Transradial access in a cath lab with moderate procedural volume: a single operator's experience.

AIM: The transradial access (TRA) for cardiovascular interventions has become increasingly popular and was shown to be effective in many clinical settings, including acute coronary syndromes. Despite offering many advantages, such as a striking reduction in access site complications, the penetration of TRA in routine practice is still low. One reason for this could be that many studies about TRA were performed in high-volume centers by expert operators, making their results not fully applicable to the real world. In order to assess the efficacy of TRA, we retrospectively reviewed the caseload of a single operator working in a community hospital with moderate procedural volume. METHODS: We considered 873 consecutive procedures, of which 406 percutaneous coronary interventions (PCI), performed by a single operator (S.R.) who had previously completed the learning curve in TRA at a high volume center. RESULTS: TRA was selected in 48.3% of patients, transfemoral approach (TFA) in 50.9% and transbrachial approach in 0.8%. TFA was used more frequently in PCI (62.5% vs 37.5%; P<0.001), largely because it was the access of choice in primary PCI. The overall procedural success rate was 94% in TRA and 98% in TFA (P=0.035); access failure was more frequent in TRA (5.9% vs 1.1%; P<0.001), whereas an increased rate of access-related vascular complications was observed in TFA as compared to TRA (1.1% vs 0%; P=0.029). CONCLUSION: After an adequate training period, the overall performance of TRA is good even in moderate-volume hospitals. Despite reducing access site complications, TRA is limited by a slightly higher rate of procedural failure as compared to TFA.

A randomized comparison between rotational and standard coronary angiography.

AIM: Selective coronary angiography is nowadays the gold standard in the definition of coronary anatomy as well as the basis for percutaneous coronary interventions. However, the diagnostic accuracy of coronary angiography can be reduced if the number of angiographic views is inadequate or if the operator does not select appropriate projections. Rotational angiography (RA) has been proposed as an alternative technique in order to provide a more complete definition of coronary anatomy reducing, at the same time, radiation exposure and contrast medium dose. METHODS: We randomly assigned 31 eligible patients, undergoing diagnostic cardiac catheterization, to RA (n=16) and traditional angiography (TA, n=15). Total procedural time, fluoroscopy time, number of cine-runs, X-ray dose and contrast medium volume were recorded in both groups. RESULTS: There were no statistically significant differences between groups in age (59+/-5.8 vs 62.8+/-9.6 years, P=ns), body mass index (26.7+/-3.5 vs 27.1+/-3.4 kg/m2, P=ns), total procedural time (20.6+/-6.6 vs 22.2+/-11.3 min, P=ns) and fluoroscopy time (3.9+/-1.5 vs 4.9+/-1.8 min, P=ns). On the contrary, number of cine-runs, X-ray dose and contrast medium volume were significantly lower in RA patients as compared with TA patients (6.2+/-1.2 vs 9.7+/-2.1, P<0.01; 530.6+/-271.6 vs 831.2+/-343.9 mGy, P<0.05; 76.9+/-22.4 vs 102.9+/-26.4 ml, P<0.01, respectively). CONCLUSIONS: RA is safe and effective in defining coronary anatomy, leading to a significant reduction in radiation exposure and contrast medium volume.

Myocardial ischemia-reperfusion damage after pacing-induced tachycardia in patients with cardiac syndrome X.

The presence of myocardial ischemia in syndrome X (chest pain, "ischemia-like" electrocardiogram changes, and normal coronary angiograms) is uncertain possibly because, when focally distributed, it may not cause contractile dysfunction or lactate production. We measured lipid hydroperoxides (ROOHs) and conjugated dienes (CDs), two sensitive, independent markers of ischemia-reperfusion oxidative stress, in paired aortic and great cardiac vein blood samples before and after pacing-induced tachycardia in nine patients with syndrome X. Diagnostic ischemic S-T segment changes during pacing were followed by a consistent increase in ROOH and CD levels in the great cardiac vein (from 4.83 +/- 1.18 micromol/l at baseline to 7.88 +/- 1.12 micromol/l and from 0.038 +/- 0.002 to 0.051 +/- 0.003 arbitrary units, respectively, P < 0.01). In controls, ROOH and CD levels did not change after pacing. The large postpacing cardiac release of lipid peroxidation products, consistently observed in all patients and similar to that previously observed after ischemia caused by percutaneous transluminal coronary angioplasty, is consistent with an ischemic origin of syndrome X.

Oxidative stress in ischemia-reperfusion injury: assessment by three independent biochemical markers.

BACKGROUND: Oxidative stress plays a key role in ischemia-reperfusion injury, causing peroxidation of tissue lipids and proteins. However, it is debated whether brief ischemic episodes are sufficient to cause detectable oxidative stress in humans, since biochemical markers used so far in the setting of percutaneous transluminal coronary angioplasty (PTCA) gave conflicting results. METHODS: We determined lipid hydroperoxides (ROOHs), conjugated dienes (CD) and total radical-trapping antioxidant capacity (TRAP), three different independent markers of oxidative stress, in aortic and great cardiac vein blood of 5 patients undergoing PTCA before a single balloon inflation lasting 115 +/- 38 s (t0), and 1 min (t1), 5 min (t5), 15 min (t15) after balloon deflation (Group 1). ROOHs and CD were also determined in aortic and great cardiac vein blood of 5 patients with mitral valve disease (Group 2). RESULTS: In Group 1, great cardiac vein levels of ROOHs and CD at t1 increased by 219% and 79%, respectively, compared to t0 (p < 0.01); this sharp and consistent increase persisted up to t15 (+189% and +63%, respectively, compared to t0; p < 0.01). Great cardiac vein levels of TRAP were significantly lower than aortic levels at t0, and exhibited a further decrease at tl. No significant differences in aortic and great cardiac vein levels of ROOHs and CD at t0 were observed between Group 1 and Group 2. CONCLUSIONS: The three methods we used showed a remarkable sensitivity for the detection of post-ischemic reperfusion injury in cardiac venous blood and may be useful for detecting small foci of ischemia-reperfusion injury in microvascular angina.

Large, sustained cardiac lipid peroxidation and reduced antioxidant capacity in the coronary circulation after brief episodes of myocardial ischemia.

OBJECTIVES: We sought to investigate whether a brief episode of myocardial ischemia produces a detectable cardiac oxidative stress in patients undergoing elective coronary angioplasty (PTCA). BACKGROUND: Although cardiac oxidative stress has been clearly demonstrated in experimental models of ischemia-reperfusion, its presence in patients after transient myocardial ischemia is still unclear. METHODS: In order to evaluate oxidative stress in ischemic cardiac regions, plasma conjugated dienes (CD), lipid hydroperoxides (ROOHs) and total antioxidant capacity (TRAP), independent indexes of oxidative stress, were measured in the aorta and great cardiac vein (GCV) before (t0), 1, (t1), 5 (t5) and 15 min (t15) after first balloon inflation in 15 patients undergoing PTCA on left anterior descending coronary artery (Group 1); six patients with right coronary artery stenosis (Group 2), which is not drained by the GCV, were studied as controls. RESULTS: In Group 1 at baseline, CD and ROOHs levels were higher in GCV than in aorta (p < 0.01 for both), and TRAP levels were lower (p < 0.01). Aortic levels of CD, ROOHs and TRAP did not change at any time after to; venous levels of CD and ROOHs levels markedly increased at t1, at t5 and remained elevated at t15 (p < 0.01 for all comparisons vs. to); venous levels of TRAP decreased at t1 and t5 (p < 0.01 vs. t0) and returned to normal at t15. In Group 2, CD, ROOHs and TRAP levels were similar in the aorta and GCV and did not change throughout the study. CONCLUSIONS: Short episodes of myocardial ischemia during PTCA induce a sustained oxidative stress, which is detectable in the venous effluent of reperfused myocardium.

Opposite changes in dopamine metabolites and met-enkephalin levels in the ventricular CSF of patients subjected to thalamic electrical stimulation.

High-frequency electrical stimulations of thalamic nuclei are currently used for the suppression of parkinsonian or essential tremor and for the relief of some types of intractable pain in man. However, the mechanisms by which such stimulations exert their therapeutic effects are essentially unknown. Attempts were made to provide some insight into these mechanisms by measuring the levels of the dopamine metabolites homovanillic acid (HVA) and 3,4-dihydroxyphenylacetic acid (DOPAC), the serotonin metabolite 5-hydroxyindoleacetic acid (5-HIAA) and met-enkephalin-like immunoreactivity in ventricular cerebrospinal fluid (CSF) of patients with Parkinson's disease (PD) or multiple sclerosis (MS) after a 30-minute therapeutic electrical stimulation of the ventralis intermedius nucleus of the thalamus. In nonstimulated control patients, the levels of these compounds did not significantly differ in two CSF samples taken 30 minutes apart. In stimulated patients, a decrease in dopamine metabolite levels associated with a relative increase in met-enkephalin-like immunoreactivity were observed in the CSF sample taken after the 30-minute stimulation as compared to the sample taken immediately before the stimulation. In contrast, the levels of 5-HIAA remained unaffected by the stimulation. These data confirmed the existence of negative interactions between dopaminergic and enkephalinergic systems in man similar to those previously demonstrated in rats. In addition, they suggest that alterations in dopaminergic or enkephalinergic neurotransmission might be involved in the therapeutic action of thalamic electrical stimulation in patients with parkinsonian symptoms and other patients.

Neurological complications of neurofibromatosis type 1 in adulthood.

Neurofibromatosis type 1 (NF1) is a genetic disease with a wide range of neurological manifestations. To examine these, and to evaluate neurological morbidity in adulthood of patients with NF1, we studied a hospital-based series of 158 patients that included 138 adult patients aged >18 years and 20 children. NF1 evaluation included a multidisciplinary clinical and a clinically oriented radiological investigation. Neurological events occurring during childhood (in both children and adults of the series) and adulthood were recorded. One or several neurological manifestations have been observed in 55% of patients (adults and children) (n = 87). These included: headache (28 patients); hydrocephalus (7); epilepsy (5); lacunar stroke (1); white matter disease (1); intraspinal neurofibroma (3); facial palsy (1); radiculopathy (5); and polyneuropathy (2). Tumours included: optic pathway tumours (20); meningioma (2); cerebral glioma (3); and malignant peripheral nerve sheath tumours (6). Life-threatening complications were observed in five adults and included four malignant peripheral nerve sheath tumours and one meningioma. Pain was the leading symptom in 11 adults and was related to malignant peripheral nerve sheath tumours, complications of intraspinal neurofibromas, subcutaneous neurofibromas and peripheral nerve neurofibromas. NF1 in adults was not associated with other disabling or life-threatening neurological complications. Symptomatic optic pathway tumours, cerebral gliomas, symptomatic aqueductal stenosis and spinal compression due to intraspinal NF were observed exclusively during childhood. In this series, the predominant neurological features of adults with NF1 were chronic pain and malignant peripheral nerve sheath tumours.

Glial and endothelial cell response to a fetal transplant of purified neurons.

Astrocytes, microglia and endothelial cells display very specific phenotypic characteristics in the intact adult CNS, which appear quite versatile when grown in culture without neurons. Indirect evidence from in vitro co-culture studies and analysis of the effects of specific neuronal removal in vivo, does accordingly favour a role of neurons for the phenotypic repression of these cells in the intact brain. In order to provide more direct evidence for such neuronal influence, we attempted to induce, in the rat brain, a reversal of the post-lesional activation of astrocytes, microglia and endothelial cells by transplantation of fetal neurons purified by immunopanning. Host microglial cells which have been activated by the lesion process, penetrated the neuronal graft during the few days after the transplantation. Reactive astrocytes began to appear in the lesioned parenchyma and gathered around the transplant. Thereafter they first sent their processes in the direction of the neuronal graft, before they migrated into the graft a few days later. At this time, which was at the end of the first week post-transplantation, the host endothelial cells sprouted "streamers" of basal lamina within the graft forming small capillaries. During the second week post-transplantation, numerous astrocytes and microglial cells, both displaying a reactive hypertrophied morphology, were observed throughout the grafts. Finally, by the end of the first month, the activated cells differentiated towards a quiescent, resting morphology. At this time the grafts contained a vascular network with morphological characteristics comparable to those observed in the intact brain parenchyma. The results indicate that the interaction of activated astroglia and microglia and endothelial cells with neurons causes the cells to re-differentiate and regain phenotypic features characteristic of intact brain parenchyma, strongly suggesting that neurons play an essential role in the phenotypic restriction of glial and endothelial cells in the adult central nervous system.