Platelet Aggregability in Patients with a VVI Pacemaker

Several studies have suggested an increased incidence of thromboembolic events in patients with VVI pacemaker (VVI patients); furthermore, other authors have demonstrated that a treatment with anticoagulants or antiplatelet drugs may be effective in reducing thromboembolic events, thus suggesting an increased formation of platelet thrombi in these patients. In this respect, platelet aggregability was investigated in ten VVI patients and ten age– and sex–matched subjects. β–thromboglobulin (β–Tg) and platelet factor 4 (PF4) plasma levels were determined as weJJ as platelet aggregation induced by ADP, collagen, epinephrine, and arachidonic acid. Plasma β–Tg JeveJs were increased in the patient group (86 ± 24 vs 24 ± 13 ng/mL; P < 0.001) in presence of normal PF4 values (14 ± 11 vs 13 ± 6 ng/mL; NS). Aggregation curves showed abnormal values of maximal amplitude, slope, and lag time. In particular, maximal amplitude was significantJy higher in VVI patients as compared with controls (ADP P < 0.01, collagen P < 0.001, adrenaline P < 0.01, arachidonic acid P < 0.05). These findings strongly suggest an increase of platelet activity in VVI patients.     

Polymorphism at the 5'' end flanking region of the insulin gene is associated with reduced insulin secretion in healthy individuals

Sixty-four unrelated healthy subjects were studied for the detection of a DNA polymorphism at the 5' end of the insulin gene. No significant difference between the groups was found in blood glucose values at fasting and after an oral glucose load. A significant association was found between fasting (P less than 0.05) and after load plasma C-peptide levels (P less than 0.01) and the presence of a 1.6 Kb insertion at the 5' end of the insulin gene. A gene dose-dependent effect was noted, class 3/3 individuals having the lowest after-load C-peptide concentration and class 1/3 an intermediate level (F for the linear trend: P = 0.007). This might suggest that insulin gene polymorphism affects insulin secretion in healthy individuals. In order to confirm this, a subgroup of six class 3/3 and eight class 1/1 individuals subsequently underwent a hyperglycaemic clamp. The tissue sensitivity to insulin was similar in the two groups but glucose-stimulated insulin secretion was markedly impaired in homozygotes for the class 3 allele. In this group, insulin secretion was, on average, only one-third of that in class 1/1 individuals (P less than 0.02). Similarly impaired in class 3/3 persons was the glucose + arginine-stimulated insulin secretion (P less than 0.05). We conclude that the polymorphism at the 5' end of the insulin gene is associated with variations in insulin secretion in healthy humans.     

Jesús Alanís and the First Recording of the His Bundle: The Scientist and the Man

The anatomy and physiology of the specialized conduction system has intrigued investigators since the 19th century and is still not fully understood. Dr. Wilhelm His Jr. is well known because he discovered the A‐V bundle, and Dr. Sunao Tawara is rightly credited with the discovery of the atrioventricular (AV) node, but who was the first to record the electrical activity of the His bundle? This paper reviews the historical background and scientific contributions made by Dr. Jesús Alanís in the middle of the 20th century working at the National Institute of Cardiology in Mexico City. Collaborating with outstanding investigators such as Arturo Rosenblueth, Dr. Alanís recorded for the first time the electrical activity of the His bundle in the isolate canine heart. That the recorded electrogram was indeed the His bundle and not the AV node was confirmed by detailed studies that set the basis for modern clinical electrophysiology. The life and research contributions of this extraordinary man are reviewed in the context of a unique group of investigators who made significant advances in cardiac electrophysiology.