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European Journal of Heart Failure 2007 9(9):865-871; doi:10.1016/j.ejheart.2007.06.003
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© 2007 European Society of Cardiology

Differences in arterial compliance, microvascular function and venous capacitance between patients with heart failure and either preserved or reduced left ventricular systolic function

Sean Balmaina,*, Neal Padmanabhana, William R. Ferrellb, John J. Mortona and John J.V. McMurraya

a British Heart Foundation Cardiovascular Research Centre, University of Glasgow Glasgow G12 8TA, Scotland, UK
b Division of Infection, Immunology and Inflammation, University of Glasgow, Scotland, UK

* Corresponding author. Tel./fax: +44 141 211 1838, +44 7811113015 (mobile). E-mail address: seanbalmain{at}hotmail.com


   Abstract
Top
 Abstract
1. Introduction
 2. Methods
 3. Results
 4. Discussion
 5. Conclusions
 References
 
Background: Up to 50% of patients with the clinical syndrome of heart failure have preserved left ventricular systolic function (HF-PSF). These patients may have abnormalities of ventriculo-vascular coupling, due to increased vascular and ventricular stiffness.

Methods: We compared arterial compliance, microvascular vasodilator function and venous capacitance (VC) in 3 groups of patients (n<=12 each) matched for the presence of coronary heart disease: 1) HF and preserved systolic function (HF-PSF), 2) HF and reduced systolic function (HF-RSF) and 3) controls (no HF, PSF). Arterial compliance was assessed by measuring aortic pulse wave velocity (PWV) with applanation tonometry. Cutaneous microvascular function was assessed using Laser Doppler imaging (LDI) coupled with iontophoresis of endothelium-dependent (acetylcholine) and -independent (sodium nitroprusside) vasodilators. VC was measured using venous occlusion plethysmography.

Results: PWV was significantly higher in HF-PSF subjects than in both HF-RSF and control groups (10.7 [1.1], 8.9 [1.7] and 8.6 [2.1] m/s respectively, p<0.05). Acetylcholine and nitroprusside induced vasodilatation were equally impaired in HF-PSF and HF-RSF, as compared to controls (p<0.01). VC was higher in HF-RSF subjects compared with HF-PSF subjects (1.75 [0.41], 1.34 [0.34] ml/100 ml forearm vol. respectively, p<0.05).

Conclusions: These findings are consistent with a more marked increase in vascular stiffness in HF-PSF than in HF-RSF and suggest that arterial stiffness, dynamic vasodilator function and venous abnormalities may be implicated in the complex pathophysiology of HF-PSF.

Key Words: Heart failure • Diastole • Arteries • Veins • Endothelium

Received October 12, 2006; Revised March 9, 2007; Accepted June 7, 2007


   1. Introduction
Top
 Abstract
 1. Introduction
2. Methods
 3. Results
 4. Discussion
 5. Conclusions
 References
 
A substantial proportion - up to 50%- of patients with the clinical syndrome of heart failure have preserved left ventricular systolic function (HF-PSF) [1,2]. Recently published data indicate that HF-PSF has increased in prevalence in the last 15 years [3], and carries a similar prognosis to heart failure with reduced systolic function (HF-RSF) [4]. The cause of heart failure in these patients is controversial. The most commonly held view is that most have diastolic dysfunction, i.e. a disorder of left ventricular (LV) relaxation and filling, as opposed to contraction and emptying [5,6]. More recently, attention has turned to examination of vascular function in patients with HF-PSF and it has been suggested that these patients have abnormal ventriculo-vascular coupling [7-13]. These pathophysiologic processes are not mutually exclusive and may both contribute to the development of the syndrome of heart failure. Reduced arterial compliance may result in abnormal ventriculo-arterial coupling, increased LV wall stress, reduced coronary flow and aggravate or even cause the clinical syndrome of heart failure [7-13].

The vascular endothelium is integral to maintaining normal vessel tone and function and, therefore, normal ventriculo-vascular interaction [14]. Vascular endothelial dysfunction has been well documented in heart failure with reduced systolic function (HF-RSF) [15-19] and is thought to be secondary to neurohumoral and inflammatory activation [20-22]. Whether HF-PSF is associated with endothelial dysfunction is, however, unknown.

Additionally, reduced compliance of veins, leading to reduced venous capacitance (VC), may also play an important role in the pathophysiology of HF-PSF. Patients with HF-PSF are more sensitive to the effects of vasodilators and diuretics on LV filling pressure, suggesting that VC is reduced [23,24]. Reduced VC is associated with reduced exercise capacity in patients with HF-RSF [25]. There have, until now, been no studies of VC in patients with HF-PSF.

We therefore tested the hypotheses that patients with HF-PSF have a greater reduction in arterial compliance, endothelial mediated vasodilatation, and VC than patients with HF-RSF.


   2. Methods
Top
 Abstract
 1. Introduction
 2. Methods
3. Results
 4. Discussion
 5. Conclusions
 References
 
2.1. Patients
This project conforms to the principles outlined in the Declaration of Helsinki and was approved by our local ethics committee. All patients gave written, informed consent.

We recruited three groups of patients: a) 12 patients with coronary heart disease (CHD) and HF-PSF, b) 12 patients with CHD and HF-RSF and c) 12 patients with CHD, preserved LV systolic function and no evidence of heart failure (control). Patients with significant valvular heart disease, atrial fibrillation, diabetes mellitus, renal failure (creatinine>250 µmol/l) and uncontrolled hypertension despite antihypertensive therapy (systolic BP>140 or diastolic BP>90 mm Hg) were excluded. Heart failure was defined as: a) relevant symptoms/signs/radiographic findings as indicated by Boston criteria, [26] ; b) need for diuretic therapy and c) increased plasma N terminal pro B-type natriuretic peptide concentration. Preserved LV systolic function was defined as a LV ejection fraction (LVEF) of ≥0.50, measured by echocardiography. Impaired LV systolic function was defined as a LVEF of <0.40. Echocardiograms were performed on a routine basis for clinical reasons in all subjects by a single operator, who was blinded to subject group allocation. LVEF was calculated using semi-quantitative assessment with 16 segment wall motion scoring [27].

CHD was defined as a) previous myocardial infarction, b) symptoms of angina pectoris with evidence of reversible myocardial ischaemia or c) evidence of coronary heart disease at coronary arteriography.

2.2. Study design
Subjects attended the Clinical Investigation and Research Unit in the morning following a light breakfast. Subjects were asked to abstain from caffeine and tobacco for 12 h and to omit their morning medication prior to their visit. Vascular function studies were carried out in a quiet, temperature-controlled (21-23 °C) room with subjects in the supine position, following at least 30 min of rest.

Arterial compliance was assessed using applanation tonometry to measure aortic pulse wave velocity. Applanation tonometry was not technically possible in one patient from the HF-RSF group. Cutaneous microvascular function was assessed using Laser Doppler imaging (LDI) coupled with transcutaneous iontophoresis of the vasodilators acetylcholine (ACh, endothelium-dependent) and sodium nitroprusside (SNP, endothelium-independent). Forearm venous capacitance was measured in all patients with venous occlusion plethysmography.

2.3. Blood pressure and heart rate measurement
Heart rate and one brachial blood pressure measurement was recorded over a 30 s time period. These measurements were performed 3 times for each subject and averaged.

2.4. Pulse wave velocity protocol
Aortic pulse wave velocity (PWV) was measured using a high fidelity micromanometer (SPC-301; Millar Instruments, Texas, USA) coupled with the SphygmoCor– system (SphygmoCor BPAS; PWV Medical, Sydney, Australia). A hand-held micromanometer-tipped probe was applied to the skin overlying the carotid and femoral arteries in turn, at the point of maximal arterial pulsation. The pulse wave recorded at each point was gated to a simultaneous electrocardiogram. This information, along with the measured body surface distance between the two points, was assimilated by the software program to calculate PWV in meters per second (m/s). This measurement was repeated 3 times and the average PWV was taken for analysis [28,29].

2.5. Venous occlusion plethysmography protocol
Forearm venous capacitance (VC) was measured with venous occlusion plethysmography, as we have previously described [30].

2.6. Laser Doppler imaging and iontophoresis protocol
Iontophoresis combined with laser Doppler imaging was performed as previously reported by our group [31-33].

Drugs used: 2.5 ml of 1% acetylcholine chloride (Sigma Chemical Co., St. Louis, MO, U.S.A.) was introduced into the anodal chamber. 2.5 ml of 1% sodium nitroprusside (Sigma) was introduced into the cathodal chamber. The vehicle for both drugs was 0.5% sodium chloride solution.

2.7. Power calculation and statistical analysis
We performed the power calculation for this study using data from a prior validation study in our department using the SphygmoCor– device to measure PWV. Between-patient standard deviation was 1.2 m/s. Therefore to detect a difference in PWV between groups of at least 1.7 m/s, with 90% power, using ANOVA with post-test correction for multiple comparisons, 11 subjects per group were required. Significance level was set at 5% (between group differences were considered significant if p value less than 0.05). Data were collated with Microsoft Excel Software for Windows (Microsoft Corp., Seattle, Washington). Statistical analysis and figure preparation was performed using Prism Graphpad software (Graphpad software Inc., San Diego, California, USA). Baseline characteristics of patients were summarized by mean (standard deviation) for continuous variables and by frequency for categorical variables. Comparisons of continuous variables between groups were made using t-tests and analysis of variance (ANOVA) with Bonferroni correction for multiple comparisons. Data are presented as mean [standard deviation] in the text and as box (median and inter-quartile ranges) and whisker (range) plots in figures.


   3. Results
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
4. Discussion
 5. Conclusions
 References
 
Baseline characteristics and concomitant medications are shown in Table 1.


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  		Table 1 Baseline characteristics

 
The proportion of women was higher in the HF-PSF group than in both the HF-RSF and control groups. Patients with HF-PSF were older than controls, but not patients with HF-RSF. The use of medications known to modify vascular smooth muscle and endothelial function, particularly angiotensin converting enzyme inhibitors (ACEI), angiotensin receptor blockers (ARB), HMG Co-A reductase inhibitors, aspirin and beta-blockers, was similar between groups. The main difference in medications between groups was the higher use of diuretics in both heart failure groups, compared with controls. All three groups had similar total serum cholesterol levels.

NT pro-BNP was significantly elevated in both the HF-PSF and HF-RSF groups compared with controls (p<0.05), in keeping with the clinical diagnosis of HF (Table 1). There was a trend to a higher mean plasma concentration of NT pro-BNP in patients with HF-RSF than was observed in the HR-PSF group (NT pro-BNP 1416.1 [1033.7] pmol/l vs. 894.2 [446.9] pmol/l, respectively). However, this difference was not statistically significant (p=0.12, t-test) and was accounted for by one outlier in the HF-RSF group, who had a plasma NT pro-BNP concentration of 4319 pmol/l. NYHA functional class and Boston score were similar in both HF groups.

3.1. Heart rate, blood pressure and pulse pressure
HF-PSF subjects had a significantly lower mean heart rate than both HF-RSF and control subjects (51.6 [6.1], 60.3 [8.5] and 60 [8] beats per minute respectively, p<0.05). The majority of patients had a history of essential hypertension, the frequency of which was similar in all groups (Table 1). Mean values for systolic blood pressure, diastolic blood pressure and mean arterial pressure did not differ significantly between groups (p=ns, Table 1). Mean pulse pressure (PP) was significantly higher in HF-PSF than in HF-RSF: 75.6 [8.2], 61.3 [17] mm Hg respectively, p<0.05 (Fig. 1).


Figure 01
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  		Fig. 1 Mean pulse pressure compared by patient group. The mean pulse pressure of subjects with heart failure and preserved systolic function (HF-PSF) was significantly higher than subjects with heart failure and reduced systolic function (HF-RSF) when compared with analysis of variance (ANOVA) despite no significant difference in mean arterial pressure (Table 1).

 
3.2. Aortic pulse wave velocity
PWV was not recordable in one male patient from the HF-RSF group.

PWV was significantly higher in HF-PSF subjects than in both HF-RSF and control groups: 10.7 [1.1], 8.9 [1.7] and 8.6 [2.1] m/s respectively, p<0.05 (Fig. 2).


Figure 02
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  		Fig. 2 Mean aortic pulse wave velocity (PWV) in meters per second (m/s) compared by patient group. PWV was significantly higher in subjects with heart failure and preserved systolic function (HF-PSF) than both heart failure and reduced systolic function (HF-RSF) and control groups, p<0.05, analysis of variance (ANOVA).

 
3.3. Peripheral microvascular responses
Vasodilatation in response to acetylcholine was similar in both HF groups. Both HF groups displayed an impaired vasodilator response to acetylcholine compared with controls (HF-RSF vs. control p=0.0003, HF-PSF vs. control p=0.00099, ANOVA) as illustrated in Fig. 3a. The HF groups also had similar peripheral vasodilatation responses to sodium nitroprusside. These endothelium-independent responses were also significantly reduced when compared with controls (HF-RSF vs. control p=0.012, HF-PSF vs. control p=0.006, ANOVA), as demonstrated in Fig. 3b.


Figure 03
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  		Fig. 3 Peripheral microvascular responses to acetylcholine (ACh) (a) and sodium nitroprusside (SNP) (b). Laser Doppler measurement of vasodilatation is expressed as arbitrary perfusion units (PU). Cumulative charge in micro-Coulombs (mC) is the total charge delivered during iontophoresis. Both heart failure groups (preserved systolic function, HF-PSF, represented by triangles, and reduced systolic function, HF-RSF, represented by squares) had impaired responses to endothelium-dependent (ACh) and -independent (SNP) vasodilatation compared with controls (represented by open circles). Responses to ACh compared by repeated measures 2-way analysis of variance: control vs. HF-PSF p=0.00099, control vs. HF-RSF p=0.0003, HF-PSF vs. HF-RSF p=ns. Responses to SNP compared by 2-way analysis of variance: control vs. HF-PSF p=0.006, control vs. HF-RSF p=0.012, HF-PSF vs. HF-RSF p=ns.

 
3.4. Venous occlusion plethysmography
VC was higher in HF-RSF subjects compared with HF-PSF subjects: 1.75 [0.41], 1.34 [0.34] ml/100 ml forearm vol. respectively, p<0.05, ANOVA (Fig. 4).


Figure 04
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  		Fig. 4 Venous capacitance (VC) compared by patient group. VC was significantly higher in subjects with heart failure and reduced systolic function (HF-RSF) than in subjects with heart failure and preserved systolic function (HF-PSF) when compared with analysis of variance (ANOVA).

 

   4. Discussion
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
5. Conclusions
 References
 
In this study, we have shown that patients with HF-PSF have a greater abnormality of arterial compliance than patients with HF-RSF and appropriate controls. We have also shown that patients with HF-PSF have profoundly reduced peripheral microvascular vasodilator function.

A notable finding was that HF-PSF was associated with elevation of PWV, which is related to the properties of the vessel wall by the Moens-Korteweg equation, and has long been accepted as a surrogate marker of arterial compliance and vascular remodelling [34]. Although pulse pressure has been reported to be increased in patients with HF-PSF, this is, to our knowledge, the first report of increased PWV in HF-PSF. More importantly, PWV was significantly elevated in our cohort of patients with HF-PSF, compared to controls and patients with HF-RSF, despite all three groups of patients being matched for underlying arterial disease (i.e. having CHD), implying that HF-PSF is indeed associated with greater impairment of arterial compliance. Supporting this theory is the fact that patients with HF-PSF had a significantly higher PP than patients with HF-RSF, independent of mean arterial pressure. PP is closely related to PWV. As PWV rises, pulse waves are reflected from the peripheral vasculature to the proximal aorta earlier in the cardiac cycle, augmenting central arterial pressure during systole rather than diastole, resulting in elevated central PP [35]. PP is also influenced by height and age, with central pressure augmentation being more marked in shorter, older individuals [36]. This may be important in HF-PSF patients who are more likely to be older and female, as noted in epidemiological studies [1,2].

Another factor influencing pulse pressure, albeit to a lesser degree than PWV, is heart rate, with slower heart rates resulting in higher pulse pressures [37]. Our patients with HF-PSF had slower heart rates than the other two groups and this may have contributed to the elevated pulse pressure values observed in this particular cohort.

We also found that HF-PSF subjects have impaired microvascular responses to both acetylcholine and sodium nitroprusside, which to our knowledge has not been shown before. This suggests that, rather than being solely a primary disorder of endothelial function, impaired control of vascular tone in HF-PSF reflects significant vascular smooth muscle dysfunction. Impaired responses to both endothelial-dependent and-independent vasodilators has been previously demonstrated in some [38-42], but not all [43-45] studies in patients with HF-RSF. This pattern of responses has not been reported before in patients with HF-PSF.

Vascular endothelial dysfunction has been extensively demonstrated in patients with HF-RSF and several potential mechanisms have been investigated. One of the most important potential mechanisms causing endothelial dysfunction is oxidative stress, leading to production of reactive oxygen species and inactivation of nitric oxide, a key factor in the control of vasomotor tone [46]. There is a significant body of evidence suggesting that oxidative stress is an important pathophysiologic process in the development of arterial endothelial dysfunction in HF-RSF [47,48]. We demonstrated that skin microvascular responses to endothelium dependent and independent vasodilators were similarly impaired in HF-PSF and HF-RSF groups. Although it is possible that the mechanisms causing impaired vascular reactivity are similar in both types of HF, evidence is currently lacking. Further studies of the mechanisms causing vascular endothelial and smooth muscle dysfunction in HF-PSF are required to clarify this issue.

We also studied venous capacitance. At first sight, the most curious observation in our study might be that venous capacitance appeared to be lower in the controls than in patients with HF-RSF. Perhaps the more interesting finding was that our patients with HF-PSF had a similar VC to the controls and lower VC than patients with HF-RSF. Patients with HF-PSF are more sensitive to the effects of vasodilators and diuretics on LV filling pressures, suggesting an abnormality of VC [23,24]. Higher VC will result in a greater capacity of the circulation to accommodate a larger circulating volume without resulting in elevation of the LV end diastolic pressure (LVEDP) [49]. It has been shown that patients with HF-RSF display a preserved venodilator response to atrial natriuretic peptide [50] and an appropriate VC rise in response to nitric oxide [51] despite impairment of arterial endothelial function. Patients with HF-PSF may have a reduced venous response to endogenous nitric oxide leading to a failure to increase VC—which could then be considered to be a dysfunctional response. Another possibility is that our cohort of patients with HF-PSF had higher resting venous pressure than patients with HF-RSF. This would result in measurements starting at a steeper point on the venous compliance curve, and less change in venous volume in response to congesting pressure. Our findings raise the possibility that patients with HF-PSF have an abnormality of venous function, but we have not defined the exact role of the venous bed in the pathophysiology of HF-PSF. Further investigation of venous function in HF-PSF is warranted.

There are three limitations to this study. The first is the differences in age and gender between subject groups. This reflects the demographics of patients with HF-PSF, who tend to be older females, as noted in previous studies [1,2]. We feel that it would be artificial to try and precisely match patients with HF-PSF to those with HF-RSF as that would result in a comparison of atypical patients with HF-PSF. In this sense our samples are probably representative of the populations from which they are drawn. We accept, however, that differences in age and gender between groups in our study may have influenced our results. The second limitation of this study is the relatively small sample size. Although we demonstrated clear differences in vascular function between subject groups, our sample size does not allow for formal regression analysis to correct for potentially confounding variables, such as age and gender. The third limitation of this study is that we did not assess ventriculo-vascular coupling directly. We feel that demonstrating preserved LV systolic function and reduced arterial compliance in patients with HF-PSF supports our hypothesis that impaired ventriculo-vascular coupling may be implicated in the pathophysiology of HF-PSF. Although the focus of this study was to assess and compare vascular function in patients with HFPSF and HF-RSF using non-invasive techniques, we accept that invasive assessment of arterial and ventricular elastance would have strengthened our findings.


   5. Conclusions
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
 5. Conclusions
References
 
Patients with HF-PSF have more marked impairment of arterial compliance, as evidenced by elevated PWV and PP, when compared to patients with HF-RSF and appropriate controls. Peripheral microvascular vasodilatation is markedly impaired in HF-PSF. The higher VC in the HF-RSF group, compared to HF-PSF patients, may represent an abnormality of venous function in HF-PSF. Our findings suggest that arterial stiffness, dynamic vasodilator function and venous abnormalities may be implicated in the complex pathophysiology of HF-PSF.


   References
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
 5. Conclusions
 References
 

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