scholarly journals P251 Right ventricular free wall dissection clearly detected and recorded by echocardiography: a fatal complication after inferior myocardial infarction

2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
Y Kawada ◽  
A Yamada ◽  
N Hoshino ◽  
M Hoshino ◽  
S Yamabe ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Blood Pressure ◽  
Right Ventricular ◽  
Left Ventricular ◽  
Ventricular Free Wall ◽  
Inferior Wall ◽  
Free Wall ◽  
Inferior Myocardial Infarction ◽  
Fatal Complication ◽  
Right Ventricular Free Wall

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.

Differential regional gene expression from cardiac dyssynchrony induced by chronic right ventricular free wall pacing in the mouse

2006 ◽  
Vol 26 (2) ◽  
pp. 109-115 ◽  
Author(s):  
Kenneth C. Bilchick ◽  
Sudip K. Saha ◽  
Ed Mikolajczyk ◽  
Leslie Cope ◽  
Will J. Ferguson ◽  
...  
Keyword(s):  
Gene Expression ◽  
Right Ventricular ◽  
Differential Expression ◽  
Stem Cell Differentiation ◽  
Left Ventricular ◽  
Ventricular Free Wall ◽  
Free Wall ◽  
Right Ventricular Free Wall ◽  
Cardiac Dyssynchrony ◽  
Clinical Prognosis

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.

Absent Pulmonary Valve with Tricuspid Atresia or Severe Tricuspid Stenosis: Report of Three Cases and Review of the Literature

2000 ◽  
Vol 3 (4) ◽  
pp. 353-366 ◽  
Author(s):  
Silvio Litovsky ◽  
Michael Choy ◽  
Jeanny Park ◽  
Mark Parrish ◽  
Brenda Waters ◽  
...  
Keyword(s):  
Right Ventricular ◽  
Pulmonary Valve ◽  
Left Ventricular ◽  
Tricuspid Atresia ◽  
Ventricular Free Wall ◽  
Ventricular Septum ◽  
Free Wall ◽  
Absent Pulmonary Valve ◽  
Right Ventricular Free Wall ◽  
The Right

Absence of the pulmonary valve occurs usually in association with tetralogy of Fallot and occasionally with an atrial septal defect or as an isolated lesion. Very rarely it occurs with tricuspid atresia, intact ventricular septum, and dysplasia of the right ventricular free wall and of the ventricular septum. We present the clinical, anatomic, and histologic findings of a new case, and for the first time, the data from two patients with absent pulmonary valve and severe tricuspid stenosis, who exhibited similar histologic findings. We also reviewed the clinical and anatomic data of 24 previously published cases and compared them with the new cases. In all three new cases, the myocardium of the right ventricle was very abnormal. In the two cases with tricuspid stenosis, large segments of myocardium were replaced with sinusoids and fibrous tissue. In the case with tricuspid atresia, the right ventricular free wall contained only fibroelastic tissue. The ventricular septum in all three patients showed asymmetric hypertrophy and in two of the three patients, multiple sinusoids had replaced large segments of myocardial cells. The left ventricular free wall myocardium and the walls of the great arteries were unremarkable. Our data indicate that myocardial depletion involving the right ventricular free wall and the ventricular septum and its replacement by sinusoids and fibroelastic tissue occur not only in cases of absent pulmonary valve with tricuspid atresia but also in cases of absent pulmonary valve with tricuspid stenosis. The degree of myocardial depletion varies and is more severe when the tricuspid valve is atretic.

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