We searched MEDLINE for reports of studies published on or before Oct 19, 2018, using the terms “heart failure”, “mitral regurgitation, “echocardiography”, “computed tomography”, “cardiac magnetic resonance”, “nuclear imaging”, “prognosis”, “mitral regurgitation”, “right ventricular failure”, and “tricuspid regurgitation”. The studies were selected according to the objectives of the Series, including the use of multimodality imaging in heart failure and how imaging techniques can help in the
SeriesMultimodality imaging in ischaemic heart failure
Introduction
Heart failure is one of the main public health problems with an increasing prevalence. A systematic analysis for the Global Burden of Disease Study 2010 indicated that approximately 37·7 million people live with heart failure.1 In the USA, projections indicate that the prevalence of heart failure will increase by 46% from 2012 to 2030.2 Although advances in medical therapy have been associated with reduction in mortality after heart failure diagnosis, still 50% of people diagnosed with heart failure will die within 5 years of diagnosis.2, 3 Ischaemic heart disease is the main cause of heart failure in high-income countries1 and was the underlying cause of death globally in 2013, accounting for 15·7% of all deaths.4 Data from 24 multicentre trials on heart failure including more than 43 000 patients showed that coronary artery disease was the underlying cause of heart failure in 62% of the patients.5 This percentage might be underestimated since the cause of heart failure was not systematically assessed in all trials.
After acute myocardial infarction, several anatomical changes in the left ventricular myocardium occur, encompassing scar formation (replacement fibrosis), dilation of the infarcted region, as well as reactive fibrosis, left ventricular hypertrophy, and dilation of the remote zone. These anatomical changes keep the wall stress at minimum and the left ventricular systolic function preserved.6 However, at long-term follow-up, these compensatory mechanisms might be exhausted leading to further left ventricular remodelling and dysfunction, causing distortion of the mitral valve apparatus and mitral regurgitation. The regurgitation imposes a volume overload to the left ventricle resulting in further progression of left ventricular remodelling with increasing mitral regurgitation. The left ventricle volume overload and increased filling pressures are transmitted to the left atrium that responds with dilation, and to the pulmonary vasculature leading to post-capillary pulmonary hypertension, which imposes an increased pressure overload to the right ventricle. If this situation is maintained for a long time, the right ventricle dilates and the subvalvular apparatus of the tricuspid valve changes along with dilation of the tricuspid valve annulus causing tricuspid regurgitation. The volume overload caused by the tricuspid regurgitation will lead to further dilation of the right ventricle and systolic dysfunction. This staged development of ischaemic heart failure (figure 1) sets the basis to tackle the sequential problems with specific therapies on top of guideline-directed medical therapy, which has already shown to improve outcome of patients with heart failure.7 The table summarises the stepwise main questions during the assessment of patients with heart failure. The first evaluation (step 1) includes the assessment of left ventricular dimensions and function followed by the assessment of the underlying cause of heart failure (ischaemic vs non-ischaemic). To decide whether coronary revascularisation is needed, ischaemia and myocardial viability are key concepts that need to be evaluated (step 2). In addition, detailed assessment of the presence and severity of mitral regurgitation (step 3) should be done to decide whether (surgical or transcatheter) mitral valve repair is indicated. Right ventricular dilation and reduced systolic function (step 4), as well as the presence and severity of tricuspid regurgitation (step 5) are associated with worse outcome, and surgical tricuspid valve repair might be considered. The role of multimodality imaging to evaluate patients with ischaemic heart failure permits individualised patient analysis regarding these therapies (revascularisation, device-therapy, and valvular repair), which will be assessed in this Series paper.8 Furthermore, the technological developments of these different imaging techniques will be highlighted.
The systematic approach described to determine the extent and severity of heart failure provides the foundation for (guideline-based) treatment; importantly, randomised controlled trials are scarce in this field and the use of imaging to guide the therapeutic decision making is mostly based on expert-consensus, but whenever trials are available, they will be addressed (appendix).
Section snippets
Step 1: assessing left ventricular remodelling
Left ventricular remodelling is defined by the changes in the typical anatomy and structure of the left ventricle with increased volumes, and alterations in wall thickness and shape that reduce its function. Myocyte hypertrophy and apoptosis, myofibroblast proliferation, and interstitial fibrosis are the histological changes that characterise left ventricular remodelling. Assessment of left ventricular remodelling is clinically relevant since left ventricular ejection fraction, end-diastolic,
Step 2: diagnosing the cause of heart failure and assessment of myocardial viability
ECG and echocardiography are the first medical evaluations for patients with heart failure symptoms: the presence of Q waves on the ECG and regional wall motion abnormalities on echocardiography usually indicate coronary artery disease. However, this diagnosis is not correct for a substantial percentage of patients. A retrospective analysis of the Duke Databank for Cardiovascular Disease of 2054 patients with a left ventricular ejection fraction of less than 45% showed that 58% of patients had
Step 3: assessment of mitral regurgitation
The left ventricular remodelling process causes apical and posterior displacement of the papillary muscles, with consequent tethering and malcoaptation of the mitral valve leaflets leading to mitral regurgitation. This so-called secondary or functional mitral regurgitation is characterised by normal mitral valve anatomy, but distorted geometry of the mitral valve apparatus, and reduced closing forces due to left ventricular remodelling. The prevalence of secondary mitral regurgitation among
Step 4: detection of right ventricular remodelling
The right ventricle is a compliant thin-walled cardiac chamber that tolerates better volume overload than pressure overload. Left ventricular systolic dysfunction and mitral regurgitation cause postcapillary pulmonary hypertension and right ventricular pressure overload. The right ventricle responds to this chronically increased pressure overload with dilation of the cavity and tricuspid valve annulus, which results in tricuspid valve regurgitation (volume overload) contributing to further
Step 5: assessment of tricuspid regurgitation
Tricuspid regurgitation that results from left ventricular dysfunction and increased pulmonary vascular resistance, as well as right ventricular dilation and dysfunction, is characterised by dilated tricuspid annulus and tethered leaflets by apically displaced papillary muscles and is categorised as secondary tricuspid regurgitation (appendix). In patients with left ventricular systolic dysfunction and indication for cardiac resynchronisation therapy or ICD, the right ventricle lead can impinge
Conclusions
In the majority of patients, heart failure is secondary to chronic coronary artery disease, referred to as ischaemic cardiomyopathy. Non-invasive imaging can stage the cardiac involvement and can guide therapeutic decision making beyond optimised medical therapy. Specifically, the development of advanced imaging with PET, CT, and CMR, but also 3D echocardiography, support detailed, personalised decision making regarding the need for revascularisation, ICD implantation, and mitral or tricuspid
Search strategy and selection criteria
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