A 60 year old man complains of progressive shortness of breath when he walks up the slope or when he walks to the nearby market. He also complains of breathlessness when he lies flat on the bed at night and has to sleep on two pillows to feel better. Occassionally, when he is sleeping, the breathlessness gets quite bad and he needs to sit up to catch his breath. He also complains that his feet are more swollen and his shoes do not fit very well anymore. On physical examination, there is a raised jugular venous pulse wave and pitting pedal edema up to the mid shin. On auscultation, there is a fourth heart sound and fine crepitations in the bases of both lung fields. The ECG shows Q waves in the anterior precordial leads and a QRS duration of 126ms. The transthoracic echocardiogram revealed an old left anterior descending artery territory scar, a moderately dilated left ventricle, moderately severe mitral regurgitation and an ejection fraction of 30%. The cardiac magnetic resonance imaging revealed an extensive scar over the anterior, apex and septal wall of the left ventricle with no viability. The coronary angiogram showed an occluded left anterior coronary artery and mild disease in the left circumflex and right coronary arteries.

Heart failure is one of the most common conditions for admissions to hospital. It is also a very common reason for admissions to hospital after an initial hospitalization episode. This is likely to be due to the aging population as well as better treatment for myocardial infarctions and coronary artery disease which allows the patient to live longer. The man above is suffering from decompensated heart failure and is in New York Heart Association functional class 3. The initial strategy would be to improve symptoms by decongesting him with diuretics and vasodilators. Diuretic therapy has been around since the 1940s but the evidenced based trial was only published in 2011! [1]. This trial showed that higher dose of diuretic was superior to low dose diuretic in inducing fluid loss and weight loss and improvement in breathlessness. It also showed that there was no difference in giving the diuretic as a divided dose or as a continuous infusion, so the conclusion was to give patients high dose diuretic in divided doses. However, it was noticed that the high dose of diuretics was more likely to cause a rise in the serum creatinine level, so it is advisable to monitor the creatinine level during therapy. The use of digitalis in heart failure has not shown to confer any survival benefit for heart failure patients but it did reduce the number of hospitalizations for worsening heart failure [2].

At this stage, it is appropriate to add vasodilators especially angiotensin converting enzyme inhibitors (ACE-I). This is because numerous studies have shown that the early addition of ACE-I resulted in a 26% reduction in death and 26% reduction in death or readmissions for heart failure [3]. ACE-I block the angiotensin-renin-aldosterone system which then leads to vasodilation which helps to decongest the heart. The ACE inhibition also leads to reverse remodelling of the heart which may then improve the heart function. The ACE-I should be started at the lowest dose and can be titrated quite aggressively to the maximum tolerable dose within the next 4 -5 days. Attention must be paid to the blood pressure to prevent significant hypotension and a rise in the serum creatinine level. The patient is also encouraged to limit his fluid intake to about 1 liter per day and to avoid adding any salt to his food. He must also weight himself daily once he has achieved his dry weight.

Once the excess fluid has been removed from the patient, the diuretics can be tailed down to a maintenance dose. It is now time to start the beta-blockers. It was always thought that beta-blockers could not be used in heart failure as they have negative inotropic properties which may then exacerbate the heart failure. That is still true but research also shows that in patients with chronic heart failure, there is upregulation of the sympathetic nervous system which leads to an increased mortality. The addition of beta-blockers will then block the sympathetic nervous system which then leads to an increased survival rate. Indeed, the CIBIS 2 study showed that in symptomatic heart failure patients, the addition of bisoprolol reduced all -cause mortality by 34% and sudden cardiac death  by 44% [4]. It was recommended that beta-blockers be started once the patient was out of heart failure and the lowest dose of beta-blocker should be used and the dose of beta-blocker be uptitrated slowly and every two weeks to reach the maximal tolerable dose. This era of studies with ACE-I and beta-blockers led to them becoming the cornerstone of heart failure therapy.

Once our patient was out of fluid congestion, his mortality still remained rather high as the heart function was abnormal. It was noticed from epidemiological data that patients with a heart rate of more than 70 bpm even when they were on beta-blockers had a reduced survival. In fact the mortality increased with an increasing heart rate. The use of a pure heart rate reducer, i*****, showed that there was a 26% reduction in admission for heart failure and a 26% reduction in deaths due to heart failure [5]. Once the patient has been maximised on ACE-I and beta-blockers and if their heart rate on the ECG was still above 70 bpm, it is advisable to start i***** and aim for a heart rate close to 60 bpm.

The patient with heart failure has an increased mortality from progressive heart failure as well as sudden cardiac death. Sudden cardiac death is usually due to ventricular arrhythmias like ventricular tachycardia or ventricular fibrillation. The survival of patients who have experienced an out of hospital cardiac arrest is dismal. The implantation of an internal defibrillator will help to remove sudden cardiac death. Our patient above has a EF of less than 35% and an infarct which makes him at high risk of sudden cardiac death. The implantation of an implantable defibrillator (ICD) resulted in a 31% reduction in all cause mortality [6]. Heart failure patients with a widened QRS complex of more than 120ms has been shown to benefit from cardiac resynchronization therapy. They are in New York Heart Association functional class II or III, like our patient, and with an ejection fraction of 30% or less. The cardiac resynchronization therapy with a defibrillator (CRT-D) was shown to reduce death by 25% and hospitalization for heart failure by 32% as compared to just implanting a (ICD) alone [7]. So the state of the art has moved and in our patient, he will probably benefit more from having a CRT-D implanted.

Heart failure is a progressive disease. The patients may have had their medications optimised and even a ICD or CRT-D implanted and may be very stable and leading a high quality of life for many years. Invariably, the heart failure will progress and become more and more difficult to treat. This usually occurs about 7 to 8 years after the initial episode of heart failure. At that stage, medications may not be useful anymore. They may have to be considered for a heart transplant if they qualify or a left ventricular assist device if they do not qualify for a heart transplant or are unable to get a donor heart urgently. The left ventricular assist devices (LVAD) have made a remarkable progress over the last 10 years. The early devices were big, noisy and could not last for more than 2 years. The latest device is very small and can fit into the palm of your hand, silent and can last for at least 10 years. In a trial of a permanent implantantion of a left ventricular assist device in severe heart failure patients who were inotrope dependent, the two year survival was 58% versus 8% survival for patients on optimal medical therapy [8]. What is more remarkable was that 83% of the patients with the LVAD were in New York Heart Association class I or II after the therapy and the percentage of patients able to walk jumped from 13% to 89% after the therapy. These amazing results have firmly entrenched LVAD as a treatment of choice for end-stage heart failure patients.

Heart failure is a chronic disease. It requires a good knowledge of the life saving therapies that are available to the patient and the meticulous implementation of these therapies to prolong their life as well as to improve their quality of life.

Dr Kenneth Ng


  1. Felker GM, Lee KL, Bull DA et al. Diuretic strategies in patients with acute decompensated heart failure. N Engl J Med 2011;364;797-805.
  2. The Digitalis Investigation Group. The effect of digoxin on mortality and morbidity in patients with heart failure N Engl J Med 1997;336:525-533.
  3. Flather MD, Yusf S, Keber l et al. Long term ACE-inhibitor therapy in patients with heart failure or left ventricular dysfunction. Lancet 2000;355(9215):1575-81.
  4. The cardiac insufficiency bisoprolol study II (CIBIS-II): a randomised trial. Lancet 1999;35399416):9-13.
  5. Swedberg K, Komajda M, Bohm M, Borer JS Ford I et al. I***** and outcomes in chronic heart failure (SHIFT): a randomised placebo-controlled study. Lancet 2010;376(9744):875-885.
  6. Moss AJ, Zareba W, Hall JW et al. Prophylactic implantation of a defibrillator in patients with myocardial infarction and reduced ejection fraction N Engl J med 2002;346:877-883.
  7. Tang ASL, Wells GA, Talajic M et al. Cardiac-resynchronization therapy for mild to moderate heart failure. N Engl J Med 2010;363:2385-2395.
  8. Slaughter MS, Rogers JG, Milano CA et al. Adavnced heart failure treated with continuous flow left ventricular assist device. N Engl J Med 2009;361:2241-2251.

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