Percutaneous brachial approach in left heart catheterization with 5 French catheters. Preliminary experience

This describes our preliminary experience with percutaneous brachial approach for cardiac catheterization, by using 5 French (F) preformed catheters. Thirty patients (pts) were studied from the left arm (Group A) with a 5F sheath and 5F Judkins catheters and 30 from the right arm (Group B) with 5F sheath and 5F Amplatz catheters. Pigtail catheters (5F) were used for the left ventricular angiograms in all patients. In 10 patients arterial velocity signals and radial and ulnar artery blood pressures were monitored with the Doppler ultrasonic velocity detector before and immediately after each procedure, and 24 hours later. Arterial puncture was carried out successfully in each patient by using a 18-gauge Potts-Cournand needle. The puncture site was as close as possible to the ante cubital fossa where the artery is less mobile. Both coronary arteries were selectively opacified and the left ventricular angiography was done on every patient. The diagnostic quality of the angiograms was evaluated by the visual analogue scale and the results were not different from those obtained with the femoral approach in our catheterization laboratory. In 3 out of 30 pts in group B it was impossible to obtain a good left coronary opacification with Amplatz catheters for anatomical reasons, thus the right femoral approach was preferred. Brachial artery occlusion occurred in 1 patient from group B and needed surgical thrombectomy carried out to restore normal radial and ulnar pulses.(ABSTRACT TRUNCATED AT 250 WORDS)     

Divergent effects of serotonin on coronary-artery dimensions and blood flow in patients with coronary atherosclerosis and control patients

BACKGROUND. Studies in animals have shown that serotonin constricts coronary arteries if the endothelium is damaged, but in vitro studies have revealed a vasodilating effect on isolated coronary segments with an intact endothelium. To investigate the effect of serotonin in humans, we studied coronary-artery cross-sectional area and blood flow before and after the infusion of serotonin in seven patients with angiographically normal coronary arteries and in seven with coronary artery disease. METHODS. We measured the cross-sectional area of the coronary artery by quantitative angiography and coronary blood flow with an intracoronary Doppler catheter. Measurements were obtained at base line and during intracoronary infusions of serotonin (0.1, 1, and 10 micrograms per kilogram of body weight per minute, for two minutes). We repeated the measurements after an infusion of ketanserin, an antagonist of serotonin receptors that is thought to block the effect of serotonin on receptors in the arterial wall but not in the endothelium. RESULTS. In patients with normal coronary arteries, the highest dose of serotonin increased cross-sectional area by 52 percent (P less than 0.001) and blood flow by 58 percent (P less than 0.01). The effect was significantly potentiated by administration of ketanserin. In patients with coronary-artery atherosclerosis, serotonin reduced cross-sectional area by 64 percent (P less than 0.001) and blood flow by 59 percent (P less than 0.001). Ketanserin prevented this effect. CONCLUSIONS. Serotonin has a vasodilating effect on normal human coronary arteries; when the endothelium is damaged, as in coronary artery disease, serotonin has a direct, unopposed vasoconstricting effect. When considered with other evidence, these data suggest that platelet-derived factors such as serotonin may have a role in certain acute coronary ischemic syndromes.     

Heart positioner: a device to easily expose all coronary arteries during beating heart operations

The increasing number of coronary operations performed on a beating heart has prompted the development of new techniques and instruments to expose the coronary arteries without major hemodynamic derangements. We describe an expandable surgical pad combined with a series of tapes that help to control rotations and positioning of the heart. The empty surgical pad is fixed at the bottom of the pericardial cavity. After injection of warm saline, the pad elevates and displaces the heart, and the tapes rotate and immobilize the heart in the desired position. Easy access to all coronary arteries with minimal effect on hemodynamics is possible.     

Reduction in infarct size by the phospholipase inhibitor quinacrine in dogs with coronary artery occlusion

It has been suggested that activation of tissue phospholipases may contribute to the development of ischemic cell injury. In the present study we sought to assess whether administration of the phospholipase inhibitor quinacrine would reduce the extent of myocardial necrosis after coronary artery occlusion. In open-chest, anesthetized dogs the left anterior descending coronary artery was ligated, and technetium-99-labeled albumin microspheres were injected into the left atrium to measure the area at risk. The animals were then randomly divided into a control group (n = 8) and a group receiving quinacrine (5 mg/kg intravenous bolus followed by a 40 micrograms/kg/min infusion for 6 hours; n = 9). The animals were killed 6 hours after occlusion, and the infarcted area was delineated by triphenyltetrazolium chloride staining. The extent of the risk region was similar in the two groups (32.3 +/- 2.1% of the left ventricle in control dogs and 34.2 +/- 3.4% in quinacrine-treated dogs). Infarct size was 86.4 +/- 8.8% of the risk region in control animals, whereas in treated dogs it averaged 62.3 +/- 6.4% of the risk region (p = 0.05). No differences were found in heart rate, arterial pressure, and rate-pressure product between the two groups. Thus administration of the phospholipase inhibitor quinacrine reduced the extent of myocardial necrosis in a model of fixed coronary artery occlusion. Preservation of membrane phospholipids, reduced formation of lipoxygenase metabolites, or both may mediate this phenomenon.     

Additive effects of simulated climate changes,elevated CO2, and nitrogen deposition on grassland diversity

Biodiversity responses to ongoing climate and atmospheric changes will affect both ecosystem processes and the delivery of ecosystem goods and services. Combined effects of co-occurring global changes on diversity, however, are poorly understood. We examined plant diversity responses in a California annual grassland to manipulations of four global environmental changes, singly and in combination: elevated CO2, warming, precipitation, and nitrogen deposition. After 3 years, elevated CO2 and nitrogen deposition each reduced plant diversity, whereas elevated precipitation increased it and warming had no significant effect. Diversity responses to both single and combined global change treatments were driven overwhelmingly by gains and losses of forb species, which make up most of the native plant diversity in California grasslands. Diversity responses across treatments also showed no consistent relationship to net primary production responses, illustrating that the diversity effects of these environmental changes could not be explained simply by changes in productivity. In two- to four-way combinations, simulated global changes did not interact in any of their effects on diversity. Our results show that climate and atmospheric changes can rapidly alter biological diversity, with combined effects that, at least in some settings, are simple, additive combinations of single-factor effects.     

Role of alpha 2-adrenoceptors in normal and atherosclerotic human coronary circulation.

BACKGROUND. Experimental studies on the effects of alpha 2-adrenoceptors on regional coronary blood flow in normal and ischemic myocardium are highly controversial. A beneficial effect on regional ischemic myocardium has been demonstrated in different animal preparations with either alpha 2-adrenoceptor blockade or stimulation. Animal studies also demonstrated that postsynaptic alpha 2-adrenoceptors mediate vasoconstriction in coronary and femoral vascular beds. The aims of the study were 1) to investigate the effects of regional alpha 2-adrenoceptor stimulation on regional coronary blood flow in subjects with angiographically normal coronary arteries, 2) to assess the effect of alpha 2-adrenoceptor blockade on coronary circulation in control subjects, and 3) to examine the influence of atherosclerosis on coronary blood flow response to alpha 2-adrenoceptor blockade. METHODS AND RESULTS. The effect of regional administration of BHT 933 (a selective alpha 2-adrenoceptor agonist) was studied in eight subjects with angiographically normal coronary arteries. The coronary blood flow velocity was measured using a subselective intracoronary 3F Doppler catheter and coronary diameter by quantitative coronary angiography. BHT 933 induced a reduction in coronary artery diameter from 2.5 +/- 0.6 mm to 1.8 +/- 0.4 mm (p less than 0.05) as well as in coronary blood flow velocity (from 6.4 +/- 0.9 cm/sec to 4.6 +/- 1.9 cm/sec, p less than 0.01). In some subjects, ST segment abnormalities occurred. In patients with angiographically normal coronary arteries (n = 6), the regional infusion of a selective alpha 2-adrenoceptor blocking agent after beta-blockade did not change coronary diameter or coronary blood flow velocity. In contrast, in patients with significant coronary stenoses (n = 6), regional infusion of an alpha 2-adrenoceptor blocking agent reduced regional coronary artery diameter (from 2.3 +/- 0.5 mm to 2.1 +/- 0.6 mm, p less than 0.01) as well as coronary blood flow velocity (from 5.8 +/- 0.8 cm/sec to 3.7 +/- 0.6 cm/sec, p less than 0.05); in addition, alpha 2-adrenoceptor blockade significantly increased coronary sinus plasma norepinephrine levels (from 300 +/- 144 pg/ml to 429 +/- 207 pg/ml, p less than 0.01). CONCLUSIONS. The selective in vivo stimulation of alpha 2-adrenoceptors produces a reduction in coronary blood flow and diameter in humans with angiographically normal coronary arteries. alpha 2-Adrenergic blockade does not change coronary blood flow in subjects with angiographically normal coronary arteries (suggesting no resting alpha 2-adrenergic vasoconstrictor tone), whereas in patients with coronary artery stenosis, regional coronary blood flow decreases after alpha 2-receptor blockade. Finally, our data also suggest that alpha 2-adrenoceptors participate in the modulation of sympathetic neuronal norepinephrine release in the human heart.     

Effects of intravenous verapamil on left ventricular relaxation and filling in stable angina pectoris

Left ventricular (LV) diastolic function is often impaired in coronary artery disease (CAD). To assess whether verapamil could improve LV diastolic properties, 12 patients with CAD undergoing right- and left-sided cardiac catheterization, as well as simultaneous radionuclide angiography, were studied before and during intravenous administration of verapamil (0.1 mg/kg as a bolus followed by 0.007 mg/kg/min). The heart rate was kept constant by atrial pacing in both studies. LV pressure-volume relations were obtained. Verapamil decreased LV systolic pressure (130 +/- 22 to 117 +/- 16 mm Hg, p less than 0.01) and the end-systolic pressure/volume ratio (2.4 +/- 1.3 to 1.6 +/- 0.5 mm Hg/ml, p less than 0.05), and increased LV end-diastolic (13 +/- 4 to 16 +/- 4 mm Hg, p less than 0.02) and pulmonary capillary pressures (10 +/- 5 to 12 +/- 5 mm Hg, p less than 0.005). Despite such negative inotropic effects, cardiac index increased (3.4 +/- 0.7 to 3.9 +/- 0.6 liters/min/m2, p less than 0.02). The time constant of isovolumic relaxation shortened (63 +/- 14 to 47 +/- 9 ms, p less than 0.02); peak filling rate increased (370 +/- 155 to 519 +/- 184 ml/s, p less than 0.001; 2.6 +/- 1.1 to 3.3 +/- 0.9 end-diastolic counts/s, p less than 0.02; and 4.1 +/- 1.6 to 5.5 +/- 1.5 stroke counts/s, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Protective role of collaterals in patients with coronary artery occlusion

We reviewed the clinical, hemodynamic and angiographic data of 105 patients with right coronary artery occlusion and of 82 patients with left anterior descending coronary artery occlusion, subdivided into 3 groups by the presence and quality of collaterals to the occluded coronary (absent, poor or good collaterals). We found that patients with right coronary artery occlusion and good collaterals had a lower frequency of diaphragmatic myocardial infarction (60%) than patients with absent collaterals (100%) (P < 0.01). In addition, in patients with old diaphragmatic myocardial infarction, both poor and good collaterals were associated with a lower frequency of severe asynergy of the diaphragmatic left ventricular segments at left ventriculography (54% and 14%, respectively), compared to patients with no collaterals to the right coronary artery (92%, P < 0.02 vs. poor collaterals, P < 0.001 vs. good collaterals). In contrast, in patients with left anterior descending coronary artery occlusion, the presence of either poor or good collaterals to the left anterior descending coronary artery was not associated with a lower frequency of old anterior myocardial infarction, or, in patients with old anterior myocardial infarction, with a less severe asynergy of the anterior left ventricular segments.Our results suggest that collaterals are effective in protecting the diaphragmatic left ventricular wall in patients with right coronary artery occlusion, but not the anterior left ventricular wall in patients with left anterior descending coronary artery occlusion.     

Effects of antiplatelet and calcium antagonist drugs on infarct size in rats

The authors performed the experimental model of infarct-like myocardial lesions in rats treated with large doses of ISP. Myocardial necrosis was assessed on the basis of serum enzyme changes as well as of gross and microscopic findings. The infarct size was measured by a direct enzymatic method assaying creatine kinase (CK) depletion in infarcted myocardium. Pretreatment of the infarcted rats with antiplatelet (Lysin Acetyl Salicylate) or calcium antagonist drugs (Verapamil or Nifedipine) allowed the reduction of the necrotic area. Since a smaller size of infarct was achieved through different types of interventions it should be suggested that ISP-myocardial damage is due to several effects of the drug involving metabolic, vascular and/or coagulative patterns.