Abstract 352: Pulmonary Vein Thrombosis can make Pulmonary Vein Acidic States, which may be Associated with Atrial Fibrillation.

2014 ◽  
Vol 115 (suppl_1) ◽  
Author(s):  
Hidekazu Takeuchi
Keyword(s):  
Carbon Dioxide ◽  
Atrial Fibrillation ◽  
Ischemic Stroke ◽  
Pulmonary Vein ◽  
Es Cells ◽  
Rare Complication ◽  
Arterial Blood Flow ◽  
Vein Thrombosis ◽  
Arterial Blood ◽  
Myocardial Layer

Atrial fibrillation can cause ischemic stroke. To prevent atrial fibrillation (AF) is crucial to prevent ischemic stroke. The pulmonary vein has a myocardial layer that can generate spontaneous or triggered action potentials. The myocardial layer is extended from the left atrial myocardium. Pulmonary vein myocardium sleeve is known to be associated with generating and maintaining AF. Pulmonary vein myocardium can be classified into two types. One is short and thin myocardium sleeve, which has no potential to cause atrial fibrillation (AF). And the other is long and thick myocardium sleeve, which has potential to cause AF. The mechanisms of such myocardium sleeve changes are not understood well. Pulmonary vein thrombosis (PVT) is believed to be rare, which was reported as a rare complication of chest surgeries such as lobectomy or lung cancers. But since 2012, I reported seven cases of PVT in elderly patients without such conditions, which suggests that PVT is not uncommon. That is a novel notion. PVT prevents arterial blood flow, which inhibits oxygen and nourishment supply and carbon dioxide excretion. Hypoxia activates hypoxia inducible factors (HIFs), and HIFs can modulate epigenetic changes, reprogramming and ES cells. Undernourishments may activate nuclear respiratory factor-1 (NRF-1) and the aryl hydrocarbon receptor (AhR). PVT can make pulmonary vein acidic states by inhibiting excretion of carbon dioxide and may modulate pulmonary vein myocardium. Under acidic states, pulmonary vein cells such as pulmonary vein myocardium cells may obtain some kinds of multipotency. After obtaining multipotency, the cells may turn into new cells to adapt changed surroundings. The changes of myocardium sleeve may be caused by acidic state conditions and HIFs, AhR and NRF-1, which seemed to modulate pulmonary vein myocardium functions. To clear these, more studies are needed.

Effects of Intraabdominanlly Insufflated Carbon Dioxide and Elevated Intraabdominal Pressure on Splanchnic Circulation 

1998 ◽  
Vol 89 (2) ◽  
pp. 475-482 ◽  
Author(s):  
Manfred Blobner ◽  
Ralph Bogdanski ◽  
Eberhard Kochs ◽  
Julia Henke ◽  
Alexander Findeis ◽  
...  
Keyword(s):  
Carbon Dioxide ◽  
Blood Flow ◽  
Vascular Resistance ◽  
Mesenteric Artery ◽  
Splanchnic Circulation ◽  
Arterial Blood Flow ◽  
Intraabdominal Pressure ◽  
Arterial Blood ◽  
Baseline Values ◽  
Air Insufflation

Background Intraabdominally insufflated carbon dioxide (CO2) during laparoscopy may have a specific effect on splanchnic circulation that may be unrelated to the effects of increased intraabdominal pressure alone. Therefore, the influences of insufflation with CO2 versus air on splanchnic circulation were compared. Methods Pigs were chronically instrumented for continuous recording of mesenteric artery, portal venous, inferior vena cava, and pulmonary arterial blood flow and portal venous pressure. After induction of anesthesia, CO2 or air was insufflated in 14 and 10 pigs, respectively. With the pigs in the supine position, intraabdominal pressure was increased in steps of 4 mmHg up to 24 mmHg by graded gas insufflation. Results During air insufflation, mesenteric artery vascular resistance was unchanged, whereas mesenteric arterial blood flow decreased with increasing intraabdominal pressure. Shortly after CO2 insufflation to an intraabdominal pressure of 4 mmHg, mean arterial pressure, mesenteric arterial blood flow, and mesenteric arterial vascular resistance were increased by 21%, 12% and 9%, respectively. Subsequently, with the onset of CO2 resorption in the third minute, mean arterial pressure declined to baseline values and mesenteric arterial vascular resistance declined to 85% of baseline values, whereas mesenteric arterial blood flow continued to increase to a maximum of 24% higher than baseline values. At steady-state conditions during CO2 insufflation, mesenteric arterial blood flow was increased up to an intraabdominal pressure 16 mmHg but decreased at higher intraabdominal pressures. Conclusions In contrast to air insufflation, intraabdominal insufflation of CO2 resulted in a moderate splanchnic hyperemia at an intraabdominal pressure < or = 12 mmHg. At higher intraabdominal pressure values, pressure-induced changes became more important than the type of gas used.

scholarly journals Clinical characteristics of patients with atrial fibrillation suffering from pulmonary vein stenosis after radiofrequency ablation

2019 ◽  
Vol 48 (3) ◽  
pp. 030006051988155
Author(s):  
Lingping Xu ◽  
Lei Cui ◽  
Junlong Hou ◽  
Jing Wang ◽  
Bin Chen ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Pulmonary Vein ◽  
Stent Implantation ◽  
Clinical Characteristics ◽  
Rare Complication ◽  
Pulmonary Veins ◽  
Pulmonary Vein Stenosis ◽  
Stent Restenosis ◽  
Asymptomatic Patients ◽  
Vein Stenosis

Objective Pulmonary vein stenosis (PVS) is a serious complication in patients with atrial fibrillation (AF) receiving radiofrequency catheter ablation (RFCA). We therefore examined these patients’ clinical characteristics in relation to PVS occurrence. Method We retrospectively analyzed the clinical symptoms, diagnostic procedures, and treatment strategies in patients with AF who developed PVS after RFCA. Results Among 205 patients with AF who underwent RFCA, five (2.44%) developed PVS (all men; age 44–64 years; AF history 12–60 months; 2 paroxysmal AF, 3 persistent AF). One patient underwent two RFCA sessions and the others received one. The time to PVS diagnosed by pulmonary vein computed tomography angiography (CTA) was 3 to 21 months. PVS symptoms included dyspnea and hemoptysis. Nine pulmonary veins developed PVS. Single mild PVS occurred in two asymptomatic patients and multiple PVS or single severe PVS in three symptomatic patients who underwent pulmonary vein angiography and stent placement. Symptoms in the three patients significantly improved after stent implantation; however, stent restenosis occurred 1 year later in one case. Conclusion PVS is a rare complication of RFCA for AF that can be diagnosed by CTA. Pulmonary vein stent implantation can remarkably improve the symptoms, but stent restenosis may occur.

P1426 Non-cardiac sourses of thromboembolic complications in atrial fibrillation

2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
O Germanova ◽  
A Germanov
Keyword(s):  
Atrial Fibrillation ◽  
Carotid Artery ◽  
Internal Carotid Artery ◽  
Kinetic Parameters ◽  
Arterial Wall ◽  
Internal Carotid ◽  
Arterial Blood Flow ◽  
Thromboembolic Complications ◽  
Arterial Blood ◽  
Permanent Form

Abstract Background Thromboischemic stroke is a significant medical problem. The most dangerous arrhythmia that causes the thromboembolism is atrial fibrillation. The source of thrombus mostly located in left atrium appendage or apex of left ventricle. But there’re a lot of cases of thromboischemic stroke in patients with atrial fibrillation without any intra-heart thrombus. Purpose To study the possibility of thromboembolic complications in patients with permanent form of atrial fibrillation without intra-heart thrombus. Materials and methods We included 48 patients with permanent form of atrial fibrillation. Mediana age - 68 ± 4,6 y.o. 32 (66,7%) were men and 16 (33,3%) women. All patients were performed 24-hours ECG monitoring to verify the atrial fibrillation. 34 (70,8%) were regularly took warfarin or NOACs to prevent the thromboembolic complications. We used CHADS-2 scale to make the prognosis of 1-year thromboembolic complications. 0 points - 0 (0%) patients, 1 point - 1 (2,1%), 2 points - 2 (4,2%), 3 points - 8 (16,6%), 4 points - 7 (14,5%), 5 points - 18 (37,5%), 6 points - 12 (25,1%). All patients were made transesophageal echocardiography. Only 3 (6,2%) of them had intra-heart thrombus. Intra-arterial blood flow we measured with Doppler-ultrasound. Most of patients – 39 (81,3%) had atherosclerotic plaques of internal carotid artery on one or both sides. In 22 (45,8%) patients were the signs of non-stability of plaques (heterogenic structure, rough surface). We valued the arterial wall kinetic parameters with sphygmography: speed, acceleration, power, work. We analyzed these parameters in different cardiocycles. Results We observed the following patterns: 1. If longer was the pause between cardiocycles in atrial fibrillation then more increase of biomechanical and kinetic parameters was observed. 2. The secondary hemodynamic arterial hypertension at the moments after long pause between cardiocycles. The longest duration of it was observed in bradysystolic atrial fibrillation (up to 38% of time). 3. In patients with hemodynamically important stenosis (about 70%) of internal carotid artery the speed after the long pause in atrial fibrillation is rising up to 4-4,5 meters per second. In comparison with sinus rhythm it is about 2,3 meters per second. Such rising of speed can cause the plaque integrity damage of parietal thrombus fragmentation. 4. Increased arterial wall deformation. The increased biomechanical parameters cause the appearance of additional waves, stand waves that may cause non-stability of plaques with further thromboembolism. 5. During the 1-year observation thromboembolic comlications appeared in 11 (22,9%) patients. Conclusion The source of thromboembolic complications can be non-cardiac in patients with multi-focus atherosclerosis and non-stable plaques.

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