INFERIOR PETROSAL SINUS SAMPLING IN ACROMEGALY

In view of the diagnostic value of bilateral simultaneous inferior petrosal sinus sampling (BSIPSS) in localising preoperatively the site of the microadenoma in pituitary dependent Cushing s disease, the clinical value of BSIPSS was evaluated in five acromegalic patients with equivocal or negative pituitary CT scans. Intersinus GH gradients were obtained for all patients (range 1.6–4.2) but in only one case was the gradient correctly localised to the side of the tumour. Gradients of several other pituitary hormones, particularly prolactin (range 1.6–4.0), also demonstrated gradients parallel to the GH intersinus gradients. Despite the paradoxical intersinus GH gradients, the surgeon was able to readily identify the tumour at the time of surgery. Thus BSIPSS is of little assistance to the surgeon for the preoperative radiological evaluation in acromegaly and these results caution against the universal adoption of the BSIPSS technique in the radiological assessment of all secretory pituitary microadenomas.     

Autonomic Manipulation Influences Both Temporal and Frequency Analyses of Late Potentials

Previous studies of late potentials have not standardized the autonomic milieu at the time of testing. We studied the effects of autonomic manipulation in seven patients with previous Q wave myocardial infarction. Late potentials were evaluated using standard temporal (TD) and spectral temporal mapping techniques (STM) in the drug free state, and during separate intravenous administration of each of the following: isoproterenol, esmolol, and atropine. Isoproterenol was nitrated to achieve a heart rate of 130% of baseline. Esmolol was infused at a rate of 250 μg/kg per minute, after a loading dose of 500 μg/kg. Atropine was given as a 2-mg bolus. In addition, five patients who received no drug infusions acted as controls, undergoing four serial signal-averaging studies in the baseline state: a "baseline" study, and then three additional studies at time intervals similar to those incurred by the study patients. Therefore, a total of 21 TD and 21 STM tests were done in the study group seven patients; three drugs per patient) during the drug infusions, and 15 TD and 15 STM tests were done in the control group (five patients; three "nonbaseline" tests per patient). A change normal to abnormal, or vice versa) in TD during a drug infusion occurred in 24% of the tests. No such change occurred in the control group (P < 0.01). A change in STM during a drug infusion occurred in 38% of tests, versus 13% of tests in the control group (P = 0.14). Overall, six of seven patients had a change in TD and/or STM diagnosis with infusion of one or more of the study drugs. Optimal clinical use of late potentials may require a standardized autonomic environment.     

Myocardial ischaemia during tracheal intubation and extubation

The incidence of myocardial ischaemia during tracheal intubationand extubation was compared using ambulatory ECG monitoringin 60 patients undergoing a variety of different surgical operations.Seven patients had myocardial ischaemia after tracheal intubationand seven patients during tracheal extubation. The patientswho developed myocardial ischaemia during tracheal extubationhad significantly greater rate-pressure products immediatelybefore tracheal extubation (P<0.05) and 1 min after trachealextubation (p<0.01) compared with those patients who didnot develop myocardial ischaemia during extubation.     

Ectopic Ventricular Beats Originating in Ischemically-Injured Left Ventricular Epicardium, 24 Hours Following Coronary Artery Occlusion in the Dog

Epicardial Ectopics. Introduction: Ventricular ectopic beats demonstrating: (1) depolarization in ischemically-injured anterior epicardium preceding His-Purkinje activation by more than 25 msec; (2) initial delta waves on the anterior chest leads of the surface ECG coincident with presystolic epicardial activation; and (3) a left bundle branch block morphology were observed in 46 of 256 anesthetized dogs evaluated 18–24 hours following anterior descending coronary artery occlusion. Methods and Results: In 18 experiments, endocardial and epicardial recordings, and signal-averaged recordings from the left ventricle were used to determine the earliest activation time/site for epicardial ectopic beats. In these ventricular ectopic beats, early epicardial activation was coupled to the preceding beat by a constant, fixed coupling interval. Electrical activity during the interectopic interval was not detected with composite or multiple bipolar recordings, or with signal averaging from the heart. The mean coupling interval was prolonged by lidocaine from 385 ± 24to 409 ± 45 msec (P < 0.01), and was decreased by epinephrine (364 ± 7 msec) and D-600 (324 ± 32 msec)(P < 0.05). Spontaneous ventricular beats of epicardial origin could be reversibly suppressed by epicardial lidocaine administration or permanently suppressed with intracoronary latex injection, eliminating presystolic potentials. Histologic examination of the epicardium revealed surviving tissue bands (0.5–2.0 mm) distributed throughout transmural infarcted epicardium. Conclusion: The present experiments demonstrate constant-coupled ectopic ventricular beats of epicardial origin, 18–24 hours following myocardial infarction. The ventricular ectopic beats may result from abnormal automaticity or electrotonic excitation from an initiating beat across an unexcitable gap with slow conduction from the “site of origin’ to reactivate the left ventricle. (JCardiovasc Electrophysiol, Vol. 3, pp. 315–333, August 1992)     

Co60 Vitamin B12 Binding Capacity of Human Leukocytes

1. Mature neutrophilic leukocytes show the highest Co⁶⁰B₁₂ binding capacity.

2. Less mature granulocytes, "blast" forms and eosinophils have little or noCo⁶⁰B₁₂ binding capacity.

3. Disintegrated mature leukocytes from chronic myelocytic leukemia andpolycythemia vera show higher B₁₂ binding capacity than intact cells.

4. Mature leukocytes from patients with chronic myelocytic leukemia andpolycythemia vera show a two-phase B₁₂ curve suggesting specific and nonspecificbinding, similar to that observed in human serum.

5. Disintegration products from mature neutrophilic leukocytes probablycontribute largely to increased B₁₂ binding capacity of serum in chronic myelocyticleukemia and polycythemia vera.

Submitted on August 30, 1961 Accepted on October 17, 1961     

Glucose tolerance, insulin sensitivity and insulin release in European non-diabetic carriers of a polymorphism upstream of CDKN2A and CDKN2B

Aims/hypothesis

The aim of this study was to investigate the association of the rs10811661 polymorphism near the CDKN2B/CDKN2A genes with glucose tolerance, insulin sensitivity and insulin release in three samples of white people with European ancestry.

Methods

Sample 1 comprised 845 non-diabetic offspring of type 2 diabetes patients recruited in five European centres participating in the EUGENE2 study. Samples 2 and 3 comprised, respectively, 864 and 524 Italian non-diabetic participants. All individuals underwent an OGTT. Screening for the rs10811661 polymorphism was performed using a TaqMan allelic discrimination assay.

Results

The rs10811661 polymorphism did not show a significant association with age, BMI and insulin sensitivity. Participants carrying the TT genotype showed a significant reduction in insulin release, measured by an OGTT-derived index, compared with carriers of the C allele, in the three samples. When these results were pooled with those of three published studies, and meta-analysed with a random-effects model, the T allele was significantly associated with reduced insulin secretion (?35.09 [95% CI 14.68?C55.52], p?=?0.0008 for CC+CT vs TT; and ?29.45 [95% CI 9.51?C49.38], p?=?0.0038, for the additive model). In addition, in our three samples, participants carrying the TT genotype exhibited an increased risk for impaired glucose tolerance (IGT) compared with carriers of the C allele (OR 1.55 [95% CI 1.20?C1.95] for the meta-analysis of the three samples).

Conclusions/interpretation

Our data, together with the meta-analysis of previously published studies, show that the rs10811661 polymorphism is associated with impaired insulin release and IGT, suggesting that this variant may contribute to type 2 diabetes by affecting beta cell function.     

Atrial Fibrosis Helps Select the Appropriate Patient and Strategy in Catheter Ablation of Atrial Fibrillation: A DE‐MRI Guided Approach

MRI for AF Patient Selection and Ablation Approach. Introduction: Left atrial (LA) fibrosis and ablation related scarring are major predictors of success in rhythm control of atrial fibrillation (AF). We used delayed enhancement MRI (DE‐MRI) to stratify AF patients based on pre‐ablation fibrosis and also to evaluate ablation‐induced scarring in order to identify predictors of a successful ablation. Methods and Results: One hundred and forty‐four patients were staged by percent of fibrosis quantified with DE‐MRI, relative to the LA wall volume: minimal or Utah stage 1; <5%, mild or Utah stage 2; 5–20%, moderate or Utah stage 3; 20–35%, and extensive or Utah stage 4; >35%. All patients underwent pulmonary vein (PV) isolation and posterior wall and septal debulking. Overall, LA scarring was quantified and PV antra were evaluated for circumferential scarring 3 months post ablation. LA scarring post ablation was comparable across the 4 stages. Most patients had either no (36.8%) or 1 PV (32.6%) antrum circumferentially scarred. Forty‐two patients (29%) had recurrent AF over 283 ± 167 days. No recurrences were noted in Utah stage 1. Recurrence was 28% in Utah stage 2, 35% in Utah stage 3, and 56% in Utah stage 4. Recurrence was predicted by circumferential PV scarring in Utah stage 2 and by overall LA wall scarring in Utah stage 3. No recurrence predictors were identified in Utah stage 4. Conclusions: Circumferential PV antral scarring predicts ablation success in mild LA fibrosis, while posterior wall and septal scarring is needed for moderate fibrosis. This may help select the proper candidate and strategy in catheter ablation of AF. (J Cardiovasc Electrophysiol, Vol. 22, pp. 16‐22, January 2011)