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Patients with chronic heart failure are at elevated risk of developing acute decompensated heart failure, often requiring hospital admission. Patients with a history of acute decompensation have additional risk of future episodes of decompensation, and death. Reasons for the transition from a stable, chronic state to an acute, decompensated state include disease progression as well as acute coronary events and dysrhythmias. While precipitating factors are frequently not identified, the most common preventable cause is non-compliance with medication and dietary regimens. Strategies for reducing decompensation, and thusly the need for hospitalization, are aimed at early identification of patients at risk for imminent decompensation. Programs for early identification of heart failure are characterized by frequent contact with patients to review signs and symptoms with a healthcare provider, and with education or adjustment of medications as appropriate. These encounters may occur face-to-face in office or in home, or via transmission of symptoms and conventional vital signs, including weight, telephonically or electronically.

Precise measurement of cardiac hemodynamics is often employed in the intensive care setting to carefully manage fluid status in acutely decompensated heart failure. Echocardiography, transesophageal echocardiography (TEE), and Doppler ultrasound are noninvasive methods for monitoring cardiac output on an intermittent basis for the more stable patient, but are not addressed in this policy. A variety of biomarkers and radiological techniques may be utilized in the setting of dyspnea when the diagnosis of acute decompensated heart failure is uncertain.

A number of novel approaches have been investigated as techniques to measure cardiac hemodynamics in the outpatient setting. It is postulated that real-time values of cardiac output or left ventricular end diastolic pressure (LVEDP) will supplement the characteristic signs and symptoms, and improve the clinician’s ability to intervene early to prevent acute decompensation. Four methods will be reviewed here: thoracic bioimpedance, inert gas rebreathing, arterial waveform during Valsalva, and implantable pressure monitoring devices.

Thoracic Bioimpedance
Bioimpedance is defined as the electrical resistance of tissue to the flow of current. For example, when small electrical signals are transmitted through the thorax, the current travels along the blood-filled aorta, which is the most conductive area. Changes in bioimpedance, measured at each beat of the heart, are inversely related to pulsatile changes in volume and velocity of blood in the aorta. Cardiac output is the product of stroke volume by heart rate, and thus can be calculated from bioimpedance. Cardiac output is generally reduced in patients with systolic heart failure. Acute decompensation is characterized by worsening of cardiac output from the patient’s baseline status. The technique is alternatively known as impedance plesthmography and impedance cardiography (ICG).

Inert Gas Rebreathing
This technique is based on the observation that the absorption and disappearance of a blood-soluble gas is proportional to cardiac blood flow. The patient is asked to breathe and rebreathe from a rebreathing bag filled with oxygen mixed with a fixed proportion of two inert gases; typically nitrous oxide and sulfur hexafluoride. The nitrous oxide is soluble in blood and is therefore absorbed during the blood’s passage through the lungs at a rate that is proportional to the blood flow. The sulfur hexafluoride is insoluble in blood and therefore stays in the gas phase and is used to determine the lung volume from which the soluble gas is removed. These gases and carbon dioxide are measured continuously and simultaneously at the mouthpiece.

Arterial Pressure during Valsalva to estimate LVEDP
Left ventricular end diastolic pressure (LVEDP) is elevated in the setting of acute decompensated heart failure. While direct catheter measurement of left ventricular end diastolic pressure is possible for patients undergoing cardiac catheterization for diagnostic or therapeutic reasons, its invasive nature precludes its outpatient use. Noninvasive measurements of LVEDP have been developed based on the observation that arterial pressure during the strain phase of the Valsalva maneuver may directly reflect the LVEDP. Arterial pressure responses during repeated Valsalva maneuvers can be recorded and analyzed to produce values that correlate to the LVEDP.

Pulmonary artery pressure measurement to estimate LVEDP
LVEDP can also be approximated by direct pressure measurement of an implantable sensor in the pulmonary artery wall. The sensor is implanted via right heart catheterization, and transmits pressure readings wirelessly to external monitors.

The following devices have received specific FDA clearance for marketing through the 510(k) process:

• June 1997, the "BioZ®" (SonoSite, Washington) thoracic impedance plethysmograph was cleared for marketing by the FDA through the 510(k) process. Several other impedance plethysmographs have been approved through the same process. The FDA determined that this device was substantially equivalent to existing devices for use in peripheral blood flow monitoring.
• In March 2006, the "Innocor®" (Innovision, Denmark) inert gas rebreathing device was cleared for marketing by the FDA through the 510(k) process. Several other inert gas rebreathing devices have been approved through the same process. The FDA determined that this device was substantially equivalent to existing devices for use in computing blood flow.
• In June 2004, the “VeriCor®” (CVP Diagnostics, Boston) noninvasive LVEDP measurement device was cleared for marketing by the FDA through the 510(k) process. The FDA determined that this device was substantially equivalent to existing devices for the following indication: “The VeriCor is indicated for use in estimating non-invasively, left ventricular end-diastolic pressure (LVEDP). This estimate, when used along with clinical signs and symptom and other patient test results, including weights on a daily basis, can aid the clinician in the selection of further diagnostic tests in the process of reaching a diagnosis and formulating a therapeutic plan when abnormalities of intravascular volume are suspected. The device has been clinically validated in males only. Use of the device in females has not been investigated."
• In April 2007, the “Endosure®” (CardioMEMS, Atlanta) wireless abdominal aortic aneurysm (AAA) pressure measurement device was cleared for marketing by the FDA through the 510(k) process. The FDA determined that this device was substantially equivalent to existing devices for the use in monitoring endovascular pressure during AAA repair. No devices have been cleared for marketing for the indication of determining LVEDP or managing heart failure.

Note: This policy only addresses use of these techniques in ambulatory care and outpatient settings.

The coverage guidelines outlined in the Medical Policy Manual should not be used in lieu of the Member's specific benefit plan language.

08/11/2011: Policy reviewed; no changes.

09/25/2012: Policy reviewed; no changes.

05/07/2013: Removed deleted CPT codes 0104T and 0105T from the Code Reference section.

Non-Covered Codes

This is not an all-inclusive list of non-covered procedure codes.

All codes billed for this procedure are considered investigational and not eligible for coverage. 

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