scholarly journals A Rare Giant Pulmonary Aneurysm with Left Lung Compression: A Case Report with Insights from the Literature

2019 ◽  
Vol 22 (3) ◽  
pp. E197-E201 ◽  
Author(s):  
Fan He ◽  
Huaidong Chen ◽  
Ximing Qian

Pulmonary artery aneurysm (PAA) is a rare condition that results from several pathologies. Here, we report a case of a rare giant PAA accompanied by left lung compression due to recurrent chest tightness for >13 years. Through this case and review of the literature, we explore the treatment options to improve the diagnosis and treatment of PAA. We found that patients with PAA may survive longer even if they also have pulmonary hypertension. In addition, it is recommended that if a PAA diameter is >5.5 cm or if the PAA diameter has increased by >0.5 cm in 6 months, the PAA should be operated on as soon as possible. Conservative treatment can be recommended in patients with congenital PAA if pulmonary arterial pressure is normal.

2020 ◽  
Vol 54 (7) ◽  
pp. 650-655
Author(s):  
Ali Ahmet Arıkan ◽  
Fatih Avni Bayraktar ◽  
Emre Selçuk

Atherosclerotic true aneurysms of the superficial femoral artery (SFA) and profunda femoris artery (PFA) are rare and difficult to detect. The synchronous presence of SFA and PFA aneurysms is even rarer. Herein, we present a case with ipsilateral true SFA and PFA aneurysms diagnosed with rupture. A review of the international literature is made, and the diagnosis and treatment options of this rare condition are discussed. A 75-year-old male was admitted to our hospital with an aneurysm on the distal SFA and the ipsilateral PFA, as well as a hematoma around the PFA. It was difficult to determine the source of the rupture before surgery, even with proper imaging. Successful ligation of the PFA and an aneurysmectomy followed by a bypass grafting for the SFA were performed. An intraoperative examination revealed that the SFA aneurysm had ruptured. In elderly males with a history of ectasia or aneurysm on the aorta or peripheral arteries, a synchronous aneurysm on the SFA or the PFA should be suspected.


2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Ekaterina Borodulina ◽  
Alexander M Shutov

Abstract Background and Aims An important predictor of cardiovascular mortality and morbidity in hemodialysis patients is left ventricular hypertrophy. Also, pulmonary hypertension is a risk factor for mortality and cardiovascular events in hemodialysis patients. The aim of this study was to investigate cardiac remodeling and the dynamics of pulmonary arterial pressure during a year-long hemodialysis treatment and to evaluate relationship between pulmonary arterial pressure and blood flow in arteriovenous fistula. Method Hemodialysis patients (n=88; 42 males, 46 females, mean age was 51.7±13.0 years) were studied. Echocardiography and Doppler echocardiography were performed in the beginning of hemodialysis treatment and after a year. Echocardiographic evaluation was carried out on the day after dialysis. Left ventricular mass index (LVMI) was calculated. Left ventricular ejection fraction (LVEF) was measured by the echocardiographic Simpson method. Arteriovenous fistula flow was determined by Doppler echocardiography. Pulmonary hypertension was diagnosed according to criteria of Guidelines for the diagnosis and treatment of pulmonary hypertension of the European Society of Cardiology. Results Pulmonary hypertension was diagnosed in 47 (53.4%) patients. Left ventricular hypertrophy was revealed in 71 (80.7%) patients. Only 2 (2.3%) patients had LVEF<50%. At the beginning of hemodialysis correlation was detected between systolic pulmonary arterial pressure and LVMI (r=0.52; P<0.001). Systolic pulmonary arterial pressure negatively correlated with left ventricular ejection fraction (r=-0.20; P=0.04). After a year of hemodialysis treatment LVMI decreased from 140.49±42.95 to 123.25±39.27 g/m2 (р=0.006) mainly due to a decrease in left ventricular end-diastolic dimension (from 50.23±6.48 to 45.13±5.24 mm, p=0.04) and systolic pulmonary arterial pressure decreased from 44.83±14.53 to 39.14±10.29 mmHg (р=0.002). Correlation wasn’t found between systolic pulmonary arterial pressure and arteriovenous fistula flow (r=0.17; p=0.4). Conclusion Pulmonary hypertension was diagnosed in half of patients at the beginning of hemodialysis treatment. Pulmonary hypertension in hemodialysis patients was associated with left ventricular hypertrophy, systolic left ventricular dysfunction. After a year-long hemodialysis treatment, a regress in left ventricular hypertrophy and a partial decrease in pulmonary arterial pressure were observed. There wasn’t correlation between arteriovenous fistula flow and systolic pulmonary arterial pressure.


1994 ◽  
Vol 76 (1) ◽  
pp. 370-379 ◽  
Author(s):  
O. Saito ◽  
W. J. Lamm ◽  
J. Hildebrandt ◽  
R. K. Albert

We compared the effects of pulsatile vs. nonpulsatile flow (Q) on pulmonary arterial pressure (Ppa)-Q relationships in zone 3 over wide ranges of pulse rate, stroke volume (SV), and Q. Excised left lungs of rabbits (n = 15) were perfused with tris(hydroxymethyl)aminomethane-buffered Tyrode solution containing 4% dextran, 1% albumin, and 10 mg/l of indomethacin and were ventilated with room air. Pulsatile Q was generated by a diaphragm pump delivering SV of 0.5, 1, or 2 ml (representing approximately 0.3, 0.6, and 1.2 times, respectively, the normal resting SV for rabbit left lung) and adjusting the pump frequency. Nonpulsatile Q was generated by raising an arterial reservoir to the required height. Mean pulmonary arterial (Ppa) and left atrial pressures were measured at end exhalation (positive end-expiratory pressure = 2.5 cmH2O) near the tips of the perfusion cannulas and were referenced to the lung base. Left atrial pressure was held constant at 7 cmH2O.Q was alternated between pulsatile and nonpulsatile, increasing Q stepwise from 100 to 600 ml/min (Q from approximately 0.3 to 2 times the normal resting Q for rabbit left lung), after which Q was reduced stepwise back to initial values. For the smallest SV there were no differences between Ppa-Q curves under pulsatile and nonpulsatile conditions. At the largest SV, Ppa was greater during pulsatile than nonpulsatile Q at Q > 100 ml/min. The slopes of the Ppa-Q curves were greater during pulsatile Q at the two larger SV values. These results can be explained by increasing Q turbulence and less ideal velocity profiles at higher peak Q resulting from the effects of rapidly changing inertial forces.


2021 ◽  
Vol 118 (17) ◽  
pp. e2023130118
Author(s):  
Zdravka Daneva ◽  
Corina Marziano ◽  
Matteo Ottolini ◽  
Yen-Lin Chen ◽  
Thomas M. Baker ◽  
...  

Recent studies have focused on the contribution of capillary endothelial TRPV4 channels to pulmonary pathologies, including lung edema and lung injury. However, in pulmonary hypertension (PH), small pulmonary arteries are the focus of the pathology, and endothelial TRPV4 channels in this crucial anatomy remain unexplored in PH. Here, we provide evidence that TRPV4 channels in endothelial cell caveolae maintain a low pulmonary arterial pressure under normal conditions. Moreover, the activity of caveolar TRPV4 channels is impaired in pulmonary arteries from mouse models of PH and PH patients. In PH, up-regulation of iNOS and NOX1 enzymes at endothelial cell caveolae results in the formation of the oxidant molecule peroxynitrite. Peroxynitrite, in turn, targets the structural protein caveolin-1 to reduce the activity of TRPV4 channels. These results suggest that endothelial caveolin-1–TRPV4 channel signaling lowers pulmonary arterial pressure, and impairment of endothelial caveolin-1–TRPV4 channel signaling contributes to elevated pulmonary arterial pressure in PH. Thus, inhibiting NOX1 or iNOS activity, or lowering endothelial peroxynitrite levels, may represent strategies for restoring vasodilation and pulmonary arterial pressure in PH.


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