She was admitted to hospital in 1979 to evaluate her progressively limited exercise capacity. On examination she was a thin girl, 144 cm in height and 29 kg in weight. Her lips were mildly cyanosed. The peripheral pulses were normal and peripheral oedema was not present. Her blood pressure was 115/80 mmHg, with a heart rate of 80 beats per minute. The first sound was closely split. A grade 4/6 rough midsystolic murmur was audible in the second intercostal space at the left sternal border. In addition, a grade 3 protodiastolic murmur was heard best in the third intercostal space. The second heart sound was split. These findings were confirmed by phonocardiography.Chest x-ray film showed normal heart size, with dilatation of the pulmonary conus. Electrocardiography showed a PR interval of 0*18 second and evidence of right atrial and ventricular hypertrophy.The M-mode echocardiogram, performed with the Echocardio Visor single element, showed multiple "blurred" echoes in diastole posterior to the anterior leaflet of the tricuspid valve (Fig. 1A). These echoes were also seen in the right ventricular outflow tract. There was no interval between the tricuspid valve opening and the appearance of these "blurred" echoes. At the level of the pulmonary valve a discrete echo structure lying anterior to the valve was detected. This echo structure moved posteriorly with the onset of systole, shortly after the opening of the pulmonary valve (Fig. IB, see arrow).When the heart was examined with a dynamically focused Multiscan system,7 an abnormal thin walled
Six cases of acute myocardial infarction with blood in the pericardial sac are described. In one case rapid death followed myocardial rupture leaving no time for the possibility of intervention. Of two other cases acute symptoms developing after myocardial rupture, one was operated on promptly and the other, whose condition improved on pericardiocentesis, after a delay of a few hours. Both are now long term survivors A fourth patient probably had two episodes of rupture which apparently sealed off. He underwent cardiac catheterization, but no epicardial leak was found. Subsequently at operation a sealed myocardial rupture was detected and sutured over. The fifth patient suffered a silent myocardial rupture. A false aneurysm was diagnosed four months later and he withstood successful surgery. In the sixth patient, the course was similar to that of case 1, namely rapid death with a clinical picture suggestive of tamponade. Postmortem examination showed a covert rupture with some evidence of attempts to plug the opening. The purpose of this report is to emphasize the varying course which myocardial rupture can take.
Thirty three consecutive patients with clinically suspected endocarditis were studied by both precordial cross sectional echocardiography and transoesophageal echocardiography. The diagnostic value of both techniques was assessed. The data were compared with findings at operation in 25 patients. In 21 patients with native valve endocarditis precordial echocardiography showed evidence of vegetations in six patients and suggested their presence in nine. Transoesophageal echocardiography identified vegetations in 18 patients. Complications were seen in four patients at precordial echocardiography and in nine patients at transoesophageal echocardiography. Precordial echocardiography did not show vegetations in any of the 12 patients with prosthetic valve endocarditis whereas transoesophageal echocardiography showed vegetations in four. Complications were seen in four patients at precordial echocardiography and in 10 at transoesophageal echocardiography. Echocardiographic findings were confirmed at operation in all 25 operated patients. In two patients both echocardiographic techniques had missed the perforation of the cusps of the aortic valve that was seen at operation, but this had no effect on patient management. Transoesophageal echocardiography is the best diagnostic approach when infective endocarditis is suspected in patients with either native or prosthetic valves.
The long-term results of a consecutive series of transannular gamma-irradiated homograft monocusp patches in tetralogy of Fallot were studied. Seven survivors out of 8 patients are doing clinically well after a mean of 22.4 years of follow-up, 5 of them being in New York Heart Association class I and 2 in class II. In one patient the completely calcified gamma-irradiated homograft monocusp patch was replaced 15 years after intracardiac repair. Echocardiographic investigation at the end of follow-up of the remaining 6 patients with a gamma-irradiated homograft monocusp patch in situ showed mild pulmonary regurgitation in 1, moderate regurgitation in 3, and severe regurgitation in 2. Residual pulmonary stenosis was present in 4 patients (gradients ranging from 10 to 40 mmHg). Right-ventricular dilatation was present in all patients. In the long-term the gamma-irradiated transannular homograft monocusp patch behaves like a simple transannular patch.
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