Echocardiographic assessment of left ventricular outflow tract in d-transposition of the great arteries

The left ventricular outflow tract in 38 patients (aged 0.3 to 13 years) with complete d-transposition of the great arteries, 31 with intraatrial (Mustard) repair, was quantitated with echocardiography, and the findings were correlated with hemodynamic and angiographic data. The left ventricular outflow tract (LVO) was measured on the echocardiogram as an anteroposterior dimension between the closure point on the mitral valve below the pulmonary arterial root (PA) and the left endocardial surface of the interventricular septum. This measurement was expressed as an LVO/PA ratio and on the basis of these measurements three groups were recognized.Group I consisted of 14 patients who had an unobstructed left ventricular outflow tract and no significant pressure differences between the pulmonary artery and left ventricle. In Group II, the 16 patients had evidence of dynamic obstruction and mild to moderate pressure differences between the pulmonary artery and left ventricle, characterized in the echocardiogram by LVO/PA ratios comparable with those of Group I, but with an abnormally prominent early posterior systolic septal bulge in the left ventricular outflow tract, abnormal systolic anterior motion of the mitral valve and coarse fluttering of the pulmonary valve. In Group III the eight patients had anatomically fixed stenosis of the left ventricular outflow tract and severe left ventricular outflow pressure gradients characterized in the echocardiogram by a reduced LVO/PA ratio and fine vibrations of the pulmonary valve. Angiographically discrete or long segmental narrowing of the left ventricular outflow tract correlated well with the echocardiographic data. Echocardiographic measurements of left ventricular posterior wall thickness also correlated well with the severity of left ventricular outflow stenosis in these three groups. The echocardiogram provides clinically useful quantitative and qualitative analysis of the left ventricular outflow tract in patients with complete transposition of the great arteries.     

Changes in the microvasculature with age

The microvasculature of various organs of the rat and of the mesentery of the cat were examined for histochemical changes as a function of age, using the periodic acid-Schiff (PAS) reaction. Arterioles, minute arteries, and nonmuscular venules were histochemically unchanged to approximately 17 months of age in the rat and 8 years in the cat. Subsequently, focal areas of PAS-positive material developed in the media of arterioles and small arteries and increased in extent and severity with age. The adventitia of nonmuscular venules normally stains slightly positive due to the mucopolysaccharide coating of collagen fibers. With age this adventitial layer becomes more intensely PAS-positive. In the 26-month-old rat and 19-year-old cat, the media of arterioles and small arteries were extensively hyalinized. Lesions of arteriosclerosis were not present. These observations, in consort with prior observations of others in various mammals, indicate that there is a regular systematic alteration of various elements of the microcirculation with age. A possible relationship between these anatomical changes and tissue exchange is considered.     

Glucose and alanine metabolism during bacterial infections in rats and rhesus monkeys

To investigate the effects of bacterial infection on glucose and alanine metabolism, a variety of studies were carried out in rat and monkey models. These included glucose turnover by a pulse-dose technique in infected rats; alanine and glucose production and utilization in control and septic monkeys; in vivo measurement of gluconeogenesis in rats, with and without an alanine load; the in vitro rate of glucose formation from various substrates by isolated liver perfusion and hepatic cells; and in vivo rates of oxidation of glucose labeled with ¹⁴C at the 1 or 6 carbon position. In rats, glucose turnover was markedly accelerated 24 hr after inoculation of either 10⁴ or 10⁷Streptococcus pneumoniae. Glucose utilization and production were also accelerated during illness and early recovery from a pneumococcal infection in monkeys. The rates of gluconeogenesis as measured by either a pulse technique in rats or continuous infusion of labeled alanine in monkey were significantly elevated during pneumococcal septicemia. During the agonal stages (10⁷) of the pneumococcal infection in rat, an alanine load resulted in a decreased rate of labeled glucose production and an increase in plasma glucose when compared to values of fasted control rats. However, early illness caused similar or increased rates of glucose production from alanine in vivo. Similar reduced rates of glucose formation were observed when the isolated livers or hepatocytes from rats during the agonal stages of infection were perfused with excess quantities of gluconeogenic substrates. Thus, in the rat, gluconeogenic capacity (ability to form glucose from excess substrates) appears to decrease only during the agonal stages of pneumococcal infection. During acute pneumococcal sepsis in the rhesus monkey, alanine production and utilization were significantly elevated and it was estimated that over 90% of the newly produced alanine was utilized for glucose synthesis. When arterial-venous differences were measured across the hindquarters, significantly more alanine was released, presumably from skeletal muscle of the septic monkey, compared to the recovery period or in the control groups. Thus, the increase in glucose synthesis in both rat and monkey appears to be correlated with substrate availability and kinetic rate, rather than gluconeogenic capacity of the liver. The major increase in glucose utilization during both S. pneumoniae and Francisella tularensis live vaccine strain (LVS) infections in rat was a progressive elevation in the rate of oxidation via the pentose phosphate shunt in the rat. Further, the rate of oxidation appeared to be correlated with the magnitude of the bacteremia, which is an indication of the severity of the infection. Therefore, since glucose oxidation is necessary for a number of metabolic processes of various cells (such as phagocytosis and RNA synthesis), the increased glucose production during pneumococcal sepsis in the rat or rhesus monkey may not represent functional wastage to remove the excess alanine produced in skeletal muscle but a necessary process in the host defense mechanism against infectious disease.     

Right bundle branch block in complete transposition

Two of 26 infants with complete transposition presented with complete right bundle branch block in the first year of life, and 10 showed incomplete right bundle branch block. In no instance was the right ventricular conduction anomaly related to surgery or cardiac catheterization and it was not present at birth. The two cases with complete right bundle branch block had prolonged and severe hypoxemia and markedly dilated right ventricles. One had depressed right ventricular function and died after a Mustard procedure from low output syndrome. Whereas incomplete right bundle branch block may reflect right ventricular hypertrophy, it is suggested that complete right bundle branch block in complete transposition may signify right ventricular dysfunction and possibly irreversible changes of the right ventricular myocardium. It may be a sequel of long-term hypoxemia and pressure overload. Once observed, it is perhaps an indication for an alternative surgical approach other than an intra-atrial repair procedure.     

Mean systolic ejection rate after aortocoronary bypass graft surgery

In 62 patients with coronary artery disease who underwent aortocoronary bypass graft surgery, we measured the mean systolic ejection rate invasively at rest and during upright exercise before and several months after operation. After bypass surgery, mean systolic ejection rate did not show any change at either supine or sitting rest and at submaximal exercise levels of walking on a treadmill. At maximal exercise, only patients with complete revascularization showed a significant increase in heart rate from 105 to 147 (+40%) and mean systolic ejection rate from 339 ml/sec to 404 ml/sec (+19%, P less than 0.001). Patients with incomplete revascularization did not show a substantial change in these variables. Beta-blocker withdrawal did not affect the result significantly.     

Tensions between academic cardiology and internal medicine

The great number of open heart operations now performed via the right atrium, makes knowledge of the arrangement of the atrial arteries, particularly the sinus node artery, every important for the surgeon. Although studied by anatomists, little attention has been paid to the surgical significance of these arteries. We have therefore examined the distribution of the right atrial arteries and the course of the sinus node artery in 50 normal adult hearts by classic dissection following, in 30 cases, postmortem angiographic studies. Two major arteries of the right atrium were found to be nearly constant. The anterior artery was present in 96% of the cases and supplied the sinus node artery in 32 cases. Of most surgical significance was the lateral artery found in 90% of the cases. This lateral artery was the principal artery to the free atrial wall and in one case gave rise to the sinus node artery.The well-established preponderance of origin of the sinus node artery from the right coronary system (66%) as opposed to the left (30%) was confirmed. Infrequently, a double supply (4%) was seen. Variability was found in the course of the nodal artery relative to the cavoatrial junction — precaval (58%), retrocaval (36%) or encircling (6%).These variations place the atrial arteries in danger when using a right or left atriotomy. The surgeon must be aware of these arteries in order to achieve the safest access to the atrial chambers prior to intracardiac procedures.     

The pancreatic islets in diabetes

Despite the fact that heterogeneity of diabetes in man has become more and more evident in recent years, its pancreatic pathology is still represented by two distinct entities, roughly corresponding to the classic juvenile-onset and maturity-onset types of the disease.In juvenile-onset, insulin-dependent diabetes, the pancreatic islets show severe and pathognomonic changes. B cells are greatly reduced in number already at clinical onset. Contrary to classic opinion they do not always disappear in the years to follow. Insulin's, a common finding in the pancreas of recent onset juvenile diabetic subjects, is compatible with a viral infection as well as with an autoimmune reaction as the cause of B cell destruction. In the pancreas of juvenile-onset diabetic subjects the islets, which in the past have been regarded as atrophic and inactive, are actually composed of cells containing glucagon and somatostatin. There is also a profound distortion of islet organization, and many endocrine cells are scattered as single cells in the exocrine tissue. These findings may well account for the abnormal secretory behavior of the glucagon-secreting A cells in insulin-dependent juvenile-onset diabetes.In maturity-onset, noninsulin-dependent diabetes, the pancreatic pathology is extremely variable and not pathognomonic. A numeric reduction of the B cells can be demonstrated in many maturity-onset diabetic subjects, but this reduction is much more moderate than in insulin-dependent juvenile-onset diabetic subjects and does not account for the disease. The same amount of B cell reduction can be found in many elderly subjects without clinical evidence of diabetes. In many maturity-onset diabetic subjects, the cytologic characteristics of the B cells suggest a decreased responsiveness to the stimulus of hyperglycemia. Islet fibrosis and hyalinosis (amyloidosis), although common, cannot explain this secretory dysfunction. The exact site of the defect in the B cells of maturity-onset diabetic subjects remains to be defined. Further investigations are necessary to assess the role of disturbed intraislet intercellular relationships in the pathogenesis of late-onset diabetes.The dual pattern of islet pathology in diabetes in man does not preclude a more profound heterogeneity in the etiology and pathogenesis of the disease.     

Intermyofibrillar and nuclear-myofibrillar connections in human and canine myocardium. An ultrastructural study

Cytoplasmic filaments, which measure 100 Å in diameter, and which differ morphologically from actin and myosin filaments, are described in normal canine myocardium and in normal and hypertrophied human myocardium. These filaments were found between Z bands, near the sarcolemma, in regions of intercalated discs, and in the vicinity of nuclear membranes. The 100 Å filaments appeared to form transverse connections between adjacent Z bands and between Z bands and outer nuclear membranes. These filaments probably function as a cytoskeleton.     

Precordial electrocardiographic mapping in the identification of patients with left main stem narrowing

This study was designed to determine if exercise testing using 16-lead precordial mapping can be used to identify patients with left main stem narrowing. In a group of 235 consecutive patients undergoing coronary angiography there were 35 patients with left main stem narrowing. The patients with left main stem disease differed from the others in that not only did they develop extensive S-T segment depression, but more specifically these changes occupied a characteristic position high on the precordium above the usual site of the precordial leads of the 12-lead electrocardiogram. This finding was then tested prospectively in a second group of 100 patients. Fourteen of the 100 patients had left main stem narrowing; the sensitivity and specificity of S- T segment changes high on the precordium in identifying patients with left main stem disease were 82 and 84% respectively. Thus precordial mapping and exercise testing is valuable in the diagnosis of patients with left main stem narrowing. The technique is simple and inexpensive and provides data not available using the conventional precordial leads of the 12-lead electrocardiogram.