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עמוד בית
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April 2006
I.M. Barbash and J. Leor

Ventricular remodeling and heart failure are the inevitable consequences of myocardial infarction. Current options to cure myocardial infarction and subsequent heart failure suffer from specific limitations. Thus, alternative, additional long-term therapeutic strategies are needed to cure this costly and deadly disease. Cardiac regeneration is a promising new therapeutic option. Through cellular and molecular therapies, the concept of in situ "growing" heart muscle, vascular tissue and manipulating the extracellular matrix environment promises to revolutionize the approach of treating heart disease. Recent studies have suggested that stem cells resident within the bone marrow or peripheral blood can be recruited to the injured heart. The regeneration of damaged heart tissue may include the mobilization of progenitor or stem cells to the damaged area or stimulation of a regenerative program within the organ. There is now evidence accumulating that the heart contains resident stem cells that can be induced to develop into cardiac muscle and vascular tissue. The present review aims to describe the potential, the current status and the future challenges of myocardial regeneration by adult stem cells.

 
 

March 2006
D. Bar-Zohar, B. Sagie, N. Lubezky, M. Blum, J. Klausner and S. Abu-Abeid

Background: Peritoneal dialysis is a widely accepted route for renal replacement. With the advent of endoscopy, many surgical techniques for the prevention of catheter failure have been proposed.

Objectives: To evaluate the outcomes of patients undergoing laparoscopic Tenckhoff catheter implantation, using the pelvic fixation technique.

Methods: Data analysis was retrospective. All procedures were performed under general anesthesia. A double-cuffed catheter was inserted using two 5 mm trocars and one 10 mm trocar, fixing its internal tip to the dome of the bladder and its inner cuff to the fascia. Catheter failure was defined as persistent peritonitis/exit-site/tunnel infection, severe dialysate leak, migration or outflow obstruction.

Results: LTCI[1] was performed in 34 patients. Mean patient age was 65 ± 17 years. In 12 of the 34 patients the indication for LTCI was end-stage renal failure combined with NYHA class IV congestive heart failure. Operative time was 35 ± 15 minutes. A previous laparotomy was performed in 9 patients. Hospital stay was 1.5 ± 0.6 days. The first continuous ambulatory peritoneal dialysis was performed after 20 ± 12 days. Median follow-up time was 13 months. There were several complications, including 5 (14%) exit-site/tunnel infections, 27 episodes (0.05 per patient-month) of bacterial peritonitis, 3 (9%) incisional hernias, 1 case of fatal intraabdominal bleeding, 2 (5.8%) catheter migrations (functionally significant), and 10 (30%) cases of catheter plugging, 8 of which were treated successfully by instillation of urokinase and 2 surgically. A complication-mandated surgery was performed in 8 patients (23.5%). The 1 year failure-free rate of the catheter was 80.8%. One fatal intraabdominal bleeding was recorded.
Conclusions: LTCI is safe, obviating the need for laparotomy in high risk patients. Catheter fixation to the bladder may prevent common mechanical failures







[1] LTCI = laparoscopic Tenckhoff catheter implantation


T. Berlin, A. Lubina, Y. Levy and Y. Shoenfeld
December 2005
S. Viskin, M. Berger, M. Ish-Shalom, N. Malov, M. Tamari, M. Golovner, M. Kehati, D. Zeltser A. Roth.

Background: Chlorpromazine is a dopamine-receptor antagonist antipsychotic agent. Because of its strong alpha-blocking and sedative actions, it has also been used as emergency therapy for extreme arterial hypertension. Published reports to date have included very small numbers of patients (i.e., 5–30).

Objectives: To analyze data on almost 500 patients who received intravenous chlorpromazine for the emergency treatment of uncontrolled symptomatic hypertension in the pre-hospital setting.

Methods: We reviewed data from 496 consecutive patients who received intravenous chlorpromazine as emergency therapy for uncontrolled symptomatic hypertension. Chlorpromazine was injected intravenously. The dose was 1 mg every 2–5 minutes until the systolic pressure was -<140 mmHg and the diastolic pressure -<100 mmHg with alleviation of symptoms.

Results: The mean dose of chlorpromazine administered was 4.5 +- 5 mg (range 1–50 mg). Only 33 patients (7%) required >10 mg. Chlorpromazine reduced the systolic blood pressure from 222.82 +- 26.31 to 164.93 +- 22.66 mmHg (P < 0.001) and the diastolic blood pressure from 113.5 +- 16.63 to 85.83 +- 11.61 mmHg (P < 0.001). The sinus rate decreased from 97.9 +- 23.5 to 92.2 +- 19.7 beats per minute (P < 0.001). These results were achieved within the first 37 +- 11 minutes.

Conclusions: Intravenous chlorpromazine is safe and effective when used as emergency treatment for uncontrolled symptomatic hypertension.

 

June 2005
M. Arad, H. Lahat and D. Freimark
 Familial cardiomyopathies represent a substantial portion of idiopathic dilated cardiomyopathy in clinical practice. Diversity of clinical presentations and variability in penetrance lead to under-recognition of this disease entity as an inherited disorder. The mechanisms by which mutations in different genes perturb cardiac function and lead to pathologic remodeling help understand the molecular pathways in disease pathogenesis and define the potential targets for therapeutic interventions. Appreciating when DCM[1] is inherited might spare unnecessary diagnostic efforts and, instead, help give appropriate attention to the timely detection of subclinically affected family members. Establishing preventive therapy in asymptomatic family members showing early signs of cardiac dysfunction might prevent death and slow down progression to end-stage heart failure.


 





[1] DCM = dilated cardiomyopathy


January 2004
A. Zeidman, Z. Fradin, A. Blecher, H.S. Oster, Y. Avrahami and M. Mittelman

Background: Anemia is a known risk factor for ischemic heart disease. Based on knowledge of the physiologic role of oxygen delivery to the myocardium, anemia may be a cause of more severe cardiovascular diseases or a marker of other processes occurring in the body that induce more severe disease.

Objectives: To investigate the relationship between anemia and the clinical picture of IHD[1], including manifestations, severity and complications.

Methods: The population studied comprised 417 similarly aged patients with IHD and anemia. The patients were categorized into subgroups of IHD according to disease severity: namely, angina pectoris, acute ischemia, acute myocardial infarction, congestive heart failure or cardiac arrhythmias. Two populations served as control groups: patients with anemia but no IHD (C-I) and patients with IHD without anemia (C-II). A standard anemia workup was conducted in all patients with IHD and anemia and a correlation was made between the hematologic parameters and the manifestations and complications of IHD.

Results: The common presenting symptom was chest pain in the study group and in C-II (94% and 86% respectively) and weakness (90%) in C-I. Patients with IHD and anemia tended to suffer from a more advanced degree of IHD (80%) compared to patients with IHD alone who had milder disease (46%). Hematologic values including hemoglobin, mean cell volume, serum iron and total iron binding capacity correlated inversely with disease severity among anemic patients with IHD. There were significant differences between the study group and C-II regarding CHF[2] (31% and 18% respectively) and arrhythmias (41% and 16% respectively). The mortality rate was higher in patients with IHD and anemia than in patients with IHD alone (13% and 4% respectively).

Conclusions: Anemia is a significant risk factor in IHD. It correlates with advanced IHD, CHF, rhythm disturbance and higher mortality rate. An aggressive therapeutic and preventive approach might improve the outcome of this disease.







[1] IHD = ischemic heart disease



[2] CHF = congestive heart failure


May 2003
D.S Silverberg, D. Wexler, M. Blum, D.Schwartz, G. Keren, D. Sheps, and A. Iaina

Background: Congestive heart failure is extremely common in octogenarians and is associated with severe fatigue, shortness of breath, recurrent hospitalizations, and death. These patients, many of whom are anemic, are often resistant to standard CHF[1] therapy including angiotensin-converting enzyme inhibitors, beta-blockers and diuretics.

Objectives: To examine whether correction of the anemia (hemoglobin <12 g/dl) in CHF patients lowers their resistance to therapy.

Methods: Forty octogenarians with anemia and severe resistant CHF were administered a combination of subcutaneous erythropoietin and intravenous iron sucrose.

Results: This combination therapy led to a marked improvement in cardiac function, shortness of breath and fatigue, a marked reduction in the rate of hospitalization and a stabilizing of renal function.

Conclusion: Anemia appears to be an important but ignored contributor to the progression of CHF, and its correction may improve cardiac and renal status as well as the quality of life in elderly patients.






[1] CHF = congestive heart failure


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