Cardiovascular magnetic resonance assessment of acute cardiovascular effects of voluntary apnoea in elite divers

Abstract

Background: Prolonged breath holding results in hypoxemia and hypercapnia. Compensatory mechanisms help maintain adequate oxygen supply to hypoxia sensitive organs, but burden the cardiovascular system. The aim was to investigate human compensatory mechanisms and their effects on the cardiovascular system with regard to cardiac function and morphology, blood flow redistribution, serum biomarkers of the adrenergic system and myocardial injury markers following prolonged apnoea.

Methods: Seventeen elite apnoea divers performed maximal breath-hold during cardiovascular magnetic resonance imaging (CMR). Two breath-hold sessions were performed to assess (1) cardiac function, myocardial tissue properties and (2) blood flow. In between CMR sessions, a head MRI was performed for the assessment of signs of silent brain ischemia. Urine and blood samples were analysed prior to and up to 4 h after the first breath-hold.

Results: Mean breath-hold time was 297 ± 52 s. Left ventricular (LV) end-systolic, end-diastolic, and stroke volume increased significantly (p < 0.05). Peripheral oxygen saturation, LV ejection fraction, LV fractional shortening, and heart rate decreased significantly (p < 0.05). Blood distribution was diverted to cerebral regions with no significant changes in the descending aorta. Catecholamine levels, high-sensitivity cardiac troponin, and NT-pro-BNP levels increased significantly, but did not reach pathological levels.

Conclusion: Compensatory effects of prolonged apnoea substantially burden the cardiovascular system. CMR tissue characterisation did not reveal acute myocardial injury, indicating that the resulting cardiovascular stress does not exceed compensatory physiological limits in healthy subjects. However, these compensatory mechanisms could overly tax those limits in subjects with pre-existing cardiac disease. For divers interested in competetive apnoea diving, a comprehensive medical exam with a special focus on the cardiovascular system may be warranted.

Trial registration: This prospective single-centre study was approved by the institutional ethics committee review board. It was retrospectively registered under ClinicalTrials.gov (Trial registration: NCT02280226 . Registered 29 October 2014).

Keywords: Apnoea; CMR; Cardiac function; Catecholamine; Hypoxia; hs-cT.

Fig. 1

Illustration of the study protocol (CMR: cardiovascular magnetic resonance)

Fig. 2

Left ventricular changes during apnoea. a) LV volumes: left ventricular volumes. b) LVEF: left ventricular ejection fraction, c) HR: heart rate, d) LVCO: left ventricular cardiac output (*p = < 0.05; **p = < 0.01; ***p = < 0.001; ****p = < 0.0001). Values are expressed as mean ± standard deviation

Fig. 3

Representative image showing a progressive LV dilation over the course of apnoea in diastolic heart phase (subject 12)

Fig. 4

Correlation of a) ΔHR (Apnoea_early – Apnoea_late) with ΔLVSV (Apnoea_early – Apnoea_late, panel and b) ΔLVEDV (Apnoea_early – Apnoea_late, panel respectively, using Spearman’s rank correlation (ΔHR with ΔLVSV: − 0.637, p = 0.008; ΔHR with ΔLVEDV: -0.592923; p = 0.0155). HR: heart rate, LVSV: left ventricular stroke volume; LVEDV: left ventricular end-diastolic volume

Fig. 5

Stroke volumes of common carotid arteries during course ao apnoea. SV-CCA: stroke volume in common carotid arteries. Values are expressed as mean ± SD

Fig. 6

Serum parameters of a) epinephrine, b) norepinephrine, c) NT pro-BNP and d) high sensitive Troponin (hsTrop) under apnoea