A patient with severe heart failure secondary to coronary heart disease is presented. Following investigation he was thought to have significant areas of myocardial hibernation and was therefore treated with coronary revascularisation, with major clinical benefit.
- heart failure
- myocardial hibernation
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Chronic heart failure is an increasing public health problem and coronary heart disease is the single commonest cause. The prognosis, even with optimal medical therapy, is poor. However, reversible ventricular dysfunction is becoming increasingly recognised as a cause of heart failure and may be amenable to myocardial revascularisation in selected patients.
A 57-year-old man was referred for further investigation of his ischaemic heart disease. Angina had first been diagnosed in 1990 and he had suffered an anteroseptal Q-wave myocardial infarction in 1993. There was a history of type 2 diabetes, hypertension, hypercholestrolaemia and peripheral vascular disease. On review in November 1994 he had not experienced angina for 9 months but had NYHA Class III dyspnoea and fatigue with frequent episodes of paroxsymal nocturnal dyspnoea, despite treatment with frusemide, enalapril, gliclazide and simvastatin. On physical examination, a third heart sound gallop was noted, along with bilateral basal lung crackles.
At cardiac catheterisation the left ventricle was dilated with globally poor wall motion. The left ventricular ejection fraction was only 9% (normal 59–75%). Left ventricular end-diastolic pressure was 34 mmHg (normal 6–12 mmHg). There were tight proximal stenoses in the right coronary artery with complete proximal occlusions of the left anterior descending and left circumflex coronary arteries. A diagnosis of severe three-vessel coronary disease with severe left ventricular impairment and grade III heart failure was made.
In view of the poor prognosis, it was felt that surgical therapy should be considered. His comorbid conditions of diabetes, hypertension, and peripheral vascular disease were thought to make cardiac transplantation a less favourable option; however his coronary disease was anatomically suitable for revascularisation if there were a realistic prospect of benefit and survival. Therefore, a thallium perfusion study was performed, with 74MBq of thallium-201 injected at rest with immediate and 4-hour-delayed imaging. This showed considerable lung activity with a severe perfusion defect at the cardiac apex and reduced activity in the remaining segments. After 4 hours, improvement was noted throughout the heart, though incomplete at the apex (figure). The study was interpreted as showing evidence of extensive myocardial viability despite the poor left ventricular function. Therefore, coronary artery bypass grafting was performed in June 1995. The immediate postoperative course was uncomplicated, without the requirement for prolonged intensive care or haemodynamic support. However, he did suffer a minor pulmonary embolus some 27 days after surgery.
At review four months after surgery he was noted to be in NYHA Class I with a normal physical examination. Radionuclide ventriculography showed a left ventricular ejection fraction of 32% (normal >45%).
The term ‘myocardial hibernation’ was first coined by Rahimtoola when commenting on the results of the large randomised trials of coronary artery surgery.1 He envisaged a state of chronic coronary hypoperfusion, insufficient to cause necrosis but leading to a prolonged reduction in myocardial contractility; this could occur even in the absence of limiting angina. He proposed that this state was reversible if the coronary blood supply could be improved. Subsequent authors have termed the hibernating heart the ‘smart heart’.2 Such reversible left ventricular dysfunction has been shown to occur in several stages of coronary heart disease, including chronic heart failure.3 In most patients with coronary heart disease, any associated left ventricular dysfunction is likely to be the result of various factors; reversible ones such as ‘hibernation’ and myocardial ‘stunning’ (persistent but slowly reversible dysfunction due to transientepisodes of ischaemia) and irreversible factors such as pre-existing myocardial necrosis.
The accurate detection of regions of myocardial hibernation is vital if such patients, often with poor left ventricular function, are to be offered coronary revascularisation with a reasonable expectation of benefit. Various methods have been described; the main methods currently in use involve either the assessment of inotropic reserve with dobutamine echocardiography or the demonstration of cellular integrity with radionuclides.The so-called ‘gold standard’ for assessment is positron emission tomography, looking for metabolic activity in dysfunctional and hypoperfused areas; pooled data indicates a sensitivity of 88% with a specificity of 73%.4Low-dose dobutamine echocardiography has reported sensitivities of 71–97%, with generally higher specificities. Of the radioisotope methods described, those using thallium-201 are the most widely available and offer acceptable predictive accuracy if appropriate protocols are used.4 If thallium-201 is used as the radionuclide it is important to realise that conventional stress-imaging protocols will seriously underestimate the extent of viable myocardium; protocols utilising rest imaging are more appropriate.5
myocardial dysfunction due to coronary artery disease can be reversible if the muscle is ‘hibernating’
even patients with previous myocardial infarctions and severe heart failure can have significant areas of viable myocardium on investigation
such patients can improve markedly after successful revascularisation
accurate non-invasive methods to detect areas of viability exist and are clinically validated
Heart failure due to coronary heart disease continues to carry a grim prognosis, even with optimal medical therapy. In carefully selected patients myocardial revascularisation can improve symptomatic status; evidence is also beginning to emerge that it can improve prognosis in those patients with truly reversible contractile dysfunction.6