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עמוד בית
Thu, 18.07.24

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January 2001
Abraham Matitiau, MD, Einat Birk, MD, Ludmyla Kachko, MD, Leonard C. Blieden, MD and Elchanan Bruckheimer, MB, BS

Background: Secundum atrial septal defect is a common congenital heart defect that causes right heart volume overload and produces symptoms usually after the third decade of life. Treatment until the last few years has been open heart surgery.

Objective: To review our early experience with transcatheter closure of ASD2 using the Amplatzer septal occluder.

Methods: Between November 1999 and February 2000, 20 children and young adults with a median age of 9.1 years (4.2-35.1 years) were referred for transcatheter closure of ASD2. Diagnosis was established by transthoracic echocardiography. Implantation was performed under general anesthesia through the femoral vein with the guidance of transesophageal echocardiography and fluoroscopy. Femoral arterial puncture was performed for blood pressure monitoring during the procedure. The device size chosen was similar to the balloon-stretched diameter of the ASD2.

Results: Implantation was completed successfully in 18 patients. Two patients were referred for elective surgery: one had an unsuitable anatomy for transcatheter closure by TEE in the catheterization laboratory and the device could not implanted properly, the other patient had a large multiperforated septal aneurysm that was retrieved. Mean ASD2 diameter by TTE and TEE was similar (13.9 + 3 mm, 13.4 + 3.5 mm) and mean stretched diameter was 18.3 + 4.3 mm. Mean Qp:Qs (pulmonary flow: systemic flow) was 2.2 + 0.6. Mean fluoroscopy time for the procedure was 14.8 + 4.8 minutes.

The patients were discharged the day after the procedure.

Four patients had a tiny leak immediately post-procedure, and none had a leak at one month follow-up. The only complication was a small pseudoaneurysm of the femoral artery in one patient, that resolved spontaneously.

Conclusion: Transcatheter closure of ASD2 with the Amplatzer septal occluder is a safe and effective alternative to surgical closure. Long-term outcome has to be evaluated.

Rasmi Magadle, MD, Paltiel Weiner, MD, Alexander Sotzkover, MD and Noa Berar-Yanay, MD
Robert Slater, DPM Yoram Ramot, MD and Micha Rapoport, MD
Aharon Kessel, MD, Elias Toubi, MD, Theo Dov Golan, MD, Aurora Toubi, MD, Jorge G. Mogilner, MD and Michael Jaffe, MB ChB, CPD, CH
Paul E. Slater, MD, MPH, Alex Leventhal, MD, MPH, MPA and Emilia Anis, MD, MPH
December 2000
Ofer Nativ MD, Edmond Sabo MD, Moshe Wald MD, Sarel Halachmi MD and Boaz Moskovitz MD

Background: The free-to-total prostate-specificantigen ratio is the best marker for optimizing prostate cancer detection. The main problem with studies of percent free PSA is the variability of reported cutoff values.

Objectives: To evaluate the influence of prostate size on the ratio of free to total PSA.

Methods: The study group included 58 patients (mean age 66.4 years) with clinically localized prostate cancer treated surgically at our institution. Total PSA and free PSA levels were measured by a solid phase enzyme immunoassay test (Hoffman-La Roche, Basel, Switzerland). The percent free PSA was compared with prostate size as determined from the surgical specimen.

Results: A direct relation was noted between prostate size and the percent free PSA value (r=0.49, P=0.0001). Mean percentage free PSA was 9%0.004 in men with normal-sized gland while in men with large prostate (60 g) the average percent free PSA was 15.90.09 (P=0.001).

Conclusions: In patients with prostate cancer the percent free PSA level is influenced by the gland size. The larger the prostate the higher the proportion of the free PSA. Such information may have influence on the recommendation for prostate biopsy in screening programs for early detection of prostate cancer.

Aliza Noy, MD, Ruth Orni-Wasserlauf, MD, Patrick Sorkine, MD and Yardena Siegman-Igra, MD, MPH.
 Background: An increase in multiple drug-resistant Klebsiella pneumoniae due to extended spectrum -lactamase production has recently been reported from many centers around the world. There is no information in the literature regarding this problem in Israel. A high prevalence of ceftazidime-resistant K. pneumoniae was noted in our Intensive Care Unit in the first few months of 1995.

Objective: To describe the epidemiology of ceftazidime-resistant K. pneumoniae in our medical center, as representing the situation in tertiary care hospitals in Israel.

Methods: We vigorously restricted the use of ceftazidime in the ICU and enforced barrier precautions. The susceptibility rate of K. pneumoniae was surveyed in the ICU and throughout the hospital before and after the intervention in the ICU.

Results: Following the intervention, the susceptibility rate of K. pneumoniae increased from 11% (3/28) to 47% (14/30) (P0.01) among ICU isolates, from 55% (154/280) to 62% (175/281) (P=0.08) among total hospital isolates, and from 61% (50/82) to 74% (84/113) (P0.05) among total hospital blood isolates, although no additional control measures were employed outside the ICU.

Conclusions: The epidemiology of ceftazidime-resistant K. pneumoniae in our medical center is similar to that reported from other centers around the world. Early awareness to the emergence of this resistance, identification of the source of the epidemic, and prompt action at the putative source site may reduce the rate of acquisition and spread of such resistance inside and outside of the source unit.

Eli Magen, MD and Reuven J. Viskoper, MD
 Renin-angiotensin-aldosterone systems play a critical role in the development and progression of cardiovascular diseases, and inhibitors of angiotensin-converting enzyme have proven effective for the treatment of these diseases. Since angiotensin II receptor antagonists can inhibit the effects of angiotensin II via ACE-independent pathways, e.g., chymase, they were considered to be more effective than ACEIs. On the other hand, ACE inhibitors can increase bradykinin, and thus, nitric oxide, which may cause potent cardioprotection, inhibition of smooth muscle proliferation and attenuation of inflammation mechanisms. It appears that angiotensin II receptor antagonists and ACEIs may mediate cardioprotection in different ways. This is the rationale to explore the possibility of a combined administration of both drugs for the treatment of chronic heart failure and other cardiovascular pathology. In this review we try to analyze the role of ACE, kinins and chymase inhibition in the pathophysiology and treatment of cardiovascular diseases.

Jayson Rapoport, MB, BS, MRCP
Atzmon Tsur, MD and Gershon Volpin, MD
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