Cerebral and Coronary Embolization of a Valvular Tumor

2002 ◽  
Vol 23 (1) ◽  
pp. 71-73 ◽  
Author(s):  
C.C. Mull ◽  
N.S. Dahdah ◽  
R.J. Scarfone
1973 ◽  
Vol 7 (1) ◽  
pp. 63-68 ◽  
Author(s):  
R. E. FALICOV ◽  
H. LIPP ◽  
L. RESNEKOV ◽  
S. KING

STEMedicine ◽  
2021 ◽  
Vol 2 (8) ◽  
pp. e99
Author(s):  
Yonggang Yuan ◽  
Zesheng Xu

Background: Thrombotic occlusion of the coronary artery, which succeeds the atherosclerotic plaquerupture or erosion, gives rise to a major portion of acute myocardial infarction (AMI) incidences.Nevertheless, coronary embolism is gaining increasing recognition as another important factor contributingto AMI. Case presentation: A 72-year-old woman with atrial fibrillation (AF) and diabetes mellitus histories,presented with chest pain radiating to the left arm and shoulder that began 6 hours prior to admission.Electrocardiogram revealed AF plus ST-segment elevation in the anterior leads.Intervention: Patient was first treated with anti-platelet agents (aspirin plus ticagrelor) and atorvastatin.Emergency coronary angiography depicted multi-site coronary embolization of the left circumflex artery(LCX) and the left anterior descending artery (LAD). Blood flow was not restored after intracoronaryinjection of 600 ug tirofiban. 40 mg recombinant human prourokinase was then administered via aspirationthrombectomy catheter. Outcome: Two weeks later, coronary angiography showed no residual obstructive lesion in the LCX andLAD with TIMI (thrombolysis in myocardial infarction) 3 flow. Conclusion: Primary percutaneous coronary intervention is the most effective measure. In the case offailed blood flow restoration, thrombolytic treatment in both intravenous and intracoronary route should beconsidered.


Author(s):  
Edouard Benit ◽  
Paulo Rocha ◽  
Didier Stroobants ◽  
Luc Jaspers ◽  
Peter Put ◽  
...  

1998 ◽  
Vol 7 (3) ◽  
pp. 240-244 ◽  
Author(s):  
LG Futterman ◽  
L Lemberg

Prinzmetal's variant angina, primarily a vasospastic disease, is a glaring example of the gaps in our knowledge regarding the etiology of coronary heart disease. Half of all patients with coronary heart disease do not have any of the established coronary risk factors. Prinzmetal's variant angina, syndrome X, coronary embolization, and congenital coronary anomalies, are a few examples of conditions that may not be associated with established risk factors. New risk factors that are emerging in an attempt to establish an etiology in this group of patients are homocysteine plasma fibrinogen, estrogen-deficiency lipoprotein (a), C-reactive protein, Chlamydia pneumoniae, factor VII endogenous tissue plasminogen, and endogenous plasminogen activator/inhibitor type I. The battle against cardiovascular disease continues!


1994 ◽  
Vol 267 (4) ◽  
pp. H1483-H1495 ◽  
Author(s):  
M. Hori ◽  
M. Kitakaze ◽  
S. Takashima ◽  
T. Morioka ◽  
H. Sato ◽  
...  

This study was undertaken to examine whether 5-amino-4-imidazolecarboxamide (AICA) riboside (acadesine), which augments adenosine release in ischemic myocardium, further attenuates ischemic injury after acute coronary microembolization. The left anterior descending coronary artery was cannulated and perfused with blood from the left carotid artery in 46 dogs, and coronary blood flow (CBF) of the perfused area was measured. In 12 dogs, 15-microns microspheres (5.0 x 10(4)/ml) were injected repeatedly until CBF approached zero. Changes in CBF, fractional shortening, lactate extraction ratio, and adenosine release were measured with and without administration of AICA riboside. In the control group (n = 7), CBF increased to 154 +/- 11 ml.100 g-1.min-1 at 16-30% of total coronary embolization, and adenosine release was 6.1 +/- 1.0 nmol.100 g-1.min-1. Administration of AICA riboside (n = 5) enhanced coronary hyperemia (187 +/- 8 ml.100 g-1.min-1, P < 0.05), adenosine release (11.9 +/- 0.9 nmol.100 g-1.min-1, P < 0.001), and myocardial adenosine content (0.434 +/- 0.069 vs. 0.118 +/- 0.019 nmol/mg wet wt, P < 0.01) and attenuated decreases in fractional shortening and lactate extraction ratio. AICA riboside preserved myocardial tissue ATP content of the embolized area. The administrations of 8-phenyltheophylline (n = 12) and alpha,beta-methyleneadenosine 5'-diphosphate (n = 10) abolished the beneficial effects of AICA riboside. Furthermore, AICA riboside increased ectosolic and cytosolic 5'-nucleotidase activity of the embolized myocardium (n = 12). Thus we conclude that AICA riboside attenuates contractile and metabolic dysfunction by enhancing adenosine release via activation of ectosolic 5'-nucleotidase and inducing local hyperemia in acute coronary microembolization.


2007 ◽  
Vol 29 (3) ◽  
pp. 292-292 ◽  
Author(s):  
Edouard Gerbaud ◽  
Mathieu Lederlin ◽  
François Laurent

2019 ◽  
Vol 99 ◽  
pp. 106595
Author(s):  
Amanda LaRose ◽  
Gail E. Geist ◽  
Yukie Ueyama ◽  
McKenna Palmieri ◽  
Bradley L. Youngblood ◽  
...  

1952 ◽  
Vol 170 (3) ◽  
pp. 536-549 ◽  
Author(s):  
Clarence M. Agress ◽  
Marvin J. Rosenberg ◽  
Howard I. Jacobs ◽  
Maxwell J. Binder ◽  
Abraham Schneiderman ◽  
...  

1972 ◽  
Vol 43 (1) ◽  
pp. 2P-3P
Author(s):  
R. E. Falicov ◽  
C. J. Mills ◽  
I. T. Gabe

2015 ◽  
Vol 8 (2) ◽  
pp. e17-e18 ◽  
Author(s):  
Daniel Garcia ◽  
Mohammad Ansari ◽  
Jaffid S. Majjul ◽  
Elman M. Urbina ◽  
Alexandre C. Ferreira ◽  
...  

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