Advanced Search
Display options
Filter resources
Text Availability
Article type
Publication date
Showing 1 to 12 of 65 entries
Sorted by: Best Match Show Resources per page
Neutrophil depletion limited to reperfusion reduces myocardial infarct size after 90 minutes of ischemia. Evidence for neutrophil-mediated reperfusion injury.


Litt MR, Jeremy RW, Weisman HF, Winkelstein JA, Becker LC.
PMID: 2598440
Circulation. 1989 Dec;80(6):1816-27. doi: 10.1161/01.cir.80.6.1816.

Reperfusion of ischemic myocardium may accelerate necrosis of injured myocytes. To determine the role of neutrophil leukocytes in this process, we examined whether neutrophil depletion during reperfusion could modify infarct size in anesthetized dogs. The proximal circumflex coronary artery...

Increased afterload aggravates infarct expansion after acute myocardial infarction.

Journal of the American College of Cardiology

Nolan SE, Mannisi JA, Bush DE, Healy B, Weisman HF.
PMID: 2971704
J Am Coll Cardiol. 1988 Nov;12(5):1318-25. doi: 10.1016/0735-1097(88)92616-2.
Free Article

After acute transmural myocardial infarction, the heart may undergo major remodeling characterized by thinning and dilation of the infarct zone and overall enlargement of the heart. The effect of increased left ventricular pressure on infarct expansion and the extent...

A method to reconstruct myocardial sarcomere lengths and orientations at transmural sites in beating canine hearts.

The American journal of physiology

Rodriguez EK, Hunter WC, Royce MJ, Leppo MK, Douglas AS, Weisman HF.
PMID: 1636767
Am J Physiol. 1992 Jul;263(1):H293-306. doi: 10.1152/ajpheart.1992.263.1.H293.

The ability to measure cyclic changes in myocardial sarcomere lengths and orientations during cardiac ejection and filling would improve our understanding of how the cellular processes of contraction relate to the pumping of the whole heart. Previously, only postmortem...

Comparison of indium-111 antimyosin antibody and technetium-99m pyrophosphate localization in reperfused and nonreperfused myocardial infarction.

Journal of the American College of Cardiology

Takeda K, LaFrance ND, Weisman HF, Wagner HN, Becker LC.
PMID: 1846888
J Am Coll Cardiol. 1991 Feb;17(2):519-26. doi: 10.1016/s0735-1097(10)80125-1.
Free Article

Recent imaging studies suggest that technetium-99m (Tc-99m) pyrophosphate yields a considerably larger estimate of myocardial infarct size than does indium-111 (In-111) monoclonal antimyosin antibody. To determine whether Tc-99m pyrophosphate may be taken up by reversibly injured myocytes, particularly in...

Cellular mechanisms of myocardial infarct expansion.


Weisman HF, Bush DE, Mannisi JA, Weisfeldt ML, Healy B.
PMID: 2968197
Circulation. 1988 Jul;78(1):186-201. doi: 10.1161/01.cir.78.1.186.

Infarct expansion is acute regional dilatation and thinning of the infarct zone. There are several possibilities for the mechanism of this alteration in cardiac shape: thinning could be caused by 1) cell rupture, 2) a reduction in the intercellular...

Myocardial infarct expansion, infarct extension, and reinfarction: pathophysiologic concepts.

Progress in cardiovascular diseases

Weisman HF, Healy B.
PMID: 2888158
Prog Cardiovasc Dis. 1987 Sep-Oct;30(2):73-110. doi: 10.1016/0033-0620(87)90004-1.

Infarct expansion and infarct extension are events early in the course of myocardial infarction with serious short- and long-term consequences. Infarct expansion, disproportionate thinning, and dilatation of the infarct segment probably begin within hours of acute infarction and usually...

The role of calcium channel abnormalities in Syrian hamster cardiomyopathy.

Clinical immunology and immunopathology

Weisman HF.
PMID: 8395359
Clin Immunol Immunopathol. 1993 Aug;68(2):170-4. doi: 10.1006/clin.1993.1114.

No abstract available.

Pathophysiology of atherosclerotic heart disease.

Cardiology clinics

Weisman HF, Bulkley BH.
PMID: 6544647
Cardiol Clin. 1984 Nov;2(4):555-69.

Coronary atherosclerosis is the major health problem of the twentieth century. Although there has been a recent decrease in mortality from this condition in many Western countries, the incidence has remained the same, and coronary atherosclerosis continues to be...

ReoPro Clinical Development: Future Directions and Therapeutic Approaches.

The Journal of invasive cardiology

Weisman HF.
PMID: 10785772
J Invasive Cardiol. 1996;8:51B-61B.

No abstract available.

Myocardial Reperfusion Injury: The Case Against Shadow Boxing.

Journal of thrombosis and thrombolysis

Weisman HF.
PMID: 10639251
J Thromb Thrombolysis. 1997 Jan;4(1):133-135. doi: 10.1023/a:1017560231064.

No abstract available.

Diabetes mellitus, glycoprotein IIb/IIIa blockade, and heparin: evidence for a complex interaction in a multicenter trial. EPILOG Investigators.


Kleiman NS, Lincoff AM, Kereiakes DJ, Miller DP, Aguirre FV, Anderson KM, Weisman HF, Califf RM, Topol EJ.
PMID: 9609084
Circulation. 1998 May 19;97(19):1912-20. doi: 10.1161/01.cir.97.19.1912.

BACKGROUND: After angioplasty, major complications and ischemic events occur more frequently in diabetic than nondiabetic patients. To determine whether treatment with abciximab is effective in reducing these events in diabetics, we analyzed characteristics and outcomes of diabetic patients enrolled...

Rapid assessment of platelet function with a modified whole-blood aggregometer in percutaneous transluminal coronary angioplasty patients receiving anti-GP IIb/IIIa therapy.


Mascelli MA, Worley S, Veriabo NJ, Lance ET, Mack S, Schaible T, Weisman HF, Jordan RE.
PMID: 9403608
Circulation. 1997 Dec 02;96(11):3860-6. doi: 10.1161/01.cir.96.11.3860.

BACKGROUND: The glycoprotein (GP) IIb/IIIa receptor antagonist abciximab (c7E3 Fab, ReoPro) is approved for use in high-risk percutaneous transluminal coronary angioplasty (PTCA). At present, no "point of care" exists for measuring pharmacological GP IIb/IIIa blockade. To address this need,...

Showing 1 to 12 of 65 entries