Speak in French when you can't think of the English for a thing.– Lewis Carroll, Through the Looking-Glass
Acute and chronic heart failure also affect other organs such as the liver. The phenomenon of liver dysfunction due to heart disease was first described by a French physician, Louis-Alfred Becquerel, in 1840 (1) and since then, the clinical, histological and haemodynamical features of the syndrome have been well documented (2–8). The French call it ‘foie cardiaque’, whereas English lacks a comparable expression. The different clinical subsets of ‘foie cardiaque’ can be classified under acute, chronic and acute-on-chronic presentations, which all have in common the underlying concept of liver disease or dysfunction secondary to a primary cardiac cause. These syndromes have been pathogenically classified as ‘forward failure’, or effects of arterial hypoperfusion and hypoxia due to a low cardiac output, and ‘backward failure’, representing the passive congestion due to elevated right atrial and central venous pressures (3, 4, 6–9). In English, we call the acute forward failure syndromes ‘shock liver’ or ‘ischaemic hepatitis’. Chronic backward failure is more common and is known by a variety of terms such as ‘passive congestion’ of the liver. The diagnoses can be confirmed by hepatic venous and right atrial pressure measurements (4, 5, 10), usually performed in conjunction with a transjugular liver biopsy. The ‘wedged’ pressure is measured in the hepatic veins by wedging a tapered catheter or inflating an occlusive balloon, and unwedging the catheter or deflating the balloon gives the ‘free’ hepatic venous pressure. The arithmetic difference between the wedged and the free pressure, known as the hepatic venous pressure gradient, reflects the portal pressure. Because congestive heart failure increases right atrial pressure, which is transmitted caudal to the hepatic veins, the free hepatic venous pressure significantly increases, thereby making the hepatic venous pressure gradient normal (4, 5).
Clinically, shock liver and ischaemic hepatitis are characterized by dramatic and rapid elevation of serum liver chemistry tests, especially the transaminases, which typically rise >1000 U/L. The presentation of acute forward failure superimposed on a previous background of chronic congestion is dominated by the features of the acute ischaemia, again with high transaminase elevations (6–8, 10, 11). Clinical features of chronic congestive heart failure, at least in the liver, are generally dominated by the venous congestion rather than any manifestation of forward failure. These patients are the most difficult to correctly diagnose. They often present nonspecifically with mildly abnormal liver chemistry, little or no jaundice and signs of portal hypertension such as ascites (10), thereby suggesting a noncardiac primary liver disease such as alcoholic liver disease. Correct diagnosis in these patients requires a high index of suspicion when a patient with known cardiac disease presents with hepatic dysfunction/disease. Some cases have no prior evidence of heart disease by routine physical examination, and are only detected by the hepatic venous pressure studies.
Correctly recognising and diagnosing ‘foie cardiaque’ is important, as the liver disease only responds to measures that improve cardiac function (3, 6, 7). Fortunately, however, current sophisticated cardiac treatments range from drugs that increase the contractility and decrease the workload to coronary angioplasty and stenting, and even heart transplantation. Therefore, the end-stage condition of cardiac cirrhosis is now rare: in our recent series of 83 patients with liver dysfunction due to heart disease, we only found one such case (10).
Following the precedent of Becquerel, many of the studies on this topic are in the French literature. Indeed, the initial haemodynamic studies of this syndrome are almost exclusively published in French. For example, the cardinal feature of a normal hepatic venous pressure gradient due to elevated free hepatic venous pressure was unreported in the English language literature until 2003 (10), whereas this finding had been described by Coelho et al. (4) and Benhamou et al. (5) in French journals four decades ago.
The problem is that while the specific subsets described above can be individually denoted by accepted English terms, we have no suitable ‘umbrella’ term that encompasses all subsets, like ‘foie cardiaque’. Instead, we must resort to unwieldy descriptions such as ‘hepatic abnormalities in congestive heart failure’ or ‘the liver when the heart fails’. In a recent study, we used the expression ‘cardiac hepatopathy (10)’, but this quasitranslation lacks a certain je ne sais quoi. The literal translation is even worse; ‘cardiac liver’ just does not make sense in English.
It is clear that worldwide, English has replaced French as the ‘lingua franca’ (a bittersweetly ironic term, especially to the French). A strength of English is its ability to borrow and incorporate foreign words. Many examples abound in everyday conversation as well as in medical usage, and often sound much better. How much more elegant is ‘torsade de pointes’ ventricular tachycardia compared to ‘twisting of the points’? And in three simple words, ‘folie à deux’ says it all. Therefore, to recognise the pioneering French work in this area, and also because English lacks a suitable equivalent expression, it is proposed that we adopt the term ‘foie cardiaque’. After all, ‘a good name is more desirable than great riches’ (12).
Dedication: This editorial is dedicated, with admiration and affection, to Prof. Jean-Pierre Benhamou on his 81st birthday. It was my great privilege to be a research fellow in his Beaujon Hospital Hepatology unit during the mid 1980s, and he was the best and most astute clinical hepatologist I have ever come across.
Potential conflict of interest: The author admits to being an unabashed Francophile.