Compared Impact of Diabetes on the Risk of Heart Failure from Acute Myocardial Infarction to Chronic Coronary Artery Disease

The association of diabetes mellitus (DM) and an increased risk of heart failure (HF) in terms of occurrence and severity are already known. However, there are no studies to investigate the risk of HF progressions at the different clinical stages of CAD and to determine if the risk of developing HF elevates similarly regardless of the clinical presentation of CAD. Gilles Lemesle and colleagues conducted research under the title “Compared Impact of Diabetes on the Risk of Heart Failure from Acute Myocardial Infarction to Chronic Coronary Artery Disease” published in Diabetes and Metabolism Journal. The summary of the study is given below:

Objective:

To describe the presence of risk of heart failure (HF) according to diabetes mellitus (DM) status in coronary artery disease (CAD) patients.

Method:

The FAST-MI cohort was analyzed for the acute and subacute MI phases. The analysis was restricted to patients without a history of HF. The analysis was conducted 1-year after MI to study the outcome and it was further restricted to patients who were discharged alive and without a history of HF and/or HF symptoms during the index hospitalization for MI. To analyze the chronic phase, investigators analyzed the CORONOR cohort restricted to patients without a history of HF.
The primary outcome was HF episodes according to DM status. The composite of all-cause death or HF was also analyzed.

Finding:

The study concludes that the risk of HF occurrence in CAD patients with DM is increased by 70% in all stages, from acute situations such as acute MI to the post-MI subacute period, and till the chronic phase of the disease. Prevention of HF occurrence should therefore be the permanent objective in these patients, with the ideal use of conventional therapy as well as new medications for HF prevention.

Limitation:

There was a lack of LVEF assessment during HF occurrence restricts the interpretation of the mechanism of left ventricular dysfunction. Secondly, the results were emerged from two different multicentre french cohorts of patients and not from a single cohort.

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