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עמוד בית
Mon, 15.04.24

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December 2015
May-Tal Rofe MD, Ran Levi PhD, Einat Hertzberg-Bigelman MSc, Pavel Goryainov MSc, Rami Barashi MD, Jeremy Ben-Shoshan MD PhD, Gad Keren MD and Michal Entin-Meer PhD
 

Background: Chronic kidney disease (CKD) is a prevalent clinical condition affecting 15% of the general population. Cardiorenal syndrome (CRS) type 4 is characterized by an underlying CKD condition leading to impairment of cardiac function and increased risk for major cardiovascular events. To date, the mechanisms leading from CKD to CRS are not completely understood. In particular, it is unclear whether the pathological changes that occur in the heart in the setting of CKD involve enhanced cell death of cardiac cells.  


Objectives: To assess whether CKD may mediate loss of cardiac cells by apoptosis. 


Methods: We established rat models for CKD, acute myocardial infarction (acute MI), left ventricular dysfunction (LVD), and sham. We measured the cardiac-to-body weight as well as kidney-to-body weight ratios to validate that renal and cardiac hypertrophy occur as part of disease progression to CRS. Cardiac cells were then isolated and the percent of cell death was determined by flow cytometry following staining with annexin-FITC and propidium iodide. In addition, the levels of caspase-3-dependent apoptosis were determined by Western blot analysis using an anti-cleaved caspase-3 antibody. 


Results: CKD, as well as acute MI and LVD, resulted in significant cardiac hypertrophy. Nevertheless, unlike the increased levels of cell death observed in the acute MI group, in the CKD group, cardiac hypertrophy was not associated with induction of cell death of cardiac cells. Caspase-3 activity was even slightly reduced compared to sham-operated controls. 


Conclusions: Our data show that while CKD induces pathological changes in the heart, it does not induce cardiac cell death. 


 

 
January 2014
Itai Horowitz, Carlos Cafri, Lior Zeller, Alina Vodonos, Zvi H. Perry and Sergio L. Kobal
Background: The effects of exercise training on cardiac structure and function have been thoroughly investigated in athletes from sport-developed nations; few data are available on sportsmen from sport-developing countries.

Objectives: To assess the incidence and magnitude of the "athlete heart" phenomenon in an elite group of Israeli cyclists.

Methods: An echocardiography study was performed in 56 cyclists (49 males, mean age 38 ± 10 years, weekly average training 13.1 ± 5.9 hours); 96 sedentary subjects served as a control group.

Results: There were significant differences in left ventricular end-diastolic diameter (LVEDD) between cyclists and the control group (48 ± 4.7 mm vs. 45 ± 4.1 mm respectively, P < 0.001), as well as in inter-ventricular septum (IVS) thickness (9.9 ± 1.2 vs. 8.9 ± 1.2 mm, P < 0.001) and LV mass index (LVMI) (79 ± 16 vs. 68 ± 13 g/m2, P < 0.001). In 5% of the cyclists LVEDD exceeded the upper normal limit of 56 mm. In 7% of the cyclists IVS thickness exceeded the upper normal limit of 11 mm. LV hypertrophy defined as LVMI 134 g/m2 was absent in the entire cyclist group.

Conclusions: Endurance sport activity in well-trained Israeli sportsmen results in a modest increment in LV dimensions and LV mass. LV dilatation and wall thickness above values compatible with primary cardiac disease are rare. These results highlight that in Israeli athletes any abnormal echocardiographic value must be thoroughly investigated and not simply assumed to be a consequence of sport activities.

March 2011
S. Siegert, D. Hazan and M. Szyper-Kravitz
March 2010
O. Jarchowsky Dolberg, A. Elis and M. Lishner
April 2007
A. Keren, M. Poteckin, B. Mazouz, A. Medina, S. Banai, A. Chenzbraun, Z. Khoury and G. Levin

Background: Left ventricular outflow gradient is associated with increased morbidity and mortality in hypertrophic cardiomyopathy. Alcohol septal ablation is the alternative to surgery in cases refractory to drug therapy. The implication of LVOG[1] measured 1 week post-ASA[2] for prediction of outcome is unknown.

Objective: To observe the pattern of LVOG course and prediction of long-term clinical and hemodynamic outcome of ASA.

Methods: Baseline clinical and echocardiographic parameters were prospectively recorded in 14 consecutive patients with a first ASA, at the time of ASA, 3 and 7 days after ASA (in-hospital) and 3 and 12 months after ASA (last follow-up).

Results: There was improvement in NYHA class, exercise parameters and LVOG in 11 of 14 patients (P < 0.005 in all). Maximal creatine kinase level was lower than 500 U/L in those without such improvement and 850 U/L or higher in successful cases. LVOG dropped from 79 ± 30 to 19 ± 6 mmHg after the ASA. LVOG was 50 ± 21 mmHg on day 3, 39 ± 26 on day 7, 32 ± 26 at 3 months and 24 ± 20 mmHg at last follow-up. LVOG identified 27% sustained procedural successes on day 3 and 73% on day 7. The overall predictive accuracy of the test for sustained success and failure was 36% on day 3 and 71% on day 7. Combination of maximal CK[3] and LVOG on day 7 showed four distinct outcome patterns: "early success" with low LVOG and high CK (73% of successful cases), "late success" with high LVOG and high CK, and "early failure" and "late failure" with both low CK and high or low LVOG, respectively
Conclusion: LVOG measurement 7 days post-ASA combined with maximal CK levels predicts late procedural outcome in the majority of patients







[1] LVOG = left ventricular outflow gradient



[2] ASA = alcohol septal ablation



[3] CK = creatine kinase


September 2001
Alexander Lowenthal, M Med Sci and Mark N. Lowenthal, MB, BCh, FRCPE
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