A case of hepatopulmonary syndrome.

UNLABELLED: This report presents the case of a 42-year-old man with liver cirrhosis who presents with breathlessness. Initial investigations are unable to explain his persistent hypoxia and a diagnosis of hepatopulmonary syndrome is considered. Saline contrast echocardiography is utilised in confirming the diagnosis. Details of this case as well as practicalities in performing and interpreting saline contrast echocardiography are reviewed. LEARNING POINTS: Key features of hepatopulmonary syndrome are liver disease, hypoxia and pulmonary vascular dilatations.Saline contrast echocardiography is a simple inexpensive procedure to perform and key to confirming the diagnosis of hepatopulmonary syndrome. Detection can be improved by performing the scan in the stand-up position.Agitated saline contrast studies are more commonly performed to identify intra-cardiac shunts. Timing of contrast arrival in the left heart chambers is key to differentiating intra-cardiac shunting from extra-cardiac pulmonary transit.

Functionally uni-leaflet mitral valves in a family: a case series.

Functionally uni-leaflet mitral valves are extremely rare. In severe cases, they are considered incompatible with life beyond the neonatal period. We present a case series of three adults with almost complete absence of the posterior mitral valve leaflet and who are asymptomatic, with no more than mild mitral regurgitation. We believe that this is the first reported instance of such findings in a single family.

Angiotensin II receptor antagonists in chronic heart failure: where do they fit?

Heart failure is a common and disabling condition with a dismal prognosis. Inhibition of the renin-angiotensin-aldosterone system (RAAS) with angiotensin converting enzyme (ACE) inhibitors has proven to be a valuable therapeutic strategy in this condition, with well-proven morbidity and mortality benefits. Nonetheless, ACE inhibitors provide incomplete blockade of the RAAS and also inhibit the degradation of bradykinin. Although increased levels of bradykinin may have haemodynamic advantages by contributing to vasodilatation, they may also be largely responsible for some of the adverse effects of ACE inhibitors. Angiotensin II (Ang II) receptor antagonists offer more complete blockade of the RAAS without the potentiation of bradykinin, and it was therefore hoped that they would provide even greater benefits for patients with heart failure. So far, much of the initial promise of the Ang II receptor antagonists in heart failure has not been realised. There has been no conclusive demonstration of their superiority to ACE inhibitors in their effects on morbidity and mortality, and their equivalence to ACE inhibitors has not been proven. The Ang II receptor antagonists have, however, proven to be better tolerated than ACE inhibitors and they are therefore likely to be a reasonable alternative for those patients with heart failure who cannot tolerate ACE inhibition. Recent evidence has indicated that the Ang II type 1 receptor antagonist valsartan is of value when used in patients already receiving either an ACE inhibitor or a beta-blocker, but has also suggested that giving all three drugs together is deleterious. Further evidence about the value of Ang II receptor antagonists in heart failure may be provided by further studies, of which several are currently ongoing.

Assessing exercise capacity, quality of life and haemodynamics in heart failure: do the tests tell us the same thing?

BACKGROUND: The objective measurement of exercise tolerance is an important component of heart failure trials. The use of laboratory-based treadmill exercise testing has attracted criticism, however, as being unrepresentative of patients' true capabilities. AIM: To examine the relationships between tests of exercise capacity, quality of life and haemodynamics in patients with stable symptomatic heart failure. METHODS: Thirty-six patients with mild-moderate chronic heart failure were studied. Exercise capacity was assessed in the laboratory by maximal treadmill tests and self-paced corridor walk tests, and in the patients' homes by hip-borne pedometers. Quality of life was assessed by a disease-specific questionnaire. Cardiac output and limb blood flow were measured by non-invasive techniques. RESULTS: Customary activity as assessed by pedometer scores correlated with quality of life questionnaire scores (r(S) = 0.47, P = 0.04), and both variables correlated with limb (calf) blood flow (pedometer scores: r(S) = 0.39, P = 0.03; quality of life scores: r(S)= 0.50, P = 0.04). The laboratory-based maximal treadmill test correlated with the self-paced corridor walk test, but neither of these tests correlated with pedometer scores, quality of life or haemodynamics. CONCLUSIONS: Different methods of assessing exercise capacity do not appear to give comparable results and bear different relationships to haemodynamic variables and quality of life. Pedometer scores of customary activity may better reflect patients' quality of life and appear to be more closely related to limb blood flow than the maximal treadmill exercise test or the corridor walk test. The sole use of laboratory-based exercise tests in therapeutic trials may give a misleading assessment of treatment efficacy in heart failure patients.