A Case of Diabetic Ketoacidosis and Acute Myocardial Infarction with

Supraventricular Tachycardia: Which Condition Appear First?

Raissa Virgy Rianda1, Isna Mahmudah1, Fahmi Aulia Rizqi1, Swastika Ayuningtyas Setyo Asri1, Muhammad Perdana Airlangga2
1Department of Emergency Services, Siti Khodijah Hospital, Sidoarjo, East Java, Indonesia, 2Department of Cardiology and Vascular Medicine, Siti Khodijah Hospital, Sidoarjo, East Java, Indonesia

INTRODUCTION
Diabetic ketoacidosis (DKA) known as one of the serious acute metabolic complication of Diabetes. It is a complex metabolic state characterized by hyperglycemia, acidosis and ketonuria. We present a case of Acute
Myocardial Infarction (AMI) and life-threateningdysrhythmias with DKA, requiring aggressivetreatment with a favorable outcome.

CASE ILLUSTRATION
A 38-year-old man presented a 2-day history of dyspnoea, retrosternal chest discomfort, nausea and intermittent vomiting. He presented supraventricular tachycardia. Laboratory results showed electrolyte imbalances and
elevated of troponin I HS (54.6). Blood gas analysis showed metabolic acidosis. The patient diagnosed with Acute Myocardial Infarction and Supraventricular tachycardia with Diabetic Ketoacidosis . The patient was
successfully treated and discharged 5 days after admission. The patient was discharged home on oral cardiac and hypoglycemic regiment after gradual weaning from insulin therapy, which was needed initially during his
acute presentation.

DISCUSSION
The interpretation of the MI relationship in DKA is quite complicated, because AMI can be either a cause or a consequence of DKA. Deaths in DKA are
most often caused by MI and the underlying pathology is not very clear. Multiple mechanisms might play a role. Several different theories have explained
this phenomenon

1. Free Fat Acid Release 2. Acidosis

Free fatty acids are the precursors for hepatic ketone body formation. The
release of free fatty acids was also observed in the acute diabetic
decompensation. A high circulating level of free fatty acid leads to the
incorporation of fatty acids into the lipid structure of the myocyte
membrane with the formation of micelle with destabilization and rupture
of this membrane (1). Circulating insulin governs the extraction rate of
glucose by cardiomyocytes (2). In case of DKA, insulin deficiency is
associated with a high level of free fatty acids and ketone bodies, which
inhibits the glucose uptake by the cell and thus deprives the myocardium of
its energy substrate. In addition, the above-mentioned excess of
catecholamine decreases the insulin reserves and increases the free fatty acid
uptake by the myocardium, which is toxic to the myocardium (2). This
phenomenon of cellular toxicity induces the cTnI production
In a another case report two patients with elevated troponin levels had no
abnormalities at the angiography and had a pH of 6.9 (4). A study also
have shown that a pH below 7.10 is an independent prognostic factor for
troponin elevation on admission in DKA (5). The interaction between
acidosis associated with PH and intracellular calcium accrued in complex
ways. Subsequent severe academia, intracellular calcium is increased by
changes in transmembrane ionic motion at the sarcoplasmic membrane
and sarcoplasmic reticulum (5). The different chemical pathways that
lead to proteolysis are stimulated by an increase of intracellular calcium.
Myocardial stunning occurs due to inhibited interactions between
calcium and contractile proteins which are triggered by severe acidosis
(6). Proteolysis and stunning both cause MI to occur.
3. Counter regulation hormones CONCLUSION
Acute decompensation of diabetes is associated by a rise The outline for the clinician should be that the sign of MI in a DKA
in counter-regulating hormones such as adrenaline, patient should always be considered an abnormal coronary until proven
cortisol and glucagon (5). These hormones increase the otherwise
oxygen demand of the myocardium (3). In diabetic
patients with a history of coronary heart disease,
coronary blood flw is compromised with an increase in
supply-demand mismatch, resulting in MI (5). REFERENCES
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