Right ventricular free wall dissection as a rupture tract in left ventricular rupture during acute myocardial infarction

2015 ◽  
Vol 17 (6) ◽  
pp. 525-531 ◽  
Author(s):  
Aya Takada ◽  
Kazuyuki Saito ◽  
Tatsuya Murai ◽  
Kunihiko Kurosaki ◽  
Katsuyoshi Kurihara ◽  
...  
2020 ◽  
Vol 2020 ◽  
pp. 1-4
Author(s):  
Mohd Al-Baqlish Mohd Firdaus ◽  
Nur Syahirah Abdul Rahim ◽  
Nurtasneem Rusdi ◽  
Nor Saadah Idris ◽  
Mohd Ridzuan Mohd Said ◽  
...  

Ventricular wall rupture possesses a high mortality rate in patients with acute myocardial infarction. We presented a case of a ninety-year-old gentleman who presented with acute inferolateral myocardial infarction in cardiogenic shock and right ventricular free wall rupture. He was treated conservatively and survived.


2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
Y Kawada ◽  
A Yamada ◽  
N Hoshino ◽  
M Hoshino ◽  
S Yamabe ◽  
...  

Abstract An 81-year-old man was transferred to our institution by ambulance because of poor feeding, general fatigue and slight disorientation lasting for a week. On arrival, he was awake and able to speak, however, his blood pressure was low at 61/43 mmHg in spite of his medical history of hypertension. His ECG showed abnormal Q waves and ST elevation in II, III, aVF leads. The echo exam detected severe hypokinesis in the left ventricular inferior wall and reduced ejection fraction at 30%. Pericardial effusion was not observed in the first echo exam. The patient was diagnosed as cardiogenic shock due to recent inferior myocardial infarction. Coronary angiography was performed, which detected total occlusion of mid right coronary artery, followed by a successful percutaneous coronary intervention (PCI) with a drug-eluting stent under the support of intra-aortic balloon pumping. Nevertheless, his blood pressure remained low and intravenous adrenaline administration was necessary during and even after PCI. To detect the cause of prolonged low blood pressure, echo was performed again immediately after PCI. The echo exam detected new findings: right ventricular posterior free wall was dissected and abnormal shunt flows were obviously observed from left ventricle to right atrium through the dissection cavity during systole. An urgent surgical repair was considered as the only option for his survival, however, his family did not accept it because the operation itself was too risky. On the next day of his admission, he passed away. Right ventricular free wall dissection is a very rare but fatal complication after inferior myocardial infarction, nevertheless, we could detect it by echocardiography with clearly recorded images. Abstract P251 Figure.


2006 ◽  
Vol 26 (2) ◽  
pp. 109-115 ◽  
Author(s):  
Kenneth C. Bilchick ◽  
Sudip K. Saha ◽  
Ed Mikolajczyk ◽  
Leslie Cope ◽  
Will J. Ferguson ◽  
...  

Routine clinical right ventricular pacing generates left ventricular dyssynchrony manifested by early septal shortening followed by late lateral contraction, which, in turn, reciprocally stretches the septum. Dyssynchrony is disadvantageous to cardiac mechanoenergetics and worsens clinical prognosis, yet little is known about its molecular consequences. Here, we report the influence of cardiac dyssynchrony on regional cardiac gene expression in mice. Mice were implanted with a custom-designed miniature cardiac pacemaker and subjected to 1-wk overdrive right ventricular free wall pacing (720 beats/min, baseline heart rate 520–620 beats/min) to generate dyssynchrony (pacemaker: 3-V lithium battery, rate programmable, 1.5 g, bipolar lead). Electrical capture was confirmed by pulsed-wave Doppler and dyssynchrony by echocardiography. Gene expression from the left ventricular septal and lateral wall myocardium was assessed by microarray (dual-dye method, Agilent) using oligonucleotide probes and dye swap. Identical analysis was applied to four synchronously contracting controls. Of the 22,000 genes surveyed, only 18 genes displayed significant ( P < 0.01) differential expression between septal/lateral walls >1.5 times that in synchronous controls. Gene changes were confirmed by quantitative PCR with excellent correlations. Most of the genes ( n = 16) showed greater septal expression. Of particular interest were seven genes coding proteins involved with stretch responses, matrix remodeling, stem cell differentiation to myocyte lineage, and Purkinje fiber differentiation. One week of iatrogenic cardiac dyssynchrony triggered regional differential expression in relatively few select genes. Such analysis using a murine implantable pacemaker should facilitate molecular studies of cardiac dyssynchrony and help elucidate novel mechanisms by which stress/stretch stimuli due to dyssynchrony impact the normal and failing heart.


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