Anterior S-T changes during acute inferior myocardial infarction

1983 ◽  
Vol 4 (4) ◽  
pp. 421-430 ◽  
Author(s):  
S. Betocchi ◽  
D. Bonaduce ◽  
M. Chiariello ◽  
E. Romano ◽  
F. Piscione ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Inferior Myocardial Infarction ◽  
Acute Inferior Myocardial Infarction

False Lumen Catheterization in a Patient Who Has Type A Aortic Dissection That Mimics Acute Inferior Myocardial Infarction: A Case Report

2015 ◽  
Vol 18 (5) ◽  
pp. 208
Author(s):  
Erhan Kaya ◽  
Hakan Fotbolcu ◽  
Zeki Şimşek ◽  
Ömer Işık
Keyword(s):  
Myocardial Infarction ◽  
Case Report ◽  
Aortic Dissection ◽  
Cardiac Catheterization ◽  
False Lumen ◽  
Type A ◽  
Inferior Myocardial Infarction ◽  
Type A Aortic Dissection ◽  
Acute Inferior Myocardial Infarction ◽  
Catheterization Procedure

We report a 61-year-old patient who suffered from a type A aortic dissection that mimicked an acute inferior myocardial infarction. During a routine cardiac catheterization procedure, diagnostic catheters can be inserted accidentally into the false lumen. Invasive cardiologists should keep this complication in mind.

scholarly journals Precordial ST-segment depression during acute inferior myocardial infarction: clinical, scintigraphic and angiographic correlations.

Circulation ◽  
1982 ◽  
Vol 66 (4) ◽  
pp. 732-741 ◽  
Author(s):  
R S Gibson ◽  
R S Crampton ◽  
D D Watson ◽  
G J Taylor ◽  
B A Carabello ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Inferior Myocardial Infarction ◽  
St Segment ◽  
Acute Inferior Myocardial Infarction

scholarly journals Right coronary artery ligation in mice: a novel method to investigate right ventricular dysfunction and biventricular interaction

2019 ◽  
Vol 316 (3) ◽  
pp. H684-H692 ◽  
Author(s):  
Pierre Sicard ◽  
Timothée Jouitteau ◽  
Thales Andrade-Martins ◽  
Abdallah Massad ◽  
Glaucy Rodrigues de Araujo ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery ◽  
Infarct Size ◽  
Right Ventricular ◽  
Right Coronary Artery ◽  
Ventricular Dysfunction ◽  
Left Ventricular ◽  
Coronary Artery Ligation ◽  
Inferior Myocardial Infarction ◽  
Acute Inferior Myocardial Infarction

Right ventricular (RV) dysfunction can lead to complications after acute inferior myocardial infarction (MI). However, it is unclear how RV failure after MI contributes to left-sided dysfunction. The aim of the present study was to investigate the consequences of right coronary artery (RCA) ligation in mice. RCA ligation was performed in C57BL/6JRj mice ( n = 38). The cardiac phenotypes were characterized using high-resolution echocardiography performed up to 4 wk post-RCA ligation. Infarct size was measured using 2,3,5-triphenyltetrazolium chloride staining 24 h post-RCA ligation, and the extent of the fibrotic area was determined 4 wk after MI. RV dysfunction was confirmed 24 h post-RCA ligation by a decrease in the tricuspid annular plane systolic excursion ( P < 0.001) and RV longitudinal strain analysis ( P < 0.001). Infarct size measured ex vivo represented 45.1 ± 9.1% of the RV free wall. RCA permanent ligation increased the RV-to-left ventricular (LV) area ratio ( P < 0.01). Septum hypertrophy ( P < 0.01) was associated with diastolic septal flattening. During the 4-wk post-RCA ligation, LV ejection fraction was preserved, yet it was associated with impaired LV diastolic parameters ( E/ E′, global strain rate during early diastole). Histological staining after 4 wk confirmed the remodeling process with a thin and fibrotic RV. This study validates that RCA ligation in mice is feasible and induces RV heart failure associated with the development of LV diastolic dysfunction. Our model offers a new opportunity to study mechanisms and treatments of RV/LV dysfunction after MI. NEW & NOTEWORTHY Right ventricular (RV) dysfunction frequently causes complications after acute inferior myocardial infarction. How RV failure contributes to left-sided dysfunction is elusive because of the lack of models to study molecular mechanisms. Here, we created a new model of myocardial infarction by permanently tying the right coronary artery in mice. This model offers a new opportunity to unravel mechanisms underlying RV/left ventricular dysfunction and evaluate drug therapy.

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