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עמוד בית
Fri, 07.08.26

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July 2026
May-Tal Rofe-Shmuel MD, Hadar Goldshtein MD, Royi Barnea MD, Vered Baset MD, Avishag Laish-Farkash MD PhD

Background: Postoperative atrial fibrillation (POAF) is well recognized after cardiac surgery; however, its incidence and clinical course following non-cardiac surgery (NCS) remain unclear.

Objectives: To evaluate the association between POAF after NCS, patient co-morbidities, and type of surgery.

Methods: In this retrospective cohort study, patients who underwent NCS at a private hospital network between 2016 and 2023 were included. Patients with a history of atrial fibrillation (AF) were excluded. Patients who developed POAF within 24-48 hours were compared with those who did not. To address baseline differences, propensity score matching (1:10) and inverse probability weighting combined with Firth’s penalized logistic regression were applied. Odds ratios with 95% confidence intervals were calculated.

Results: POAF developed in 174 patients within 24–48 hours postoperatively, compared with 391,329 controls. Older age, ischemic heart disease, diabetes, and prior stroke were associated with increased odds of POAF, although significance diminished after multivariable adjustment. Weighted regression confirmed these findings with narrower confidence intervals. Higher POAF risk was observed after laparoscopic pancreatectomy, hepatectomy, rectopexy, synovectomy, and gastrectomy. Total knee replacement was the most common procedure among POAF cases, representing 22% of cases and a fourfold increased risk.

Conclusions: Advanced age and cardiovascular co-morbidities were associated with increased POAF risk after NCS, although attenuated after adjustment. Consistent findings across statistical models support the robustness of the results. Targeted monitoring in high-risk patients may improve postoperative outcomes.

May 2023
May-Tal Rofe-Shmuel MD, Michael Shapira MD, Gad Keren MD

Romidepsin is an intravenously administered antineoplastic agent, which acts by inhibiting histone deacetylases, thus preventing removal of acetyl groups from histones. The accrual of acetyl groups on histones causes cell cycle arrest and apoptotic cell death. It was approved for use in the United States in 2009 for treatment of refractory or relapsed cutaneous and peripheral T cell lymphomas [1-3].

The most common side effects are mild to moderate in severity and include nausea, vomiting, fatigue, fever, myelosuppression (e.g., anemia, neutropenia, thrombocytopenia), elevated liver enzymes, constipation, and rash. More severe adverse events can include marked neutropenia, thrombocytopenia, serious infections such as line sepsis, acute renal failure, tumor lysis syndrome, and cardiac arrhythmias [1].

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. 


 

 
June 2008
D. Sharif, G. Rofe, A. Sharif-Rasslan, E. Goldhammer, N. Makhoul, A. Shefer, A. Hassan, S. Rauchfleisch and U. Rosenschein

Background The temporal behavior of the coronary microcirculation in acute myocardial infarction may affect outcome. Diastolic deceleration time and early systolic flow reversal derived from coronary artery blood flow velocity patterns reflect microcirculatory function.

Objectives To assess left anterior descending coronary artery flow velocity patterns using Doppler transthoracic echocardiography after primary percutaneous coronary intervention, in patients with anterior AMI[1].

Methods Patterns of flow velocity patterns of the LAD[2] were obtained using transthoracic echocardiography-Doppler in 31 consecutive patients who presented with anterior AMI. Measurements were done at 6 hours, 36–48 hours, and 5 days after successful PPCI[3]. Measurements of DDT[4] and pressure half times (Pt½), as well as observation for ESFR[5] were performed.

Results In the first 2 days following PPCI, the average DDT, 600 ± 340 msec, were shorter than on day 5, 807 ± 332 msec (P < 0.012). FVP[6] in the first 2 days were dynamic and bidirectional: from short DDT (< 600 msec) to long DDT (> 600 msec) and vice versa. On day 5 most DDTs became longer. Pt½ at 6 hours was not different than at day 2 (174 ± 96 vs. 193 ± 99 msec, P = NS) and became longer on day 5 (235 ± 98 msec, p = 0.012). Bidirectional patterns were also observed in the ESFR in 6 patients (19%) at baseline, in 4 (13%) at 36 hours, and in 2 (6.5%) on day 5 after PPCI.






[1] AMI = acute myocardial infarction

[2] LAD = left anterior descending

[3] PPCI = primary percutaneous coronary intervention

[4] DDT = diastolic deceleration time

[5] ESFR = early systolic flow reversal  

[6] FVP = flow velocity pattern


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