Re-evaluation of a possible high incidence of hypertension in hypothyroid patients.

In an attempt to re-evaluate a possible high incidence of hypertension in hypothyroid patients, blood pressure was measured in 38 slightly hypothyroid patients, in 17 moderate hypothyroid patients, and in 26 severe hypothyroid patients. The data were then compared with the findings in 73 known euthyroid subjects and in 1,601 possibly euthyroid subjects. Blood pressure and incidence of hypertension increased progressively with age in known euthyroid subjects and in possibly euthyroid subjects. Similarly, blood pressure increased progressively with age in slight and moderate hypothyroid patients, but the incidence of hypertension was high in the sixth decade in slightly hypothyroid patients for some unknown reason. In contrast, blood pressure and the incidence of hypertension were low in the fifth and sixth decades in severe hypothyroid patients. This low blood pressure was elevated slightly when Sv1 + Rv5 and C/T were shifted toward normal by T4 treatment for 3 to 4 months. It is suggested that the hypothyroid state does not accelerate the development of hypertension.     

Acute effects of the calcium antagonist, nifedipine, on blood pressure, pulse rate, and the renin-angiotensin-aldosterone system in patients with essential hypertension

Ten milligrams nifedipine was administered orally to young and old persons with or without hypertension, and the acute effects of nifedipine on the renin-angiotensin-aldosterone system were studied one half to 3 hours later. Nifedipine reduced blood pressure and increased pulse rate in young and old persons with or without hypertension. Simultaneously, nifedipine produced a significant increase of plasma renin activity in young persons with or without hypertension but failed to do so in old persons with or without hypertension. As a result, angiotensin I and II increased significantly in young persons but not in old persons. Hydralazine elevated aldosterone concentration by stimulating the renin-angiotensin system but nifedipine failed to do so despite its effect on the renin-angiotensin system in young individuals. Since calcium is required to secrete aldosterone, it is suggested that nifedipine blocked aldosterone secretion by the agent's calcium antagonizing action.     

Concurrent hypersecretion of aldosterone and cortisol from the adrenal cortical adenoma.

Hypertension, hypokalemia, suppressed plasma renin activity and increased plasma aldosterone were found in a middle-aged woman. Following removal of the tumor in the left adrenal gland these abnormalities disappeared. Concurrently, however, the plasma cortisol level did not show normal diurnal change, although the value at 6 A.M. was within the normal range. Administration of 2 mg dexamethasone failed to depress the plasma cortisol level and urinary 17-OHCS concentrations. Postoperatively, plasma cortisol and urinary 17-OHCS were below normal. Histologic examination of the tumor indicated the presence of two types of adenoma cells; one was a large watery clear cell with rich lipid and possibly with aldosterone secretion and the other was an acidophilic cell with poor lipid and possibly with cortisol secretion. It is suggested that, in addition to oversecretion of aldosterone, the tumor autonomously secreted cortisol, although the amount of cortisol secreted was not large enough to produce typical Cushing's syndrome.     

Cross-sectional echocardiography: Physical principles, anatomic planes, limitations and pitfalls

Although M mode echocardiography has achieved a prominent role in the diagnosis and management of patients with cardiovascular disease, the limited area of view afforded by M mode techniques has restricted the application of ultrasound in many areas. The development of two dimenslonal echocardiography has obviated many of the limitations inherent in the narrow view of the M mode technique. It has enabled imaging of the heart from additional transducer locations, permitted determination of shape and anatomy and provided the ability to determine motion along two axes. Several types of two dimensional echocardiographs have been developed, and each type offers both advantages and disadvantages. Although two dimensional echocardiography has provided a larger area of view with ultrasound, it has also introduced new limitations including a larger and bulkier transducer, a much reduced sampling rate and a difficult display medium (videotape). In addition, new considerations regarding ultrasonic resolution have been raised. Two dimensional techniques have resulted in new pitfalls in ultrasonic diagnosis related to instrument artifacts as well as to performance and interpretation of the examination. The spurious appearance of cardiac masses because of these ultrasonic artifacts represents a particularly prominent diagnostic pitfall that must be avoided in daily practice. It is anticipated that the new wider field of view provided by two dimensional echocardiography combined with a Standard high resolution capability of ultrasound (2 to 4 mm) will result in an increasingly large role for echocardiography in the management of patients with heart disease.     

Comparative mechanisms of action of antiarrhythmic drugs

The antiarrhythmic actions of different compounds are best compared in terms of their dominant electrophysiologic effects on myocardial fibers from different parts of the heart. Such primary actions may be modified considerably by changes in the serum electrolyte concentrations, pH, interactions with serum proteins, or other extracardiac factors. Clinically, however, it appears useful to categorize antiarrhythmic drugs into four groups in terms of their currently known mechanisms of action. Quinidine is the prototype of Group 1 drugs. Its main effect is the reduction of the maximal rate of depolarization of the cardiac action potential so that it slows conduction velocity and increases the effective refractory period with only minor effects on repolarization. Procainamide, disopyramide, carbamazepine, and Kö 1173 all have similar effects to those of quinidine on heart muscle. Lidocaine and diphenylhydantoin may be considered to constitute a subgroup (Group 1B) of “quinidine-like” drugs. In small concentrations they increase membrane responsiveness but in concentrations in the therapeutic range they have a quinidine-like depressant action on the cardiac membrane, particularly if serum levels of potassium are physiologically appropriate. Group 2 drugs are exemplified by β-adrenergic receptor blocking compounds. In blocking concentrations their only electrophysiologic effect is the reduction in the slope of the pacemaker potential; in very much higher concentrations they reduce the maximal rate of depolarization of the cardiac action potential but the precise clinical significance of this is still uncertain. Amiodarone and bretylium prolong the duration of the action potential in the ventricular muscle and Purkinje fibers without causing a significant change in other electrophysiologic parameters. This leads to a “pure” prolongation of the absolute refractory period which may be regarded as an independent antiarrhythmic mechanism (Group 3). Verapamil, a novel antiarrhythmic compound, is a specific calcium antagonist in the heart. It does not reduce the maximal rate of depolarization of the action potential but slows the spontaneous diastolic depolarization in heart muscle. The effects of verapamil are sufficiently different from those of other known agents to allow the tentative conclusion that its fundamental mode of action represents a fourth (Group IV) class of antiarrhythmic action.     

Selective total removal of a growth-hormone-secreting adenoma: evidence that acromegaly is a primary pituitary disease.

Acromegaly is caused by hypersecretion of growth hormone by the pituitary. There is some debate as to whether the primary etiology of the disease is abnormal hypothalamic stimulation of the pituitary or a primary pituitary tumor. This paper presents a case of acromegaly in which growth hormone dynamics in response to stimulation and suppression tests were abnormal. After transsphenoidal adenomectomy of a small tumor, growth hormone levels returned to normal and suppression and stimulation test results reverted to normal within 1 wk postoperatively and remained normal for 2 yr. The findings suggest that the acromegaly in this case was due to a primary pituitary dysfunction. Microsurgical removal of growth-hormone-secreting tumors provides a unique opportunity to study the etiology of acromegaly.     

The influence of electrode placement in the reconstruction and analysis of body surface potential maps from limited thoracic arrays

Despite their capacity to indicate abnormality outside the scope of routine electrocardiography body surface maps remain extensive, time-consuming research procedures. By contrast, a 35-electrode grid which sums precordial ST segment deviations has received wide attention as a clinical monitor of acute myocardial infarction. First, this study examined the feasibility of recovering essential data from a small electrode array to construct maps equal to those obtained from a much larger array. Such a small-array technique would offer economy, easy application, plus the comprehensiveness and clinical correlation of the large system. Second, the relationships between map, small-array and a 35-component equivalent multipolar generator were explored for a transformation system which both expands the small-array data to map displays and reduces such data to non-redundant waveforms. Comparisions were made between direct maps and those derived from two 35-electrode sets in normal subjects and patients with myocardial infarction or cardiomyopathy. Electrode placement did not conform to the conventional rectangular grid; for one, the electrodes encircled the thorax symmetrically; in the other they were statistically selected for signal information content. We found 1) symmetrical electrode placement and analytic reconstruction of maps from multipolar lead components consistently reproduced known maps well (.91 correlation, 120 microvolts error); but 2) empirical electrode placement and statistical prediction of known maps averaged .99 correlation and 20 microvolts error for the normal training population and .97 and 60 microvolts for the abnormal test sample. Worsening occurred when placement and prediction methods were mixed; however, maps reconstructed by the empirical-statistical approach reduced to a reasonable approximation of equivalent generator scalar leads     

Metabolic changes in the rat anterior pituitary and prolactin production following estradiol treatment

The effects of estradiol treatment on the synthesis and release of prolactin and GH in castrated male rats were studied in connection with the anterior pituitary enzymes that represent the hexosemonophosphate shunt, glycolytic, oxidative, and lysosomal activity. LDH and G6P-DH activities increased by 15%–30% at 12 hr and by 70% at 72 hr after estrogen administration. PK activity showed a statistically significant elevation of 20%–40% only after 48–72 hr. ICDH, MDH, acid phosphatase activities, and water-soluble protein concentrations were unchanged. Serum prolactin concentration increased about 400% 24 hr after estradiol injection, and the pituitary synthesized 1000%–1500% more radioactive prolactin in vitro than did control glands. However, no significant increase in prolactin synthesis was observed 12 hr after estradiol treatment.It is suggested that the primary effect of estradiol is on the synthesis of prolactin and that the increased rate of secretion is secondary. Radioimmunoassayable prolactin in the incubated gland tissue and its medium was greatly increased after estradiol treatment. A slight but statistically significant accumulation and decreased release of radioactive GH were also observed. The results suggest a correlation of pituitary prolactin production with the tissue's metabolic activity.     

The incidence and clinical significance of ECG-VCG changes of myocardial infarction following aortocoronary saphenous vein bypass surgery

The electrocardiogram and vectorcardiogram were analyzed in 35 consecutive patients before and after undergoing elective aortocoronary saphenous vein bypass grafting for angina pectoris. Typical changes of perioperative myocardial infarction were seen in 40 per cent (ECG) and 46 per cent (VCG). Changes of ST segments and T wave could not be correlated with QRS changes of infarction. Surgery with or without infarction resulted in a loss in R wave voltage in anterior and lateral precordial leads (V₄, V₅, and V₆) as well as in a symmetric shrinkage of the vector loop in the transverse and frontal planes.Comparing one year follow-up results of those with versus those without perioperative VCG changes of infarction showed that late death, clinical evidence of myocardial damage, and reinfarction were more frequent in the infarction group. However, no difference in N.Y.H.A. functional classification, congestive heart failure alone, or persistence of angina pectoris could be demonstrated between the two groups. The ECG and VCG changes of perioperative infarction are common with this operation and helped to predict late morbidity and death.     

The peritoneal absorption of insulin in diabetic man: A potential site for a mechanical insulin delivery system

The potential of the peritoneum as a site for an “artificial beta cell” was studied. Three 14-hr studies were performed in an insulin-dependent diabetic male maintained on chronic peritoneal dialysis. All studies were performed between dialyses and throughout three standard American Diabetes Association (ADA) 600 calorie meals. The degree of insulin absorption from the peritoneal space was assessed by measuring the changes in plasma-free insulin concentration during these studies. The results of this study demonstrate that normalization of plasma insulin profiles may be observed with the administration of insulin into the peritoneal space. This absorbed insulin exerts hypoglycemic activity that suppresses the meal-induced rise in plasma glucose concentration. Thus, the peritoneal space may be a feasible route into which insulin may be delivered by an artificial beta cell.