Atrial reentry in chronic repetitive supraventricular tachycardia

Atrial reentrance as a mechanism of the tachycardia was demonstrated in a 28-year-old patient suffering from chronic repetitive supraventricular tachycardia. Criteria for diagnosis included the following: (1) Repetitive supraventricular tachycardia was induced and terminated by properly timed atrial extrastimuli. (2) Return cycles of all atrial extrastimuli not abolishing the tachycardia were fully compensatory. (3) A-H prolongation was not a prerequisite to induce the tachycardia. (4) The contours of P and A waves during tachycardia differed from those in sinus rhythm, but atrial activation remained antegrade. (5) A concealed anomalous pathway could not be proved.     

Folic acid deficiency and neutrophil dysfunction

Polymorphonuclear leukocyte functions were studied in 92 patients with protein-calorie malnutrition. Serum folic acid levels were higher than 3 ng/ml in 38 patients and 3 ng/ml or less in 54 patients. Significant differences were found between these two groups of patients with regard to phagocytosis (81.5 +/- 1.9 versus 69.2 +/- 2.0 percent, p less than 0.001) and bactericidal ability (90.6 +/- 1.1 versus 84.5 +/- 2.3 percent, p less than 0.05). Correction of folic acid deficiency in 22 patients was associated with recovery of normal phagocytosis (p less than 0.001) but not bactericidal function. Adding folic acid to the serum of eight patients also restored normal phagocytic function (p less than 0.001). A correlation was found in vivo and in vitro between changes over time in folic acid levels and in phagocytosis.     

Role of beta-adrenoreceptor antagonism in the prevention of reperfusion ventricular arrhythmias: effects of acebutolol, atenolol, and d-propranolol on isolated working rat hearts subject to myocardial ischemia and reperfusion

The role of catecholamines in the genesis of ventricular arrhythmias during the reperfusion period following coronary occlusion remains incompletely understood. An isolated rat heart preparation, free from the influence of autonomic innervation or of circulating catecholamines, was used to assess the effects of beta-adrenoceptor blockade. The hearts were prelabeled with tritiated norepinephrine ( NE3H ), and the total radioactivity and that in NE3H were measured in the effluent coronary flow. The left main coronary artery was ligated for 10 minutes after which reperfusion followed. The liberation of NE3H and the development of ventricular tachycardia and fibrillation were monitored throughout. The cardioselective beta-antagonist agent, acebutolol, in a high concentration (1.1 X 10(-4)M), had good beta-antagonist effect in response to the added isoproterenol (10(-6)M); this concentration of acebutolol also suppressed sustained reperfusion ventricular arrhythmias but unexpectedly increased the release of NE3H . Atenolol, another cardioselective agent, did not prevent reperfusion ventricular arrhythmias even in a high concentration of 40 mg/L (1.5 X 10(-4)M). The d-isomer of propranolol, with poorer beta-antagonist properties than the l-isomer, prevented such ventricular arrhythmias in a concentration of 1.3 X 10(-5)M, which was low when compared to that of atenolol. It is proposed that the beta-antagonist activity of the compounds tested could not explain the inhibition of reperfusion ventricular arrhythmias and that another quality such as membrane-stabilizing activity may be involved.     

Urinary excretion and efflux from the leg of 3-methylhistidine before and after major surgical operation

Changes in the effluxes from the leg of 3-methylhistidine and tyrosine were studied in relation to alterations in the 24-hour excretion of 3-methylhistidine and total nitrogen in 11 patients before and after undergoing major surgical operation. On the first day after operation, efflux of 3-methylhistidine from the leg was significantly decreased by 40% compared to preoperative values. In contrast, tyrosine efflux was doubled at the same time as a transient 20% increase in oxygen uptake of the leg and a marked increase in catecholamine excretion were observed. These changes coincided with a 40% elevation in the excretion of both 3-methylhistidine and nitrogen. Leg metabolism returned to the preoperative pattern within a week. These results suggest that the loss of amino acids from the lean tissues of the leg is the result of a fall in protein synthesis accompanied by an adaptive fall in protein breakdown. Although the increase in nitrogen excretion in response to major surgical trauma reflects the negative amino acid balance of skeletal muscle, the changes in urinary 3-methylhistidine do not correlate with changes in efflux of 3-methylhistidine from the leg. These results suggest that the use of 3-methylhistidine excretion as a specific index of skeletal muscle protein breakdown in postoperative patients may be invalid. Tissues other than skeletal muscle appear to make a substantial contribution to the 3-methylhistidine excretion postoperatively.     

Serial changes in markers of disease activity with corticosteroid treatment in sarcoidosis

Serial changes in various markers of disease activity with corticosteroid therapy were assessed in 12 patients with active sarcoidosis. After six weeks of treatment with 40 mg daily of prednisone, all but one patient demonstrated symptomatic and radiographic improvement. For the entire patient group, there were corresponding improvements in forced vital capacity, from 59.2 +/- 5.5 to 70.5 +/- 5.3 percent of the predicted value (p less than 0.001, Student paired t test), serum angiotensin-converting enzyme levels, from 66.0 +/- 12.1 to 28.2 +/- 4.0 U/ml (p = 0.003), 67gallium lung scanning scores, from 3.6 +/- 0.2 to 0.8 +/- 0.3 (p less than 0.001), serum gamma globulin levels, from 2.40 +/- 0.2 to 1.5 +/- 0.1 g/dl (p less than 0.001), and erythrocyte sedimentation rate, from 26.8 +/- 2.7 to 14.8 +/- 3.0 mm per hour (p less than 0.001). Changes in percent of bronchoalveolar lavage fluid lymphocytes were less impressive (from 28.7 +/- 4.9 to 21.2 +/- 5.1, p = 0.034), but the geometric mean number of bronchoalveolar lavage fluid-IgG-secreting cells decreased from 23,861 to 3,830 (p = 0.013). Serial evaluations in five patients treated with decreasing doses of alternate-day prednisone for an additional 10 1/2 months indicated that changes in 67gallium lung scanning scores corresponded most closely to the clinical course in five of five patients. Determination of serum angiotensin-converting enzyme levels also closely paralleled the clinical course in four of five patients, whereas the other parameters measured were more variable markers of clinical response. However, abnormalities of bronchoalveolar lavage fluid-IgG-secreting cells often persisted in the absence of clinically evident disease, and the percentages of bronchoalveolar lavage fluid lymphocytes were frequently normal in patients who responded subsequently to corticosteroids. Larger prospective studies are warranted to more extensively evaluate various measurements of disease activity, especially bronchoalveolar lavage fluid analysis, in sarcoidosis.     

Effects of oleic acid infusion on plasma free fatty acids and blood ketone bodies in the fasting rat.

Oleic acid emulsions stabilized with albumin were infused into fasted rats. Blood samples taken before and during infusion were analyzed for free fatty acids (FFA), ketone bodies, glucose, and insulin. Turnover rates of FFA and ketone bodies were also determined using constant infusion of radioactive tracers. During oleic acid infusions at a rate of 2 mumoles/min/100 g body weight, FFA concentrations increased for a short time and then decreased to preinfusion levels. The decreases in concentrations were due to decreases in the endogenous rates of appearance of FFA into the blood. When oleic acid was infused at a rate of 3.5 mumoles/min/100 g body weight, FFA concentrations increased and remained elevated throughout the infusion. Ketone body concentrations more than doubled during infusions at 2 and 3.5 mumoles/min/100 g body weight and showed no signs of decreasing even when FFA concentrations decreased. Insulin concentrations doubled during infusion and glucose concentrations decreased. Insulin injected during infusion had little effect on concentrations of FFA or ketone bodies. It was concluded that infusions of oleic acid inhibit adipose tissue lipolysis and increase blood ketone concentrations in intact fasted rats. The injection of insulin does not inhibit ketogenesis when blood FFA levels are maintained by infusion.     

Perioperative myocardial infarction related to coronary bypass surgery.

Frank lead electrocardiograms were recorded from 149 normal and abnormal adult males using four different electrode placements. All chest electrodes were placed at: (1) the fourth intercostal space level, (2) the fifth intercostal space level, (3) the fourth intercostal space level with V₄ substituted for C, and (4) the fifth intercostal space level with V₄ substituted for C.Differences in mean values of many commonly used amplitudes and orientations were not statistically significant among the four recording methods, but amplitude differences for individual subjects were often large and difficult to predict. When V₄ is substituted for C, as commonly done in some laboratories, R_x decreased and R_z increased by more than 10 per cent in about 40 per cent of the cases. In about 70 per cent of the cases, R_x and R_z changed significantly when electrode level was shifted from the fifth to the fourth intercostal space. For these 70 per cent, it does not appear possible to accurately predict increase or decrease of R_x, R_z, or QRS_m.Analysis programs which depend on individual amplitude measurements are likely to be significantly affected by electrode placement. It is suggested that criteria for analysis programs developed using a specified version of the Frank system should ideally be applied only to electrocardiograms recorded in the same manner.     

Evaluation of the chronotropic property of captopril in hypertensive patients

Captopril was administered (50 mg orally) to 88 untreated hypertensive patients (70 with essential hypertension, eight with renal arterial disease, 10 with renal parenchymal disease) and to 25 hypertensive patients treated with sympatholytic or beta-blocking agent (20 with essential hypertension, five with renal arterial disease). In the former group, captopril caused a decrease in heart rate (HR) in 18 patients and an increase in only two. As a whole, captopril caused significant decreases in blood pressure without increase in HR. Significant negative correlation was observed between change in HR and plasma renin activity obtained before captopril administration (n = 79, r = -0.425, p less than 0.0001). Hypotensive and chronotropic effects of captopril were almost identical in untreated and treated patients. Hypotensive effects caused by captopril and nifedipine (20 mg orally) were almost identical. Nifedipine caused reflex tachycardia, while captopril caused slight bradycardia. Absence of compensatory tachycardia appears to be related to reduction of endogenous angiotensin II by captopril.U     

Ventricular arrhythmias during ergonovine-induced episodes of variant angina

Of 95 consecutive patients with active variant angina who underwent ergonovine testing in the coronary care unit while off treatment, 24 (25%) developed serious ventricular arrhythmias: ventricular tachycardia in eight, bigeminy in seven, pairs in five, and frequent ventricular extrasystoles in four. Ergonovine-induced arrhythmias were observed more often in patients with anterior than inferior ST segment elevation (p less than 0.05). ST segment elevation was significantly higher (10.3 +/- 8.1 vs 3.1 +/- 2.1 mm) in patients who developed arrhythmias. All ventricular arrhythmias began within 3 minutes after the onset of ST segment elevation. The intravenous administration of nitroglycerin eliminated arrhythmias in 22 of 24 cases; in only two patients did ventricular arrhythmias develop after the administration of nitroglycerin. Serious ventricular arrhythmias were found during spontaneous variant angina attacks in 14 of 24 patients with ergonovine-induced arrhythmias compared to 16 of 71 patients without ergonovine-induced arrhythmias (p less than 0.001). We conclude that arrhythmias during ergonovine testing are most often caused by ischemia and not reperfusion. Patients with arrhythmias during ergonovine-induced attacks are more likely to have arrhythmias during spontaneous attacks.     

Sex and insulin sensitivity

To analyze whether enhanced adiposity in females as compared with males is associated with a decreased sensitivity to insulin, a group of healthy normal weight females (n = 13, age 21 ± 1 years) and males (n = 11, age 23 ± 1 year, mean ± SEM) was studied. In each subject, body composition (% fat and % muscle), maximal aerobic power (V_O2 max) and whole body insulin-mediated glucose metabolism were measured. The group of women had a higher percentage of fat to total body weight (P < 0.001) and a lower percentage of muscle (P < 0.001) than the group of men. The higher percentage of fat in women compared with males was due to enhanced peripheral fat accumulation in the arm and thigh regions. V_O2 max levels were comparable in both groups (48 ± 1 mL/kg/min for women, 53 ± 2 mL/kg/min for men, P = NS). The rate of glucose metabolism (M) was comparable in women (8.78 ± 0.74 mg/kg/min), and men (8.31 ± 0.89 mg/kg/min) when expressed per kilogram of total body weight, but when expressed per kilogram of muscle tissue (M_m), it was 45% higher in women (29.4 ± 2.4 mg/kg/min) than in men (20.2 ± 1.6 mg/kg/min, P < 0.005). Partial correlation analysis indicated that the percentage of fat was inversely related to M and M_m in both women (P < 0.05) and men (P < 0.05), but not to percentage of muscle or V_O2 max. Conclusions: (1) Insulin-mediated glucose disposal is inversely related to adiposity in normal weight healthy males and females. (2) Women and men utilize equal amounts of glucose despite a higher adiposity in females. (3) Since muscle tissue utilizes most of intravenously administered glucose, this result indicates enhanced glucose uptake by muscle tissue in females compared with males. (4) Elevated glucose uptake by muscle in women may provide a mechanism by which women are protected against excessive hyperglycemia despite their smaller amount of glucose-consuming tissue.