Sleep apnoea severity has a non-linear relationship with acute myocardial infarction risk

Dr Neomi Shah (Icahn School of Medicine at Mount Sinai, USA) presented a small study suggesting that moderate sleep apnoea may be cardioprotective in acute myocardial infarction through enhanced collaterals [1].

Dr Shah and colleagues hypothesised that ischaemic preconditioning of the myocardium may have a protective effect in some sleep apnoea (SA) patients during myocardial infarction (MI). The researchers conducted a study to assess whether sleep apnoea is associated with reduced infarct size and enhanced coronary collaterals during an MI by quantifying infarct size (% of left ventricle [LV] infarcted divided by the volume of LV mass). They assessed the score of coronary collaterals using the Rentrop Score (range 0-3, higher scores indicating augmented collaterals).

The study recruited 33 patients (age >21) with ST-elevation MI who underwent percutaneous coronary intervention. Level 3 SA testing was done during hospitalisation. Patients were stratified by SA severity: none (apnoea-hypopnoea index [AHI]<5, n=8), mild (5≤AHI<15, n=10), moderate (15≤AHI<30, n=8), and severe (AHI>30, n=7) (hypopneas with 4% desaturation). Comparing the no-SA vs SA groups, the mean age was 47.5±10.9 years vs 56.6±11.0 years, mean BMI (kg/m²) 26.4±6.11) vs 29.3±5.82, male gender 87.5% vs 88%. The median infarct size in no-SA was 22% vs 28% in the SA group (P=0.79). Across all SA categories, moderate SA group had the lowest infarct size (median 15.5; IQR 9-23) vs mild SA (median 27, IQR 23.8-32.5) and severe SA (median 34, IQR 31-53, P=0.289). Similarly, moderate SA group had the highest Rentrop grade compared with no-SA, mild SA, or severe SA (P=0.23). After excluding central SA, moderate SA patients had a significantly higher proportion of Rentrop grade 2 (indicating higher collaterals) compared with other SA categories (P=0.03).

The study results generate preliminary evidence for a non-linear relationship between SA severity and infarct size where only moderate SA appears to be associated with reduced infarct size and enhanced coronary collaterals. Dr Shah noted that these data were consistent with animal models of hypoxic preconditioning. The study suggests that moderate SA may be cardioprotective in acute MI through enhanced collaterals, but this requires confirmation in larger studies adjusted for intergroup differences.

In an interview, Dr Shah added, “I think that sleep apnoea for the last 2 decades has been a well-established independent risk factor for cardiovascular disease, and we have done many, many studies that have shown that sleep apnoea is an independent risk factor for stroke, for arrhythmias, for sudden cardiac death, for atrial fibrillation, for myocardial infarction. But unfortunately, in the recent few years, the clinical trials in which we are trying to treat the sleep apnoea condition with continuous positive airway pressure, therapy did not reduce the occurrence of some of these events. So, it is a little puzzling, because we have shown that it is a risk factor for cardiovascular disease, but when we treated, it did not really make the impact that we were hoping for it to make. We are in a state of a little bit of confusion, and we are really trying to dig deep in terms of the mechanisms—as to what it is about the obstructive sleep apnoea that was causing this increased risk factor.”

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   1. Shah NA. A4460, ATS 2019, 17-22 May, Dallas, USA.

Posted on 23 July 201917 May 2024