type 2, and cardiac damage induced by SIRS is

likely to be the most probable mechanism of acute myocardial

infarction. Additionally, a hypodynamic circulation, especially

one reflected in a notable reduction in the ejection fraction

(32%) by echocardiography, as in this case, may also be related

to myocardial infarction.

In recent years, many researchers have suggested that local

and systemic inflammation may play an important role in the

occurrence, development and complications of acute coronary

syndrome (ACS).

12

However, coronary angiography is essential

to avoid the potentially lethal consequences of thrombolytic

therapy in this type of myocardial infarction.

In summary, according to the results of glycated haemoglobin

and the patient’s medical history, we may infer that the patient

had a medical history of diabetes that was not well controlled.

Pneumonia infection was induced by diabetes; therefore, we

speculated that the patient developed SIRS secondary to

diabetes-induced infection. As a result, a large number of

inflammatory factors, including C-reactive protein, may have

damaged the patient’s pancreas, heart, liver, kidney and skeletal

muscle, leading to MODS.

Conclusion

The present case demonstrates that SIRS may lead to multiple

organ damage, and even to a clinical performance of coronary

artery disease mimicking acute myocardial infarction. Urgent

diagnosis by angiography is required. To enable prompt

diagnosis and effective treatment in similar cases, clinicians

should be aware of this type 2 myocardial infarction. Patients

who smoothly obtain an inflammatory reaction peak under

active treatment will likely experience good results.

No external financial support was provided. We thank the patient for his

cooperation and for providing the photographic material.

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Table 1. Clinical classification of myocardial infarction (MI), as

proposed at the 2007 ESC/ACCF/AHA/WHF consensus conference

Type of MI Description

Type 1

Spontaneous MI related to ischaemia due to a primary

coronary event such as plaque erosion and/or rupture,

fissuring or dissection

Type 2

MI secondary to ischaemia due to either increased oxygen

demand or decreased supply, e.g. coronary artery spasm,

coronary embolism, anaemia, arrhythmias, hypertension

or hypotension

Type 3

Sudden unexpected cardiac death

Type 4a MI associated with primary percutaneous coronary inter-

vention (PPCI)

Type 4b MI associated with stent thrombosis as documented by

angiography or at autopsy

Type 5

MI associated with coronary artery bypass grafting (CABG)