Monitoring Heart Failure using an Implantable Device Measuring Intrathoracic Impedance - Technical and Clinical Overview

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Management of heart failure consumes 1% to 2% of the healthcare budget in developed countries, with the largest share due to the cost of hospitalisations.1 A pan-European survey has shown that up to 65% of patients hospitalised with heart failure have a past history of chronic heart failure.2 Such admissions are usually long, with an average duration of 11 days. In-hospital mortality was reported as 6.9% and by 12 weeks the mortality had risen to 13.5%, with a risk of re-hospitalisation of 24%.2 Recent efforts to reduce the risk of re-hospitalisation have largely focused on multidisciplinary disease management teams working with patients to ensure adherence to medication and the early detection of signs of decompensation, particularly in the early period after hospital discharge.3

Unfortunately, the monitoring of heart failure syndrome control in clinical practice is usually relatively unsophisticated. Physicians rely on the subjective assessment of exercise tolerance and breathlessness, changes in body weight and clinical examination to detect increasing dependent oedema or lung crackles. Such measures are far from perfect - in chronic heart failure many patients may not have marked clinical signs or symptoms, despite high and possibly rising pulmonary capillary wedge pressures.4

Various, more sophisticated, methods of assessing heart failure control have been proposed, including serial measurement of B-type natriuretic peptide,5 implantable haemodynamic monitors6 and implantable intrathoracic impedance monitors.

Implantable Intrathoracic Impedance Monitoring

Intrathoracic impedance falls as the amount of fluid in the lungs increases, due to fluid being a good conductor of electrical current,7-9 raising the possibility that this technology may be clinically useful in providing an early warning of decompensation.

It is now possible to add the facility to monitor intrathoracic impedance to either cardiac resynchronisation devices or implantable cardioverter defibrillators using OptiVol™ technology, which is unique to Medtronic.

Transthoracic impedance is measured between the coil of the right ventricular lead and the can of the cardiac resynchronisation therapy (CRT) device or implanted cardioverter defibrillator (ICD) (see Figure 1). This measurement is made multiple times each day and recorded for up to 14 months. The device can be interrogated in detail by a technician, or at a more basic level by either the patient or physician using a simple hand-held device.

The OptiVol Fluid Index™ represents the accumulation of consecutive day-to-day differences between the daily and reference impedance. In other words, as the lungs become wetter or stay wetter the index increases. The physician can activate the patient alert in the device and when a threshold is crossed the device will audibly alarm. The index is reset if the daily impedance readings become higher than the impedance trend, thus reducing the risk of an alarm when the lungs are drying out. The OptiVol Fluid Index and average daily impedance measurements are shown in Figure 2.

Clinical Trial Data

There are several on-going clinical trials of the OptiVol technology, with data available from the Medtronic Impedance Diagnostics in Heart Failure Patients (MID-HeFT) Study that followed-up 33 patients with New York Heart Association (NYHA) class III or IV heart failure for 21 months. Ten of those patients had 25 hospitalisations for heart failure during that time. Retrospective analysis of the OptiVol data revealed that intrathoracic impedance dropped in the two weeks prior to the admissions with decompensation. On average, the drop in impedance was 13.9 ± 6.7%.10 There was also a good correlation between the drop in pulmonary capillary wedge pressure on treatment in hospital for acute decompensation and the risein intrathoracic impedance during admission(R=-0.7, p<0.001).11

Retrospective application of the recommended 60Ω OptiVol threshold has been studied in the MID-HeFT population - the algorithm would have detected 12 of the first 14 heart failure hospitalisations with a median of 18.5 days warning before hospitalisation (range one to 59 days).12 At the same detection threshold, one 'false positive' alert would have occurred on average in the non-hospitalised patients for every 417 days of patient monitoring. This compares very favourably with relying on patient self-report of worsening symptoms - in 50% of all cases, patients first noticed worsening symptoms only 2.5 days prior to hospitalisation. In 28% of all cases, patients first noticed worsening symptoms only within 24 hours prior to hospitalisation.

It must be remembered that the OptiVol fluid index cannot provide an alarm for a patient becoming too 'dry', nor can it determine the underlying cause of fluid accumulation such as non-adherence to diuretics or concurrent chest infection. The OptiVol facility should be viewed as an adjunct to good clinical skills and not as a replacement.


Larger scale prospective studies in both North America and Europe are currently examining the clinical utility of OptiVol intrathoracic impedance measurement and monitoring technology. Initial results are promising and are relevant to an increasing number of heart failure patients who are being considered for cardiac resynchronisation or implantable defibrillator therapy. OptiVol raises the possibility of patients being able to monitor the control of fluid retention more precisely, with the detection of decompensation before symptoms deteriorate. The hope is that this will allow both the physician and patient time to adjust therapy and prevent the need for subsequent hospitalisation.

Case Study

A 47-year-old civil servant presented in August 2004 with a four-week history of dyspnoea on exertion, paroxysmal nocturnal dyspnoea and nausea. He was admitted to his local hospital where a diagnosis of heart failure was made. Transthoracic echocardiography (TTE) showed a dilated, globally hypokinetic left ventricle (LV), also with poor systolic function of the right ventricle (RV). The viral and autoimmune screen were normal, as was the serum ferritin. He was transferred to the local cardiac centre for further work-up, including cardiac catetherisation. This revealed normal coronary arteries, a dilated globally hypokinetic LV with end-diastolic pressure of 25 mmHg and moderate pulmonary hypertension. He was initially stabilised on an angiotensin-converting enzyme (ACE) inhibitor, low-dose beta-blocker and diuretic and was discharged. He deteriorated and was re-admitted two weeks later with increasing breathlessness and several episodes of presyncope. He was transferred to a specialised heart failure unit.

At the time of transfer his systemic blood pressure was 95/60mmHg, the jugular venous pressure was raised to the angle of the jaw and the apex beat was diffuse and displaced to the anterior axillary line. The chest was clear on auscultation but there was dependent oedema to the knee bilaterally. The chest radiograph revealed gross cardiomegaly but no pulmonary oedema. The electrocardiogram (ECG) showed sinus rhythm with first-degree heart block (PR interval 250msec) and large voltage QRS complexes with non-specific ST flattening laterally. A 24-hour Holter recording revealed five self-terminating runs of ventricular tachycardia (VT) and one short episode of complete heart block. Biochemistry was normal, except for a serum creatinine of 127╬╝mol/l (calculated creatinine clearance 66ml/min).

Cardiac magnetic resonance (MR) confirmed the echocardiographic findings of severe biventricular systolic dysfunction and dilatation, with no evidence of fibrosis or recent infarction on gadolinium imaging. The patient had a maximal oxygen consumption of 11.6ml/kg/min on cardiopulmonary exercise testing (predicted 33.2ml/kg/min) with a raised VE/VCO2 slope of 55.

Cardiac resynchronisation therapy with a cardioverter defibrillator (Medtronic InSync Sentry™), and with OptiVol technology, was implanted on 30 September 2004. Within two days his dependent oedema resolved and his blood pressure rose to 110/80mmHg, permitting an increase in his ACE inhibitor dose. His maximal oxygen consumption increased to 21.5ml/kg/min and the VE/VCO2 slope decreased to 38. He was discharged with regular review in the heart failure clinic.

Six weeks later he was re-admitted from a clinic visit, with a short history of increasing breathlessness on exertion. Adjustment to his diuretic regime lead to rapid improvement in his symptoms. Maximal oxygen consumption was 19ml/min/kg. He was assessed for transplantation but was not listed due to his mild symptoms and ability to work.

In the middle of January 2005 his symptoms deteriorated and he required an increased dose of diuretics to control his symptoms. After two weeks of stability his symptoms deteriorated again and interrogation of the CRT device revealed loss of capture of the left ventricular lead. He required further increased dose of diuretics to stabilise his symptoms, pending repositioning of the lead in the middle of February 2005. After this his symptoms improved and the dose of diuretic was decreased again.


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