Reduced peripheral arterial blood flow with preserved cardiac output during submaximal bicycle exercise in elderly heart failure

Background The underlying pathophysiology of heart failure with preserved ejection fraction (HFpEF) remains poorly understood. Changes in peripheral arterial function concomitantly with the evaluation of cardiopulmonary reserve and biomarkers related to wall stress, extra-cellular matrix turnover (ECM), subclinical inflammation and oxidative stress have not been investigated in patients with HFpEF nor compared with age-matched healthy volunteers (HV). We hypothesized that patients with HFpEF would have impairments in cardiac reserve with reduced peripheral arterial function associated with broad-spectrum biomarkers activation. Methods Eighteen male and female HFpEF patients (aged 70 ± 9 yr) NYHA class II and III were recruited. Data from patients were compared with those from 14 age and sex matched HV. A maximal exercise testing with gas exchange analysis was completed on a treadmill using a RAMP protocol and heart rate recovery (HRR) was measured at 1 and 2 minutes following exercise. Peripheral arterial function was assessed using near infrared radionuclide plethysmography. Biomarkers included BNP, NT-proBNP, hsCRP, TBARS, 8-epi-prostaglandin F2α, MMP 1, 2, 9 and TIMP 1, 2, 3, 4) were analyzed. Results Selected data are presented in the Table 1 and 2. Conclusions Compared to healthy volunteers, patients with HFpEF demonstrated a significant decrease in aerobic capacity but an increase in basal peripheral arterial blood flow, subclinical inflammation and oxidative stress. The increase in resting arterial blood flow may be a compensatory mechanism for the decrease in cardiac reserve and the pro-inflammatory/oxidant milieu in these patients.

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Changes in Cardiopulmonary Reserve and Peripheral Arterial Function Concomitantly with Subclinical Inflammation and Oxidative Stress in Patients with Heart Failure with Preserved Ejection Fraction

International Journal of Vascular Medicine ◽

10.1155/2014/917271 ◽

2014 ◽

Vol 2014 ◽

pp. 1-8 ◽

Cited By ~ 4

Author(s):

Damien Vitiello ◽

François Harel ◽

Rhian M. Touyz ◽

Martin G. Sirois ◽

Joel Lavoie ◽

...

Keyword(s):

Oxidative Stress ◽

Heart Failure ◽

Blood Flow ◽

Ejection Fraction ◽

Arterial Blood Flow ◽

Preserved Ejection Fraction ◽

Arterial Blood ◽

Patients With Heart Failure ◽

Peripheral Arterial ◽

And Oxidative Stress

Background. Changes in cardiopulmonary reserve and biomarkers related to wall stress, inflammation, and oxidative stress concomitantly with the evaluation of peripheral arterial blood flow have not been investigated in patients with heart failure with preserved ejection fraction (HFpEF) compared with healthy subjects (CTL).Methods and Results. Eighteen HFpEF patients and 14 CTL were recruited. Plasma levels of inflammatory and oxidative stress biomarkers were measured at rest. Brain natriuretic peptide (BNP) was measured at rest and peak exercise. Cardiopulmonary reserve was assessed using an exercise protocol with gas exchange analyses. Peripheral arterial blood flow was determined by strain gauge plethysmography. Peak VO2(12.0±0.4versus19.1±1.1 mL/min/kg,P<0.001) and oxygen uptake efficiency slope (1.55±0.12versus2.06±0.14,P<0.05) were significantly decreased in HFpEF patients compared with CTL. BNP at rest and following stress, C-reactive-protein, interleukin-6, and TBARS were significantly elevated in HFpEF. Both basal and posthyperemic arterial blood flow were not significantly different between the HFpEF patients and CTL.Conclusions. HFpEF exhibits a severe reduction in cardiopulmonary reserve and oxygen uptake efficiency concomitantly with an elevation in a broad spectrum of biomarkers confirming an inflammatory and prooxidative status in patients with HFpEF.

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Immediate Effects of Electrical Stimulation, Diathermy, and Physical Exercise on Lower Limb Arterial Blood Flow in Diabetic Women With Peripheral Arterial Disease: A Randomized Crossover Trial

Journal of Manipulative and Physiological Therapeutics ◽

10.1016/j.jmpt.2014.08.008 ◽

2015 ◽

Vol 38 (3) ◽

pp. 195-202 ◽

Cited By ~ 7

Author(s):

Elaine Caldeira de Oliveira Guirro ◽

Rinaldo Roberto de Jesus Guirro ◽

Almir Vieira Dibai-Filho ◽

Siane Cristina Santarosa Pascote ◽

Delaine Rodrigues-Bigaton

Keyword(s):

Blood Flow ◽

Electrical Stimulation ◽

Peripheral Arterial Disease ◽

Lower Limb ◽

Crossover Trial ◽

Arterial Disease ◽

Arterial Blood Flow ◽

Arterial Blood ◽

Randomized Crossover Trial ◽

Peripheral Arterial

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Abstract 67: Vasopressin impairs Brain, Heart and Kidney Perfusion in Acute Heart Failure

Circulation ◽

10.1161/circ.116.suppl_16.ii_937-b ◽

2007 ◽

Vol 116 (suppl_16) ◽

Author(s):

Stig Müller ◽

Ole-Jakob How ◽

Stig E Hermansen ◽

Truls Myrmel

Keyword(s):

Blood Flow ◽

Cardiac Output ◽

Heart Function ◽

Left Ventricular Pressure ◽

Left Ventricular ◽

Arterial Blood Flow ◽

Organ Blood Flow ◽

Arterial Blood ◽

Time Flow ◽

The Brain

Arginin Vasopressin (AVP) is increasingly used to restore mean arterial pressure (MAP) in various circulatory shock states including cardiogenic shock. This is potentially deleterious since AVP is also known to reduce cardiac output by increasing vascular resistance. Aim: We hypothesized that restoring MAP by AVP improves vital organ blood flow in experimental acute cardiac failure. Methods: Cardiac output (CO) and arterial blood flow to the brain, heart, kidney and liver were measured in nine pigs by transit-time flow probes. Heart function and contractility were measured using left ventricular Pressure-Volume catheters. Catheters in central arteries and veins were used for pressure recordings and blood sampling. Left ventricular dysfunction was induced by intermittent coronary occlusions, inducing an 18 % reduction in cardiac output and a drop in MAP from 87 ± 3 to 67 ± 4 mmHg. Results: A low-dose therapeutic infusion of AVP (0.005 u/kg/min) restored MAP but further impaired systemic perfusion (CO and blood flow to the brain, heart and kidney reduced by 29, 18, 23 and 34 %, respectively). The reduced blood flow was due to a 2.0, 2.2, 1.9 and 2.1 fold increase in systemic, brain, heart and kidney specific vascular resistances, respectively. Contractility remained unaffected by AVP. The hypoperfusion induced by AVP was most likely responsible for observed elevated plasma lactate levels and an increased systemic oxygen extraction. Oxygen saturation in blood drawn from the great cardiac vein fell from 31 ± 1 to 22 ± 3 % dropping as low as 10 % in one pig. Finally, these effects were reversed forty minutes after weaning the pigs form the drug. Conclusion: The pronounced reduction in coronary blood flow point to a potentially deleterious effect in postoperative cardiac surgical patients and in patients with coronary heart disease. Also, this is the first study to report a reduced cerebral perfusion by AVP.

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