SUMMARY We report a case in which pulmonary embolectomy was crucial in the successful outcome of an operation to remove a right sided atrial myxoma. The association between such myxomata and embolisation is emphasised and guidelines for the rational investigation and treatment of such lesions are given.The occurrence of peripheral emboli is relatively common and well documented with left atrial myxoma,'-3 and it is not surprising, therefore, that right atrial myxoma should give rise to pulmonary emboli.4 Indeed, the association of pulmonary emboli with right atrial myxoma has been recognised at necropsy for many years; Chiari5 reported the first case in 1931. The clinical recognition of this association, however, is less well documented4 6 7 and a search of the published reports discloses only two pulmonary embolectomy8 9 performed during an operation to remove a right sided myxoma, and in neither case was the outcome successful. We report here the successful removal of a right atrial myxoma in a case where pulmonary embolectomy was crucial.Case report A 52 year old housewife was admitted with sudden swelling of the right arm accompanied by a dull ache. She complained of increasing tiredness for the six months before admission, with progressive exertional dyspnoea for the last three weeks. Her Chest radiography showed moderate cardiomegaly (cardiothoracic ratio of 155/280) without any specific chamber enlargement, while the electrocardiogram showed sinus rhythm with a Q wave in lead III and T wave inversion in the anterior chest leads.A technetium-99mMAA venogram through a distal right arm vein showed an abnormality of flow in the right axillary vein, suggesting thrombosis, and a contrast venogram via the right median cubital vein confirmed thrombosis of the brachial and axillary veins, which extended as far as the superior vena cava. A pulmonary perfusion scan, using technetium99mMAA, showed diminished flow to the entire left lung in keeping with massive pulmonary embolism, while flow to the right lung appeared normal. Echocardiography showed the presence of a large filling defect of the right atrium, prolapsing into the ventricle during diastole. Cardiac catheterisation was carried out via the left median basilar vein and the right femoral artery. The systolic pulmonary arterial pressure and the mean right atrial pressure were 15 and 14 mmHg.respectively. Contrast injection showed a large irregular filling defect occupying two thirds of the right atrium and prolapsing through the tricuspid valve. In addition, there was stagnation of blood flow in this area. A biopsy was taken using a "Bioptome" introduced viE

Thirty one (78%) of 40 consecutive patients (aged 13-79, mean 44 years) with infective endocarditis had congestive heart failure at presentation. Twenty six (65%) had had rheumatic heart disease and 17 (43%) patients had prosthetic valves. Eight (20%) patients had undergone dental procedures within three months of presentation. Blood cultures were positive in only 22 (55%) of the patients. In nine (41%) of them streptococci of the viridans group were isolated and in seven (32%) patients endocarditis was due to Staphylococcus aureus. Eight patients had Q fever endocarditis. Sixteen patients required operation because of haemodynamic deterioration while they were in hospital; 11 patients had native valves and five had prosthetic valves. Seven had emergency operations and were pyrexial at that time. Four of the seven died in hospital. Of the 12 who were alive and well after surgery only two required further surgery two and three years after the initial operation. Twelve (30%) of the 40 patients died in hospital; in 10 death was mainly due to left ventricular failure or congestive heart failure. All patients died who had renal failure (four cases), myocardial infarction (two cases), complete heart block (one case), or ventricular fibrillation (two cases) before operation. Six (33%) of the 18 patients with culture negative endocarditis died. Two of the four patients seen and treated more than 12 weeks after the onset of symptoms died, as did three of the five patients with prosthetic valves who required surgery while in hospital. Three patients with neurological complications survived and only two (29%) of the seven patients with blood cultures that were positive for Staphylococcus aureus died. Of these 40 high risk patients optimal antibiotic treatment and early surgery for haemodynamic difficulty ensured that 28 (70%) were discharged from hospital alive and well.

Clinical and echocardiographic findings were compared with those found at operation in 18 consecutive patients with active endocarditis undergoing valve replacement for continuing left ventricular failure. A close correlation was shown between vegetations detected by echocardiography and those found at operation. In 10 of 11 patients with clinically suspected severe aortic regurgitation and vegetations only on the aortic valve and in two of three patients with severe mitral regurgitation echocardiography provided confirmation of the clinical diagnosis. In the three patients with clinically suspected aortic and mitral regurgitation, however, cardiac catheterisation was necessary to confirm the severity ofthe valvular regurgitation. In a further three patients cardiac catheterisation was carried out as the severity of the single valve lesion was difficult to assess or there were associated problems, that is chest pain with myocardial infarction and a sinus of Valsalva aneurysm. Four patients had either an abscess, annular infection, a sinus, or a ventricular septal defect at the time of operation, which were not detected by echocardiography. Nevertheless, because of their size it would be doubtful if these would have been identified by cardiac catheterisation. Echocardiography allowed repeated assessment of the patient so that the optimal time for operation could be determined without the risks ofleft heart catheterisation. Fourteen ofthe 18 patients (78%) survived to leave hospital. The follow-up extended to 44 months. During this time reinfection, prosthetic dehiscence, or paravalvular leaks did not occur. Thus, in the majority of patients with left sided active infective endocarditis and continuing left ventricular failure resulting from severe valvular disease the clinical findings together with echocardiography provide a satisfactory preoperative assessment.

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suMMARY Four patients with rupture of the interventricular septum after myocardial infarction are described. This condition carries a grave prognosis. Surgical repair of the septum is almost always urgently required if the left-to-right shunt is large (QP/QS>3). Results are better if surgery can be deferred for six weeks to allow the infarcted area to heal and the tissues to become firmer. This delay may be achieved by using a combination of agents to reduce afterload and to exert a positive inotropic effect. The timing of surgical intervention was an important factor in the survival of three of the four patients.Ventricular septal defect after acute myocardial infarction was first described by Latham in 1846. hours of admission, complete heart block developed, preceded by sinus bradycardia and first and second degree atrioventricular block. The ventricular rate fell to 50/min and the blood pressure to 80/60 mmHg. Temporary atrioventricular sequential pacing was started. The blood pressure rose to 120/80 mmHg. Three days later sinus rhythm returned. The same day severe central chest pain recurred. The electrocardiogram showed sinus tachycardia at 120/min, with further ST segment elevation in leads II, III, and aVF. The blood pressure was 105/80 mmHg. The jugular venous pressure was raised with prominent 'a' and 'v' waves. A loud pansystolic murmur accompanied by a thrill was noted at the lower left sternal edge. A Swan-Ganz balloon tip catheter was inserted at the bedside. A large left-to-right shunt (QP/QS 4-8:1) was confirmed at ventricular level (Table 2). Systolic blood pressure had fallen to 65 mmHg. Digoxin and diuretics were started along with a dobutamine infusion. In view of the size of the shunt, persistent hypotension, and increasing congestive cardiac failure operation was carried out 10 hours after the development of the ventricular septal defect. At operation the right ventricle was greatly enlarged. The inferior surface of the heart was the site of a large haemorrhagic infarct covering most of the base and extending into the mitral annulus. The left ventricle was opened through its inferior surface using a longitudinal incision through the area of infarction parallel to the posterior descending coronary artery. The mitral apparatus and the papillary muscles appeared 570 on 10 May 2018 by guest. Protected by copyright.