The impact of an experimentally induced increase in arterial blood pressure on left ventricular twist mechanics

Abstract

New Findings r What is the central question of this study?Increases in blood pressure elicited by isometric hand-grip exercise (IHG) have been shown to impair ventricular twist mechanics. However, the utility of the IHG model is confounded by a concurrent increase in heart rate, which independently influences ventricular mechanics. r What is the main finding and its importance?We show that a period of post-IHG circulatory occlusion isolates the effect of an arterial blood pressure increase from heart rate and magnifies the impairment of left ventricular twist when compared with IHG alone. A protocol using IHG followed by brief circulatory occlusion may serve as a useful tool in examining and understanding the relationships between afterload and cardiac function in various disease states.The effects of isometric hand-grip exercise (IHG) coupled with a period of postexercise circulatory occlusion (OCC; known to sustain exercise-induced increases in blood pressure while facilitating a decrease in heart rate) on left ventricular (LV) twist mechanics was examined. Two-dimensional speckle-tracking echocardiography was used to assess LV apical and basal rotation and LV twist in 19 healthy participants (23 ± 2 years old) at rest, during 3 min of IHG (performed at 40% maximal voluntary contraction) and 3 min of OCC immediately following IHG. The IHG elicited significant (P < 0.001) increases in mean arterial pressure (rest, 91 ± 1 mmHg; IHG, 122 ± 2 mmHg) and heart rate (rest, 65 ± 2 beats min −1 ; IHG, 91 ± 4 beats min −1 ). Mean arterial pressure remained elevated during OCC (116 ± 2 mmHg; P < 0.001 versus rest), whereas heart rate returned to resting levels (68 ± 3 beats min −1 ; P = 0.159 versus rest). Apical rotation decreased significantly (P < 0.01) by 10 ± 5% during IHG and 21 ± 4% during OCC, whereas basal rotation remained unchanged from rest. Left ventricular twist decreased from rest to IHG (12 ± 5%; P = 0.015) and OCC (21 ± 4%; P = 0.001), whereas a decrease in LV untwist rate was observed only during OCC. An increase in blood pressure generated by IHG, and maintained by a period of OCC, impairs aspects of LV twist mechanics. Postexercise circulatory occlusion isolated the effect of the arterial blood pressure rise (from heart rate), magnifying the impairment of LV twist mechanics when compared with IHG, whilst also negatively impacting LV relaxation. We propose that a protocol using isometric exercise followed by circulatory occlusion provides a method for studying the effects of blood pressure changes on LV twist mechanics.

Acute cardiac functional and mechanical responses to isometric exercise in prehypertensive males

“…(2012) and Balmain et al. (2016) in healthy populations confirm data from clinical populations, where a decrease in cardiac mechanics is associated with an increase in LV after‐load (Takeuchi et al. 2007), which is an important finding when considering the continuum of hypertensive heart disease from raised after‐load to adverse LV remodeling to cardiac failure.…”

“…Similar results were reported with a single isometric hand‐grip exercise session followed by a period of post exercise circulatory occlusion (Balmain et al. 2016). Studies by both Weiner et al.…”

Alterations in Cardiac Deformation, Timing of Contraction and Relaxation, and Early Myocardial Fibrosis Accompany the Apparent Recovery of Acute Stress-Induced (Takotsubo) Cardiomyopathy: An End to the Concept of Transience

“…Thirdly, our controls were matched for cardiac co-morbidities (mostly history of hypertension). The latter two characteristics eliminate important confounders in assessing LV strain and twist mechanics which are known to be affected by inotropic therapy [30][31][32][33][34] and LV afterload 35,36 .…”

Interaction between left ventricular twist mechanics and arterial haemodynamics during localised, non‐metabolic hyperaemia with and without blood flow restriction

“…Additionally, LV twist appears to be related to the regional O 2 distribution across the LV muscle (Beyar & Sideman, 1986) and has been implicated in stress sensing (Vendelin et al 2002). Owing to the potentially detrimental effects of high arterial resistance on LV function, a number of studies have examined the effects of increased afterload on LV twist and untwisting rate (Gibbons Kroeker et al 1995;Dong et al 1999;Weiner et al 2012;Balmain et al 2016). Whilst these studies have consistently reported a reduction in LV twist when afterload was increased, they have examined the LV apex only (Gibbons Kroeker et al 1995) or quantified subendocardial twist and not the complete transmural contributions (Dong et al 1999) or employed methods that produced systemic arterial effects that probably impacted indirectly on the heart through circulating anaerobic metabolites (Gibbons Kroeker et al 1995;Weiner et al 2012;Balmain et al 2016).…”

“…Owing to the potentially detrimental effects of high arterial resistance on LV function, a number of studies have examined the effects of increased afterload on LV twist and untwisting rate (Gibbons Kroeker et al 1995;Dong et al 1999;Weiner et al 2012;Balmain et al 2016). Whilst these studies have consistently reported a reduction in LV twist when afterload was increased, they have examined the LV apex only (Gibbons Kroeker et al 1995) or quantified subendocardial twist and not the complete transmural contributions (Dong et al 1999) or employed methods that produced systemic arterial effects that probably impacted indirectly on the heart through circulating anaerobic metabolites (Gibbons Kroeker et al 1995;Weiner et al 2012;Balmain et al 2016). Consequently, a fundamental question that remains to be answered is whether in vivo LV twist mechanics respond to changes in local peripheral arterial haemodynamics that do not exceed an individual's normal afterload and when the normal metabolic demand of tissue is maintained.…”