Cardiovascular Journal of Africa: Vol 30 No 1 (January/February 2019)

CARDIOVASCULAR JOURNAL OF AFRICA • Volume 30, No 1, January/February 2019

AFRICA

heparin was initiated at full dose within six hours of the end of

the operation and continued up to the postoperative third day.

When thepatientwas extubatedon the first daypostoperatively,

oral sildenafil and warfarin were started. A 3-l/min nasal oxygen

tube was applied after the extubation. She was transferred to

a general ward from the intensive care unit on the third day

postoperatively.

Postoperative echocardiography, V/Q scan and computerised

tomographic angiography (CTA) showed marked improvement

in our patient. There were no perfusion defects in the lungs on

the V/Q scan after the operation (Fig. 3). She was discharged

uneventfully on the postoperative 10th day.

The patient was controlled at three, six, 12 and 24 months

after the operation. She was evaluated according to NYHA

functional class on echocardiography. She was in NYHA class

I at the second-year check-up after the operation. The systolic

PAP was 25 mmHg in the first year postoperatively. We designed

the prothrombin time/international normalised ratio to range

from two to three to control the warfarin effect postoperatively.

Discussion

PTE is normally eliminated by active fibrinolytic systems.

Complete dissolution of a thromboembolism has been shown

in four to eight days after a thromboembolic event in one study

using pulmonary scanning. This study showed 0.5 to 4% of

patients developed CTEPH, while 22% of patients continued to

have signs of the disease.

PEA is potentially the most successful

procedure for patients with CTEPH. These procedures are

currently performed with low mortality rates in clinics with

experienced surgeons.

5,6

If chronic thromboembolic disease leads to CTEPH, it

aggravates and leads to right ventricular failure due to a decline

in vascular compliance across the pulmonary arterial circulation

and increased vascular resistance.

Thromboembolic disease

also leads to redistribution of blood flow within the pulmonary

vasculature, resulting in the development of overflow and

post-obstructive vasculopathy in the small pulmonary vessels,

similar to that seen in pulmonary arterial hypertension.

The

progressive increase in pulmonary vascular resistance affects the

clinical course of CTEPH. If CTEPH is left untreated, it could

result in progressive pulmonary hypertension, right ventricular

dysfunction and death.

Protein S acts as a co-factor to activated protein C to form

the protein C–protein S complex. Thrombin generation via the

inhibition of factor Va and factor VIIIa by binding to Ca

and

phospholipids is prevented by the protein C–protein S complex.

Our patient had protein C and protein S deficiencies. A

mortality rate of 5 to 9% seemed to be an acceptable risk for

surgical treatment of her disease.

Surgical treatment was planned

for our patient because of a poor prognosis on medical treatment.

Control and prevention of recurrent PTE is very important.

Pre-operative implantation of an inferior vena cava filter and

lifelong administration of warfarin is important to prevent

recurrent attacks. In our patient, we did not use an inferior vena

cava filter because she did not have acute or sub-acute DVT.

Conclusion

Patients diagnosed with CTEPH should have the diagnosis

confirmed and the best therapeutic option determined according

to the haemodynamic and morphological data provided by an

invasive pulmonary angiogram and/or CTA. PEA for patients

with CTEPH may be associated with acceptable peri-operative

morbidity and mortality rates, and improved haemodynamic

indices and survival rate.

This article was presented at the 16th National Congress of Vascular and

Endovascular Surgery on 26–29 October 2013 in Istanbul, Turkey.

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