Article, Cardiology

The utility of inferior vena cava diameter and the degree of inspiratory collapse in patients with systolic heart failure

a b s t r a c t

Introduction: Both inferior vena cava diameter and the degree of inspiratory collapse are used in the estima- tion of right atrial pressure.

Aim: The purpose of this study is to evaluate the utility of IVC diameter, using echocardiography as a marker of volume overload and the relationship between these parameters and N-terminal pro-B natriuretic peptide (NT-proBNP) in patients with systolic heart failure .

Methods: We included 136 consecutive patients with systolic HF (left ventricular ejection fraction, b 50%), includ- ing 80 patients with acutely decompensated HF and 56 patients with compensated HF as well as 50 subjects without a diagnosis of HF. All patients underwent transthoracic echocardiography to assess both their IVC diam- eters and the degree of inspiratory collapse (>=50%, b 50%, and no change [absence] groups); Nt-proBNP levels were measured, and these data were compared between the 2 groups.

Results: inferior vena cava diameter and NT-proBNP were significantly higher among the patients with HF than among the Control subjects (21.7 +- 2.6 vs 14.5 +- 1.6 mm, P b .001 and 4789 [330-35000] vs 171 [21-476], P b

.001). The mean IVC diameter was higher among the patients with decompensated HF than among the patients with compensated HF (23.2 +- 2.1 vs 19.7 +- 1.9 mm, P b .001). The values of NT-proBNP were associated with different collapsibility of IVC subgroups among HF patients. The NT-proBNP levels were 2760 (330-27336), 5400 (665-27210), and 16806 (1786-35000), regarding the collapsibility of the IVC subgroups: greater than or equal to 50%, less than 50%, and absence groups, P b .001, respectively, among HF patients. There was a signif- icant positive correlation between IVC diameter and NT-proBNP (r = 0.884, P b .001). A cut off value of an IVC diameter greater than or equal to 20.5 mm predicted a diagnosis of compensated HF with a sensitivity of 90% and a specificity of 73%.

Conclusions: Inferior vena cava diameter correlated significantly with NT-proBNP in patients with HF. Inferior vena cava diameter may be a useful variable in determining a patient’s volume status in the setting of HF and may also enable clinicians to distinguish patients with decompensated HF from those with compensated HF.

(C) 2015

Introduction

heart failure has become increasingly common in society; the rising incidence of HF is a worsening Public health problem. In spite of advances in both HF diagnosis and treatment, the morbidity and mortal- ity of the disease remain high [1]. Among patients hospitalized after a traditional physical examination, there exist a number of difficulties in the evaluation of patients’ vascular volume loads. In patients with

* Corresponding author at: Duzce State Hospital, Cardiology Clinics, Duzce, Turkey. Tel.: +90 506 276 59 29; fax: +90 380 529 13 00.

E-mail address: [email protected] (F. Besli).

Acute decompensated HF, the measurement of both invasive pulmonary capillary wedge pressure and right atrial pressure is the criterion standard for making a diagnosis of HF, but they are not practical. Pro-B natriuretic peptide (pro-BNP) is extremely important in the diagnosis of HF as well as in patients admitted for acute decompensated systolic HF. In patients with acute decompensated HF, obtaining a series of pro-BNP measurements is useful during follow-up, as these values are compatible with the measurement of both invasive and noninvasive left ventricular (LV) filling pressures [2,3]. In addition, an ultrasono- graphic assessment of Inferior vena cava diameter may be an ob- jective, quantifiable means of measuring right atrial pressure [4]. Inferior vena cava diameter is a marker of venous congestion [5]. Inferi- or vena cava diameter may also reflect volume overload [6]. The use of the degree of IVC collapsibility (in response to intrathoracic pressure)

http://dx.doi.org/10.1016/j.ajem.2015.02.006

0735-6757/(C) 2015

in conjunction with IVC diameter provides clinicians with more accurate noninvasive information regarding right atrial pressure [4,7]. Pellicori et al [5] determined that IVC diameter was a strong predictor of Disease prognosis and provides information similar to that of N-terminal pro-B natriuretic peptide (NT-proBNP) among patients with HF.

In this study, we aimed to determine the utility of both IVC diameter and the degree of inspiratory collapse, using echocardiography as a marker of volume overload and the relationship between these parameters and NT-proBNP in patients with HF.

Methods

We included 136 consecutive patients admitted with a diagnosis of HF (including 80 patients with decompensated HF and 56 patients with compensated HF) as well as 50 subjects without a diagnosis of HF, who served as our control group, who visited either cardiology or the emergency department at Uludag University School of Medicine Hospital, Bursa, between 15th October 2012 and 15th April 2013. Informed consent was provided by each subject before beginning this study. The study conformed to the principles outlined in the Declaration of Helsinki and was approved by the appropriate ethics committee for clinical research. The clinical diagnosis of HF was made based on each patient’s clinical history, chest roentgenogram, electrocardiogram, and echocardiogram. The inclusion criteria included patients diagnosed with systolic HF (LV ejection fraction [EF], b 50%). The exclusion criteria for the study included subjects with isolated diastolic HF; Tricuspid valve stenosis; primary pulmonary hypertension; and pulmonary hy- pertension due to collagen tissue disease, congenital heart disease, acute coronary syndrome, and pulmonary disease (lung disease, chronic obstructive lung disease, asthma, either acute or Chronic pulmonary embolism, and pneumonia). Heart failure severity was evaluated clini- cally using the New York Heart Association classification. Outpatients with class I to II HF and no signs of congestion were placed into the com- pensated HF group. Decompensated HF was defined as an admission for worsening pertinent symptoms. [8] Subjects who presented to our de- partment and did not have the aforementioned signs or symptoms or any of the above exclusion criteria were included as members of the control group.

For each of the subjects enrolled in the study, age, sex, and medical

history (diabetes mellitus, hypertension, hyperlipidemia, additional diseases, smoking history, and medications) were determined via a chart review. NT-proBNP was measured using an enzyme-linked immunosorbent assay (Biovendor Laboratory Medicine INS, Brno, Czech Republic) performed at 4?C. The results were expressed as micrograms per milliliter.

Each echocardiogram was performed by 1 of 2 trained cardiologists, using a Vivid 3 model (Vivid 3 Echocardiography; General Electric, Milwaukee, WI). Using standard transthoracic windows, LV end- diastolic diameter, LV end-systolic diameter, and LV EF were each mea- sured [9]. In most patients, systolic function was determined using the EF obtained via 2-dimensional echocardiography, using the Modified SImpson rule, due to LV wall motion abnormalities. Inferior vena cava dimensions were measured in the subcostal view, 10 mm from the junction between the IVC and the right atrium, during quiet respiration. Respiratory collapse of IVC was described as being greater than or equal to 50%, less than 50%, or no change (absence) [4,10,11]. Clinicians blinded to each patient’s diagnosis of HF evaluated the images. The IVC diameters were measured by different clinicians blinded to each patient’s diagnosis.

A statistical analysis was performed using the Statistical Package for Social Sciences for Windows (version 13; SPSS, Chicago, IL). The base- line, echocardiographic, and laboratory characteristics of the study sub- jects are presented as percentages for the dichotomous variables and as the means +- SDs or as medians with interquartile ranges, for the con- tinuous variables, based on the distribution of the data. The categorical

variables are expressed as numbers and percentages. The continuous data with a normal distribution were compared using the Student t test and the analysis of variance, whereas the skewed data were com- pared using the Mann-Whitney U test and the Kruskal-Wallis test. The categorical variables were compared using the ?2 test. The degree of correlation between IVC size and the variables was measured using a correlation coefficient, using either a parametric or a nonparametric (Pearson and Spearman) coefficient. An analysis of variance was used to perform comparisons across the 3 groups regarding IVC collapse. Re- ceiver operating characteristics (ROC) curves were developed to assess the area under the curve to detect LV EFs less than 50% for both NT-proBNP and IVC dimensions. All probabilities were 2 tailed, and P values b .05 were considered statistically significant.

Results

We included 136 patients with HF and 50 subjects without HF, who served as the control group. The clinical characteristics of the study pop- ulation are included in Table 1; 69.1% of the patients with HF were male, and 33.3% of the patients had Atrial fibrillation . According to the New York Heart Association classification, 8.1% of the patients with HF were in class I, 33.1% of the patients were in class II, 43.4% of the patients were in class III, and 15.4% of the patients were in class IV (Table 1).

Compared with the controls, the patients with HF were older (63 +- 12.4 vs 56 +- 15.8, P = .008). In the HF group, both serum creatinine (1.1 +- 0.4 vs 0.8 +- 0.1, P b .001) and NT-proBNP (4789 [330-35000]

vs 171 [21-476], P b .001) levels were significantly higher than in the control group. The mean LV EF was 29.8% +- 7.7% among the patients with HF. Compared with the control subjects, the mean IVC diameter was significantly higher (21.7 +- 2.6 vs 14.5 +- 1.6 mm, P b .001). Regard- ing the respiratory collapse of the IVC, the percentage of patients with HF with either less than 50% or no collapse was higher than those of the control group (P b .001) (Table 1).

Among the 136 patients admitted to the hospital, 80 patients had de- compensated HF, and 56 patients had compensated HF. No significant differences in age, sex, cause of HF, AF frequency, and medications were noted between the 2 groups. In the decompensated HF group, both LV diastolic diameter (LVDD) (61.3 +- 7.7 vs 56.7 +- 7.8, P b .001)

Table 1

Baseline, echocardiographic, and laboratory characteristics of subjects

Control (n = 50)

HF (n = 136)

P

Age (y)

56.2 +- 15.8

63 +- 12.4

.007

Sex (female/male) (n)

Respiratory collapse of IVC (n) Absent

26/24

1

42/94

32

.008

b.001

b50%

11

53

>=50%

38

51

AF (n)

0

46

b.001

Medications (%)

acetylsalicylic acid

34

89

b.001

ACEI/ARB

40

85

b.001

?-blockers

34

80

b.001

Calcium-channel blockers

12

28

.019

Digoxin

0

33

b.001

Diuretics

functional capacity (%) Class I

0

50

92

8.1

b.001

Class II

0

33.1

b.001

Class III

0

43.4

Class IV

0

15.4

LV EF (%)

61.6 +- 5.3

29.8 +- 7.7

b.001

LVDD (mm)

43.6 +- 4.7

59.4 +- 8

.001

LVSD (mm)

29 +- 4.1

48.3 +- 9.8

b.001

IVC (mm)

14.5 +- 1.6

21.7 +- 2.6

b.001

NT-proBNP (pg/mL)

171 (21-476)

4789 (330-35000)

b.001

Hemoglobin level (mg/dL)

12.9 +- 1.3

12.3 +- 8.3

.577

Creatinine (mg/dL)

0.8 +- 0.1

1.1 +- 0.4

b.001

Abbreviations: ACEI, angiotensin-converting enzyme inhibitors; ARB, angiotensin receptor blockers.

Table 2

Baseline, echocardiographic, and laboratory characteristics of subjects with compensated and decompensated HF

Compensated HF (n = 56)

Decompensated HF P

(n = 80)

Fig. 2. The correlation between IVC diameter and NT-proBNP levels.

Age (y)

62.4 +- 11.2

62.2 +- 13.2

.37

Sex (female/male) (n) Respiratory collapse of IVC (n, %)

Absent

18/38

3 (5.4)

24/56

29 (36.2)

.79

b 50%

22 (39.2)

31 (38.8)

b.001

>=50%

31 (55.4)

20 (25)

AF (%)

30.4

36.2

.475

Medications (%)

Acetylsalicylic acid

91.1

88.8

.661

ACEI/ARB

85.7

85

.908

?-blockers

80.4

81.2

.896

Calcium-channel blockers

28.6

28.8

.982

Digoxin

32.1

35

.729

Diuretics

89.3

96.2

.108

Others

8.9

10

.834

Etiology of HF (%)

Ischemic cardiomyopathy

75

62.5

.125

dilated cardiomyopathy

25

37.5

LV EF

33.5 +- 7.4

27.2 +- 6.9

b.001

LVDD (mm)

56.7 +- 7.8

61.3 +- 7.7

.001

LVSD (mm)

45 +- 9.4

50.7 +- 9.5

.001

IVC (mm)

19.7 +- 1.9

23.2 +- 2.1

b.001

NT-proBNP (pg/mL)

1945 (330-8278)

11428 (1786-35000)

b.001

Hemoglobin level (mg/dL)

13.8 +- 2.7

11.2 +- 1.9

.085

Creatinine (mg/dL)

1 +- 0.3

1.2 +- 0.5

.023

and LV systolic diameter (LVSD) (50.7 +- 9.5 vs 45 +- 9.4, P = .001) were significantly higher; LV EF (27.2 +- 6.9 vs 33.5 +- 7.4, P b .001) was lower than in the patients with compensated HF. Among the patients with de- compensated HF, serum NT-proBNP was significantly higher than among the patients with compensated HF (11 428 [1786-35000] vs 1945 [330-8278], P b .001) (Table 2).

The mean IVC diameter was higher in the patients with decompen- sated HF than in the patients with compensated HF (23.2 +- 2.1 vs 19.7

+- 1.9 mm, P b .001). Regarding the respiratory collapse of the IVC, the percentage of patients with either less than 50% or no collapse in de- compensated HF was higher than that of the patients with compensated HF (P b .001) (Table 2).

The NT-proBNP and IVC diameter values were associated with differ- ent collapsibility among the IVC subgroups. Although the collapsibility of the IVC decreased, both serum NT-proBNP and the IVC diameter sig- nificantly increased among HF patients. The IVC diameters were 20.1 +-

Fig. 1. N-terminal pro-B natriuretic peptide level based on the degree of inspiratory col- lapse among HF patients.

2.0, 21.9 +- 2.3, and 24.2 +- 2.0, P b .001; and the NT-proBNP levels were 2760 (330-27336), 5400 (665-27210), and 16806 (1786-35000), re-

garding the collapsibility of the IVC subgroups as follows: greater than or equal to 50%, less than 50%, and absent groups, P b .001 (Fig. 1).

Inferior vena cava diameter significantly and positively correlated with NT-proBNP in all patients (r = 0.884 and P b .001) (Fig. 2). In ad- dition, IVC diameter correlated positively with age (r = 0.201, P =

.006), LVDD (r = 0.645, P b .001), LVSD (r = 0.659, P b .001), and

serum creatinine (r = 0.357, P b .001) and correlated negatively with LV EF (r = -0.802, P b .001).

An ROC analysis was undertaken for serum NT-proBNP; the “cut off” value was 2755 ug/mL for NT-proBNP, with a sensitivity of 96% and a specificity of 77%, in distinguishing patients with decompensated HF from patients with compensated HF. Regarding IVC diameter, the “cut off” value was greater than or equal to 20.5 mm, with a sensitivity of 90% and a specificity of 73%, in distinguishing patients with decompen- sated HF from patients with compensated HF (Fig. 3).

Discussion

Our results indicated that the mean diameter of the IVC was higher among the patients with HF than among the control subjects and was also higher among the patients with decompensated HF than among the patients with compensated HF. Regarding the respiratory collapse of the IVC, the percentage of patients with either less than 50% or no col- lapse was higher among the patients with decompensated HF than among the patients with compensated HF. NT-proBNP correlated posi- tively with IVC diameter and negatively with the degree of inspiratory collapse. These findings indicate that both IVC diameter and the degree of inspiratory collapse may be associated with volume load among pa- tients with HF.

Patients presenting with dyspnea are evaluated in terms of weight gain, orthopnea, jugular venous distension, and heart gallops, as these parameters and findings enable clinicians to make a diagnosis of HF. B-type natriuretic peptide measurements are also helpful in making and confirming an accurate diagnosis [12]. Pro-BNP, a diuretic peptide, is synthesized in the ventricular myocardium; in response to systolic HF, which may be characterized by increased ventricular volume, in- creased end-diastolic pressure, and increased LV wall stress, it is re- leased into the plasma [13,14]. Pro-BNP levels increase with advancing stages of HF [15]. In our study, we observed that NT-proBNP levels were higher among patients with decompensated HF than among pa- tients with compensated HF. These findings indicate that volume loads are higher among patients with decompensated HF than among

Fig. 3. An ROC curve analyses of IVC diameter and NT-proBNP to differentiate between patients with decompensated HF and patients with compensated HF.

patients with compensated HF. NT-proBNP levels were higher in our study than in previous studies [16,17]. We speculated that this finding may be related to ethnicity. In addition, the socioeconomic level of our sample was low; therefore, our patients with HF were usually admitted to the hospital in advanced stages of HF.

Inferior vena cava diameter changes in response to both pressure fluctuations and volume overload in the right atrium [18]. The use of the degree of collapsibility of the IVC (in response to intrathoracic pres- sure) in conjunction with IVC diameter offers more accurate noninva- sive information regarding right atrial pressure [6,18,19,7]. In patients with hypervolemia, the IVC dilates and becomes less elastic due to alter- ations in venous return with inspiration [19]. Measuring the IVC rapidly provides clinicians with useful information, particularly in the emergen- cy department when evaluating patients with dyspnea of an unknown cause [20]. Among patients with signs of congestion, in particular, IVC diameter is an important indicator of volume load and correlates with pro-BNP among patients with HF [5,21,22]. In the study by Hebl et al [21], the correlation between IVC diameter and NT-proBNP was signifi- cant among patients with systolic HF compared with patients with diastolic HF. Furthermore, Pellicori et al [5] demonstrated that increased IVC diameter was associated with poor outcomes among patients with HF.

In our study, compared with the control group, IVC diameter was significantly higher in the HF group. The diameter of the IVC was higher among patients with decompensated HF than among patients with compensated HF. There was a significant positive correlation between IVC diameter and NT-proBNP; a negative correlation was noted be- tween IVC diameter and LV EF. In addition, the degree of collapse of the IVC correlated positively with NT-proBNP. These findings may be in- dicative of the usefulness of IVC diameter and the degree of inspiratory collapse as markers of volume overload in patients with systolic HF. In the study by Pellicori et al [5], the mean IVC diameter was 15 mm in pa- tients without HF and 19 mm in patients with HF; in the study by Hebl et al [21], the mean diameter was 18.5 mm in patients with HF. In our study, the mean IVC diameter was 21.7 mm in patients with HF and

14.5 mm in the control group. Hospitalization is a major problem in the setting of HF. The early de-

tection of these patients is very important. Elevated jugular venous

pressure has been associated with clinical symptoms in various studies but has also been found to vary among said studies. IVC diameter is an easier and more objective means of predicting right atrial pressure [18,23,24]. In HF, increased pulmonary capillary wedge pressure results in increased Pulmonary arterial pressure [25]. In addition, with the in- creases in pressure in both the right atrium and the right ventricle, the combination of neuroendocrine activation and the deterioration of renal perfusion and water and salt uptake causes an increase in the di- ameter of the IVC. Therefore, IVC diameter may be both an easy and con- venient means with which to identify congestion in the setting of HF.

To the best of our knowledge, ours was the first study to evaluate IVC collapsibility in patients with compensated and decompensated HF. Furthermore, the relationship between IVC diameter and natriuretic peptide was evaluated in patients with compensated HF and patients with decompensated HF. The IVC diameter was 23.2 +- 2.1 among the patients with decompensated HF and 19.7 +- 1.9 mm among the pa- tients with compensated HF. Based on our findings, a cut off value of an IVC diameter of greater than or equal to 20.5 mm predicted a diagno- sis of compensated HF with a sensitivity of 90% and a specificity of 73%. We believe that IVC diameter may be a useful method with which to dif- ferentiate between patients with decompensated HF and patients with compensated HF.

These findings demonstrated that assessing IVC diameter was valu- able in distinguishing between the decompensated HF group and the compensated HF group. To the best of our knowledge, our study was the first to compare IVC diameter and the collapsibility of the IVC be- tween patients with compensated HF and patients with decompensated HF. We believe that in addition to performing a clinical evaluation, mea- suring IVC diameter may be helpful in differentiating between patients with decompensated HF and patients with compensated HF.

Limitations

Our study had several limitations. First, patients with isolated diastolic HF were not included. Second, to assess both left and right ventricular fill- ing pressures, invasive hemodynamic measurements were not routinely applied in our study population. Third, right ventricular function could not be evaluated in detail. Finally, we did not perform serial IVC or NT-

proBNP measurements, nor did we collect information regarding medica- tions that may influence both NT-proBNP and IVC diameter during each patient’s index admission. Randomized, controlled trials are necessary, particularly studies that involve larger groups of patients.

Conclusion

Inferior vena cava diameter may be useful in determining volume status in the setting of HF and in distinguishing decompensated HF from compensated HF.

References

  1. Cleland JG, McDonagh T, Rigby AS, Yassin A, Whittaker T, Dargie HJ. National Heart Failure Audit Team for England and Wales. The national heart failure audit for England and Wales 2008-2009. Heart 2011;97:876-86.
  2. Dokainish H, Zoghbi WA, Lakkis NM, Ambriz E, Patel R, Quinones MA, et al. Incre- mental Predictive power of B-type natriuretic peptide and Tissue Doppler echocardi- ography in the prognosis of patients with congestive heart failure. J Am Coll Cardiol 2005;45:1223-6.
  3. Gackowski A, Isnard R, Golmard JL, Pousset F, Carayon A, Montalescot G, et al. Com- parison of echocardiography and plasma B-type natriuretic peptide for monitoring the response to treatment in acute heart failure. Eur Heart J 2004;25:1788-96.
  4. Kircher BJ, Himelman RB, Schiller NB. Noninvasive estimation of right atrial pressure from the inspiratory collapse of the inferior vena cava. Am J Cardiol 1990;66:493-6.
  5. Pellicori P, Carubelli V, Zhang J, Castiello T, Sherwi N, Clark AL, et al. IVC diameter in patients with chronic heart failure: relationships and prognostic significance. JACC Cardiovasc Imaging 2013;6:16-28.
  6. Pudil R, Tichy M, Praus R, Blaha V, Vojacek J. NT-proBNP and echocardiographic param- eters in patients with acute heart failure. Acta Medica (Hradec Kralove) 2007;50:51-6.
  7. Kimura BJ, Shaw DJ, Agan DL, Amundson SA, Ping AC, DeMaria AN. Value of a cardio- vascular limited ultrasound examination using a hand-carried Ultrasound device on clinical management in an outpatient medical clinic. Am J Cardiol 2007;100:321-5.
  8. Gheorghiade M, Zannad F, Sopko G, Klein L, Pina IL, Konstam MA, et al. Acute heart failure syndromes: current state and framework for future research. Circulation 2005;112:3958-68.
  9. Lang RM, Bierig M, Devereux RB, Klein L, Pina IL, Konstam MA, et al. Recommenda- tions for chamber quantification: a report from the American Society of Echocardiography’s guidelines and standards committee and the chamber quantifi- cation writing group, developed in conjunction with the European Association of Echocardiography, a branch of the European Society of Cardiology. J Am Soc Echocardiogr 2005;18:1440-63.
  10. Blehar DJ, Dickman E, Gaspari R. Identification of congestive heart failure via respira- tory variation of inferior vena cava diameter. Am J Emerg Med 2009;27:71-5.
  11. Fields JM, Lee PA, Jenq KY, Mark DG, Panebianco NL, Dean AJ. The interrater reliability of inferior vena cava ultrasound by bedside clinician sonographers in emergency department patients. Acad Emerg Med 2011;18:98-101.
  12. Wang CS, FitzGerald JM, Schulzer M, Mak E, Ayas NT. Does this dyspneic patient in the emergency department have congestive heart failure? JAMA 2005;294: 1944-56.
  13. Iwanaga Y, Nishi I, Fuoruichi S, Noguchi T, Sase K, Kihara Y, et al. B-type natriuretic peptide strongly reflects diastolic wall stress in patients with chronic heart failure: comparison between systolic and Diastolic heart failure. J Am Coll Cardiol 2006;47: 742-8.
  14. Yasue H, Yoshimura M, Sumida H, Kikuta K, Kugiyama K, Jougasaki M, et al. Localization and mechanism of secretion of B- type natriuretic peptide in compari- son with those of A-type natriuretic peptide in normal subjects and patients with heart failure. Circulation 1994;90:195-203.
  15. Karabulut A, Kaplan A, Aslan C, Iltumur K, Toprak G, Toprak N. The association between NT-proBNP levels, functional capacity and stage in patients with heart fail- ure. Acta Cardiol 2005;60:631-8.
  16. Januzzi Jr JL, Camargo CA, Anwaruddin S, Baggish AL, Chen AA, Krauser DG, et al. The N-terminal Pro-BNP investigation of dyspnea in the emergency department (PRIDE) study. Am J Cardiol 2005;95(8):948-54.
  17. Kim HN, Januzzi Jr JL. Natriuretic peptide testing in heart failure. Circulation 2011 May 10;123(18):2015-9.
  18. Stein JH, Neumann A, Marcus RH. Comparison of estimates of right atrial pressure by physical examination and echocardiography in patients with congestive heart failure and reasons for discrepancies. Am J Cardiol 1997;80:1615-8.
  19. Jardin F, Vieillard-Baron A. Ultrasonographic examination of the venae cavae. Inten- sive Care Med 2006;32:203-6.
  20. Jang T, Aubin C, Naunheim R, Char D. Ultrasonography of the internal jugular vein in patients with dyspnea without jugular venous distension on physical examination. Ann Emerg Med 2004;44:160-8.
  21. Hebl V, Zakharova MY, Canoniero M, Duprez D, Garcia S. Correlation of natriuretic peptides and inferior vena cava size in patients with congestive heart failure. Vasc Health Risk Manag 2012;8:213-8.
  22. Goonewardena SN, Gemignani A, Ronan A, Vasaiwala S, Blair J, Brennan JM, et al. Comparison of hand-carried ultrasound assessment of the inferior vena cava and N-terminal pro-brain natriuretic peptide for predicting readmission after hospi- talization for acute decompensated heart failure. Am Coll Cardiol Img 2008;1: 595-601.
  23. Drazner MH, Rame JE, Stevenson LW, Dries DL. Prognostic importance of elevated jugular venous pressure and a third heart sound in patients with heart failure. N Engl J Med 2001;345:574-81.
  24. Drazner MH, Hellkamp AS, Leier CV, Shah MR, Miller LW, Russell SD, et al. Value of clinician assessment of hemodynamics in advanced heart failure: the ESCAPE trial. Circ Heart Fail 2008;1:170-7.
  25. Damy T, Goode KM, Kallvikbacka-Bennett A, Lewinter C, Hobkirk J, Nikitin NP, et al. Determinants and prognostic value of pulmonary arterial pressure in patients with chronic heart failure. Eur Heart J 2010;31:2280-90.

Leave a Reply

Your email address will not be published. Required fields are marked *