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עמוד בית
Thu, 21.11.24

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July 2006
Y. Turgeman, P. Levahar, I. Lavi, A. Shneor, R. Colodner, Z. Samra, L. Bloch and T. Rosenfeld
 Background: Adult calcific aortic stenosis is a well-known clinical entity but its pathophysiology and cellular mechanism have yet to be defined.

Objectives: To determine whether there is an association between the presence and severity of adult calcific aortic stenosis and Chlamydia pneumoniae seropositivity

Methods: Forty adult patients (23 women, 17 men) were divided into three groups according to echocardiographic aortic valve area: Group A – 7 symptomatic subjects (age 67 ± 7 years) with normal aortic valve and normal coronary angiogram, Group B – 16 patients (age 73 ± 6) with moderate ACAS[1] (AVA[2]> 0.8 £ 1.5 cm2), and Group C – 17 patients (age 76 ± 7) with severe ACAS (AVA £ 0.8 cm2). We tested for immunoglobulins M, G and A as retrospective evidence of C. pneumoniae infection using the micro-immunofluorescence method. Past C. pneumoniae infection was defined by IgG titer > 16 £ 512.

Results: No patients in Group A showed positive Ig[3] for C. pneumoniae. IgM was not detected in any of the patients with ACAS (groups B and C) while 2 of 17 patients (12%) in group C showed IgA for the pathogen. High titers of IgG were found in 14 of 33 (42%) of the patients with moderate or severe ACAS: 5 of 16 (31%) in group B and 9 of 17 (53%) in group C (P = 0.2). Both groups had the same prevalence of coronary artery disease (66%). AVA was lower in IgG-seropositive patients than in the seronegative group (0.88 ± 0.3 cm2 vs. 1.22 ± 0.4 cm2, respectively, P = 0.02).

Conclusions: Past C. pneumoniae infection may be associated with a higher prevalence and greater severity of ACAS.


 





[1] ACAS = adult calcific aortic stenosis

[2] AVA = aortic valve area

[3] Ig = immunoglobulin


March 2005
D. Antonelli, S. Atar, N.A. Freedberg and T. Rosenfeld
Background: Torsade de pointes is rarely associated with chronic amiodarone treatment, despite the effect of amiodarone on QT interval prolongation.

Objective: To identify risk factors and associated conditions that may cause TdP[1] in patients on chronic amiodarone treatment.

Methods: We reviewed the data of six consecutive patients on chronic amiodarone treatment who were admitted to the intensive cardiac care unit due to syncope and TdP.

Results: The patients’ median age was 73.5 years, and five were women. Concomitantly, loratadine was given to two patients and trazodone to one patient. Associated and attributing conditions to the development of TdP were hypokalemia in three patients, drug-induced bradycardia in one and reduced left ventricular function in four.

Conclusions: TdP associated with chronic amiodarone treatment may occur when amiodarone is co-administered with drugs that may potentially prolong QT interval. Additional risk factors for amiodarone-associated TdP include female gender, hypokalemia, reduced left ventricular function and bradycardia.

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[1] TdP = torsade de pointes

February 2003
Y. Turgeman, S. Atar, K. Suleiman, A. Feldman, L. Bloch, N. A. Freedberg, D. Antonelli, M. Jabaren and T. Rosenfeld

Background: Current clinical guidelines restrict catheterization laboratory activity without on-site surgical backup. Recent improvements in technical equipment and pharmacologic adjunctive therapy increase the safety margins of diagnostic and therapeutic cardiac catheterization.

Objective: To analyze the reasons for urgent cardiac surgery and mortality in the different phases of our laboratory’s activity in the last 11 years, and examine the impact of the new interventional and therapeutic modalities on the current need for on-site cardiac surgical backup.

Methods: We retrospectively reviewed the mortality and need for urgent cardiac surgery (up to 12 hours post-catheterization) through five phases of our laboratory’s activity: a) diagnostic (years 1989–2000), b) valvuloplasties and other non-coronary interventions (1990–2000), c) percutaneous-only balloon angioplasty (1992–1994), d) coronary stenting (1994–2000), and e) use of IIb/IIIa antagonists and thienopiridine drugs (1996–2000).

Results: Forty-eight patients (0.45%) required urgent cardiac surgery during phase 1, of whom 40 (83%) had acute coronary syndromes with left main coronary artery stenosis or the equivalent, and 8 (17%) had mechanical complications of acute myocardial infarction. Two patients died (0.02%) during diagnostic procedures. In phase 2, eight patients (2.9%) were referred for urgent cardiac surgery due to either cardiac tamponade or severe mitral regurgitation, and two patients (0.7%) died. The combined need for urgent surgery and mortality was significantly lower in phase 4 plus 5 as compared to phase 3 (3% vs. 0.85%, P = 0.006).

Conclusion: In the current era using coronary stents and potent antithrombotic drugs, after gaining experience and crossing the learning curve limits, complex cardiac therapeutic interventions can safely be performed without on-site surgical backup.
 

April 2001
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