Hemodynamic response to muscle reflex is abnormal in patients with heart failure with preserved ejection fraction

Abstract

The aim of the present investigation was to assess the role of cardiac diastole on the hemodynamic response to metaboreflex activation. We wanted to determine whether patients with diastolic function impairment showed a different hemodynamic response compared with normal subjects during this reflex. Hemodynamics during activation of the metaboreflex obtained by postexercise muscle ischemia (PEMI) was assessed in 10 patients with diagnosed heart failure with preserved ejection fraction (HFpEF) and in 12 age-matched healthy controls (CTL). Subjects also performed a control exercise-recovery test to compare data from the PEMI test. The main results were that patients with HFpEF achieved a similar mean arterial blood pressure (MAP) response as the CTL group during the PEMI test. However, the mechanism by which this response was achieved was markedly different between the two groups. Patients with HFpEF achieved the target MAP via an increase in systemic vascular resistance (+389.5 ± 402.9 vs. +80 ± 201.9 dynes·s·cm for HFpEF and CTL groups respectively), whereas MAP response in the CTL group was the result of an increase in cardiac preload (-1.3 ± 5.2 vs. 6.1 ± 10 ml in end-diastolic volume for HFpEF and CTL groups, respectively), which led to a rise in stroke volume and cardiac output. Moreover, early filling peak velocities showed a higher response in the CTL group than in the HFpEF group. This study demonstrates that diastolic function is important for normal hemodynamic adjustment to the metaboreflex. Moreover, it provides evidence that HFpEF causes hemodynamic impairment similar to that observed in systolic heart failure. This study provides evidence that diastolic function is important for normal hemodynamic responses during the activation of the muscle metaboreflex in humans. Moreover, it demonstrates that diastolic impairment leads to hemodynamic consequences similar to those provoked by systolic heart failure. In both cases the target blood pressure is obtained mainly by means of exaggerated vasoconstriction than by a flow-mediated mechanism.

Metaboreflex-mediated hemodynamic abnormalities in individuals with coronary artery disease without overt signs or symptoms of heart failure

“…Thus, the total recovery lasted 6 min. This protocol has been used several times in the past in similar experimental settings to study hemodynamic consequences of metaboreflex recruitment in both healthy subjects and patients (14,15,29,30,33,49,50).…”

“…Hemodynamic assessment. Throughout the PEMI and CER tests, hemodynamics were measured using the transthoracic impedance cardiography method, which has been previously used in similar experimental settings dealing with the metaboreflex activation in both healthy subjects and disease states (14,16,18,29,32,33,49,50). The impedance method allows for noninvasive calculation of SV on the basis of the Sramek-Bernstein equation (5).…”

“…It has been previously reported that an exaggerated SVR increment in response to the PEMI test is attributable to the impaired systolic and diastolic function (16,50). However, although the consequences of overt CAD-induced systolic and diastolic impairment during PEMI have been already investigated (16,50), to the best of our knowledge, nothing is known about the hemodynamic consequences of CAD with no overt signs of heart failure. A study of this kind would help to establish whether the PEMI test was able to detect preclinical signs of myocardial dysfunction.…”

“…Because in the PEMI setting the recruitment of the heart rate (HR) reserve is absent (15-17, 26, 38, 62), this method appears particularly useful to study the hemodynamic responses to metaboreflex activation when impairments in cardiac preload, inotropism, and afterload are present. These cardiac reserves are in fact all recruited in healthy individuals during PEMI (1,13,14,25,31,32,36,37,41,49,50,53,59,60).…”

“…By using the PEMI method, hemodynamic dysregulation has been demonstrated in different cardiovascular and metabolic and nervous diseases. In particular, it has been observed that, whenever the preload and inotropic reserves cannot be recruited, the hemodynamic regulation relies more on the afterload reserve and arteriolar vasoconstriction (14,16,31,33,50). This appears to be the consequence of the incapacity to enhance stroke volume (SV), which normally is stable or increases during PEMI in healthy individuals (13,17).…”