Changes in the QRS complex and ST segment in transmural and subendocardial myocardial infarctions. A clinicopathologic study.

The QRS complex and ST segment in the ECGs of 80 patients who died of an acute myocardial infarction (MI) were studied in relation to the extent of the MI (subendocardial vs. transmural). Changes in the QRS complex developed in nine out of the 15 cases with an acute subendocardial MI. Five of these cases fulfilled the conventional QRS criteria for a myocardial infarction. A definite ST segment depression (a J point depression of 2 mm. or more in at least one lead, and a horizontal or downward sloping ST segment with a minimum duration of 0.08 sec.) occurred most frequently in connection with a circumferential subendocardial MI (88 per cent), but it was also found in a regional subendocardial (43 per cent) and transmural MI (43 per cent). In 17 per cent of the cases with a transmural MI, this was the only ECG abnormality. It is concluded that cases with a subendocardial MI cannot always be distinguished from transmural MI on the basis of the presence or absence of the QRS changes, and that an ST segment depression, as defined in this study, can give additional information in the evaluation of an acute phase of an MI.     

Brain deviations in adult obese-hyperglycemic mice (ob/ob)

In the brain of adult obese-hyperglycemic mice (ob/ob) deviations, such as reduced brain weight, diminished myelination, and reduced amount of DNA were found. These findings cannot be explained by hypothyroidism in adults since above mentioned deviations could only have been caused by a reduced thyroidal activity in the first weeks of postnatal life. Therefore, our data are in support of the earlier hypothesis of congenital hypothyroidism.     

Significance of a terminal R wave in lead V1 of the electrocardiogram.

A terminal r wave in Lead V1 lower than 0.6 mV. was studied in the ECGs of four groups: (1) 104 healthy children, (2) 207 healthy young adults, (3) 171 patients with no autopsy evidence of a cardiopulmonary disease, and (4) 1,078 autopsy patients with a cardiopulmonary disease. Cases with a complete right bundle branch block were excluded. A terminal r wave occurred in 2.9 per cent healthy children, 1.4 per cent of healthy young adults, 0.6 per cent of patients without and in 5.9 per cent of patients with autopsy evidence of a cardiopulmonary disease. The occurrence of a terminal r wave was most common in pulmonary patients (10 per cent). But it was also found in patients with an anterior or a posterior myocardial infarction and in some cases of left ventricular hypertrophy. In the autopsy series RVH occurred in 57 per cent of patients with a Qr pattern, in 30 per cent of patients with a terminal r wave higher than the initial one, and in none of the patients with a terminal r wave lower than the initial one. It is concluded that the height of the terminal r wave has clinical significance. A terminal r wave higher than the initial one in Lead V1 is associated with a cardiopulmonary disease in subjects over 30 years of age, while an r wave lower than the initial one seems to be an innocent finding.     

C-peptide secretion and insulin antibodies as determinants of stability in diabetes mellitus

The relative significance of residual beta-cell secretory activity and human insulin antibodies in determining diabetic stability has been examined in 35 diabetic subjects. The response of plasma C-peptide immunoreactivity following 50 g oral glucose has been used as an index of beta-cell function. Glucose-stimulated C-peptide secretion was observed in 58% of stable diabetics, but in no labile diabetics. When present, C-peptide secretion following a glucose load in diabetics was of smaller amplitude and slower in onset, but more prolonged than in normal subjects. In secretors, stability of diabetes was significantly correlated with the magnitude of the C-peptide response. As a group, labile diabetics had lower insulin antibody levels than stable patients, but stability and antibody levels were not correlated in individual patients. In non-secretors there was no difference in antibody levels between the stable and labile groups. Neither the equilibrium binding affinities nor the dissociation rate constants differed significantly for antibodies from stable and labile diabetics. Thus stability of diabetes depends upon residual beta-cell secretory activity, but not on the concentration or binding characteristics of insulin antibodies.     

Sudden death during ambulatory monitoring. Analysis of six cases

The ambulatory electrocardiographic recordings of six patients with coronary artery disease who died during monitoring were analyzed. In four patients, sinus rhythm was interrupted by sinoatrial, atrioventricular, nodal, or infra-His conduction abnormalities leading to bradyarrhythmic sudden death. Two patients died of sustained ventricular tachycardia or ventricular fibrillation. These data emphasize that the arrhythmias involved in the sudden death syndrome may be more heterogenous than currently appreciated.     

Cardiac rehabilitation: its role in evaluation and management of the patient with coronary heart disease

Comprehensive cardiac rehabilitation is not for every patient, but rather for those who require more than the services of a physician and a nurse. The services which eventually are required may be provided simply in some cases by paramedical persons and in the more complicated cases by an experienced multidisciplinary team. The main evaluative expertise of cardiac rehabilitation specialists is the functional evaluation of the patient—that is, the physical, psychological, social, and vocational functioning by a variety of specialized techniques. The major therapeutic recommendation is usually endurance-building exercise training for secondary prevention. The educational and supportive aspects of the rehabilitation process may make the difference between non-limiting impairment and disability.     

Short-term influences of dichloroacetate on genetically hyperlipemic rats

The effects of short-term (7 days) administration of dichloroacetate (DCA) on carbohydrate and lipid metabolism in the Zucker obese and lean rat were investigated. Metabolic effects of the drug were more pronounced in the obese than in the lean rat. DCA decreased fasting blood glucose concentrations in both lean and obese rats, but more so in the fat animals, probably because of higher initial levels. The hypoglycemic action of DCA is likely attributable to a direct effect on liver and peripheral tissues and not to an indirect action caused by a decrease in the glucagon-to-insulin ratio because the drug induced just the opposite effect. DCA decreased plasma triglycerides (TG) and free fatty acids (FFA) in the hyperlipemic rats but not in lean rats. Intrahepatic triglyceride content diminished after drug treatment in fat rats, suggesting decreased hepatic TG synthesis. Hyperketonemia, induced in both lean and fat rats by DCA treatment, was also greater in the obese animal. This response was probably caused by accelerated hepatic ketone body production due to increased β-oxidation, and not to enhance FFA substrate supply. These data demonstrate that DCA is capable of correcting many of the underlying abnormalities in carbohydrate and fat metabolism in the obese Zucker rat.     

Comparisons of prostaglandin vasoactive effects and interactions in the in vivo microcirculation of the rat urinary bladder

A combination of techniques for in vivo transillumination, topical application of vasoactive agents, and direct microscopic observation of microcirculatory responses was utilized to evaluate the vasomotor actions of prostaglandins (PGs) E₁, E₂, F_1α, F_2α, A₁, and A₂ on rat urinary bladder arterioles and venules. The effects of PGE₁ and histamine (HIS) on arteriolar responsiveness to norepinephrine (NE), serotonin (5-HT), and PGF_2α were measured. Histochemical studies were completed to determine the primary site of prostaglandin (PG) metabolic deactivation in the urinary bladder. Arteriolar dilatation occurred with HIS, PGE₁, PGE₂, PGA₁, PGA₂, and PGF_1α, all of which (with the exception of HIS) demonstrated significant dose-related responses. Overall, PGE₁ and PGE₂ were of greatest potency. Significant dose-related arteriolar constriction occurred with NE > PGF_2α > 5-HT (in order of decreasing potency). HIS, PGE₁, PGE₂, and PGA₁ produced significant venular dilatation; PGE₁ and HIS were dose related. Only NE resulted in significant venoconstriction. Arteriolar responsiveness to NE and PGF_2α decreased after pretreatment with PGE₁ but was unchanged by HIS pretreatment, whereas application of 5-HT following pretreatment with PGE₁ or HIS produced equivalent levels of arteriolar constriction. The primary site of deactivation of PGE₁ was histochemically localized to bundles of smooth muscle fibers in the muscular coat of the rat urinary bladder wall.     

The mechanism of recovery of hepatic T4-5'-deiodinase during glucose-refeeding: role of glucagon and insulin

Refeeding studies were performed on male Sprague-Dawley rats that had been fasted for 72 hours to characterize the specific effect of carbohydrates on T₃ metabolism. Fasting is associated with low serum T₃ levels and reduced hepatic T₄-5′-deiodinase activity (T₄ → T₃). Carbohydrate refeeding (20% glucose in H₂O) normalized both the serum T₃ and hepatic T₄-5′-deiodinase activity within 72 hours, whereas fat (10% Intralipid) and amino acids (5.5% Travasol) had no effect after 72 hours of refeeding. Refeeding with a mixed diet (Purina Rodent Chow) occasionally reactivated hepatic T₄-5′-deiodinase activity, however, normalization of enzyme activity did not occur within 72 hours. Time-course studies demonstrated that hepatic T₄-5′-deiodinase activity was not stimulated until 24 hours of carbohydrate refeeding had elapsed and that 48 to 72 hours were required for normalization. The mechanism of the carbohydrate-refeeding effect was characterized by analyzing the alterations in the kinetics Michaelis constant (Km) and maximal velocity (Vmax) of hepatic T₄-5′-deiodinase and the changes in the hepatic content of nonprotein sulfhydryl groups (NP-SH), which are possible enzyme cofactors. There was no relationship between the hepatic enzyme activity and the NP-SH response during the refeeding period. Moreover, homogenate enrichment with the sulfhydryl compound, dithiothreitol (DTT), did not alter the temporal profile of the enzyme recovery consequent to refeeding. Refeeding with carbohydrate had no effect on the Km of hepatic T₄-5′-deiodinase but had a significant effect on the Vmax. Refeeding with glucose induced an increase in enzyme Vmax over the time-course, which became significant (P < 0.005) compared with the enzyme Vmax of the fasted group by 72 hours. During carbohydrate refeeding, a positive correlation was noted between the ratio of serum insulin to glucagon and hepatic-T₄-5′-deiodinase activity (r = 0.82, P < 0.001), whereas a negative correlation was found between enzyme activity and the ratio of serum glucose to insulin (r = ?0.9, P < 0.001). Furthermore these correlations also applied during refeeding with fat and amino acids. Thus, the carbohydrate-refeeding reactivation of hepatic T₄-5′-deiodinase in fasted rats is a delayed process that requires a refeeding period equivalent to the duration of fasting for enzyme normalization to occur. Recovery was due to an increase in the hepatic content of active enzyme rather than an enhancement of cofactor supply. The glucoregulatory hormones, glucagon and insulin, may modulate these carbohydrate induced changes on hepatic T₄-5′-deiodinase. Moreover, the differential reaction of hepatic T₄-5′-deiodinase to specific nutriments may be mediated by these glucoregulatory hormones.