The Lewis A. Conner Memorial Lecture

Abstract

While there are many anatomic varieties of congenital malformations of the heart and great vessels, most may be divided, from a functional point of view, into 3 types: (1) Conner also had keen insight into the specific problems of the individual patient. He was a pioneer more than 40 years ago in emphasizing facts which then were controversial and which we accept today as commonplace. His interests in the pulmonary complications of the patient with typhoid fever led to a clear appreciation of the relationship of peripheral venous thrombosis to pulmonary embolism.He indicated that peripheral venous thrombosis might be clinically latent and yet be responsible for pulmonary embolism.' 2 The pulmonary embolism might be recurrent and not necessarily fatal. In stressing these facts, he brought out the concept that in a patient with a disease seemingly unrelated to the lungs, there might be pulmonary manifestations that were, in fact, somehow related to the basic nonpulmonary disease.

Pulmonary Hypertension in Congenital Heart Disease

“…The pulmonary arteries in uncomplicated atrial septal defect, ventricular septal defect, and patent ductus arteriosus show only patchy intimal thickening similar to that in control subjects (Welch and Kinney, 1948;Edwards, 1955). The changes found on microscopical examination of the lungs in our 11 cases with pulmonary hypertension were uniform, nor did they differ in any important respect from those found in solitary pulmonary hypertension (Evans et al, 1957).…”

“…Edwards (1950) has pointed to the similarity between the apparently hypertrophied arteries of the patient with hypertension and the thick-walled arteries of the fcotus, and has postulated that in patients who will develop hypertension, the foetal state persists into childhood. Edwards (1957) believes that the obliterative lesions develop later as a specific effect of severe chronic hypertension.…”

“…Edwards (1950) has pointed to the similarity between the apparently hypertrophied arteries of the patient with hypertension and the thick-walled arteries of the fcotus, and has postulated that in patients who will develop hypertension, the foetal state persists into childhood. Edwards (1957) believes that the obliterative lesions develop later as a specific effect of severe chronic hypertension. The main objection to Edwards' theory is that apparently similar thick-walled arteries are found in pulmonary hypertension associated with mitral stenosis, and it is very difficult to believe that the arterial abnormality here is an independent condition present from birth.…”

“…If it is assumed that the inherent responsiveness of the arteries to a raised pressure is not universal, but varies from one subject to another, it may explain the development of pulmonary hypertension. Occlusive changes would then be regarded as a late development leading to reversal of the shunt, as Dammann and Ferencz (1956) and Edwards (1957) have suggested.…”

The Aetiology of Pulmonary Thrombosis in Cyanotic Congenital Heart Disease with Pulmonary Stenosis

“…Furthermore, it is not generally appreciated in the group of patients in whom pulmonary stenosis is associated with a large ventricular septal defect that the stenosis may not be severe enough to attenuate the propagated systolic pulse of the ventricles into the pulmonary circulation (Broadbent and others, 1953;Edwards, 1957). Hence, the small pulmonary blood vessels remain thickwalled from birth in such patients to give rise to an early stage of hypertensive pulmonary vascular disease, as in Group 1.…”