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BACKGROUND: Chronic pulmonary regurgitation often leads to myocardial dysfunction and heart failure. It is not fully known why secondary hypertrophy cannot fully protect against the increase in wall stress brought about by the increased end-diastolic volume in ventricular dilation. It has been assumed that mural architecture is not deranged in this situation, but we hypothesised that there might be a change in the pattern of orientation of the aggregations of cardiomyocytes, which would contribute to contractile impairment.METHODS: We created pulmonary valvular regurgitation by open chest, surgical suturing of its leaflets in seven piglets, performing sham operations in seven control animals. Using cardiovascular magnetic resonance imaging after 12 weeks of recovery, we demonstrated significantly increased right ventricular volumes in the test group. After sacrifice, diffusion tensor imaging of their hearts permitted measurement of the orientation of the cardiomyocytes.RESULTS: The helical angles in the right ventricle approached a more circumferential orientation in the setting of right ventricular RV dilation (p = 0.007), with an increased proportion of surface-parallel cardiomyocytes. In contrast, this proportion decreased in the left ventricle. Also in the left ventricle a higher proportion of E3 angles with a value around zero was found, and conversely a lower proportion of angles was found with a numerical higher value. In the dilated right ventricle the proportion of E3 angles around -90° is increased, while the proportion around 90° is decreased.CONCLUSION: Contrary to traditional views, there is a change in the orientation of both the left ventricular and right ventricular cardiomyocytes subsequent to right ventricular dilation. This will change their direction of contraction and hinder the achievement of normalisation of cardiomyocytic strain, affecting overall contractility. We suggest that the aetiology of the cardiac failure induced by right vetricular dilation may be partly explained by morphological changes in the myocardium itself.

A young lady presented with 1-month history of fever on transthoracic echocardiography along with colour interrogation, she was found to have a small ventricular septal defect and large vegetations on pulmonary valve with severe pulmonary valvular regurgitation. Other cardiac valves were normal. On further detailed study, there was an echolucent paravalvular area, suggestive of paravalvular abscess. These findings were confirmed subsequently during surgery. This case with isolated pulmonary valvular infective endocarditis and associated paravalvular abscess is a very rare finding.

The right ventricle (RV) tolerates acute pulmonary valvular regurgitation fairly well, however, in the long-term dilatation and failure often ensues. There is little known of the structural and functional myocardial alterations following this pathophysiology, and therefore animal models are sought. We aimed to develop an animal experimental model for RV dilatation emphasizing feasibility, reproducibility and human compatibility. Free pulmonary valve insufficiency and RV dilatation were created with a novel external suture plication technique in nine 5 kg piglets. Six matched animals served as controls. After 10 weeks cardiac dimensions and physiology were assessed with in vivo cardiovascular MRI and conductance technique. RV end-diastolic volume increased 31% in the intervention group (P=0.03). The regurgitation fraction was 37% in the intervention group compared to -2% in controls (P

IPVR is a rare clinical entity that was first diagnosed during life in 1955. In the past 35 years, only 69 patients have been reported. With increasing clinical awareness, as well as use of PDE, the confirmation of its clinical diagnosis has become easier and more accurate without having to take recourse to invasive cardiac studies as in the past. For this reason, it is becoming increasingly apparent that IPVR is not so rare as has been suggested in the past. IPVR is more common in men than in women, in whites than blacks, and in the young than the elderly. The mean age of IPVR patients is 27 years (range, 4 to 85). The majority of the patients are asymptomatic and the diagnosis is usually suspected upon the discovery of a crescendo-decrescendo, low-pitched, early to mid diastolic murmur in the second and third left intercostal space, which increases during inspiration, particularly in the presence of a hyperdynamic right ventricle and in the absence of peripheral circulatory phenomenon of aortic regurgitation. The ECG often shows right axis deviation, incomplete right bundle branch block, and rarely, right ventricular hypertrophy and strain. However, a normal ECG does not preclude its diagnosis. Approximately 30% of the IPVR patients have normal 12-lead ECGs. The diagnosis may be further suggested by the posteroanterior chest roentgenogram when dilated and large central pulmonary arteries are noted to pulsate vigorously (hilar dance) on chest fluoroscopy. In the past, the diagnosis of IPVR could only be confirmed at cardiac catheterization by demonstrating equalization of late diastolic pressures in the right ventricle and pulmonary artery, and with selective angiocardiography by demonstrating reflux of contrast material from the main pulmonary artery into the right ventricle. However, the diagnosis now can be accurately confirmed by noninvasive PDE, and more recently by CDFM, particularly when the regurgitation jet is detected 1 to 2 cm or more below the pulmonic valve and it occupies 75% or greater of the entire duration of diastole. Because the majority of the patients with IPVR are asymptomatic, they need not be subjected to invasive studies; however, these should be considered before any active surgical intervention. Besides periodic follow-up and infective endocarditis prophylaxis, no other intervention is needed in most cases of IPVR. However, with the first indication of right ventricular failure, surgical intervention should be actively considered, either in the form of prosthetic valve replacement when IPVR is solely due to valvular abnormality or a composite graft when IPVR is due to both valvular dysfunction, as well as pulmonary artery dilatation. The long-term prognosis of IPVR appears excellent, particularly in those who are young and have a congenital variety of IPVR. However, the ultimate prognosis remains uncertain, particularly in those with acquired IPVR. Even this lesion is well tolerated in middle-age and elderly individuals; however, rarely right heart failure may ensue, particularly in those who have severe regurgitation to the degree that compromises the capcity of the right ventricle to tolerate it. Until the results of a large long-term cooperative study of several patients with IPVR becomes available, it will be difficult to be certain about the prognosis in any given patient.

Background . The insertion of bioprosthetic valves into the pulmonic position is not performed commonly because of uncertainty concerning the necessity and durability of such valves. Methods . We reviewed the long-term outcome of 10 patients who underwent pulmonary valve replacement with bioprostheses between March 1985 and March 1997. A Carpentier-Edwards supraannular bioprosthesis was used in 7 patients, a Hancock II bioprosthesis was used in 2 patients, and a Carpentier-Edwards pericardial bioprosthesis was used in 1 patient. The mean patient age at the time of pulmonary valve replacement was 38.9 ± 16.3 years (range, 15 to 63 years). The diagnoses were pulmonary valvular regurgitation after corrective surgery for tetralogy of Fallot in 7 patients, right ventricular outflow tract stenosis and absent right pulmonary artery combined with a double-outlet right ventricle in 1 patient, pulmonary valvular regurgitation with pulmonary artery dilatation in 1 patient, and aortic valve stenosis treated with our modification of the Ross procedure using a pulmonary bioprosthesis in 1 patient. Survivors were followed up for a mean of 5 years and 5 months. Results . One patient underwent reoperation because of infective endocarditis of the bioprosthesis. No bioprosthetic valve dysfunction has been observed on Doppler echocardiography during a maximum follow-up period of 12.2 years, except in the patient who underwent replacement at 15 years of age. Conclusions . Bioprostheses in the pulmonic position are durable in adult patients because they face a minimal hemodynamic load, but they may undergo early leaflet degeneration in younger patients.

Surgical repair was performed on 8 patients with tetralogy of Fallot and congenital or acquired absence of the left pulmonary artery. Prior palliative systemic-pulmonary artery shunts had been performed in the 5 patients with acquired absence of the pulmonary artery, and in none was repair of the damaged pulmonary artery possible. A valve-containing conduit (Hancock) was used in each patient to prevent pulmonary valvular regurgitation during the early postoperative period. All patients survived operation and have exhibited marked symptomatic and hemodynamic improvement. This contrasts with the poor results of corrective operation previously reported in patients in this diagnostic category. We believe that the present improved results are due in large part to the valved conduit, and we therefore recommend its use during repair in children or adults with tetralogy and a single pulmonary artery.

Angiocardiographic findings in 9 infants with patent ductus arteriosus following maternal rubella are described. In 8 patients, certain anomalies of the pulmonary valve and main pulmonary artery were present which represent possibly a specific sign of post-rubella infection. These anomalies are: (1) a foreshortened main pulmonary artery, (2) a high, posteriorly placed, vertically tilted, pulmonary valve, (3) pulmonary valvular regurgitation, and (4) thickened pulmonary valves. In addition, 2 cases showed localized ectasia of the left subclavian artery.

Postoperative haemodynamic evaluation was performed on 15 patients 7 to 14 years (mean, 11 years) after total intracardiac repair of Fallot's tetralogy. The average age of the patients at the time of postoperative catheterization was 20 years (range 12 to 29) and they were all asymptomatic. Before operation 11 patients were severely cyanosed and disabled and 4 had mild cyanosis with anoxic spells. The cardiac output and right heart pressures were measured at rest and after 5 minutes of submaximal exercise on a bicycle ergometer. It was shown that the degree of residual obstruction of the pulmonary outflow tract was slight and that the right ventricular/pulmonary arterial systolic gradient (RV/PA gradient) exceeded 20 mmHg (2-6 kPa) at rest in only 3 patients. The mean cardiac index at rest was 5-4 l min-1 m-2 which increased to 8-3 l min-1 m-2 during exercise. The response of the cardiac output during exercise was either normal or supranormal in 14 of the 15 patients. In the remaining patient the response was marginally below the normal range. Pulmonary valvular regurgitation was present in 8 patients but there was no detectable difference in the cardiac function of these patients compared with patients with competent pulmonary valves. Six of the patients investigated had also had cardiac catheterizations performed 1 to 4 years after operation. The results of the present study show that remarkably little change has occurred in their haemodynamic status in the intervening years. Though these results are encouraging, further studies are required to determine the eventual outcome of the RV pressure and volume overload.

A patient is reported with isolated pulmonary valvular regurgitation acquired probably as a result of endocarditis at age 22 years. The patents remained essentially asymptomatic with physical findings compatible with haemodynamically significant pulmonary regurgitation until death at age 85 years. A necropsy confirmed the presence of isolated severe pulmonary valvular destruction. This long-term follow-up lends further support to the concept that significant volume overload of the right ventricle from pulmonary regurgitation is well tolerated and usually does not require surgical intervention.