Discussion
Tuberculosis is the most common cause of constrictive pericarditis,
accounting for 38% to 83% of cases in endemic countries [7].
Transient constrictive pericarditis occurs in 10% of
tuberculosis-related pericarditis, while progression to chronic
constrictive pericarditis occurs in 20% to 50% of patients despite
antituberculosis treatment [7]. Furthermore, chronic constrictive
pericarditis can persist for several years, leading to heart failure
[7]. Although the right and left ventricular diastolic pressures are
equalized in this disease, symptoms of RV dysfunction are dominant.
Tuberculous constrictive pericarditis typically presents with dense
fibrosis that progressively impaired diastolic filling of the heart.
Therefore, pericardiectomy in combination with anti-tuberculosis drugs
is the recommended treatment for tuberculous constrictive pericarditis
and persistent symptoms.
The main advantages of pericardiectomy are (1) improvement of symptoms,
(2) better chance of a complete cure than with medication, and (3) keep
constriction from getting worse and damaging heart muscle. On the other
hand, bleeding complications, atrial arrhythmias, kidney failure, RV
dysfunction, and death are potential postoperative complications.
Pericardiectomy can lead to increased left ventricular end-diastolic
volume and improved Frank-Starling reserve, providing an increase in
exercise stroke volume, cardiac output, and aerobic capacity [8].
Bozbuga et al. showed an improvement in the functional status in 88% of
patients undergoing pericardiectomy after a 1-year follow-up [9]. A
meta-analysis that investigated the effects of pericardiectomy in
patients with constrictive tuberculous pericarditis showed that patients
had a significant improvement in the New York Heart Association (NYHA)
grade one year following pericardiectomy (HR 8.04, 95% CI [5.20 to
12.45], I2= 0%) [10].
The mortality rate in patients with chronic constrictive pericarditis
undergoing pericardiectomy varies between 4 and 8% [11,12].
However, it is important to note that the mortality associated with
pericardiectomy has markedly decreased over the past decades [13].
RV dysfunction is one of the
main postoperative complications after pericardiectomy [8,14].
However, this problem commonly occurs during the early postoperative
phase. Azzu A et al. showed that approximately 80% of patients have
evidence of RV dysfunction early post-pericardiectomy [15]. The main
pathophysiological mechanisms possibly involved in RV dysfunction after
pericardiectomy are myocardial atrophy secondary to prolonged
constriction as well as a rapid increase in venous return to the right
heart after pericardial decompression [16]. This external
constriction leads, over time, to a reduction in myocardial mass due to
low diastolic volumes. For this reason, when the ventricle is exposed to
a greater volume postoperatively, ventricular dilation occurs and
cardiac output decreases. Thus, it is important to choose the ideal
period for pericardiectomy, given that if the surgical option is
postponed for a long time, the greater the risk of irreversible
ventricular remodeling and the greater the probability of low output
syndrome [17]. Another post-pericardiectomy complication is
tricuspid insufficiency, which occurs due to sudden right ventricular
dilation.
Although cardiopulmonary bypass is associated with higher rates of
postoperative complications, in our case it was necessary in order to
facilitate a complete pericardiectomy. Studies have demonstrated the
benefit of complete pericardiectomy in terms of long-term survival and
symptom improvement [18,19].
The prognosis after surgery depends on age, the degree of myocardial
involvement, the severity of liver dysfunction caused by the
constriction, the preoperative NYHA functional class, the presence of
extensive pericardial calcifications, which condition the incomplete
removal of the pericardium, or of pericarditis caused by exposure to
radiation [20].
We report a peculiar case of a patient with constrictive tuberculous
pericarditis who presented RV dysfunction two weeks after
pericardiectomy. RV dysfunction occurred in the late
post-pericardiectomy, although it is more common early
post-pericardiectomy. Rapid and accurate identification of RV
dysfunction confirmed by TTE associated with the rapid initiation of
diuretics and inotropic therapy, in addition to drainage of the pleural
effusion complicated by empyema and administration of appropriate
antibiotics, allowed the prompt and complete recovery of the patient.
Our case demonstrates the importance of special attention for RV
dysfunction in patients with constrictive pericarditis undergoing
pericardiectomy.