scholarly journals 1115 Ultra-slow low-dose thrombolytic therapy as an option of treatment in intracardiac thrombus: a case report

2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
R Alves Pinto ◽  
S Torres ◽  
M Formigo ◽  
C X Resende ◽  
T Proenca ◽  
...  
Keyword(s):  
Pulmonary Artery ◽  
Right Ventricle ◽  
Coronary Sinus ◽  
Low Dose ◽  
Systolic Function ◽  
Nyha Class ◽  
Right Atrial ◽  
Right Pulmonary Artery ◽  
The Right ◽  
Intracardiac Thrombi

Abstract We present a case of a 57-year-old male with previously known primary severe mitral regurgitation, who was admitted to the ICU due to massive venous thromboembolism with associated right ventricle dysfunction and with two large mobile right atrial thrombi (2.4 x 1.5 cm and 3.6 x 3.7 cm). Despite of five days with a therapeutic aPTT achieved with unfractionated heparin (UFH), a TTE showed deterioration of the right ventricle systolic function, persistence of the right atrial masses with similar dimensions together with new mobile thrombi on the coronary sinus and on the right pulmonary artery. Due to deterioration of his clinical condition and given the refractoriness to the classical treatment with UFH, it was decided to administer an ultra-slow low-dose thrombolysis protocol, which consisted in a 24-hour infusion of 24 mg of alteplase at a rate of 1 mg per hour, without bolus. The treatment was continued by 48 consecutive hours, with clinical improvement and important reduction of the right atrial masses with resolution of the coronary sinus and right pulmonary artery thrombi. The patient started hypocoagulation with warfarin bridging with low molecular weight heparin (LMWH). Seven days after alteplase discontinuation there was complete resolution of the intracardiac thrombi. One month after ICU admission a successful mitral valve replacement surgery was conducted. Three months after discharge, the patient is in functional New York Heart Association (NYHA) class I with no cardiovascular events or hospitalizations. This case demonstrates that ultra-slow low-dose thrombolysis is a valid bailout treatment option in patients with large intracardiac thrombi refractory to anticoagulation. Abstract 1115 Figure. TTE showing right atrial masses

scholarly journals P686 Right atrial, right ventricular and pulmonary cement embolism: a rare complication of percutaneous vertebroplasty

2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
S Akhunova ◽  
R Khayrullin ◽  
N Stekolshchikova ◽  
M Samigullin ◽  
V Padiryakov
Keyword(s):  
Pulmonary Artery ◽  
Right Ventricle ◽  
Right Atrium ◽  
Percutaneous Vertebroplasty ◽  
Rare Complication ◽  
Clinical Manifestations ◽  
Stable Condition ◽  
Right Atrial ◽  
Cement Embolism ◽  
The Right

Abstract A 68-year-old man was admitted to the hospital with complaints of pain in the lumbar spine. He had L5 disc herniation, Spinal stenosis of the L5 root canal - S1 on the right in the past medical history. Percutaneous vertebroplasty at the level of L3 and Th8 vertebral bodies was performed six months ago due to painful vertebral hemangioma. The man is suffering from arterial hypertension, receives antihypertensive therapy. During routine transthoracic echocardiography, a hyperechoic structure with a size of 9.5 x 0.9 cm was found in the right atrium and right ventricle. Chest computed tomography with contrast enhancement revealed signs of bone cement in the right atrium and right ventricle, in the right upper lobe artery, in the branches of the upper lobe artery, in the paravertebral venous plexuses. Considering the duration of the disease, the stable condition, the absence of clinical manifestations and disorders of intracardiac hemodynamics, it was decided to refrain from surgical treatment. Antiplatelet therapy and dynamic observation were recommended. Conclusion Percutaneous vertebroplasty is a modern minimally invasive surgical procedure for the treatment of degenerative-dystrophic diseases of the spine. However, the cement can penetrate into the paravertebral veins and migrate to the right chambers of the heart and the pulmonary artery. This clinical case demonstrates asymptomatic cement embolism of the right chambers of the heart and pulmonary artery after percutaneous vertebroplasty, detected incidentally during routine echocardiography. Abstract P686 Figure.

Coexistence of Primary Sarcomatoid Carcinoma of the Right Ventricle and Absence of Right Pulmonary Artery

2015 ◽  
Vol 32 (11) ◽  
pp. 1728-1731 ◽  
Author(s):  
Guobing Hu ◽  
Fang Song ◽  
Xiangming Zhu ◽  
Baiyu Yang ◽  
Yinhua Liu ◽  
...  
Keyword(s):  
Pulmonary Artery ◽  
Right Ventricle ◽  
Sarcomatoid Carcinoma ◽  
Right Pulmonary Artery ◽  
The Right

Absence of the coronary sinus with coronary venous drainage into the main pulmonary artery

2012 ◽  
Vol 23 (5) ◽  
pp. 759-762
Author(s):  
Kiyoshi Ogawa ◽  
Takashi Hishitani ◽  
Kenji Hoshino
Keyword(s):  
Coronary Angiography ◽  
Pulmonary Artery ◽  
Right Ventricle ◽  
Contrast Medium ◽  
Coronary Arteries ◽  
Coronary Sinus ◽  
Main Pulmonary Artery ◽  
Venous Drainage ◽  
Anterior Wall ◽  
The Right

AbstractWe describe the case of a 9-year-old girl demonstrating isolated absence of the coronary sinus with abnormal coronary venous drainage into the main pulmonary artery. Coronary angiography showed normal coronary arterial trees and contrast medium from both coronary arteries drained into the main pulmonary artery via an abnormal cardiac vein on the anterior wall of the right ventricle.

Limitations of thermodilution cardiac output measurements in the rat

1984 ◽  
Vol 246 (6) ◽  
pp. H754-H760 ◽  
Author(s):  
B. E. Hayes ◽  
J. A. Will ◽  
W. C. Zarnstorff ◽  
G. E. Bisgard
Keyword(s):  
Cardiac Output ◽  
Pulmonary Artery ◽  
Right Ventricle ◽  
Heat Loss ◽  
Thoracic Aorta ◽  
Vascular System ◽  
Vena Cava ◽  
Right Atrial ◽  
Thermodilution Cardiac Output ◽  
The Right

Heat loss from the vascular system could introduce an error in thermodilution cardiac output determinations. Cardiac output measured in the rat via the thermodilution technique following right atrial injection yielded different values (P less than 0.001), depending whether sampling was from the pulmonary artery (460 +/- 31 ml X min-1 X kg-1), right ventricle (311 +/- 19), or thoracic aorta (245 +/- 15). Recirculation errors could not account for the differences. Heat loss from the vascular system was measured from extravascular thermistors within both the thorax and the abdomen. These dilutions were 22-57% in peak height of aortic curves recorded at approximately the same location. Differences in calculated cardiac output between sampling sites could be attributed to rapid heat conduction directly from the right atrium and inferior vena cava to the thoracic aorta with progressive loss of indicator from both the right ventricle and pulmonary artery.

scholarly journals Right Atrial and Ventricular Adaptation to Chronic Right Ventricular Pressure Overload

Circulation ◽  
2005 ◽  
Vol 112 (9_supplement) ◽  
Author(s):  
Sydney L. Gaynor ◽  
Hersh S. Maniar ◽  
Jeffrey B. Bloch ◽  
Paul Steendijk ◽  
Marc R. Moon
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Right Ventricular ◽  
Right Atrium ◽  
Systolic Function ◽  
Pressure Overload ◽  
Right Atrial ◽  
Chronic Pulmonary Hypertension ◽  
The Right ◽  
Conduit Function

Background— Increased mortality in patients with chronic pulmonary hypertension has been associated with elevated right atrial (RA) pressure. However, little is known about the effects of chronic right ventricular (RV) pressure overload on RA and RV dynamics or the adaptive response of the right atrium to maintain RV filling. Methods and Results— In 7 dogs, RA and RV pressure and volume (conductance catheter) were recorded at baseline and after 3 months of progressive pulmonary artery banding. RA and RV elastance (contractility) and diastolic stiffness were calculated, and RA reservoir and conduit function were quantified as RA inflow with the tricuspid valve closed versus open, respectively. With chronic pulmonary artery banding, systolic RV pressure increased from 34±7 to 70±17 mm Hg ( P <0.001), but cardiac output did not change ( P >0.78). RV elastance and stiffness both increased ( P <0.05), suggesting preserved systolic function but impaired diastolic function. In response, RA contractility improved (elastance increased from 0.28±0.12 to 0.44±0.13 mm Hg/mL; P <0.04), and the atrium became more distensible, as evidenced by increased reservoir function (49±14% versus 72±8%) and decreased conduit function (51±14% versus 28±8%; P <0.002). Conclusions— With chronic RV pressure overload, RV systolic function was preserved, but diastolic function was impaired. To compensate, RA contractility increased, and the atrium became more distensible to maintain filling of the stiffened ventricle. This compensatory response of the right atrium likely plays an important role in preventing clinical failure in chronic pulmonary hypertension.

scholarly journals P1701 Biatrial thrombus detection in a patient with atrial paroxysmal fibrillation and asymptomatic massive pulmonary embolism

2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
I Refatllari ◽  
A Banushi ◽  
H Gjergo ◽  
A Goda
Keyword(s):  
Pulmonary Artery ◽  
Troponin I ◽  
Nyha Class ◽  
Good Condition ◽  
High Rate ◽  
Right Atrial ◽  
Close Monitoring ◽  
Ecg Changes ◽  
Noninvasive Test ◽  
The Right

Abstract Introduction Computed tomography (CT) is a noninvasive test for detection of LA and LAA thrombus.Although the transesophageal echocardiogram is the gold standart method, it can have rare but potential life threatening complications.Case report:A 62 y.o woman presented to the ER complaining of palpitations started less then 12h ago with no chest pain or dispnea.She was diagnosed with high rate paroxysmal atrial fibrillation (HR∼120/min).The ECG showed AF with no specific changes,the troponin I (TPI) level was negative and a TTE revealed a dilated left atria.The other lab results were within normal range(TBC and blood chemistry).Her past medical history included hypertension and diabetes type 2 for 10 years and 6 months respectively both on regular treatment and obesity.Also 2 months ago she was diagnosed with Hashimoto thyroiditis and close monitoring of TSH was recommended but no treatment.Subsequently,LMWH (enoxaparin) and amiodarone loading dose for cardioversion were started.After 24h the pt was still in AF,with a controlled heart rate and no complains.However ECG changes were noticed (evolutive T negative waves in leads D1,D2,aVL,V3-V6).A D-Dimer was requested and came back negative,O2 saturation was 97%.The asymptomatic pt was transferred to the Cardiology ward for further evaluation.TPI remained negative.Due to the cardiac risk factors and the ECG changes it was decided to perfom a coronary angiography which resulted normal.An electrical cardioversion was considered.Both TEE and pulmonary angio CT were requested prior.Because of the ECG changes the CT was performed first and showed central and peripheric bilateral pulmonary artery clots present also in both the left and right atrial auricles.Due to the massive thromboembolism(PE) unfractioned heparin was immediately started (aPTT 50-70s).A new TTE showed a PAP of 50 mmHg.Approximately 10h after the heparin infusion,the pt became hypotensive and started complaining of dyspnea,tachypnea,cough,pleuritic pain and fever(high temperature 39.5-40ᵒC).Considering the deteriorating conditions she was consulted by a cardiac surgery team and it was decided to perform an emergency surgical pulmonary embolectomy despite the high risk.Within 24h,the pt underwent a surgical embolectomy of the right and left pulmonary branches after incision of the pulmonary artery, as well as a clot embolectomy of the right and left atria auricles (confirmed by intraoperatory TEE).She was put on an iv heparin regimen and recovered well.She was discharged 2 weeks later in good condition,with a PAP of 40 mmHg,on acenocoumarol with persistent AF.1.5 years later she is in NYHA class I,in sinus rhythm taking rivaroxaban 20 mg/d.Discussion: Biatrial thrombus detection in both atrial auricles is rare as well as in this case a massive PE without a stroke.CT can be used as an alternative modality for detecting thrombus in selected high risk patients because it shows a good diagnostic accuracy with high sensitivity and specificity. Abstract P1701 Figure. Biatrial clots on CT and removed ones

Differential sympathetic regulation of automatic, conductile, and contractile tissue in dog heart

1988 ◽  
Vol 255 (5) ◽  
pp. H1050-H1059 ◽  
Author(s):  
J. L. Ardell ◽  
W. C. Randall ◽  
W. J. Cannon ◽  
D. C. Schmacht ◽  
E. Tasdemiroglu
Keyword(s):  
Pulmonary Artery ◽  
Pulmonary Vein ◽  
Contractile Force ◽  
Right Atrial ◽  
Canine Heart ◽  
Superior Pulmonary Vein ◽  
Right Pulmonary Artery ◽  
The Common ◽  
The Right ◽  
Contractile Tissue

Sympathetic pathways mediating chronotropic, dromotropic, and inotropic responses during ansae subclavia stimulation were determined by sequential dissection around major cardiac vessels. Right sympathetic (RS) projections influencing ventricular contractile force converge at the common pulmonary artery and within the pulmonary artery nerves (PAN). RS projections influencing left atrial contractile force course within the PANs. RS pathways to pacemaker and right atrial contractile tissue were localized between the superior vena cava and ascending aorta. RS projections influencing conductile tissue converge between the common pulmonary artery and proximal right pulmonary artery. Left sympathetic (LS) projections to ventricular contractile tissue were localized at the common pulmonary artery, within the PANs, and in the ventral lateral cardiac nerve (VLCN). LS pathways influencing heart rate and conductile tissue were localized at the left pulmonary artery and coursing between the right pulmonary artery and left superior pulmonary vein. LS projections to atrial contractile tissue were localized within the PANs and coursing between the right pulmonary artery and left superior pulmonary vein. We conclude that there are parallel, yet distinct, projections of sympathetic efferents to automatic, conductile, and contractile tissue of the canine heart.

Sign in / Sign up

Export Citation Format

Share Document