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. 2022 Oct 25;10(1):716–720. doi: 10.1002/ehf2.14219

Pressures do not equal volumes: implications for heart failure management in patients with CardioMEMS

Muhammad Shahzeb Khan 1, Michel G Khouri 1, Leilani Gomez 1, Marat Fudim 1,2,
PMCID: PMC9871682  PMID: 36283969

Abstract

Pulmonary arterial pressures are often used as surrogates for intravascular blood volume. However, the relationship between pressure and volume remains controversial. To contextualize and provide concrete examples and impact on clinical management, we report two cases of heart failure (one in heart failure with reduced ejection fraction and one in heart failure with preserved ejection fraction) where pressure‐based measurements did not accurately represent the intravascular status and affected clinical management.

Keywords: Heart failure, Pressure, Volume, CardioMEMS

Introduction

Decongestion is the mainstay of heart failure (HF) therapy. However, assessment of congestion and response to loop diuretics remains highly subjective with most clinicians relying on a combination of multiple parameters such as physical examinations, blood chemistries, weight change, net fluid loss, or invasive haemodynamics. Many of these parameters often provide discordant information and have their own set of limitations. 1 Given the robust experience with intra‐cardiac haemodynamics and their predictive value for cardiac decompensation and chronic outpatient monitoring with CardioMEMS (Abbott), an implantable pulmonary arterial pressure monitor has gained increasing interest. The technology allows for remote, real‐time haemodynamic information. Several studies have shown that pulmonary arterial diastolic pressure (PAD) guided management of HF has the potential to reduce HF hospitalization burden and overall costs. 2 , 3 The CardioMEMS HF System was initially approved by the Food and Drug Administration (FDA) in 2014 for use in patients with a prior HF hospitalization within the last year, who had New York Heart Association (NYHA) Class III symptoms. Recently, the FDA expanded CardioMEMS indication to HF patients with NYHA Class II, who have elevated levels of natriuretic peptide. 4

Pulmonary arterial pressures and PAD specifically as a substitute of pulmonary capillary wedge pressure (PCWP) are used as surrogates for intravascular blood volume. With this information in hand, clinicians most commonly adjust diuretics, yet the relationship between pressure and volume remains controversial. This has important clinical implications for the management of HF patients with CardioMEMS. Recently, Yaranov et al showed that there was discordance between intra‐cardiac pressures and direct measurement of circulating volume in HF. 5 To contextualize and provide concrete examples and impact on clinical management, we report two cases of HF [one in HF with reduced ejection fraction (HFrEF) and one in HF with preserved ejection fraction (HFpEF)] where pressure‐based measurements did not accurately represent the intravascular status and affected clinical management.

Case 1

Past medical history

A 47‐year‐old woman, recently retired from the Army, with no significant past medical history was diagnosed with kappa light chain multiple myeloma in January 2020. She was initially treated with RVd (lenalidomide, bortezomib, and dexamethasone) chemotherapy regimen. However, course was complicated by several chemotherapy side effects and disease progression. She eventually underwent autologous stem cell transplant in August 2020. Transthoracic echocardiogram several months prior to transplant had shown a normal left ventricular ejection fraction of 65% with global longitudinal strain of −17.4%. She was not on any HF medication.

Case presentation

A few months after her autologous stem cell transplant, she was admitted to the hospital with signs and symptoms of HF. She had gain roughly 40 lb and had significant dyspnoea on exertion. At that time, transthoracic echocardiogram showed a left ventricular ejection fraction of 30% with a global longitudinal strain of −7.9%. Cardiac magnetic resonance imaging showed biventricular dysfunction with calculated left ventricular ejection fraction 14% with no evidence of inducible ischaemia or late gadolinium enhancement suggestive of infiltrative disease or scar. She was aggressively diuresed and discharged on metoprolol and lisinopril after she returned to her baseline weight. However, she continued to have symptoms and was again admitted for HF next month. At that time, she underwent right heart catheterization with right atrial (RA) mean pressure of 13 mmHg, PCWP 14 mmHg, and cardiac index of 2.5 consistent with restrictive physiology. Endomyocardial biopsy results showed mild to moderate myocyte hypertrophy, non‐specific granular degeneration and vacuolar change and mild lipofuscin. No evidence of active myocarditis, giant cells, granulomatous inflammation, or amyloid deposition was present. She continued to have HF hospitalizations and was tolerating low doses of guideline directed medical therapy for systolic heart failure on blood pressure support with midodrine. Considering tenuous volume status with fluctuating weights and a narrow therapeutic window for diuresis constrained by orthostasis and renal dysfunction, CardioMEMS was placed in June 2021 in the left pulmonary artery. Right heart catheterization at that time showed RA mean pressure of 9 mmHg, RV 34/7 mmHg, PA 32/16 with a mean of 23 mmHg, PCWP 10 mm Hg, and cardiac index of 2.8 L/min. Blood pressure was 102/64 mmHg with a heart rate of 77 beats per minute.

Management

CardioMEMS data showed stable normal‐range diastolic PA pressures on furosemide 40 mg daily. Unfortunately, she continued to have ongoing fatigue and multi‐systemic symptoms, which severely impaired her quality of life. Blood volume analysis (BVA) results are shown in Table 1 . BVA (BVA‐100TM, Daxor Corporation) is clinically approved and utilizes the gold‐standard indicator dilution technique with an iodine131‐tagged albumin tracer to provide quantitative measurement of total BV (TBV), plasma volume (PV), and red blood cell volume (RBCV). 6 The BVA report provides absolute values (mL) and deviation from ideal TBV, PV, and RBCV (expressed as absolute deviation and excess or deficit in mL and %‐deviation). 7 A TBV deviation ≥8% indicates either an excess or deficit of volume. Armed with the BVA data, we elected to de‐escalate diuretics despite relatively high PAD, which at the time of BVA was 18 mmHg. Her furosemide dose was decreased to 20 mg daily from 40 mg daily with marked improvement in symptoms, and since then, she did not have any more HF hospitalizations to date. Figure 1 shows the implant time and decrease in PAD thereafter despite de‐escalation of diuretics. No interval change in guideline directed medical therapy was done due to hypotension. She remained on fludrocortisone 0.1 mg BID for adrenal insufficiency and midodrine 5 mg TID for her low blood pressures and low‐dose HF GDMT (metoprolol succinate 25 mg daily, lisinopril 2.5 mg daily, spironolactone 12.5 mg daily).

Table 1.

Blood volume analysis results for Case 1

BVA result (mL) Patient ideal (mL) Deviation from ideal (mL) Excess/deficit %
Total blood volume 3081 4862 −1781 −36.6
Red blood cell volume 1012 1752 −740 −42.2
Plasma volume 2069 3110 −1041 −33.5

BVA, blood volume analysis.

Interpretation guide for BV deviation, Normal: 0–8%; Mild: >8–16%; Moderate: >16–24%; Severe: 24–32%; Extreme: >32%.

Figure 1.

Figure 1

Recordings from CardioMEMS for Case 1. The figure shows the implant time, and changes in pulmonary artery pressures after that. PA, pulmonary artery.

Case 2

Past medical history

A 64‐year‐old woman with a history of apical hypertrophic cardiomyopathy, HFpEF, NYHA Class III HF symptoms, and atrial fibrillation status post‐pulmonary vein isolation and linear ablation across the posterior wall was referred to our HF clinic for additional management. Transthoracic echocardiogram demonstrated normal left ventricular function with left ventricular ejection fraction of 70%, mild tricuspid regurgitation, and left atrial volume index of 36 mL/m2. She was taking apixaban 5 mg daily, atorvastatin 40 mg daily, empagliflozin 10 mg daily, furosemide 20 mg daily, lisinopril 10 mg daily, metoprolol succinate 25 mg daily, and spironolactone 25 mg every other day.

Case presentation

The patient suffered from exertional dyspnoea NYHA III paired with frequent visits to the ER for IV diuretics, HF‐related hospitalization, and alternating episodes of hypotension and orthostasis/pre‐syncope. Review of her recent event monitor showed no significant conduction abnormalities, very low burden of atrial fibrillation, and no ventricular tachyarrhythmias. We discussed that her symptoms are more likely haemodynamic than arrhythmic. A decision was made to implant a CardioMEMS. Right heart catheterization at that time showed RA mean pressure of 5 mmHg, RV 32/3 mmHg, PA 32/13 with a mean of 21 mmHg, PCWP 11 mm Hg, and cardiac index of 2.1 L/min. Blood pressure was 108/63 mmHg with a heart rate of 67 per minute. On follow‐up, CardioMEMS showed that her PAD were in 20 mmHg, but however she was euvolaemic on our exam. It appeared that her symptoms were in association with a very tenuous fluid status. BVA results are shown in Table 2 .

Table 2.

Blood volume analysis results for Case 2

BVA result (mL) Patient ideal (mL) Deviation from ideal (mL) Excess/deficit %
Total blood volume 4119 4840 −721 −14.9
Red blood cell volume 1347 1744 −397 −22.8
Plasma volume 2772 3096 −324 −10.5

BVA, blood volume analysis.

Interpretation guide for BV deviation, Normal: 0–8%; Mild: >8–16%; Moderate: >16–24%; Severe: 24–32%; Extreme: >32%.

Management

Given the low TBV, we decided to de‐escalate diuretics. Diuretics were weaned off in a matter of weeks with stable to lower trend on the PAD (Figure  2 ). Ultimately, patient's furosemide dose was decreased to 10 mg daily despite high natriuretic peptide levels and PAD. She started feeling better, and eventually, her furosemide was stopped with improvement in her symptoms, and no more hospitalizations or ER visits. Diuretic down‐titration did not result in up‐titration of any other medications.

Figure 2.

Figure 2

Recordings from CardioMEMS for Case 2. The figure shows the implant time, and changes in pulmonary artery pressures after that. PA, pulmonary artery.

Discussion

These two cases show the variable pressure/volume phenotypes and show that pressures do not necessarily equate to volumes. This has very important implications for managing ambulatory HF patients with CardioMEMS. There has been a common belief since a long time that all patients with HF are generally volume overloaded and require treatment with diuretics especially in the context of worsening of symptoms and relatively normal to high PAD. These cases challenge that belief and suggest that treatment with diuretics universally may in fact lead to a worsening of symptoms in patients who are euvolaemic or even hypovolaemic. It is important to understand that centring volume‐adjusting medications on proxy measures of pressure may not accurately account for the complex nature of congestion. These cases also indicate that an appropriate titration (up and down) of diuretics is needed in patients with HF, and some patients may have a narrower therapeutic window.

Several prior studies demonstrated a poor association between intra‐cardiac pressures and direct measurement of circulating blood volume, including patients with HF. 8 In simpler terms, high pressures do not necessarily imply a volume overloaded state. In a recent study by Yaranov et al., authors found that using PAD of 15 mmHg and total blood volume of +/−8% deviation from ideal were the appropriate cut‐offs. 5 Patients with >+8% of ideal TBV had in total only one hospitalization in follow‐up (rate of 0.2 events/patient), whereas patients with a TBV 8% or less (N = 15) had a higher rate of 0.93 events/patient. There was a lack of correlation between PAD and blood volume metrics (PAD vs. total blood volume, R 2 = 0.002; PAD vs. plasma volume, R 2 = 0.001; PAD vs. red blood cell volume, R 2 = 0.025).

A discordant blood volume and pressure state (low volume with high pressure) implies a low vascular compliance state with venoconstriction and arterial constriction. Pressures alone are unable to unmask vascular compliance. 9 Use of a two‐dimensional approach using pressure and volume assessment could get closer to the understanding of vascular compliance. What could potential actions for patients with a low‐normal volume but high pressure state be? We demonstrate two cases where diuretics were successfully weaned. Alternative or parallel actions could be to use arterial or venous dilators if tolerated. Finally, the above scenario could indicate a ‘cold and dry’ situation where use of advanced HF therapies or inotropes is the next appropriate action. 5

Also, it is important to note that HF patients usually have low renal perfusion pressures, which in turn activates the sympathetic and renin–angiotensin–aldosterone system (RAAS), leading to a vicious cycle of water and salt retention. Too much diuretics in this context can be detrimental as it can lead to hyper‐activation of RAAS. Although some may argue that this may not be that pronounced in the setting of beta‐blockers and RAAS inhibition, it has been shown that higher plasma renin activity is an independent predictor of outcomes in HF patients regardless of the baseline therapy. 10 It is also important to note that lung ultrasound may represent a useful and non‐invasive tool in the assessment of pulmonary congestion in patients with HFrEF and HFpEF. A lung ultrasound guided strategy has been shown to possibly reduce the risk of HF hospitalizations. 11

In conclusion, these two cases reinforce that pressure‐based assessment of congestion in ambulatory patients with HF who have CardioMEMS do not accurately represent intravascular volume always and clinical context and volume assessment via other means could be considered. Use of a combined pressure and volume assessment allowed for a more comprehensive and faster ascertainment of the underlying physiology, potentially allowing us to adjust medical therapy faster and with greater confidence. Nevertheless, it is important to recognize that pressure changes longitudinally can still help predict HF exacerbations. In the future, more studies are needed for better volume‐based phenotyping for management of patients with HF.

Conflict of interest

Dr Fudim was supported by the National Heart, Lung, and Blood Institute (NHLBI) (K23HL151744), the American Heart Association (20IPA35310955), Bayer, Bodyport, BTG Specialty Pharmaceuticals, and Verily. He receives consulting fees from Abbott, Alleviant, Audicor, AxonTherapies, Bayer, Bodyguide, Bodyport, Boston Scientific, Coridea, CVRx, Daxor, Deerfield Catalyst, Edwards LifeSciences, Feldschuh Foundation, Fire1, Gradient, Intershunt, Medtronic, NXT Biomedical, Pharmacosmos, PreHealth, Shifamed, Splendo, Vironix, Viscardia, and Zoll.

Funding

None.

Khan, M. S. , Khouri, M. G. , Gomez, L. , and Fudim, M. (2023) Pressures do not equal volumes: implications for heart failure management in patients with CardioMEMS. ESC Heart Failure, 10: 716–720. 10.1002/ehf2.14219.

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