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.