A Healthy Young Lady with ‘Unprovoked’ Persistent Bilateral Pulmonary Embolism - Why?

Muhammad Farid Bin Mohd Fauad ◽  
Hazlyna Baharuddin ◽  
Mohd Arif Mohd Zim ◽  
Bushra Johari

Pulmonary embolism (PE) was reported in about 9% patients with antiphospholipid syndrome (APS). Seronegative APS is an entity which demonstrates clinical manifestations highly suggestive of APS but persistently negative APS antibodies. A 31-year-old lady presented with a two-month history of exertional dyspnoea. She had two consecutive miscarriages at 12 and 14 weeks, previously. Physical examination revealed a thin lady who was tachycardic, tachypneic, hypoxic but normotensive. There was a loud P2 without signs of heart failure. Investigations revealed a type 1 respiratory failure, sinus tachycardia with right ventricular strain pattern, cardiomegaly with normal lung fields, and dilated right atrium and right ventricle with increased in pulmonary arterial pressure of 70mmHg from echocardiography. CT pulmonary angiography (CTPA) confirmed the presence of PE over bilateral pulmonary arteries. She continued to have exertional dyspnoea and was readmitted 9 months later with worsening dyspnoea. APS antibodies performed during both admissions were negative. Seronegative APS was diagnosed. Interestingly, two CTPAs performed at 6 months and 9 months after initial presentation revealed persistent bilateral pulmonary embolism. The provoking factors for PE should be sought because ‘unprovoked’ PE especially in young individuals need further attention. APS, including seronegative APS, should be considered. Persistence of symptoms of PE also warrants further attention as chronic thromboembolic pulmonary hypertension (CTEPH) may be the cause. Currently, there are available medical and surgical treatment of CTEPH, therefore establishing its diagnosis is important and it is best performed in pulmonary hypertension expert centre.International Journal of Human and Health Sciences Supplementary Issue-2: 2021 Page: S25

1963 ◽  
Vol 18 (3) ◽  
pp. 544-552 ◽  
D. F. J. Halmagyi ◽  
B. Starzecki ◽  
G. J. Horner

The cardiopulmonary consequences of coli-lipopolysaccharide and staphylococcus toxin administration were studied in sheep. Circulatory changes consisted mainly of a marked rise in pulmonary arterial and pulmonary arterial wedge pressure (with left atrial pressure unchanged), and a fall in cardiac output and in systemic arterial pressure. Fall in the latter closely followed the onset of pulmonary hypertension. The respiratory response consisted mainly of a severe fall in lung compliance produced by terminal airway closure. Continued perfusion of the nonventilated alveoli resulted in venous admixture. Premedication with antihistaminic, antiserotonin, or adrenolytic agents failed to affect the response. Norepinephrine or hypertensin administered after toxin injection had virtually no effect while isoproterenol treatment reduced pulmonary arterial pressure, increased cardiac output, arterial oxygen saturation, and, in cases of endotoxin shock, promptly raised systemic arterial pressure. Endotoxin-resistant sheep proved nonresponsive to minor pulmonary embolism and to incompatible blood transfusion. It is suggested that a common mediator agent is responsible for the similar cardiopulmonary consequences of these three diverse conditions. Submitted on November 26, 1962

1998 ◽  
Vol 84 (3) ◽  
pp. 815-821 ◽  
Marco Maggiorini ◽  
Serge Brimioulle ◽  
Didier De Canniere ◽  
Marion Delcroix ◽  
Robert Naeije

Pigs have been reported to present with a stronger pulmonary vascular reactivity than many other species, including dogs. We investigated the pulmonary vascular impedance response to autologous blood clot embolic pulmonary hypertension in anesthetized and ventilated minipigs ( n = 6) and dogs ( n = 6). Before embolization, minipigs, compared with dogs, presented with higher mean pulmonary arterial pressure (Ppa; by an average of 9 mmHg), a steeper slope of Ppa-flow (Q˙) relationships, and higher 0-Hz impedance (Z0) and first-harmonic impedance (Z1), without significant differences in characteristic impedance (Zc), and a lower ratio of pulsatile hydraulic power to total hydraulic power. Embolic pulmonary hypertension (mean Ppa: 40–55 mmHg) was associated with increased Z0 and Z1 in both species, but the minipigs had a steeper slope of Ppa/Q˙ plots and an increased Zc. At identical Q˙ and Ppa, minipigs still presented with higher Z1 and Zc and a lower ratio of pulsatile hydraulic power to total hydraulic power. The energy transmission ratio, defined as the hydraulic power in the measured waves divided by the hydraulic power in the forward waves, was better preserved after embolism in minipigs. No differences in wave reflection indexes were found before and after embolism. We conclude that minipigs, compared with dogs, present with a higher pulmonary vascular resistance and reactivity and adapt to embolic pulmonary hypertension by an increased Zc without earlier wave reflection. These differences allow for a reduced pulsatile component of hydraulic power and, therefore, a better energy transfer from the right ventricle to the pulmonary circulation.

1995 ◽  
Vol 268 (2) ◽  
pp. H817-H827 ◽  
C. Melot ◽  
M. Delcroix ◽  
J. Closset ◽  
P. Vanderhoeft ◽  
P. Lejeune ◽  

We investigated whether the Starling resistor model (Mitzner et al. J. Appl. Physiol. 51: 1065–1071, 1981) or a distensible vessel model (Haworth et al. J. Appl. Physiol. 70: 15–26, 1991) best describes pulmonary vascular pressure-flow (Q) relationships in embolic pulmonary hypertension. Mean pulmonary arterial pressure (Ppa)-Q plots at constant left atrial pressure (Pla) and Ppa-Pla plots at constant Q were investigated in seven dogs before and after 500-micron glass bead pulmonary embolism. Embolization to a mean angiographic obstruction of 78% increased the slope and extrapolated pressure intercept (P(i)) of Ppa-Q plots and increased the inflection point of Ppa-Pla plots, above which an increase in Pla is transmitted to Ppa in a ratio of approximately 1:1. The Starling resistor and the distensible vessel model provided a reasonably good fit to the Ppa-Q and Ppa-Pla coordinates before and after embolism. However, contrary to the prediction of the Starling resistor model, no correlation was found between the inflection point of Ppa-Pla plots and P(i). We therefore conclude that an increased closing pressure is unlikely to contribute to embolic pulmonary hypertension.

The main indications for pulmonary artery imaging are acute pulmonary thromboembolic disease and assessment of chronic pulmonary artery hypertension. Other indications, such as investigation of haemoptysis and pulmonary arterial vascular malformations are not addressed in this chapter. Although recurrent acute thromboembolic disease may eventually lead to pulmonary hypertension, the two are essentially separate patient groups for the purpose of CT scanning. This chapter covers CT pulmonary angiography, peripheral venous imaging, and chronic pulmonary hypertension.

2021 ◽  
Vol 14 (6) ◽  
pp. e243083
Joshua Chang ◽  
Dayna J Isaacs ◽  
Joseph Leung ◽  
David R Vinson

A healthy, active woman in her 70s reported intermittent exertional dyspnoea for 2 months, notable during frequent open-water swimming. Symptoms were similar to an episode of travel-provoked pulmonary embolism 3 years prior. She denied chest pain, cough, fever, extremity complaints and symptoms at rest. Due to the COVID-19 pandemic, her healthcare system was using secure telemedicine to evaluate non-critical complaints. During the initial video visit, she appeared well, conversing normally without laboured breathing. An elevated serum D-dimer prompted CT pulmonary angiography, which identified acute lobar pulmonary embolism. After haematology consultation and telephone conversation with the patient, her physician prescribed rivaroxaban. Her symptoms rapidly improved. She had an uneventful course and is continuing anticoagulation indefinitely. The pandemic has increased the application of telemedicine for acute care complaints. This case illustrates its safe and effective use for comprehensive management of acute pulmonary embolism in the primary care setting.

2001 ◽  
Vol 86 (07) ◽  
pp. 444-451 ◽  
Samuel Goldhaber

SummarySuccessfully utilized contemporary pulmonary embolism thrombolysis reverses right heart failure rapidly and safely. This therapeutic approach may lower mortality from pulmonary embolism and reduce morbidity from chronic pulmonary hypertension. Pulmonary embolism thrombolysis remains a debatable indication because large clinical trials using survival as an endpoint have not been carried out. Instead, thrombolysis trials have been undertaken with surrogate endpoints such as reduction in clot burden, reduction in pulmonary arterial pressure, and improvement in right ventricular function. In an era where hundreds of thousands of myocardial infarction patients have participated in thrombolysis trials that focus on survival as the principal endpoint, the much smaller trials of PE thrombolysis have not been sufficiently definitive to achieve a consensus. Pharmaceutical companies have not considered this area of investigation to be a good return on investment, because PE is a much less common problem than acute coronary syndromes. No government funding agency has targeted PE thrombolysis as a priority for clinical research.Currently, the only contemporary thrombolytic regimen for pulmonary embolism that is approved by the Food and Drug Administration is tissue plasminogen activator, in a dose of 100 mg/2 h. New thrombolytic agents under development for pulmonary embolism include reteplase, saruplase, and recombinant staphylokinase. Future clinical trials will require multicenter collaboration and focus on clinically relevant endpoints such as reduction of mortality and recurrent venous thromboembolism.

2012 ◽  
Vol 23 (5) ◽  
pp. 692-696 ◽  
Gregory J. Skinner ◽  
Robert M. Tulloh ◽  
Andrew J. Tometzki ◽  
Ingram Schulze-Neick ◽  
Gareth J. Morgan

AbstractThe presence of an atrial septal defect in pulmonary hypertension has benefits and detractions. Even in idiopathic pulmonary arterial hypertension, a significant left-to-right shunt at atrial level may increase the pulmonary arterial pressure and exacerbate the disease. However, it is well recognised that the presence of an atrial communication may be protective in subgroups with severe disease, allowing maintenance of cardiac output during times of increased pulmonary resistance. In the present paper, we present the case of a young boy with significant idiopathic pulmonary arterial hypertension and an atrial septal defect. We report our technique of septal occlusion using a device to decrease left-to-right shunting with concomitant stent insertion in that device to maintain the potential for right-to-left shunting during times of high pulmonary arterial pressure.

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