Walter Markiewicz
Rappaport Faculty of Medicine
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Featured researches published by Walter Markiewicz.
American Journal of Cardiology | 2010
Saleem Dabbah; Haim Hammerman; Walter Markiewicz; Doron Aronson
Increased red blood cell distribution width (RDW) has been associated with adverse outcomes in heart failure and stable coronary disease. We studied the association between baseline RDW and changes in RDW during hospital course with clinical outcomes in patients with acute myocardial infarction (AMI). Baseline RDW and RDW change during hospital course were determined in 1,709 patients with AMI who were followed for a median of 27 months (range 6 to 48). The relation between RDW and clinical outcomes after hospital discharge were tested using Cox regression models, adjusting for clinical variables, baseline hemoglobin, mean corpuscular volume, and left ventricular ejection fraction. Compared to patients in the first RDW quintile, the adjusted hazard ratios for death progressively increased with higher quintiles of RDW (second quintile 1.1, 95% confidence interval [CI] 0.6 to 2.1; third quintile 1.8, 95% CI 1.0 to 3.2; fourth quintile 2.0, 95% CI 1.1 to 3.4; fifth quintile 2.8, 95% CI 1.6 to 4.7, p for trend <0.0001). An increase in RDW during hospital course was also associated with subsequent mortality (adjusted hazard ratio 1.13 for 1-SD increase in RDW, 95% CI 1.02 to 1.25). Similar results were obtained for the end point of heart failure. The association between increased RDW and worse outcome was evident in patients with and without anemia. In conclusion, there is a graded, independent association between increased RDW and mortality after AMI. An increase in RDW during hospitalization also portends adverse clinical outcome.
Circulation | 2005
Mahmoud Suleiman; Haim Hammerman; Monther Boulos; Michael Kapeliovich; Abeer Suleiman; Yoram Agmon; Walter Markiewicz; Doron Aronson
Background—Stress hyperglycemia in patients with acute myocardial infarction has been associated with increased mortality. Most studies looked at the relationship between admission glucose (AG) and outcome; limited information is available about the clinical significance of fasting glucose (FG). Methods and Results—We prospectively studied the relationship between FG and 30-day mortality in 735 nondiabetic patients with acute myocardial infarction. FG (≥8-hour fast within 24 hours of admission) and AG were measured in each patient. At 30 days, 9 deaths (2%) occurred in patients with normal FG, and 11 (10%), 14 (13%), and 31 (29%) deaths occurred in the first, second, and third tertiles of elevated FG, respectively. Compared with normal FG (<110 mg/dL), the adjusted OR for 30-day mortality progressively increased with higher tertiles of elevated FG (first tertile, 4.6; 95% CI, 1.7 to 12.7; P=0.003; second tertile, 6.4; 95% CI, 2.5 to 16.6; P<0.0001; third tertile, 11.5; 95% CI, 4.7 to 20.0; P<0.0001). Compared with patients categorized as having normal AG (<140 mg/d), the adjusted ORs for tertiles of elevated AG were as follows: first tertile, 1.4 (95% CI, 0.5 to 3.8; P=0.54); second tertile, 3.0 (95% CI, 1.3 to 7.0; P=0.01); and third tertile, 4.4 (95% CI, 2.0 to 9.7; P<0.0001). Compared with patients with normal FG and AG, the adjusted ORs for 30-day mortality were 0.71 (95% CI, 0.15 to 3.4; P=0.67) in patients with elevated AG and normal FG, 3.4 (95% CI, 1.1 to 10.4; P=0.03) for patients with normal AG glucose and elevated FG, and 9.6 (95% CI, 3.5 to 26.0; P<0.0001) for patients with both elevated FG and AG. Comparing nested models showed that including AG failed to improve the prediction of the model based on FG (&khgr;2=5.4, 3 df, P=0.15). In contrast, the addition of FG classes to the model based on AG improved model prediction (&khgr;2=22.4, 3 df, P<0.0001). Conclusions—There is a graded relation between elevated FG and AG and 30-day mortality in patients with acute myocardial infarction. FG is superior to AG in the assessment of short-term risk. (Circulation. 2005;111:754-760.)
International Journal of Obesity | 2004
Doron Aronson; Peter Bartha; Oren Zinder; Arthur Kerner; Walter Markiewicz; Ophir Avizohar; Gerald J. Brook; Yishai Levy
OBJECTIVE: To investigate the relationship between C-reactive protein (CRP) and various characteristics of the metabolic syndrome.DESIGN: Population-based cross-sectional study.SUBJECTS: A total of 1929 subjects undergoing a medical examination in a preventive medicine clinic (age, 50±10 y; 63% males).RESULTS: The proportion of subjects with CRP levels above the cut point generally used to indicate an obvious source of infection or inflammation (>10 mg/l) was 3, 7, and 15% in subjects who were normal weight, overweight, and obese, respectively. Subjects with obesity had markedly higher CRP level compared to patients without obesity regardless of whether they had the metabolic syndrome. However, there was no significant difference in CRP levels between nonobese subjects without the metabolic syndrome and subjects in whom the diagnosis of the metabolic syndrome was based on criteria other than obesity (adjusted geometric mean CRP 1.75 vs 2.08 mg/l, P=0.79). Similarly, CRP levels did not differ among obese subjects with and without the metabolic syndrome (adjusted geometric mean CRP 3.22 vs 3.49 mg/l, P=0.99). There was a linear increase in CRP levels with an increase in the number of metabolic disorders (P trend <0.0001), which was substantially diminished after controlling for body mass index (BMI) (P trend=0.1). Stepwise multivariate linear regression analysis identified BMI, triglyceride levels, HDL cholesterol levels (inversely), and fasting glucose as independently related to CRP levels. However, BMI accounted for 15% of the variability in CRP levels, whereas triglycerides, HDL cholesterol and fasting glucose levels accounted for only ∼1% of the variability in CRP levels.CONCLUSION: Obesity is the major factor associated with elevated CRP in individuals with the metabolic syndrome. CRP levels in the range suggesting a source of infection or inflammation (>10 mg/l) are more common among obese subjects than in nonobese subjects.
Arteriosclerosis, Thrombosis, and Vascular Biology | 2004
Arthur Kerner; Ophir Avizohar; Ron Sella; Peter Bartha; Oren Zinder; Walter Markiewicz; Yishai Levy; Gerald J. Brook; Doron Aronson
Objective— The objective of this study was to test whether the frequent association between liver enzyme elevations and various components of the metabolic syndrome is associated with higher C-reactive protein (CRP) levels. Methods and Results— Alanine aminotransferase (ALT), alkaline phosphatase (Alk-P), and high-sensitivity CRP were measured in 1740 subjects. Adjusted geometric mean CRP was calculated for subjects with normal and elevated ALT and for subjects with normal and elevated Alk-P, adjusting for age, sex, smoking, physical activity, body mass index, fasting glucose, triglycerides, the presence of hypertension and low HDL cholesterol, and use of aspirin or hormone replacement therapy. Adjusted CRP levels were higher in subjects with elevated ALT (2.21 versus 1.94 mg/L, P=0.028) or elevated Alk-P (2.58 versus 1.66 mg/L, P<0.0001). Logistic regression showed that compared with subjects with normal liver function tests, the adjusted odds for high-risk CRP (>3 mg/L) were significantly higher in subjects with elevated ALT (OR, 1.5; 95% CI, 1.2 to 1.9, P=0.002) or elevated Alk-P (OR, 2.1; 95% CI, 1.7 to 2.6, P<0.0001). Conclusions— Elevations of liver enzymes are associated with higher CRP concentrations. Hepatic inflammation secondary to liver steatosis is a potential contributor to the low-grade inflammation associated with the metabolic syndrome.
Journal of the American College of Cardiology | 1991
Benjamin Brenner; Zeev Blumenfeld; Walter Markiewicz; Shimon A. Reisner
To evaluate cardiac involvement in primary antiphospholipid syndrome, two-dimensional and Doppler echocardiographic studies were performed in 34 consecutive patients with this syndrome. All patients had an increased level of serum anticardiolipin antibodies with no evidence of malignancy or systemic lupus erythematosus. The clinical manifestations of primary antiphospholipid syndrome were arterial thrombosis in 14 patients, venous thrombosis in 6 and recurrent fetal loss in 14. Valvular lesions were observed on two-dimensional echocardiography in 11 patients (32%) (9 women and 2 men), aged 24 to 57 years (mean +/- 1 SD 36 +/- 10). Abnormal echocardiographic findings were observed in 9 (64%) of 14 patients with arterial thrombosis versus 1 (17%) of 6 patients with venous thrombosis and 1 (7%) of 14 patients with recurrent fetal loss. The most common echocardiographic abnormality was mitral leaflet thickening, found in five patients; this was associated with mitral regurgitation in three and with combined mild mitral stenosis and regurgitation in one patient. Localized subvalvular mitral thickening was observed in one patient and calcification of the anulus in another. Aortic valve thickening was observed in two patients, one of whom also had a moderate degree of aortic regurgitation. Vegetation-like lesions on the mitral or aortic valve were found in two patients. It is concluded that valvular lesions are commonly found in primary antiphospholipid syndrome, particularly when the syndrome is manifested by peripheral arterial thrombosis. The location and appearance of valvular lesions in this syndrome are heterogeneous. Most patients have no clinically significant valvular disease. Two-dimensional and Doppler echocardiographic studies are often informative in these patients.
Journal of the American College of Cardiology | 1987
Walter Markiewicz; Udo Sechtem; Robin Kirby; Nikita Derugin; Gary C. Caputo; Charles B. Higgins
Nuclear magnetic resonance (NMR) imaging is a new, noninvasive approach for imaging the cardiovascular system. Being a three-dimensional technique, NMR imaging has the capability of measuring volumes without the need for assumptions regarding ventricular geometry. In this study, the technique was validated in 19 excised dog hearts, filled with silicone-rubber, imaged using a multislice spin-echo sequence. The volume of the cavity in each slice was calculated from the number of pixels outlined for each slice multiplied by the pixel volume. Ventricular volumes measured by NMR imaging were highly correlated with cast volumes measured by water displacement: right ventricle (RV):RVNMR = 1.05 RVcast - 1.62; r = 0.99, SEE = 0.96 ml; left ventricle (LV):LVNMR = 0.98 LVcast + 0.35, r = 0.98, SEE = 1.48 ml. After validation in casts, NMR imaging volumes were measured in eight living dogs using a multiphasic gated technique to obtain images at 5, 105, 205, 305 and 405 ms after the QRS complex. Cardiac output (CO) and stroke volume (SV) measured by NMR imaging were significantly correlated with thermodilution (TD) measurements (CONMR = 0.63 COTD + 0.51 liters/min; r = 0.78, SEE = 0.57 liters/min; SVNMR = 0.67 SVTD + 1.95 ml; SEE = 5.58 ml). Right and left stroke volumes were closely related (LVSVNMR = 0.9 RVSVNMR + 1.75; r = 0.94, SEE = 4.32 ml), with the slope and intercept of the regression line showing no difference from 1 and 0, respectively. However, volumes determined by NMR imaging underestimated the thermodilution measurements, presumably reflecting the inability to obtain a true systolic image with the present sampling rate.(ABSTRACT TRUNCATED AT 250 WORDS)
American Journal of Cardiology | 2008
Doron Aronson; Eldad J. Dann; Lilach Bonstein; Miry Blich; Michael Kapeliovich; Rafael Beyar; Walter Markiewicz; Haim Hammerman
Divergent views remain regarding the safety of treating anemia with red blood cell (RBC) transfusion in patients with acute coronary syndrome (ACS). We used a prospective database to study effect of RBC transfusion in patients with acute myocardial infarction (MI; n = 2,358). Cox regression models were used to determine the association between RBC transfusion and 6-month outcomes, incorporating transfusion as a time-dependent variable. The models adjusted for baseline variables, propensity for transfusion, and nadir hemoglobin previous to the transfusion. One hundred ninety-two patients (8.1%) received RBC transfusion. Six-month mortality rates were higher in patients receiving transfusion (28.1% vs 11.7%, p <0.0001). The adjusted hazard ratio (HR) for mortality was 1.9 in transfused patients (95% confidence interval [CI] 1.3 to 2.9). Interaction between RBC transfusion and nadir hemoglobin with respect to mortality (p = 0.004) was significant. Stratified analyses showed a protective effect of transfusion in patients with nadir hemoglobin < or=8 g/dL (adjusted HR 0.13, 95% CI 0.03 to 0.65, p = 0.013). By contrast, transfusion was associated with increased mortality in patients with nadir hemoglobin >8 g/dL (adjusted HR 2.2, 95% CI 1.5 to 3.3; p <0.0001). Similar results were obtained for the composite end point of death/MI/heart failure (p for interaction = 0.04). In conclusion, RBC transfusion in patients with acute MI and hemoglobin < or =8 g/dL may be appropriate. The increased mortality observed in transfused patients with nadir hemoglobin above 8 g/dL underscores the clinical difficulty of balancing risks and benefits of RBC transfusion in the setting of ACS.
Catheterization and Cardiovascular Interventions | 2005
Mithal Nasser; Michael Kapeliovich; Walter Markiewicz
We describe two patients with in‐stent thrombosis occurring 4 and 21 months after implantation of sirolimus‐eluting stents. Both cases occurred following noncardiac surgery. In both cases, aspirin had been stopped prior to surgery. Both patient sustained a severe myocardial infarction; one died. The occurrence of late thrombosis of sirolimus‐eluting stents is of concern.
Kidney International | 2009
Alexander Goldberg; Elena Kogan; Haim Hammerman; Walter Markiewicz; Doron Aronson
Acute kidney injury is a common complication of acute myocardial infarction and is generally associated with adverse outcomes. We studied the incidence and clinical significance of transient versus persistent acute kidney injury in 1957 patients who survived an ST-elevation acute myocardial infarction. We divided the patients into 5 groups based on changes in serum creatinine level during hospitalization. Mild acute kidney injury (creatinine 0.3-0.49 mg/dl above baseline) occurred in 156 patients and was transient (resolved during their hospital stay) in 61. Moderate/severe acute kidney injury (creatinine more than or 0.5 mg/dl above baseline) was found in 138 patients and was transient in 60. Compared to patients without acute kidney injury, the adjusted hazard ratio for mortality was 1.2 in patients with mild, transient acute kidney injury and 1.8 in patients with mild, persistent injury where the creatinine remained elevated. Patients with persistent moderate/severe acute kidney injury had the highest mortality (hazard ratio 2.4), whereas patients with transient moderate/severe injury had an intermediate risk (hazard ratio of 1.7). A similar relationship was present between acute kidney injury and admissions for heart failure. Our study shows that dynamic changes in renal function during acute myocardial infarction are strongly related to long-term mortality and heart failure.
American Heart Journal | 1986
Walter Markiewicz; Riva Borovik; Semadar Ecker
Experience was reviewed in the management of pericardial tamponade in 36 patients with emphasis on factors governing short and long-term survival. Malignant pericardial effusion was the most common etiology and accounted for pericardial tamponade in 14 of the 36 patients (39%). Of the 36 patients, three received medical therapy alone, 18 were treated by one or more needle pericardiocentesis, pericardial drains were inserted in six patients, and thoracotomy was performed in nine. Needle pericardiocentesis was attempted as the initial therapy in all but two patients and was initially successful in relieving tamponade in 30 patients. Twenty-four patients died during a follow-up of from 1 day to 6 years. Delay in diagnosing tamponade was frequent and accounted for three deaths. Two more patients died from recurrent tamponade following initial relief. Eighteen patients died primarily from complications related to their basic illness, though recurrent pericardial effusion was a contributory factor in five. One patient died following pericardiectomy. The remaining 12 patients are well and free of pericardial disease. Short-term survival in pericardial tamponade is mostly dependent upon early diagnosis and relief of tamponade. Long-term survival depends upon the prognosis of the primary illness, irrespective of the mode of treatment used.