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The diagnosis of constrictive pericarditis is not easy to make. This rare condition can be suggested by clinical, echocardiograohic, hemodynamic, and radiological signs. It must be distinguished from restrictive cardiomyopathy as therapeutic options are radically different. We present an ambiguous case of constrictive pericarditis with macroscopically normal pericardium recognized 10 years after open-chest cardiac surgery: a large pericardiectomy rapidly induced clinical improvement.

Beta blockers are thought to exert beneficial effects on the ischemic heart. The authors examined the effects of landiolol (ONO 1101), a highly selective beta1 antagonist, propranolol, a nonspecific beta blocker, and esmolol, a selective beta1 antagonist, on postischemic contractile recovery. Drugs were given prophylactically.Ischemia-reperfusion in isolated guinea pig hearts was induced by stopping the perfusion for 45 min and reperfusing for 60 min. Hearts (n = 7 in each group) were treated with or without propranolol (1 or 10 microM), esmolol (5 or 50 microM), or landiolol (20, 100 or 500 microM) ten minutes before inducing ischemia.At the end of reperfusion, left ventricular pressure (LVP) recovered to 64 +/- 3% of the baseline value in the control group. With 1 and 10 microM propranolol, LVP recovered to 90 +/- 5% and 100 +/- 6% of the baseline value at 60 min after reperfusion, respectively. Fifty microM but not 5 microM of esmolol resulted in restoration of LVP to 97 +/- 17% of the pre-ischemic value at 60 min after reperfusion. In hearts pretreated with 100 and 500 microM landiolol, LVP was restored to 109 +/- 5% and 104 +/- 5% of the baseline value, respectively. Landiolol 100 microM did not depress LVP in the pre-ischemic period.The present study shows that landiolol, an ultra-short-acting cardioselective beta1 blocker, has cardioprotective effects on ischemia-reperfusion injury in isolated guinea pig hearts. All three beta blockers were equally protective but the intermediate dosage of landiolol preserved LVP during the pre-ischemic period.

Amiloride 5-(N,N-dimethyl)(AMD), an Na+/H+ pump inhibitor, was used to evaluate the maturity and sensitivity of the Na+/H+ pump in neonatal myocardial cells.Using the isolated contraction isometric heart model, the hearts of neonatal rabbits (10-12 days) were stopped by cardioplegia with and without AMD (20 mumoles/l), then submitted to 40 minutes of ischaemia at 37 degrees C or 120 minutes of ischaemia at 20 degrees C before being reperfused for 30 minutes at 37 degrees C. When AMD was added to the cardioplegic solution, it was also added (20 mumoles/l) to the Krebs solution for the first five minutes of reperfusion. Functional assessment of myocardial contractility and relaxation was performed before aortic clamping and after 30 minutes of reperfusion. Coronary venous drainage during reperfusion was collected to evaluate CPK levels.To 37 degrees C or 20 degrees C, Na+/H+ pump inhibition was marked by improvement of all myocardial contractility and relaxation parameters at the end of the reperfusion period. A significantly reduced CPK release wase also observed during reperfusion associated with Na+/H+ pump inhibition.This study demonstrates maturation of the Na+/H+ pump in neonatal myocardial cells and confirms the role of this ion exchange pump in the pathogenesis of ischaemia-reperfusion lesions. The study at 20 degrees C demonstrated the sensitivity of the Na+/H+ pump to a low transmembrane proton gradient.

Pure infundibular stenosis of the right ventricle is a rare congenital anomaly. Right midventricular stenosis with intact interventricular septum is even rarer. It consists of obstruction of the trabecular zone of the right ventricle by a hypertrophied moderator band with or without abnormal muscle bundles. This anomaly can now be diagnosed by transthoracic echocardiography, while haemodynamic and angiographic diagnosis is reserved for doubtful cases. Two cases of midventricular stenosis are reported. In both patients, the diagnosis was suspected bu ultrasonography which showed a right intraventricular gradient of about 80 mmHg without identifying the exact site (infundibular or midventricular). The diagnosis was corrected by the operative findings. A good postoperative course was observed for both patients.

We report the case of a patient with refractory ascitis due to a constrictive pericarditis who underwent a liver transplantation with the initial diagnosis of cryptogenic cirrhosis. The cardiac origin was suspected 5 months post surgery when a liver biopsy showed lesions in favor of a post sinusoidal shunt. The diagnosis was confirmed by the increased values of the right intra-ventricular pressures. We discuss the causes of the delay of the diagnosis and, in particular, the difficulty to interpret vascular liver lesions. Such vascular lesions were present on the needle biopsy performed prior to transplantation but wrongly interpreted as cirrhosis.

Left ventricular hypertrophy (LVH) is a physiological process of adaptation of the heart to mechanical load increase. Despite depression of left ventricular (LV) contractile performance, work efficiency is preserved and ventriculoarterial coupling is almost normal in hypertensive patients with LVH. To assess the differences between patients with and without LVH, LV contractile performance, the ventriculoarterial coupling and mechanical efficiency were compared in 2 groups of hypertensive patients with similar body surface area and arterial pressures, 23 without LVH (group 1) and 30 with LVH (group 2) and compared to data of 20 normotensive subjects. Left ventricular angiography coupled with simultaneous recording of pressures with micromanometer were used to determine end-systolic stress-to-volume ratio (ESSVR), end-systolic elastance (Ees), effective arterial elastance (Ea), external work (EW) and pressure-volume area (PVA). Left ventricular contractile performance assessed by Ees/100 g myocardial mass and EESVR were lower in group 2 than in group 1 (1.23 +/- 0.28 vs 1.89 +/- 0.48 mmHg/mL/100 g and 6.22 +/- 1.07 vs 9.56 +/- 0.97 g/cm2/mL/m2, respectively, both p0.0001, control subjects: 1.47 +/- 0.41 and 6.97 +/- 1.22, respectively). Ventriculoarterial coupling evaluated through Ea/Ees ratio (0.51 +/- 0.05 in group 1 vs 0.53 +/- 0.08 in group 2, 0.49 +/- 0.09 in control subjects), and work efficiency evaluated through EW/PVA ratio (0.80 +/- 0.02 in group 1 vs 0.78 +/- 0.03 in group 2, 0.80 +/- 0.03 in control subjects), were similar in the 2 groups and were comparable to control subject values. In conclusion, this study shows that ventriculoarterial coupling and work efficiency are comparable in hypertensive patients with and without LVH. These results suggest that in patients without LVH the matching between left ventricle and arterial receptor is preserved through an enhancement of myocardial contractility which is energetically costly. Conversely, LVH seems to be a useful adaptation which minimizes the energetical cost of high pressure generation.

The study of diastolic function is an essential step in Doppler echocardiographic investigation of cardiac failure. Although the recording of transmitral flow remains the basis of analysis of diastolic function, it should be completed by other Doppler parameters. In fact, the simple analysis of transmitral flow is not sufficient because of the interplay of other factors, especially the preload. The authors describe the complementary ultrasonographic approaches for analysis of diastolic function, especially the ventricular filling pressures, by recording of pulmonary venous flow, the kinetics of the mitral annulus and the propagation of intra-ventricular flow.

The aim of this study was to analyse the possible relationship between inversion of the end diastolic wave of pulmonary venous flow (Avp) recorded by transoesophageal echocardiography in the left superior pulmonary vein and left ventricular end-diastolic pressures (LVEDP) at cardiac catheterisation. In this series of patients, there was a poor correlation between the E/A ratio of transmitral blood flow and LVEDP. On the other hand, there was a better correlation between LVEDP and the difference of duration of the end diastolic Avp wave and the A wave of mitral flow. An even better correlation was found between LVEDP with respect to the contribution of atrial systole and the difference of duration Avp-A. When the pressure due to atrial contraction exceeds 15 mmHg, the difference between the durations of pulmonary and mitral A waves increases. Therefore, when the duration of the end diastolic Avp is greater than that of the mitral A wave, a LVEDP of over 15 mmHg may be predicted with a sensitivity of 88% and a specificity of 74%.