Adenosine induced chest pain--a comparison between intracoronary bolus injection and steady state infusion.

OBJECTIVE: Adenosine may induce chest pain in at least two ways, either by direct stimulation of sensory afferents before actual ischaemia occurs or secondary to ischaemia. The aim was to study if the mechanism of pain induction may depend on the method of adenosine administration. METHODS: Increasing doses of adenosine were given to seven male patients with ischaemic heart disease referred for coronary angiography: first as a bolus intracoronary injection (2.5-50 mumol), second as a 1 ml.min-1 steady state infusion (0.01-20 mumol.min-1) and third as an intravenous steady state infusion (0.076-0.76 mumol.kg-1 x min-1). Pain, rate-pressure product, coronary sinus blood flow, and ECG were monitored. Lactate was analysed in coronary sinus and arterial blood. RESULTS: After intracoronary bolus injection there were no signs of myocardial ischaemia, whereas during intracoronary steady state infusion, and in spite of a lower, but definite, degree of pain, 5/7 patients showed myocardial lactate production and three patients showed ST depression. During the intravenous steady state infusion 6/6 patients showed ST depression. CONCLUSIONS: These findings suggest that when using adenosine for studies on the mechanisms of chest pain in patients with ischaemic heart disease it is preferable to use an intracoronary bolus injection technique rather than a steady state infusion, as the risk of inducing ischaemia with the latter model cannot be ignored.     

Immunological parameters in girls with Turner syndrome

Disturbances in the immune system has been described in Turner syndrome, with an association to low levels of IgG and IgM and decreased levels of T- and B-lymphocytes. Also different autoimmune diseases have been connected to Turner syndrome (45, X), thyroiditis being the most common.     

Does chronic hypoxaemia induce transformations of fibre types?

The study comprised nine patients with chronic obstructive lung disease. Quadriceps muscle biopsies were studied with respect to fibre type composition before and after haemodilution that brought haemoglobin (Hb) to within normal limits. Ten days elapsed between the two biopsy occasions. The arterial oxygen tension (PaO2) and saturation (SaO2) were depressed to 8.4 +/- 2.0 kPa and 89 +/- 11% in the patients with chronic obstructive lung disease and increased to 9.2 +/- 2.1 and 91 +/- 8% with haemodilation. The type II fibre proportion was 71 +/- 12% before haemodilation and significantly higher than normal (reference group, see Aniansson et al. 1981). Following haemodilation the proportion of type II fibres decreased significantly to 60 +/- 14%. The proportion of type II fibres was directly related to the haemoglobin content before, but not after, haemodilation and was inversely related to PaO2 and SaO2 both before and after haemodilation. In conclusion, hypoxaemia may be a factor underlying the high proportion of type II fibres found in patients with chronic obstructive lung disease.     

Effects of training at simulated altitude on performance and muscle metabolic capacity in competitive road cyclists

Summary Differences between the effects of training at sea level and at simulated altitude on performance and muscle structural and biochemical properties were investigated in 8 competitive cyclists who trained for 3–4 weeks, 4–5 sessions/week, each session consisting of cycling for 60–90 min continuously and 45–60 min intermittently. Four subjects, the altitude group (AG), trained in a hypobaric chamber (574 torr=2300 m above sea level), and the other four at sea level (SLG). Before and after training work capacity was tested both at simulated altitude (574 torr) and at sea level, by an incremental cycle ergometer test until exhaustion. Work capacity was expressed as total amount of work performed. Venous blood samples were taken during the tests. Leg muscle biopsies were taken at rest before and after the training period. AG exhibited an increase of 33% in both sea level and altitude performance, while SLG increased 22% at sea level and 14% at altitude. Blood lactate concentration at a given submaximal load at altitude was significantly more reduced by training in AG than SLG. Muscle phosphofructokinase (PFK) activity decreased with training in AG but increased in SLG. All AG subjects showed increases in capillary density. In conclusion, work capacity at altitude was increased more by training at altitude than at sea level. Work capacity at sea level was at least as much improved by altitude as by sea level training. The improved work capacity by training at altitude was paralleled by decreased exercise blood lactate concentration, increased capillarization and decreased glycolytic capacity in leg muscle.     

Lower threshold for adenosine-induced chest pain in patients with angina and normal coronary angiograms

Objective—To investigate whether patients with angina-like chest pain and normal coronary angiograms are more sensitive to adenosine as an inducer of chest pain.

Design—Increasing doses of adenosine were given in a single blind study as intravenous bolus injections. Chest pain and the electrocardioraphic findings were noted.

Patients—Eight patients with anginalike chest pain but no coronary stenoses (group A), nine patients with angina and coronary stenoses (group B), and 16 healthy volunteers (group C).

Results—In the absence of ischaemic signs on the electrocardiogram adenosine provoked angina-like pain in all patients in groups A and B. The pain was located in the chest, and its quality and location were described as being no different from the patient's habitual angina. In group C, 14 of 16 subjects reported chest pain. The lowest dose resulting in chest pain was lower in group A (0·9 (0·6) mg) than in group B (3·1 (1·5) mg) (p < 0·005) and in group C (6·2 (3·7) mg) (p < 0·005). The maximum tolerable dose was lower in group A (4·7 (2·1) mg) than in group B (9·2 (3·8) mg) (p < 0·05) and in group C (12·0 (4·1) mg) (p < 0·005).

Conclusions—Patients with anginalike chest pain and normal coronary angiograms have a low pain threshold and low tolerance to pain induced by adenosine.

     

Effects of intramyocardial injection of phVEGF-A165 as sole therapy in patients with refractory coronary artery disease--12-month follow-up: angiogenic gene therapy

OBJECTIVE: To test the safety and bioactivity of phVEGF-A165 after intramyocardial injection during 12-month follow-up. DESIGN: Open-labelled study. SUBJECTS: Inclusion criteria were angina pectoris, Canadian Cardiovascular Society (CCS) class III-IV, unamenable to further revascularization, ejection fraction (EF) >30%, perfusion defects extending over >10% of the anterolateral left ventricle wall detectable with adenosine single photon emission computerized tomography (SPECT) and at least one patent vessel visible by coronary angiography. Seven of 39 patients referred for gene therapy were included. INTERVENTION: Via a mini-thoracotomy under general anaesthesia. phVEGF-A165 was injected directly into the myocardium at four sites in the anterolateral region of the left ventricle. RESULTS: Operative procedures were uneventful. Perioperative release of myocardial markers and electrocardiogram (ECG) changes were detected in two patients. There were no perioperative deaths but one patient died 7 months postoperatively because of myocardial infarction. Plasma vascular endothelial growth factor (VEGF)-A levels increased two to threefold peaking 6 days postoperatively (P < 0.004) and returning to baseline by day 30. A significant reduction in angina pectoris was reported. The CCS class improved from 3.3+/-0.2 to 1.9+/-0.3 (P < 0.01) and nitroglycerine intake decreased from 39+/-15 to 12+/-5 tablets week(-1) (P < 0.001) 2 months after gene transfer. Improvements remained after 12 months when nitroglycerine consumption approached zero. Improved myocardial function in the phVEGF-A165 injection region was documented in all patients (P < 0.016) by tissue velocity imaging (TVI). Reduced reversible ischaemia was detected by adenosine SPECT in four patients. Improved collateralization was detected in four patients with coronary angiography. CONCLUSION: Intramyocardial injection of phVEGF-A165 is safe and may lead to improved myocardial perfusion and function with longstanding symptomatic relief in end-stage angina pectoris. Based on these results this therapeutic potential is being tested in a double-blind placebo controlled multicentre trial.     

Prognostic role of on-line vectorcardiography as regards repeat revascularization after successful coronary angioplasty

This study evaluated the prognostic significance of continuous on-line vectorcardiography (VCG) during elective coronary angioplasty (percutaneous transluminal coronary angioplasty, PTCA). Patients (n = 192, mean age 58 +/- 10), treated with elective and initially successful PTCA, were included. VCG monitoring was started before start of the PTCA procedure and was carried out during the entire procedure. ST vector magnitude (ST-VM) was monitored. A 6-month follow-up was obtained. Main outcome measures were the frequency of cardiac events and revascularization during follow-up. During follow-up, 1 patient died, 6 suffered a nonfatal myocardial infarction and 50 were revascularized. Angiography revealed restenosis in 88% of the patients who had a revascularization. In the total patient group, the VCG predictor of revascularization was the total ischemic time of all ST-VM episodes (p = 0.05). Clinical predictors of revascularization were diabetes mellitus (p < 0.01), a more severe type of lesion (type B; p < 0.01), percent post-PTCA stenosis (p < 0.05), nominal balloon size (p < 0.01), maximum balloon pressure (p < 0.05) and no stent implanted (p < 0.001). In a multivariate analysis all the above significant univariate variables of revascularization were entered. Total ischemic time of ST-VM (p < 0.01) was the best variable giving independent prognostic information. In the nonstent group, total ischemic time of ST-VM (p < 0.01) was the only independent predictor of a further revascularization. In conclusion, VCG monitoring during elective PTCA gives on-line information that identifies patients at an increased risk of a revascularization during 6 months after the initial procedure.