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Professor Dirk Brustsaert
FESC and Immediate Past President HFA of the ESC
Silent Majority: cardiac suction failure
Sunday 15 June in the Auditorium from 08:30 - 10:00
| Here is an insight :
In numerous recent clinical trials, patients with chronic heart failure (CHF) have been arbitrarily subdivided into two groups, depending on the LV Ejection Fraction (LVEF) being either ‘preserved’ (> 40-50%) or ‘depressed’ (< 35-40%). This arbitrary distinction, erroneously coined as either diastolic or systolic heart failure as if heart failure consisted of two distinct diseases, originated from the selection bias of a ‘bimodal’ distribution of LVEF among patients with CHF. As in all recent clinical CHF trials, however, a clearly unimodal LVEF distribution among patients with CHF has been demonstrated, there is no rationale nor pathophysiological basis for this almost dogmatic approach of separating patients with heart failure into two disease categories (FIG 1). This viewpoint has been endorsed further by recent observations of a continuous unimodal progression, also matched for LVEF, of various measurements of TDI-derived indices as well as of cardiomyocyte morphology.
It follows that patients with CHF are to be seen as different phenotypes within a continuous spectrum of one single disease, with at one end of the spectrum patients with predominant concentric hypertrophy -hence stiffer hearts-, and at the other end patients with predominant eccentric hypertrophy –hence less stiff, dilated hearts- , and importantly, between these two extremes of the spectrum a wide transition zone of hybrids with each patient following his/her individual pathway and occupying a position within the spectrum depending on various modifiers (FIG 2). E.g. female gender, hypertension/LVhypertrophy, diabetes, age rather favor positioning towards the end of the spectrum with the stiffer, non-dilated hearts. Only about 15 to 20 % of the latter patients will slowly progress towards the other end of the spectrum with the dilated hearts.
Keeping in mind that traditional physiology has amply demonstrated that the normal mammalian heart functions as a suction-compression pump, the stiffer hearts in the above CHF spectrum primarily suffer from FAILING SUCTION and have in general preserved LVEF, whereas the dilated hearts suffer from failure of both SUCTION and COMPRESSION and have a lower LVEF. Most patients with CHF occupy intermediate positions within the spectrum. Moreover, regardless of their position within the spectrum, all patients can develop the whole range of NYHA I-to-IV symptoms and mortality is high in all.
Cardiac suction failure results i) from impaired load-dependence of systolic LV relaxation (FIG 3) through inappropriate loading conditions, impaired inactivation processes and excessive spatial and temporal non-uniformity of load/inactivation during LV relaxation and early filling, ii)as well as from cardiovascular stiffening and impaired cross-talk of LV hypertrophy and increased arterial impedance through the reflected arterial waves (FIG 4,5,6).
These pathophysiological mechanisms of CHF due to cardiac suction failure and to combined suction-compression failure as well as the implications for diagnosis and guidelines for management (FIG 7,8) will be discussed in detail.
Accordingly, at an early stage in the majority of patients with CHF, i.p. those caused by either chronic hypertension/hypertrophy or in the early stages of cardiac ischemia, suction rather than compression failure of the cardiac pump is often a first ominous sign of impaired cardiac pump function.
Don't miss Prof. Brutsaert's presentation
Sunday 15 June at 08:30 in the Auditorium.
Cardiomyopathies: the 'unknown' face of heart failure
The cardiomyopathies: classification and clinical diagnosis
The term cardiomyopathy was first used over forty years ago, to describe myocardial disorders not caused by haemodynamic disturbances such as valve disease and hypertension, or by multi-system diseases. Heart muscle disorders with an identifiable aetiology were initially termed specific heart muscle diseases, but were later renamed specific cardiomyopathies. Remarkably, this nomenclature has survived to the present day with only minor changes. Recently, expert committees of the AHA and the ESC Working Group on Myocardial and Pericardial Diseases have proposed updates of the cardiomyopathy classification system. The shared motivation was to resolve outstanding ambiguities in the existing classification and to incorporate knowledge derived from advances in molecular genetics. Both proposals continue to define cardiomyopathies according to the morphology and physiology of the ventricles, but place new emphasis on the importance of genetic disease as a cause of cardiomyopathy. The major differences relate to the handling of primary and secondary disease and the classification of ion channel disorders. This presentation will compare and contrast the two approaches and will describe the implications of the ESC classification for everyday clinical practice.
By Doctor Perry Mark Elliot
The Heart Hospital , London , UK
for more information on the session , consult the Scientific Programme Online
Controversies in Heart Failure with Normal EF:
Here is a highlight on Prof.F Zannad 's argument on "treatment is different to heart failure with reduced EF"
Heart failure (HF) with normal (or preserved) ejection fraction (EF) is an entity presenting and evolving with concentric left ventricular (LV) remodelling and mainly diastolic LV dysfunction (DHF) while HF with low EF presents and evolves as an eccentric LV remodelling and combined systolo-diastolic dysfunction (SHF). DHF features distinct isoform shifts of the cytoskeletal proteins, distinct expression pattern of the matrix metalloproteinases system as well as prominent changes in large artery stiffening. DHF is characterised by cardiomyocyte hypertrophy as opposed to reduced myofilamentary density in SHF, Clinically, the contributions of specific individual and common aetiologies as well as the role of co-morbidities are different in DHF and SHF. Many of the pathophysiological features of DHF may be favourably influenced by agents with proven benefit in SHF. However, despite a visible improvement in prognosis under current therapy of SHF, no improvement in the pattern of outcome in DHF has been reported so far. Treatments of DHF should target
- specific mechanisms of transition from risk factors to DHF, such as LVH and diabetic cardiomyopathy,
- mechanisms of progression from DHF to SHF and
- specific mechanisms triggering decompensation, such as abrupt blood pressure rise.
Professor Faiez Zannad
CIC , Hopital Jeanne D'Arc
Domartin les Touls, France
Of course there are always 2 sides in a debate. In Milan you will be able to hear more on Professor Zannad's ideas as well as what the other side has to say ....
Highlight on Session "How is heart failure changing"
Insight from Professor Komajda on his presentation " The burden of the aging population"
" The clinical profile of heart failure patients has dramatically changed over the past decades. Nowadays, the average age of patients hospitalised for this condition is over 70 years and in a large European survey of more than 11000 patients hospitalised for HF across 24 ESC countries, more than 25 % were over 80. Thus, a growing proportion of HF patients is made of elderly patients. All surveys suggest that management of this subgroup of patients is not optimal. Elderly HF patients do not receive the quality of care recommended by international guidelines both for investigations and treatment strategies. Of course, comorbidities or side effects explain partly this situation and, indeed, management of heart failure in the elderly, frail patient is often complicated. Nevertheless, it seems that age in itself leads to self limiting behaviour by care providers. There is therefore room for improvement and we need a better interaction between cardiologists, geriatricians, general practitioners and nurses in order to provide a better service to this growing group of heart failure patients"
Find out more about Professor Komajda's perspective in Milan on Sunday 15 June 08:30 - 10:00 in the Main Auditorium.
Professor Michel Komajda - FESC
Centre Hospitalier Universitaire
Pitie Salpetriere
Paris, France
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