The floppy mitral valve. Study of incidence, pathology, and complications in surgical, necropsy, and forensic material.
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Biomedical subjects
Publications and source records attributed to M V Braimbridge.
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The comprehensive experience of coronary artery surgery in a Cardiothoracic Unit over a 31-month period is reviewed. Hospital mortality for elective bypass grafting was 3.9% overall and 2.5% in those with good pre-operative left ventricular function. Major influences on hospital mortality were pre-operative left ventricular function, extent of coronary artery disease and extent of the surgical procedure undertaken in terms of number of aortocoronary grafts inserted, coronary endarterectomy and particularly concomitant valve surgery or aneurysm resection. Follow-up experience shows 74% of grafted patients to be symptom-free and 85% symptomatically improved one year after surgery with 70% symptom-free and 80% improved at two years. Early post-operative deaths appear related to early graft closure and recurrence of symptoms postoperatively to late graft closure or progression of coronary disease in the native circulation. The study provides a guide to the relative risks of coronary artery surgery for symptomatic coronary artery disease and expected symptomatic results in the early follow-up period.
In studies in the isolated rat heart that were designed to optimize the composition of the infusion conditions for a cardioplegic protective solutuin, we have observed a complex relationship between the duration and volume of infusion and the extent of tissue protection. Our results would indicate that solutions, such as that formulated at St. Thomas' Hospital, which are based on extracellular electrolyte content, afford (after a brief equilibration period) a constant degree of protection, irrespective of infusion volume or duration. In contrast other solutions, such as the Bretschneider solution, which have extremes of electrolyre concentration, are associated with a complex dose-response relationship. In the latter instance, infusion of small volumes for short durations affords an increasing degree of protection against ischemia. Increasing the infusate volume may result in a progressive loss of protection. Excessive infusion may lead to an exacerbation of ischemia-induced damage. Our studies suggest that the relative patterns and rates of re-equilibration of various ions, especially sodium and calcium, during infusion may play a major role in determining the efficacy of the infusate.
The increasing use of coronary infusates for the protection of the human heart drug ischemic cardiac arrest has placed great emphasis on the need for a rational and safe formulation of any infusion solution. Using a rat heart model of cardiopulmonary bypass and ischemic cardiac arrest, we have found magnesium to be a highly effective component of protective infusates which can be additive to hypothermia and other protective agents. However, the concentration of magnesium bears a complex relationship to the degree of protection, a fact which stresses the need for the establishment of the correct concentration for optimal protection.
Cardioplegic protective infusates are designed to induce rapid diastolic arrest and also to reduce or delay the onset of ischemic damage. As this study shows, the use of such infusates can greatly improve postischemic recovery of cardiac function. A number of investigators include glucose, insulin, or mannitol in their infusates in an attempt to increase the amount of protection afforded to the ischemic myocardium. Using an isolated, working rat heart model of cardiopulmonary bypass and ischemic cardiac arrest, we have shown that under certain conditions these additives can be deterimental to tissue protection. The deleterious effects of glucose and mannitol are dose dependent and can be modified by the inclusion of insulin in the infusate. The damaging effects of glucose appear to be both osmotic and metabolic in origin and those of mannitol, purely osmotic. The effects of insulin are complex and may affect a number of cellular processes.
The increasing use of cardioplegic protective infusates for reducing ischemic tissue injury requires that all infusates be carefully assessed for any protective or damaging properties. This study describes ultrastructural, enzymatic, and functional assessments of the efficacy of three infusates (Bretschneider, Kirsch, and St. Thomas' Hospital) in a rat heart model of cardiopulmonary bypass and ischemic cardiac arrest. The study reveals a close concordance of results as assessed by the three totally different indices of tissue damage. The results also indicate that, in the rat heart model, the St. Thomas' Hospital solution is an effective protective agent under all conditions studied but the Bretschneider solution is effective only under hypothermic conditions and the Kirsch solution is ineffective under all conditions studied and may exacerbate tissue injury. The studies further suggest that the potentially damaging effects of calcium-free myocardial infusates may be due to their induction of a "calcium paradox."
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Left ventricular endomyocardial biopsies have been obtained from patients with cardiomyopathy and hypertrophy due to aortic valve disease. These biopsies have been examined by electron microscopy and the ultrastructural abnormalities compared. In congestive cardiomyopathy no specific abnormalities were found although myofibrillary degeneration and membrane-bound vacuoles were more commonly present. Crossing of whole groups of sarcomeres was found only in asymmetric septal hypertrophy, but was not present in all cases. Amyloid deposits were demonstrated easily by electron microscopy in patients with restrictive cardiomyopathy. In the patients with hypertrophy due to aortic valve disease, no specific features were found and ultrastructural abnormalities did not differentiate between normal and impaired left ventricular functions.
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Five different types of myocardial protection were employed in this series of 168 patients undergoing aortic valve replacement. Two methods of assessing myocardial preservation were used: cellular biological estimations and quantitative polarization measurements. Both parameters showed that either of two methods, continuous perfusion at 32 degrees C. with a beating heart or cardioplegic hypothermic arrest, protected the myocardum best. Intermittent perfusion at 30 degrees C. with a fibrillating heart was the worst means of preservation. Our investigations (both clinical and experimental) have also shown that changes in birefringence, indicative of deteriorating myocardial function, are often detectable before parallel cytochemical changes are apparent.
A number of cardioplegic and protective solutions have been described for the reduction of cellular damage during ischemic cardiac arrest. These solutions are designed to induce diastolic arrest rapidly and to combat the various deleterious effects of ischemia. The efficacy of three different infusates (Bretschneider, Kirsch and St. Thomas' Hospital) has been compared. The results indicate that, whereas some solutions are able to afford striking protection, others may be ineffective and may exacerbate damage. Until the mechanisms underlying ischemic damage and its prevention are understood, it would seem undesirable to advocate the use of solutions containing extremes of concentration or solutions devoid of ions normally found in the extracellular fluid.
Myocardial preservation by continuous coronary perfusion is compared with cold cardioplegia. The 1 L. of St. Thomas' cardioplegic protective solution used for infusion into the coronary arteries was at 4 degrees C. and had a normal electrolyte content except for raised concentrations of magnesium and potassium and the addition of procaine. Myocardial preservation was assessed by cytochemical grading of myocardial biopsy specimens and also by the requirement for significant inotropic support postoperatively. In aortic valve replacements with an aortic occlusion time of 1 1/2 hours, both techniques afforded a similar degree of preservation, except that the inner half of the myocardium was markedly better preserved by cold cardioplegia. After 2 hours in double valve replacements, a single cardioplegic infusion was not as effective as continuous coronary perfusion, but this could be corrected by a second infusion of the cardioplegic solution after an hour.
The clinical histories of two patients with angiosarcoma of the pericardium are described. Both were previously well young men who presented with cardiac tamponade caused by haemorrhagic pericardial effusions. If a pericardiectomy is undertaken for diagnosis, wide excision of the pericardium is recommended. This will provide a large specimen for histological examination and may prevent subsequent development of constriction.
A case of necrotizing sarcoid angiitis and granulomatosis (NSG) presenting as a peripheral lung 'tumour' in a 63-year-old man is recorded, and the clinical and pathological features are compared with those of Liebow's original cases. Resection may be avoided if the diagnosis is made by biopsy as the disease is possibly steroid responsive and the prognosis appears favourable. The aetiology is obscure but an immune disturbance is suspected.
An isolated perfused working rat heart model was used to investigate the extent to which various protective agents, used either singly or in combination, were able to increase the resistance of the heart to periods of transient ischemia. The aim of the studies was to develop a solution which, if infused into the coronary vessels just prior to the onset of ischemia, would rapidly induce arrest and would also counteract several of the deleterious cellular changes known to occur during myocardial ischemia. Agents with induce cardiac arrest, modify cellular ion loss, affect substrate utilization, energy production and energy stores, affect coronary vessel diameter and cell swelling, prevent dysrhythmias, and affect metabolic rate were investigated. The additive effects of these agents were evaluated. An aqueous solution was formulated which contained high concentrations of potassium and magnesium, in combination with adenosine triphosphate, creatine phosphate and procaine. This solution increased the recovery of the ischemic (37 degrees C for 30 min) rat heart from 0% to 93%. The safe period of ischemia could be further increased by the use of hypothermia.
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