Biomedical subjects
Publications and source records attributed to M Honey.
A patient is reported with pulmonary arterial occlusions and aneurysms and recurrent haemoptysis. He gave a history of recurrent arthropathy and febrile illnesses; though he had had no other features of Behçet's or Hughes-Stovin syndrome his disease probably fell into this broad diagnostic category.
A case of Noonan's syndrome with aneurysmal dilatation of the sinuses of Valsalva is described. Enlargement of the left heart border on the postero-anterior chest radiograph was initially interpreted as dilatation of main pulmonary artery but aortography confirmed the presence of large aneurysms of two of the sinuses of Valsalva. Connective tissue abnormalities, known to occur in Noonan's syndrome, could be responsible for aortic abnormalities in this syndrome.
A young man with Takayasu's disease had severe right and left coronary ostial stenoses. Severe angina was relieved by operation at which the right coronary ostium was enlarged by a pericardial patch extending across the stenosis from aorta to coronary artery; the aortic end of a vein graft to the left coronary artery was attached to this patch. This technique may reduce the risk of recurrence of ostial stenosis or of stenosis at graft origins.
We have examined 5 patients with typical angina pectoris and found them to have left coronary ostial stenosis without evidence of any other coronary arterial disease and without evidence of aortic disease (Takayasu aortitis, syphilitic aortitis, or familial hypercholesterolaemia). All five patients were female aged between 38 and 53 years, a striking difference from the normal 7:1 male:female ratio for atherosclerotic coronary artery disease. It may be that these patients represent a rare but distinct syndrome. The angiographic diagnosis can be difficult but a pressure drop as the catheter tip engages the ostium and lack of spill-over of contrast into the sinus of Valsalva are findings that should lead the angiographer to suspect ostial stenosis.
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A patient with sinuatrial disease and implanted pacemaker was treated with amiodarone (maximum dose 1000 mg, maintenance dose 800 mg daily) for 10 months, for control of supraventricular tachyarrhythmias. He developed pneumonitis, pleural and pericardial effusions, and a predominantly proximal motor neuropathy. Immediate but gradual improvement followed withdrawal of amiodarone and treatment with prednisolone. Review of this and previously reported cases indicates the need for early diagnosis of amiodarone pneumonitis, immediate withdrawal of amiodarone, and prompt but continued steroid therapy to ensure full recovery.
Treatment with the combination of aspirin and dipyridamole is believed to reduce the incidence of coronary vein graft occlusion. A double blind randomised controlled trial was carried out in which aspirin 990 mg and dipyridamole 225 mg daily or placebo were added to the routine postoperative management (warfarin for three months) of 320 patients undergoing coronary bypass grafting. The trial treatment was given for 12 months, after which the results were assessed by coronary and graft angiography. The two randomised groups, each of 160 patients, were comparable in age, sex, symptomatic state, angiographic findings, and operative procedure. Repeat coronary arteriography was carried out on 266 patients, 133 in each group. All grafts and distal anastomoses were patent in 68% (91/133) of the placebo patients and in 75% (100/133) of those receiving active treatment. Overall graft patency was 87% (306/352) and 89% (342/385) respectively. Retrospective subgroup analysis showed patency rates of 72% (26/36) and 78% (39/50) of grafts to vessels requiring preliminary endarterectomy, and 80% (36/45) and 91% (40/44) of distal anastomoses to vessels measured at operation to have a diameter of less than or equal to 1 mm. None of these differences was significant at the 5% level. Thus in this group of patients with high graft patency rates, treatment with aspirin and dipyridamole conferred no appreciable advantage.
The angiocardiographic and clinical findings in 218 patients with significant obstruction confined to the left anterior descending coronary artery were reviewed to study the influence of the site of obstruction and of the collateral circulation on clinical presentation and prognosis. One hundred and fifty-six patients had been managed medically, 51 had had aortocoronary bypass operations, and 11 had had left ventricular aneurysms excised. The artery was divided into three segments: left anterior descending 1 (LAD1) from its origin to the first septal branch, left anterior descending 2 (LAD2) from the first septal to the first diagonal branch, and left anterior descending 3 (LAD3) the remaining distal vessel. Cardiogenic shock occurred only in patients with LAD1 lesions, but apart from this the clinical presentation bore no consistent relation to the site of disease. Patients with proximal lesions were more likely to have a "positive" exercise test, had more severely impaired left ventricular function, and had a worse prognosis than those with more distal disease. Non-visualisation of collateral vessels in patients with left anterior descending occlusion was associated with extensive infarction, and patients who presented with infarction had more severely impaired ventricular function than those who presented with angina and subsequently had an infarction. Left ventricular function was poor at the time of angiography in 11 of 12 of those who subsequently died; it is therefore unlikely that the prognosis of patients with isolated left anterior descending obstruction could be improved by expanding the indication for aortocoronary bypass from that of severe angina.
One hundred consecutive patients, admitted to the coronary care unit with cardiac pain at rest but no evidence of recent myocardial infarction have been followed up for nine to 26 (mean 14) months. They were treated initially with bed rest, beta-adrenergic blockade, and nitrates. In 54 patients pain subsided within 24 hours. Coronary angiography was carried out in 46. Thirty-five had coronary artery lesions and three had spasm in normal coronary arteries. One had hypertrophic cardiomyopathy and seven had normal findings. Seventeen patients with previous angina and severe coronary disease were operated on, with one death and one perioperative infarction; two died late, 12 were symptom free, and two had angina. Seven of 18 patients treated medically had recurrent angina and underwent operation. Of the 11 unoperated patients, one died, three had angina, and seven were symptom free. Two of the eight patients who were not catheterised developed infarction, four had angina, and three were symptom free. Recurrent pain continued for more than 24 hours in 46 patients, and all underwent angiography. Forty-three had coronary artery disease and 34 underwent early bypass surgery; there were two operative deaths and three perioperative infarctions. Twenty-six symptom free at follow-up. Of the nine unoperated patients with coronary disease, four developed infarction, two were operated on for recurrent angina, two were symptom free, and one had mild angina. Optimal management of patients with pain at rest can be determined only with knowledge of the coronary artery anatomy and of left ventricular function. Many respond initially to intensive medical treatment and coronary angiography can be performed electively. In those with continuing pain, urgent angiography is required and can be done safely.
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Two cases are described in which severe mechanical haemolytic anaemia developed shortly after operation for repair of non-rheumatic mitral regurgitation. One patient had a "floppy" valve and the other cleft mitral leaflets, and both had chordal rupture. In both there was residual regurgitation after repair though in one this was initially only trivial. Clinically manifest haemolysis ceased after replacement of the valve by a frame-mounted xenograft. There are two previously reported cases in which haemolytic anaemia followed an unsuccessful mitral valve repair operation. Subclinical haemolysis or mild haemolytic anaemia may occur with unoperated valve lesions, but hitherto frank haemolytic anaemia has been observed only when turbulent blood flow is associated with the presence of a prosthetic valve or patch of prosthetic fabric. In these four cases, however, polyester or Teflon sutures were the only foreign material, and it is suggested that when these are used for the repair of leaflets, particularly in non-rheumatic mitral valve disease, they may increase the damaging effect of turbulence on circulating red blood cells.
Diazoxide was injected into the pulmonary artery in nine patients with primary pulmonary hypertension. There was no significant change in pulmonary artery pressure, which fell by more than 10 mmHg in only two patients. The pulmonary blood flow increased in all patients as a result of a fall in pulmonary vascular resistance (by 4 to 17 units). Systematic vasuclar resistance also fell as expected in all patients. Oral diazoxide was given to seven patients, two of whom showed sustained clinical improvement while remaining on treatment (400 to 600 mg daily). Five patients were unable to tolerate the drug, because of nausea and sickness (two), peripheral oedema requiring large doses of diuretics (four), diabetes (three), and postural hypotension (one). Hirsutes was troublesome in the two patients remaining on treatment. Diazoxide may be useful in the management of some patients with primary pulmonary hypertension, but its use is limited by the frequency of side effects. Our results suggest that examination of othe potent vasodilators may be worth while.
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Forty patients with persistent or recurrent angina after an aortocoronary bypass procedure underwent a second operation. The cause of recurrent angina, defined by angiography, was thought to be isolated graft failure in 13 patients, progression of disease in ungrafted vessels in 4, incomplete revascularisation in 2, and stenoses distal to patent grafts in 1. More than one factor was responsible in 20 patients. There was 1 early postoperative death and 3 perioperative myocardial infarctions. Thirty-four patients have been followed for more than 3 months (4 to 63 months). Of these, 17 had previously bypassed vessels regrafted and 5 are sympton free, 4 have mild angina, and 8 have severe angina. Ten patients had previously ungrafted vessels grafted and 4 are sympton free, 3 have mild angina, 2 have severe angina, and 1 is limited by breathlessness. Seven patients had a combined procedure and 4 are sympton free, 1 has mild angina, and 2 have severe angina. Reoperation can be carried out safely but the results are less satisfactory than for a primary procedure.
Three hundred and forty-three patients who had aortocoronary bypass graft operations for disabling angina were followed up for from 6 months to 5 years (average 2 years). 80 per cent had multiple grafts and 20 per cent had additional endarterectomy. The overall mortality within one month of operation was 5 per cent, and in those who had vein graft procedures only was 4 per cent. 11 per cent had a postoperative myocardial infarction (6% perioperative) and there were 3 per cent late deaths. At 3 years 90 per cent are surviving. 80 per cent are asymptomatic without treatment. The mean angina grade was 0.3 at the latest follow-up, compared with 2.5 before operation; maximum exercise tolerance was also significantly improved (P less than 0.001). When angina recurred, it did so in 80 per cent of the cases within 12 months of operation and was usually attributable to inadequate revascularisation. Ventricular function as assessed by preoperative ventriculography was the factor most clearly related to survival rate and the early excellent results of coronary bypass operations seem to be maintained up to 5 years. It is, therefore, reasonable to continue to advise operation if only for relief of angina.
Six new cases of the "scimitar syndrome" are described. The anatomical and haemodynamic features of these and other reported cases are reviewed. Within the spectrum of the disorder there is a group of patients in whom the bronchopulmonary manifestations are relatively unimportant. In five of our patients there was a left-to-right shunt exceeding 2:1 and the anomalous pulmonary venous connection was corrected surgically. The presence or absence of an associated atrial septal defect may be difficult to establish but influences the choice of surgical technique. When the atrial septum is intact, the anomalous vein should be reimplanted if possible into the back of the left atrium; otherwise a pericardial or teflon patch can be used to redirect the anomalous venous return through an existing or created atrial septal defect to the left atrium.
We report the clinical features and the results of investigation and surgery in 20 patients with significant left main coronary artery stenosis. All had moderate to severe angina; 8 had pain at rest. Three had dyspnoea as a major symptom. The electrocardiogram was abnormal in 17, with evidence of previous myocardial infarction in 10. Of the 11 patients exercised, 8 developed chest pain. Nine patients had a normal left ventriculogram. At coronary angiography all patients had major disease elsewhere in addition to the left main coronary artery stenosis. There were no deaths or major complications associated with this investigation. One patient was unsuitable for surgery because of diffuse left ventricular hypokinesia, one had a fatal myocardial infarction while awaiting operation, and there was one preoperative death. Sixteen of the 17 surgical survivors are free from angina. There has been a significant improvement in the maximum exercise capacity in the 10 patients who had pre- and postoperative exercise tests.