REVIEW ARTICLE

Pdf version

MANAGEMENT OF CHRONIC HEART FAILURE IN PRIMARY CARE: WHAT EVIDENCE DO WE HAVE FOR HEART FAILURE WITH PRESERVED SYSTOLIC FUNCTION?

AS Ramli MBBS (Newcastle-upon-Tyne), DFFP (UK), DRCOG (UK), MRCGP (UK), Fellow in Chronic Disease Management (Monash University, Melbourne), Head of Primary Care Medicine Discipline, Associate Professor & Consultant Family Medicine Specialist, Faculty of Medicine, Universiti Teknologi MARA (UiTM), Sungai Buloh, Selangor, Malaysia (Anis Safura Ramli)
B Jackson BMedSc, MBBS, MD, FRACP, FAHA, Medical Director, Chronic Heart Failure Program, Southern Health, Associate Professor, Faculty of Medicine, Nursing and Health Sciences, Monash University, Melbourne, Australia (Bruce Jackson)
CT Toh MPharm, FSHP, Senior Pharmacist, Chronic Heart Failure Program, Dandenong Hospital, Melbourne, Australia (Cjeng Tiong Toh)
D Ambigga MBBS (Mangalore), MMed Family Medicine (UKM), Fellow in Community Geriatrics and Rehabilitation Medicine (Monash University, Melbourne), Senior Lecturer & Family Medicine Specialist, Faculty of Medicine, Universiti Teknologi MARA (UiTM), Sungai Buloh, Selangor, Malaysia (Ambigga Devi)
L Piterman AM, MBBS, M.Med (Primary Care), M.Ed.St, FRCP (Edin), FRACGP, MD, Professor & Head of School of Primary Health Care, Pro Vice-Chancellor, Berwick Campus, Monash University, Melbourne, Australia (Leon Piterman)

Address for correspondence: Associate Professor Dr Anis Safura Ramli, Level 2, Clinical Training Centre, Faculty of Medicine, Universiti Teknologi MARA, 47000 Sungai Buloh, Selangor, Malaysia. Email: rossanis_yuzadi@yahoo.co.uk

Conflict of interest: None

CASE SCENARIO

Madam YW, a 70-year-old woman with a long history of hypertension, type 2 diabetes mellitus and osteoarthritis; presented to her primary care physician complaining of increasing shortness of breath while walking over the last six months. She noted swelling in her feet and ankles. Her breathlessness worsened over the last three days, where she has been unable to lie flat in bed at night and has been sleeping on three pillows.

This lady lives with her 76-year-old husband who has recently been diagnosed with colon cancer. Her daughter, who lives nearby, noted that her mother has been deeply affected by the news. She complained of feeling tired all the time, and has been unable to cope with looking after him and doing her usual house chores. She is a non-smoker and does not drink alcohol.

Her current medications are as follows:

• Hydrochlorothiazide 50 mg od.
• Metformin 1 g bd.
• Gliclazide 160 mg bd.
• Diclofenac  50 mg tds. prn.

She admitted that she has not been taking her medications regularly and has frequently defaulted on her follow up appointments.

On examination, this lady has a body mass index (BMI) of 31 kg/m² and waist circumference of 98 cm. Her pulse rate was regular at 95 beats per minute, blood pressure was 170/90 mmHg and her jugular veins were noticeably distended. Her apex beat was displaced to the sixth left intercostals space and auscultation of the heart revealed normal heart sounds. There were bibasal crepitations heard on auscultation of her lungs, and lower limbs examination revealed bilateral pitting oedema of feet and ankles.

Chest X-ray (CXR) and Electrocardiogram (ECG) were performed. Results are shown in Figure 1 and 2 respectively.

Figure 1: Madam YW’s Chest X-ray showing bilateral pulmonary congestion and cardiomegaly

Figure 2: Madam YW’s 12-lead ECG showing large voltages, left axis deviation, ST-T strain pattern in lateral chest leads (without digoxin) and interventricular conduction delay typical of left ventricular hypertrophy (LVH)

Madam YW was suspected to have an acute heart failure and was then admitted to the nearest hospital for stabilisation and confirmation of diagnosis. One week later, she was discharged from the hospital to her primary care physician with the following information:

Trans-thoracic echocardiography report:
Concentric LV hypertrophy with normal left ventricular ejection fraction (LVEF) of 55%.
Bi-atrial dilatation, impaired LV filling and elevated filling pressure.

Cardiac stress perfusion study (thallium):
No evidence of reversible ischaemia. LVEF of 55% is confirmed.

Blood results:
HbA_1c: 7.5%       Renal profile (RP): normal       Liver function test (LFT): normal       Full blood count (FBC): normal
Fasting serum lipid (FSL): TC 6.1, LDL-C 3.0, TG 2.1, HDL-C 1.19 (mmol/litre)

Urinalysis:
Urine protein negative, urine microalbumin negative.

Medication on discharge:

• Frusemide 40 mg bd.
• Hydrochlorothiazide 50 mg od.
• Bisoprolol 2.5 mg od.
• Perindopril 4 mg od.
• Metformin 1 g bd.
• Gliclazide 160 mg bd.
• Simvastatin 40 mg nocte.
• Aspirin 75 mg od.
• Slow K 600 mg od.
• Paracetamol 1 g qds.

Clinical Questions

1. How do we make the diagnosis?
2. How common and how significant is this condition?
3. How do we manage this lady?

REVIEW OF EVIDENCE

Diagnosing Heart Failure

Heart Failure (HF) is a common chronic condition encountered in primary care. The prevalence of HF in developing countries is gradually rising as a result of an ageing population, and an escalating epidemic of coronary heart disease, hypertension, type 2 diabetes and obesity.¹ In Malaysia, HF accounts for 6%-10% of all medical admissions.^2,3 The economic burden of HF is substantial, in which the cost of hospitalisations represents the greatest proportion of total expenditure.⁴

This case illustrates a common primary care presentation of an Acute Heart Failure (AHF), which is defined as rapid onset of symptoms and signs due to acute deterioration of cardiac function.⁵ Patients with AHF may present de novo or as an acute decompensation of chronic heart failure (CHF).⁵ In the case of Madam YW - an elderly, obese woman with long history of hypertension and type 2 diabetes, it is more likely that she has an acute decompensation of an undiagnosed CHF which may have developed gradually. There are several common factors which can precipitate an acute cardiac decompensation, and in this scenario it may have been contributed to her uncontrolled hypertension, excessive salt and water intake, and adverse effects of non-steroidal anti-inflammatory drug (NSAID). Exercise capacity should be assessed to determine functional class in CHF patients (Table 1)⁵, and this lady is most likely to be in the New York Heart Association (NYHA) Class III (marked limitation of physical activities such as walking and doing her house chores).

Table 1: The New York Heart Association (NYHA) functional classification

NYHA grading	Functional description	Untreated 1 year mortality
Class I	No limitation. Ordinary physical activity does not cause fatigue, dyspnoea or palpitation.	5-10%
Class II	Slight limitation of physical activity. Such patients are comfortable at rest. Ordinary physical activity results in fatigue, dyspnoea, palpitation or angina.	10-15%
Class III	Marked limitation of physical activity. Less than ordinary physical activity leads to symptoms.	15-20%
Class IV	Inability to carry on any physical activity without discomfort. Symptoms of CHF present at rest.	20-50%

HF however, may present insidiously in the elderly, obese and in women, making it difficult to interpret.⁵ It is absolutely vital that primary care physicians recognize these characteristics early and have a high index of suspicion especially in patients with cardiovascular co-morbidities and risk factors.

Patients suspected to have AHF require hospital admission for i) stabilisation of haemodynamics ii) management of symptoms aimed at reducing pulmonary venous pressure and congestion iii) identification and management of the underlying cause or precipitating factors and iv) confirmation of diagnosis by echocardiography.^5-7 CXR and ECG should be performed in primary care where available;⁵ and when the patient is relatively stable. Natriuretic peptides, which may be useful as a ‘rule-out’ test in doubtful cases,⁵ is not commonly available in Malaysian primary care setting.

This lady’s echocardiogram confirmed that she has a normal systolic function with pre-dominantly diastolic dysfunction. Diastolic dysfunction can also occur in asymptomatic patients; therefore, it is important to distinguish this terminology with diastolic heart failure (DHF).^8,9 Controversies surrounding the optimal diagnostic criteria for DHF is a subject of ongoing debate in the literature.^10,11,12 The recently updated consensus statement by the European Society of Cardiology suggests that the diagnosis of DHF is made when three criterias are fulfilled simultaneously; i) presence of sign or symptoms of congestive HF ii) objective evidence of normal or mildly abnormal left ventricular systolic function (LVEF >50%) and iii) objective evidence of left ventricular diastolic dysfunction (abnormal relaxation, filling, diastolic distensibility or stiffness).¹² It is well known that the gold standard assessment for left ventricular diastolic dysfunction is by cardiac catheterization,¹² but this invasive procedure is not practical or widely available especially in developing countries. The Malaysian Clinical Practice Guidelines (CPG) for Management of HF recommends trans-thoracic echocardiography as a mean of diagnosis for diastolic dysfunction.⁵ It is also important to rule out cardiac ischaemia as a potential underlying cause for HF,^5,6 therefore cardiac stress perfusion study was performed in this case.

DHF has also been described as Heart Failure with Preserved left ventricular Systolic Function (HF-PSF) in the literature. ^5,6,13,14 There is an ongoing debate regarding the most appropriate terminology for this condition.¹⁵

How common and how significant is HF-PSF?

Current epidemiological evidence from various parts of the world have established that HF-PSF is just as common as HF with reduced left ventricular Systolic Function (HF-RSF), representing 50% of all patients with heart failure.^14,16-22 Compared to the latter, individuals presenting with HF-PSF are more likely to be female, older, have hypertension and atrial fibrillation; and less likely to have coronary heart disease.^{14,16,17,18,20,22} The prevalence of HF-PSF was found to have increased over time, and was significantly higher among community patients.¹⁸ A survey in everyday practice has also shown that elderly, female patients with HF were more likely to be managed in primary care as compared to secondary care.²³

The clinical presentation of patients with HF-PSF is similar to those with HF-RSF.¹⁴ In pathophysiological terms, the symptoms and signs of HF-PSF result from elevated left ventricular filling pressure due to diminished relaxation and reduced distensibility during diastole, while its contractility during systole (ejection fraction) is preserved.⁸

A growing body of evidence now shows that HF-PSF carries a comparably poor prognosis to HF-RSF.^18-22 The recently published data from OPTIMIZE-HF registry comparing 21,149 patients with HF-PSF and 20,118 patients with HF-RSF shows that both groups had similar hospital readmission rates (29.2% vs. 29.9%; p=0.591) and similar mortality risks (9.5% vs. 9.8%; p=0.459).²⁰ Another study from Japan shows similar outcome where the combined all cause mortality or rehospitalisation rates did not differ between the two groups (adjusted HR1.082 and 95%CI 0.858-1.365; p=0.507).²² Five year survival rates were also not significantly different in patients with HF-PSF compared to HF-RSF (43% vs. 46%; p=0.95).²¹

How do we manage this lady?

Regardless of whether the diagnosis is HF-PSF or HF-RSF, long term management of patients with CHF in primary care is intricate as they often present with multiple co-morbidities which require persistent lifestyle modification and multiple drug therapies. As illustrated in the case of Madam YW, not only that she has osteoarthritis and metabolic syndrome (central obesity, dyslipidaemia, hypertension and type 2 diabetes);²⁴ she is also frail and not coping with her activities of daily living. The fact that her husband is terminally ill adds to her psychological stress and she may be at risk of developing depression. Prevalence of depression has been reported to be as high as 39% in patients with CHF, and it is related to a higher risk of functional decline.²⁵ Therefore, all individuals presenting with CHF should be routinely screened for depression.⁶