Abstract
Background
Inferior vena cava (IVC) ultrasonography has been used for the diagnosis and prognosis of acute heart failure (HF). Its usefulness in chronic HF is less known.
Hypothesis
IVC ultrasonography is a useful tool in the care of patients with chronic HF.
Methods
For this prospective cohort study, 95 patients with chronic HF were included consecutively as they attended scheduled medical visits. Ultrasound was done with a 5‐MHz convex probe device, calculating IVC collapse index (IVCCI). Follow‐up time was 1 year. Outcome events were worsening HF, hospital admission for HF, HF mortality, and all‐cause mortality.
Results
Worsening HF occurred in 70.9% of patients with IVCCI <30% and 39.1% of patients with IVCCI >50%, with a hazard ratio (HR) of 2.8 (95% CI: 1.3–6.2) adjusted by multivariable analysis. Regarding hospitalization, 45.3% of patients with IVCCI <30% required admission, compared with 5.9% of patients with IVCCI >50%; the adjusted HR was 13.9 (95% CI: 1.7–113.0). Mortality was higher in the IVCCI <30% group, with 25.7% all‐cause mortality and 18.6% HF mortality, whereas in the IVCCI >50% group these values were 13% and 4.7%, respectively. However, these differences did not reach statistical significance. ROC analysis was performed and the AUC for IVCCI was not higher than that for NTproBNP for any of the outcomes studied.
Conclusions
IVC ultrasonography is a useful tool in follow‐up of patients with chronic HF, allowing identification of patients at high risk of worsening and hospitalization. However, its usefulness is not higher than that of NTproBNP.
Keywords: Chronic Heart Failure, Inferior Vena Cava, POCUS, Ultrasonography
1. INTRODUCTION
Heart failure (HF) is a prevalent chronic disease that is the leading cause of hospitalization among patients age >65 years.1 Acute decompensated HF (ADHF), characterized by volume overload and secondary congestive signs, is the principal cause of admission for patients with HF. Knowing outpatients' volume status to adjust treatment and to avoid decompensation is a challenge. Physical examination and radiological findings have a limited value for estimating the volemia status.2, 3 Alternatively, several studies have shown a good correlation between volume overload and natriuretic peptides in HF. However, although the cutoff point of natriuretic peptides for ADHF diagnosis is well established, values for outpatients with chronic HF are less defined.4
Alternatively, inferior vena cava (IVC) ultrasonography is a simple and useful tool in patients with HF. An increase in IVC diameter or a reduction of IVC inspiratory collapse allow detection of volume overload. Therefore, these parameters have been proposed in the management of HF, based on their capacity to detect hemodynamic congestion. IVC ultrasound is a simple technique with a short learning curve. There is an excellent degree of reproducibility and agreement between scans performed by expert sonographers and health professionals with minimal training.5, 6
IVC diameter has been correlated with atrial and left ventricular filling pressures7, 8, 9, 10, 11 and N‐terminal pro‐B‐type natriuretic peptide (NTproBNP) values.12 Consensus documents recommended for the diagnosis of ADHF a degree of collapse <50% or a maximum IVC diameter of >20 mm.13 Several studies have shown the power of IVC ultrasonography for diagnosis of ADHF in patients with dyspnea in the emergency department, either alone14, 15 or in combination with lung ultrasound.16, 17, 18 Other studies suggest the capacity of IVC ultrasonography to differentiate between ADHF and stable chronic HF.19 Besides, in ADHF patients, IVC diameter at admission has shown prognosis utility for readmission, renal impairment, and mortality.20, 21, 22, 23 IVC diameter has been correlated with the clinical evolution of ADHF, showing improvement in diameter and collapsibility after diuretic treatment.24, 25, 26, 27, 28 Finally, other studies have demonstrated the prognosis power of IVC ultrasonography, prior to discharge after hospitalization for ADHF, to predict readmission.29, 30
Despite extensive research in this area, the role of IVC ultrasonography in chronic HF is less studied and cutoff points for outpatients with stable chronic HF are not established. Patients with long‐term chronic HF could present altered vena cava dimensions despite being in normovolemic states. But on the other hand, this tool could reveal data of subclinical congestion in outpatients with chronic HF. Given the difficulty of knowing the volemia status of patients with chronic HF, IVC ultrasound could be a powerful tool to optimize treatment and prevent hospitalization and death. Khandwalla et al. found a strong relationship between IVC diameter and the risk of hospitalization for ADHF in patients with chronic HF.31 However, they did not evaluate the predictive utility of IVC ultrasonography for mortality, or compare it with natriuretic peptides. Nath et al. measured the IVC diameter in patients undergoing ambulatory echocardiography and demonstrated a relationship between this parameter and all‐cause mortality, but they did not compare it with natriuretic peptides.32 Pellicori et al. have shown in several articles the poor prognosis of this measurement in relation to the dilation of IVC in patients with chronic HF. For this purpose, they used a variable that combined hospital admission for HF and death due to cardiovascular causes.33, 34, 35 In one of these studies they compared the IVC measurement with natriuretic peptides, demonstrating similar utility.33
The aim of this study is to analyze the usefulness of IVC ultrasonography parameters in patients with chronic HF to predict HF worsening, hospital admission, and death, and to compare it with NTproBNP.
2. METHODS
We conducted a prospective cohort study at University Hospital La Princesa in Madrid, Spain. The study received approval from the Research Ethics Committee of the hospital and was performed according to the principles outlined in the Declaration of Helsinki.
We included outpatients with chronic HF attending a specialist clinic between May 2014 and April 2015. A written consent was required prior to enrollment. Inclusion criteria were age > 18 years and prior diagnosis of HF. Diagnosis of chronic HF was made through the history of decompensation with compliance with Framingham criteria and increase of NTproBNP levels adjusted for age, and the presence of structural heart disease demonstrated by echocardiogram. Patients who had been admitted to hospital within the 3 months prior to recruitment were excluded.
2.1. Data collection
Patients were included consecutively as they attended scheduled medical visits. Recruitment was performed between May 2014 and April 2015. Clinical routine data were collected, such as age at inclusion, sex, comorbidities, atrial fibrillation (AF), etiology of cardiac disease, echocardiographic data, and current treatment. Clinical routine visit procedures included the assessment of congestive symptoms (dyspnea, edema), New York Heart Association functional class, general physical examination, weight, and height. Various analytical parameters were recorded, including hemoglobin, creatinine, estimated glomerular filtrate rate (eGFR), ionogram, and NTproBNP levels.
2.2. IVC ultrasound
Ultrasound study was conducted in the right paramedian longitudinal plane using a 5‐MHz convex probe device (SonoSite Inc., Bothell, WA). An intercostal plane was used if the longitudinal plane was not feasible. IVC diameter was measured 2 cm from the junction with the right atrium. Using M‐mode ultrasound display, the maximum IVC diameter (maxIVC) and minimum IVC diameter (minIVC) were determined during a nonforced breathing cycle. The IVC collapse index (IVCCI) was calculated as a change in diameter between inspiration and expiration divided by maximum diameter [(maxIVC – min IVC) / maxIVC]. Ultrasound study was performed by one of the investigators with advanced training in the technique. This physician was not involved in the medical management of study subjects. Results were blinded to patients and medical staff attending.
2.3. Follow‐up
Follow‐up time for each patient was 1 year after inclusion date. Outcome events checked were worsening HF, defined as an increase in the dose of diuretic required because of symptoms; HF hospital admission; HF mortality; and all‐cause mortality. Data regarding HF hospitalizations or deaths were confirmed through patients' follow‐up and review of patients' electronic medical records. All‐cause mortality was confirmed through the institution's electronic medical records and the Social Security Death Index.
2.4. Statistical analysis
Classically, the IVC parameters cutoff points for the diagnosis of ADHF are 2 cm for maxIVC and 50% for IVCCI.13 Several authors have suggested smaller cutoff points for the diagnosis of ADHF.14, 15 IVC reference values for the follow‐up of chronic HF are not established and the tendency is to equate them with those of acute HF. Due to this, and under medical criteria, the patients were initially divided into 3 groups using IVCCI as reference parameter: patients with IVCCI >50% (without hypervolemia), IVCCI between 30% and 50% (mild hypervolemia), and IVCCI <30% (moderate/severe hypervolemia). We chose IVCCI as reference parameter because it is the most used in the different studies. It also corrects observer‐dependent variability in minimum or maximum IVC measurements. Another reason for this choice was to reduce the potential bias of chronic HF, which can cause chronic stasis and dilatation of IVC without accompanying congestive status. In any case, data of the utility of minIVC and maxIVC are also shown.
Qualitative variables were expressed as percentages; continuous variables were expressed as mean ± SD (or median and interquartile range, in the case of NTproBNP). Differences in qualitative variables were analyzed using the χ2 test, or Fisher exact test when the expected frequency was <5. Quantitative variables were analyzed by analysis of variance (ANOVA) test, taking into account the homogeneity and normality of the distribution. Non–normally distributed data, as in the case of NTproBNP, were analyzed using the Kruskal‐Wallis test. The relationships between IVC parameters and other variables were assessed by Pearson or Spearman correlation coefficients.
Kaplan–Meier curves with log‐rank statistic were made, and hazard ratios (HR) were calculated using the group with IVCCI >50% as reference. Associations between IVCCI and outcome events were analyzed with Cox proportional hazards models adjusting for age, sex, AF, tricuspid regurgitation, and other potentially confounding variables that showed differences between groups with P < 0.2. To compare prognosis accuracy of IVC parameters and NTproBNP, receiver operating curve (ROC) analysis was plotted and areas under the curve (AUC) were performed and compared for each outcome variable. Statistical calculations were performed with Stata software version 13.0 (StataCorp LP, College Station, TX).
3. RESULTS
Ninety‐nine cases of chronic HF were identified for inclusion. However, in 4 of them, we could not obtain ultrasound parameters of IVC due to poor visibility. Therefore, the final study population consisted of 95 patients. Baseline characteristics are presented in Table 1. The majority were female (58.9%), with high average age (84.3 ± 6.4 years) and with high prevalence of arterial hypertension (92.6%), AF (75.8%), and HF due to diastolic dysfunction (64.2%). HF with reduced ejection fraction was present in 14.8% of patients. Regarding IVC collapsibility, 24.2% presented with IVCCI >50%; 38.9% with IVCCI 30% to 50%; and 36.8% had IVCCI <30%. There were no clinically or statistically significant differences between groups in terms of age, comorbidities, treatment, or characteristics of heart disease (Table 1). There were also no differences in clinical semiology or analytical parameters except for NTproBNP. This showed higher levels in those patients with lower degrees of IVC collapse (849 pg/mL vs 1693 pg/mL vs 2655 pg/mL; P = 0.02). IVCCI showed a significant correlation with NTproBNP, with a coefficient of −0.23 (P = 0.01). However, there was no significant correlation between IVCCI and left ventricular ejection fraction (LVEF; coefficient 0.11, P = 0.315) or eGFR (coefficient 0.12, P = 0.261; Figure 1). On the other hand, NTproBNP showed significant correlation with both LVEF (coefficient − 0.27, P = 0.013) and eGFR (coefficient − 0.36, P < 0.001).
Table 1.
Clinical characteristics, laboratory parameters, and medications of study population
| Total, N = 95 | IVCCI ≥50%, n = 23 | IVCCI 30%–50%, n = 37 | IVCCI <30%, n = 35 | P Value | |
|---|---|---|---|---|---|
| Age, y | 84.3 ± 6.4 | 83.8 ± 7.7 | 84.7 ± 5.9 | 84.2 ± 6.2 | 0.871a |
| Female sex | 56 (58.9) | 13 (56.5) | 23 (62.2) | 20 (57.1) | 0.878b |
| Comorbidities | |||||
| CKD | 38 (40.0) | 8 (34.8) | 16 (43.2) | 14 (40) | 0.809b |
| COPD | 17 (17.9) | 6 (26.1) | 8 (21.6) | 3 (8.6) | 0.176b |
| DM | 32 (33.7) | 8 (34.8) | 13 (35.1) | 11 (31.4) | 0.938b |
| Arterial HTN | 88 (92.6) | 22 (95.7) | 33 (89.2) | 33 (94.3) | 0.688c |
| Cerebrovascular disease | 17 (17.9) | 6 (26.1) | 7 (18.9) | 4 (11.4) | 0.355b |
| Dementia | 9 (9.5) | 2 (8.7) | 5 (13.5) | 2 (5.7) | 0.616c |
| Cardiopathy | |||||
| IHD | 19 (20.0) | 3 (13.0) | 10 (27.0) | 6 (17.1) | 0.416c |
| AF | 72 (75.8) | 18 (78.3) | 24 (64.9) | 30 (85.7) | 0.113b |
| LVEF, % | 58.0 ± 14.8 | 79.7 ± 15.6 | 56.0 ± 14.6 | 59.0 ± 14.6 | 0.574a |
| LVEF <40% | 16 (17.0) | 5 (21.7) | 7 (18.9) | 4 (11.8) | 0.606c |
| Diastolic dysfunction | 61 (64.2) | 17 (73.9) | 21 (56.8) | 23 (65.7) | 0.335c |
| LA size, mm | 43.9 ± 13.7 | 42.4 ± 8.6 | 45.4 ± 17.3 | 43.2 ± 12.1 | 0.901d |
| Tricuspid regurgitation | 23 (24.5) | 7 (30.4) | 7 (18.9) | 9 (26.5) | 0.567b |
| Treatment | |||||
| β‐Blockers | 67 (69.8) | 12 (52.2) | 29 (78.4) | 22 (68.8) | 0.105b |
| ACEIs/ARBs | 63 (65.6) | 18 (78.3) | 27 (73.0) | 18 (56.3) | 0.185c |
| Aldosterone antagonists | 51 (53.1) | 11 (47.8) | 19 (51.4) | 18 (56.3) | 0.835c |
| Loop diuretics | 81 (84.4) | 20 (87.0) | 29 (78.4) | 28 (87.5) | 0.593c |
| Thiazides | 17 (17.7) | 7 (30.4) | 6 (16.2) | 4 (12.5) | 0.224b |
| CCBs | 11 (11.5) | 3 (13.0) | 4 (10.8) | 4 (12.5) | 0.960b |
| Semiology | |||||
| NYHA class | 0.293c | ||||
| I | 4 (4.2) | 2 (8.7) | 2 (5.4) | 0 (0) | |
| II | 66 (69.5) | 15 (65.2) | 23 (62.2) | 28 (80.0) | |
| III | 25 (26.3) | 6 (26.1) | 12 (32.4) | 7 (20.0) | |
| Lower‐extremity edema | 25 (26.3) | 5 (21.7) | 9 (25.0) | 11 (31.4) | 0.690a |
| SBP, mm Hg | 126.1 ± 19.8 | 127.1 ± 18.7 | 124.8 ± 20.8 | 126.8 ± 19.8 | 0.880a |
| DBP, mm Hg | 71.7 ± 11.7 | 73.4 ± 10.2 | 69.1 ± 11.7 | 69.5 ± 19.9 | 0.240a |
| Heart rate, bpm | 74 ± 12.9 | 72 ± 15.0 | 72.4 ± 11.9 | 77.0 ± 12.1 | 0.242a |
| Weight, kg | 71.7 ± 18.2 | 75.5 ± 15.9 | 70.6 ± 19.2 | 70.6 ± 18.7 | 0.562a |
| BMI, kg/m2 | 27.0 ± 5.6 | 28.2 ± 5.1 | 27.0 ± 5.8 | 26.4 ± 5.8 | 0.505a |
| Laboratory parameters | |||||
| Hb, g/dL | 12.7 ± 1.6 | 12.9 ± 1.4 | 12.7 ± 1.5 | 12.5 ± 1.9 | 0.701a |
| Urea, mg/dL | 67.6 ± 30.8 | 63.8 ± 40.4 | 69.1 ± 26.8 | 68.5 ± 28.1 | 0.347d |
| Cr, mg/dL | 1.2 ± 0.5 | 1.1 ± 0.5 | 1.2 ± 0.4 | 1.3 ± 0.7 | 0.517d |
| GFR, mL/min/1.73 m2 | 55.4 ± 21.9 | 59.5 ± 23.1 | 55.2 ± 18.9 | 52.9 ± 24.4 | 0.468d |
| Na, mEq/L | 140.2 ± 3.5 | 140.8 ± 3.0 | 140.3 ± 2.3 | 139.8 ± 4.4 | 0.698d |
| NTproBNP, pg/mL, median (IQR) | 1632 (765–3038) | 849 (618–1666) | 1637 (774–2733) | 2655 (1058–4129) | 0.020d |
| IVC parameters | |||||
| maxIVC, cm | 1.9 ± 0.5 | 1.8 ± 0.4 | 1.8 ± 0.5 | 2.1 ± 0.5 | 0.005a |
| minIVC, cm | 1.3 ± 0.5 | 0.8 ± 0.2 | 1.1 ± 0.4 | 1.7 ± 0.5 | 0.001d |
| IVCCI | 0.4 ± 0.2 | 0.6 ± 0.1 | 0.4 ± 0.1 | 0.2 ± 0.1 | 0.001d |
Abbreviations: ACEI, angiotensin‐converting enzyme inhibitor; AF, atrial fibrillation; ANOVA, analysis of variance; ARB, angiotensin II receptor blocker; BMI, body mass index; CCB, calcium channel blocker; CKD, chronic kidney disease; COPD, chronic obstructive pulmonary disease; Cr, creatinine; DBP, diastolic blood pressure; DM, diabetes mellitus; GFR, glomerular filtrate rate; Hb, hemoglobin; HTN, hypertension; IHD, ischemic heart disease; IQR, interquartile range; IVC, inferior vena cava; IVCCI, inferior vena cava collapse index; LA, left atrium; LVEF, left ventricular ejection fraction; maxIVC, maximum inferior vena cava diameter; minIVC, minimum inferior vena cava diameter; Na, sodium; NTproBNP, N‐terminal pro‐B‐type natriuretic peptide; NYHA, New York Heart Association; SBP, systolic blood pressure; SD, standard deviation.
Data are presented as n (%), mean ± SD, or median (IQR).
ANOVA test.
χ2 test.
Fisher exact test.
Kruskal‐Wallis test.
Figure 1.
Correlation between IVCCI and LVEF and eGFR. Abbreviations: eGFR, estimated glomerular filtrate rate; IVCCI, inferior vena cava collapse index; LVEF, left ventricular ejection fraction
Regarding outcome variables after 1 year of follow‐up, worsening HF occurred in 56 patients (58.9%; 95% confidence interval [CI]: 48.9–68.3), requiring an increase in the dose of diuretic. With respect to admission, HF hospitalization occurred in 18 patients (18.9%; 95% CI: 12.3–28.0). HF mortality was 11.6% (95% CI: 6.6–19.6), and all‐cause mortality affected 18 patients (18.9%; 95% CI: 12.3–28.0).
Analyzing these outcome variables based on IVC collapsibility, worsening HF that required an increase in the diuretic dose occurred in 39.1% of the patients with IVCCI >50%, in 62.2% of patients with IVCCI 30% to 50%, and in 70.9% of patients with IVCCI <30% (P = 0.032). The HR of the group with IVCCI <30% with respect to the IVCCI >50% group was 2.7 (95% CI: 1.3–5.9; Table 2). Figure 2 shows the incident curves. After adjusting for age, sex, AF, tricuspid regurgitation, LVEF, and chronic obstructive pulmonary disease (COPD), the HR maintained its statistical significance with a value of 2.8 (95% CI: 1.3–6.2). Regarding hospitalization, 5.9% of patients with IVCCI >50% required admission, compared with 45.3% of patients with IVCCI <30%. The HR was 12.1 (95% CI: 1.5–92.9). After adjusting for the same variables, the HR maintained its statistical significance with a value of 13.9 (95% CI: 1.7–113.0).
Table 2.
Cumulative incidence and univariate HR of IVCCI, for worsening HF, HF hospitalization, all‐cause mortality, and HF mortality at 1‐year follow‐up
| Outcome | IVCCI >50% | IVCCI 30%–50% | IVCCI <30% | Log‐Rank Test | |||
|---|---|---|---|---|---|---|---|
| Cumulative Incidence (95% CI) | HRa | Cumulative Incidence (95% CI) | HRa (95% CI) | Cumulative Incidence (95% CI) | HRa (95% CI) | ||
| Worsening HF | 39.1 (22.6–61.7) | 1 | 62.2 (47.0–77.4) | 2.0 (0.9–4.4) | 70.9 (55.2–85.0) | 2.7 (1.3–5.9) | 0.032 |
| HF hospitalization | 5.9 (0.9–35.0) | 1 | 24.9 (11.9–47.8) | 5.0 (0.6–41.9) | 45.3 (27.1–68.5) | 12.1 (1.5–93.9) | 0.006 |
| All‐cause mortality | 13.0 (4.4–35.2) | 1 | 16.2 (7.6–32.6) | 1.3 (0.3–5.3) | 25.7 (14.3–43.6) | 2.2 (0.6–8.3) | 0.374 |
| HF mortality | 4.7 (0.7–29.2) | 1 | 11.4 (4.5–27.6) | 2.6 (0.3–23.7) | 18.6 (8.8–36.8) | 4.6 (0.6–38.1) | 0.276 |
Abbreviations: CI, confidence interval; HF, heart failure; HR, hazard ratio; IVCCI, inferior vena cava collapse index.
Univariate HR with IVCCI >50% as reference population.
Figure 2.
Kaplan–Meier curve analysis of IVCCI, for worsening HF, HF hospitalization, all‐cause mortality, and HF mortality at 1‐year follow‐up. Abbreviations: HF, heart failure; IVCCI, inferior vena cava collapse index
With regard to deaths, all‐cause mortality and HF mortality were 13% and 4.7%, respectively, in the IVCCI >50% group; whereas those in the IVCCI 30% to 50% group were 16.2% and 11.4%, respectively. Mortality was higher in the IVCCI <30% group, with 25.7% all‐cause mortality and 18.6% HF mortality. However, these differences did not reach statistical significance (Table 2, Figure 2). The HR of the IVCCI <30% group compared with the IVCCI >50% group was 2.2 (95% CI: 0.6–8.3) for all‐cause mortality and 4.6 (95% CI: 0.6–38.1) for HF mortality.
To compare predictive accuracy of IVCCI and other IVC parameters and NTproBNP, ROC analysis was plotted (Figure 3, Table 3). The maxIVC and minIVC AUCs were not clinically or statistically superior to those of IVCCI for any of the outcome variables studied (Table 3). Regarding worsening HF, IVCCI AUC was 0.62, slightly lower than that of NTproBNP, which was 0.71. This difference was not statistically significant (P = 0.246). About HF hospitalization, AUC for IVCCI was 0.66, whereas AUC for NTproBNP was 0.81 (P = 0.094). In the analysis of all‐cause mortality, AUC for NTproBNP was 0.91, significantly higher than that of IVCCI (0.62; P = 0.001). Specifically in HF mortality, the AUC for NTproBNP was higher than that of IVCCI (0.84 vs 0.65), very close to statistical significance (P = 0.053).
Figure 3.
Comparison of prognostic capacity of IVC parameters and NTproBNP by AUCs for each outcome variable. Abbreviations: AUC, area under the curve; IVC, inferior vena cava; IVCCI, inferior vena cava collapse index; NTproBNP, N‐terminal pro‐B‐type natriuretic peptide
Table 3.
AUCs of IVC parameters and NTproBNP for worsening HF, HF hospitalization, all‐cause mortality, and HF mortality at 1‐year follow‐up
| AUC (95% CI) | ||||
|---|---|---|---|---|
| NTproBNP | IVCCI | minIVC | maxIVC | |
| Worsening HF | 0.71 (0.60–0.82) | 0.62 (0.50–0.74) | 0.67 (0.55–0.78) | 0.62 (0.50–0.74) |
| HF hospitalization | 0.81 (0.72–0.90) | 0.66 (0.51–0.81) | 0.65 (0.50–0.80) | 0.57 (0.42–0.72) |
| All‐cause mortality | 0.91 (0.82–0.99) | 0.62 (0.45–0.78) | 0.61 (0.43–0.78) | 0.56 (0.40–0.73) |
| HF mortality | 0.84 (0.71–0.96) | 0.65 (0.49–0.81) | 0.69 (0.51–0.87) | 0.64 (0.46–0.82) |
Abbreviations: AUC, area under the curve; CI, confidence interval; HF, heart failure; IVC, inferior vena cava; IVCCI, inferior vena cava collapse index; maxIVC, maximum inferior vena cava diameter; minIVC, minimum inferior vena cava diameter; NTproBNP, N‐terminal pro‐B‐type natriuretic peptide.
4. DISCUSSION
In patients with chronic HF, IVC ultrasound shows prognostic utility to predict HF hospitalization or worsening. Patients with IVCCI <30% have a risk of clinical worsening 2.8× higher than patients with IVCCI >50%. In the case of HF hospitalization, the risk is increased 13.9×. This increased risk is maintained after adjusting for age, sex, AF, tricuspid regurgitation, LVEF, and COPD. IVC ultrasound shows a lower degree of utility in predicting mortality. Although there is a tendency for an association, it does not reach statistical significance. In either case, the prognostic power of IVC ultrasonography is not superior to NTproBNP in the different outcome variables studied.
The prognostic power of IVC ultrasonography for HF hospitalization has been shown by other authors,31, 32, 33, 34, 35 but only 1 of these studies compared the utility of the IVC measurement with NT‐proBNP.33 In this study, Pellicori et al. analyzed the use of IVC ultrasound for a combined variable of cardiovascular mortality and HF hospitalization.33 Their study population had a mean age of 73 years, was predominantly male (71%), had lower prevalence of AF (40%), and had a predominance of HF with reduced ejection fraction (64.6%). In our study, the analysis of a combined variable of HF mortality and HF hospitalization is also significant, with an adjusted HR for IVCCI <30% of 7.5 (95% CI: 1.7–34.2), lower than the HR of IVCCI <30% for isolated HF hospitalization, 13.9 (95% CI: 1.7–113.0). Therefore, we understand that in our sample, these significant findings appear at the expense of the strong association between IVCCI and HF hospitalization. In Pellicori study, all‐cause mortality was significantly associated with IVC ultrasonography. The AUC for maxIVC was 0.76 for cardiovascular mortality and HF admission and was 0.73 for all‐cause mortality. The AUC for NTproBNP was 0.73 and 0.75, respectively, with no significant differences. In the present study, the AUC for maxIVC was 0.61 for HF mortality or admission, and 0.61 for all‐cause mortality, whereas AUCs for NTproBNP were 0.84 and 0.91, respectively. In any case, in none of the studies was IVC ultrasonography superior to NTproBNP in patients with chronic HF.
Thus, a slight decrease in the usefulness of the IVC parameters is observed in our study. The reasons for this discrepancy may be multiple. First, an avoidable interobserver variation of ultrasound examinations may exist. In the present study, the population is older, with many other comorbidities (predominantly HF with preserved ejection fraction) and increased risk of mortality from other causes. There is also a high prevalence of AF, which in other studies has been shown to interfere with the measurement of IVC.32
IVC parameters have shown high diagnostic and prognostic power in the acute HF setting, even at the end of the acute phase, prior to discharge.14, 15, 29, 30 In light of our study, this power is reduced in chronic HF. This finding can be explained by a common phenomenon of diagnostic and prognostic tests, in which tests or examinations lose utility in less severe cases within the spectrum of HF disease. In addition, regarding the technique of IVC measurement, IVC parameters are better measured during a nonforced breathing cycle,36 in which chronic HF patients may show a lot of individual variability. This may explain the higher reliability of IVC parameters in acute HF in patients with severe dyspnea (mainly New York Heart Association class III/IV), where the respiratory pattern of patients is probably more homogeneous. This detail about IVC ultrasound has already been evidenced during the management of resuscitation in patients with shock, where IVC parameters are monitored to guide fluid therapy, but especially in patients with mechanical ventilation.36, 37, 38 It is postulated that this patient profile, controlling the respiratory rate, allows a more reliable analysis of the IVC. This would be an additional adjustment to understand that the diameter and collapsibility of the IVC are influenced by cardiac preload but is biased by the respiratory cycle of the patient. Probably, with a less serious volume overload and less respiratory compromise, IVC ultrasound could be more exposed to individual variability and thus the benefit could be reduced.
These aspects should not detract from the information provided by IVC ultrasound, only delimit its field of utility. We have seen that it is related to the risk of decompensation and, consequently, can help the clinician in decision‐making. In those centers with availability of NTproBNP determination, the use of IVC ultrasound can help to clarify the volume status in cases of discrepancy between semiology and NTproBNP. On the other hand, in those centers where NTproBNP is not available, the measurement of IVC ultrasound parameters can improve the physical examination of the patient and help identify those with an increased risk of decompensation.
4.1. Study limitations
A limitation of this study is the characteristic makeup of the population (older, with many comorbidities and with predominance of an HF pattern with preserved ejection fraction). However, as there is no standardized treatment for these patients, they provide a model of HF that allows studying prognosis with more accuracy in congestive states. This is because the natural course of this disease with preserved ejection fraction has not been shown to be altered by any particular therapeutic regimen. Another limiting aspect could be the sample size, although it was sufficient to make relevant comparisons and reach statistical conclusions. Perhaps a larger sample would show that the relationship between IVCCI and mortality is statistically significant, but even then, it is unlikely to be superior to NTproBNP.
5. CONCLUSION
IVC ultrasonography is a useful tool in the follow‐up of patients with chronic HF, allowing the identification of patients at high risk of worsening and hospitalization for HF. However, its usefulness is not superior to that of NTproBNP.
Conflicts of interest
The authors declare no potential conflicts of interest.
Curbelo J, Aguilera M, Rodriguez‐Cortes P, Gil‐Martinez P, Suarez Fernandez C. Usefulness of inferior vena cava ultrasonography in outpatients with chronic heart failure. Clin Cardiol. 2018;41:510–517. 10.1002/clc.22915
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