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עמוד בית
Wed, 12.06.24

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May 2010
H. Vaknin-Assa, A. Assali, E. Lev, I. Ben-Dor, D. Brosh, I. Teplitsky and R. Kornowski

Background: The best therapeutic alternative for patients suffering from in-stent restenosis after drug-eluting stent implantation remains to be elucidated.

Objective: To characterize the pattern, treatment and outcomes of DES[1]-related in-stent restenosis in patients treated at our institution.

Methods: We determined the incidence and major adverse clinical events in 71 consecutive patients with DES failure among 2473 patients who were treated with 2548 drug-eluting stents between 2004 and 2007. We analyzed the clinical data, procedural parameters and clinical outcomes.

Results: The type and number of stents implanted were as follows: Cypher (n=1808), Endeavor (421) and Taxus (319) of these, 53 (2.9%), 10 (2.4%), and 8 (2.5%) patients respectively presented with restenosis. The mean time to restenosis was 11.3 ± 9.9 months. Patients’ mean age was 65 ± 11 years 75% were male, and 68% had diabetes mellitus. Unstable angina was the clinical presentation in 52 (73%). At 6 months, 3 patients had developed myocardial infarction (4.2%), repeat restenosis at follow-up was diagnosed in 8 patients (11.3%), the overall major adverse clinical events rate was 18.3% (13 patients), and 2 patients died (2.8%).

Conclusions: Drug-eluting stent-related restenosis is relatively infrequent but remains a clinical challenge. It occurs more frequently in complex lesion subsets, but the overall intermediate-term prognosis is tolerable.

[1] DES = drug-eluting stent

October 2004
I. Teplitsky, A. Asali, H. Vaknin, G. Golovchiner, S. Fuchs, A. Battler and R. Kornowski

Background: Left main coronary artery disease is considered a surgical indication in most centers. However, in some cases prohibited from surgery or in patients with prior bypass grafting, there is a need for percutaneous coronary intervention in LMCA[1] disease scenarios.

Objectives: To assess the clinical outcomes among patients undergoing stent-based LMCA angioplasty.

Methods: We identified 34 consecutive patients who underwent PCI[2] in LMCA at our institution. Procedural data and clinical outcomes were obtained for all patients.

Results: The mean age was 71 ± 12 years. There were 27 elective and 7 emergent procedures performed on 23 “protected” LMCA and 11 “unprotected” LMCA. In emergent procedures, the prevalence of cardiogenic shock (29% vs. 0%, P = 0.04) in patients with prior coronary bypass (29% vs. 8.5%, P = 0.007) was significantly higher compared to elective cases. Procedural success in emergent procedures was significantly lower than in elective procedures (71 vs. 100%, P = 0.04). In emergent versus elective procedures, the in-hospital mortality rate was higher (43 vs. 0%, P = 0.006). The rate of cumulative major adverse cardiac events at 1 and 6 months was 43% and 71% in emergent cases versus 0% and 33% in elective cases (P < 0.05 for both comparisons). In patients with “unprotected” LMCA the overall major cardiac events at 1 month was higher compared to “protected” LMCA patients (27 vs. 0%, P = 0.02). Multivariate analysis revealed emergent procedure as an independent predictor for mortality and adverse cardiac events (odds ratio 6.7; 95% confidence interval 1.2–36; P = 0.02).

Conclusions: Percutaneous interventions in LMCA are feasible and relatively safe in carefully selected cases. Procedural outcomes and clinical prognosis is highly dependent on the nature of disease prior to angioplasty (e.g., elective vs. emergent procedure) as well as on protection of the LMCA by patent grafts.

[1] LMCA = left main coronary artery

[2] PCI = percutaneous coronary intervention

December 2003
V. Teplitsky, D. Huminer, J. Zoldan, S. Pitlik, M. Shohat and M. Mittelman

Background: Transcobalamin II is a serum transport protein for vitamin B12. Small variations in TC-II[1] affinity were recently linked to a high homocysteine level and increased frequency of neural tube defects. Complete absence of TC-II or total functional abnormality causes tissue vitamin B12 deficiency resulting in a severe disease with megaloblastic anemia and immunologic and intestinal abnormalities in the first months of life. This condition was described in hereditary autosomal-recessive form. Low serum TC-II without any symptoms or clinical significance was noted in relatives of affected homozygotes.

Objectives: To study 23 members of a four-generation family with hereditary vitamin B12 deficiency and neurologic disorders.

Methods: Thorough neurologic, hematologic and family studies were supplemented by transcobalamin studies in 20 family members.

Results: Partial TC-II deficiency was found in 19 subjects. Apo TC- II (free TC-II unbound to vitamin B12) and total unsaturated B12 binding capacity were low in all tested individuals but one, and holo TC-II (TC-II bound by vitamin B12) was low in all family members. The presentation of the disease was chronic rather than acute. Early signs in children and young adults were dyslexia, decreased IQ, vertigo, plantar clonus and personality disorders. Interestingly, affected children and young adults had normal or slightly decreased serum vitamin B12 levels but were not anemic. Low serum B12 levels were measured in early adulthood. In mid-late adulthood megaloblastic anemia and subacute combined degeneration of the spinal cord were diagnosed. Treatment with B12 injections resulted in a significant improvement. The pedigree is compatible with an autosomal-dominant transmission. This family study suggests a genetic heterogeneity of TC-II deficiency.

Conclusions: We report the first family with a hereditary transmitted condition of low serum TC-II (partial TC-II deficiency) associated with neurologic and mental manifestations in childhood. Partial TC-II deficiency may decrease the amount of stored cobalamin, resulting in increased susceptibility to impaired intestinal delivery of cobalamin and predisposing to clinically expressed megaloblastic anemia at a later age. Partial TC-II deficiency should be suspected in families with megaloblastic anemia and in individuals with neurologic and mental disturbances – despite normal serum vitamin B12 levels. Low serum UBBC[2] and apo TC-II should confirm the diagnosis. Early vitamin B12 therapy may prevent irreversible neurologic damage.

[1] TC II = transcobalamin II

[2] UBBC = unsaturated B12 binding capacity

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