Fig. 3.1
(a) The e-GFR in the last 10 years. The renal function is progressively deteriorating albeit the clinical symptoms of right sided heart failure were present only during the last couple of years. (b) The cours of gamma-GT in the last 10 years. It’s the most reliable parameter, like the e-GFR for the cardiorenal syndrome, for the cardio-hepatic syndrome as the right sided heart failure/chronic hepatic congestion over time progress. (c) The classical heart failure biomarker is less reliable in the setting of chronic right sided heart failure as a marker of the progression. The NT-proBNP is chronically 20–25 times the normal value (N < 14) elevated, but escalated very late in the disease course
In June 2016, she was admitted with severe heart failure and progression of her renal insufficiency. The electrocardiogram (see Fig. 3.2) of the severe TR patient at the latest follow-up, showing prominent right bundle branch block with right sided strain pattern, present from the very early in the course of the heart transplantation. She was treated with intravenous inotropic and diuretics and heart failure symptoms could be fairly compensated. However, this was at the expense of her renal function, with estimated e-GFR values of 20—30 mL/min, only with the support of continuous intravenous inotropics. On the other hand, without inotropic support, her renal functions deteriorated to e-GFR 15 mL/min and her symptoms escalated. After extensive discussion with the patient and family, we decided at last for tricuspid valve surgery. This was done in July 2016, with a valve replacement by a bioprothesis. The postoperative period was complicated by transient delirium and acute kidney failure, but she recovered very well. At 3-months follow-up, she was remained stable without signs of herat failure and her renal function was improved to serum creatinine of 125 mmol/L and a e-GFR of 39 mL/min.
Fig. 3.2
The electrocardiogram of the severe tricuspid regurgitation patient at the last follow-up, showing prominent right bundle branch block with right sided strain pattern, which was present from the very early in the course after the heart transplantation
Her preoperative (see Fig. 3.3a through c and Videos S1– S3) as well as postoperative (see Fig. 3.3d through f and Videos S4– S6) echocardiographic finding are shown.
Fig. 3.3
(a, b, and c, Movies S1, S2, and S3) Apical four chamber view demonstrating the severe dilated right ventricle and atrium with severe tricuspid regurgitation. The parasternal short-axis view shows enlarged right ventricle with diastolic collaps (“D-sign”) of the interventricular septum. (d, e and f, Movies S4, S5, and S6) Postoperative images, showing relatively reduced right ventricular size, with trace resting tricuspid regurgitation and disappearance of the “D-sign”
Epidemiology
TR prevalance is reported very variable, from 19 to 84% of all HTx recipients [1]. However, in our clinical cohort of 688 patients, severe TR was present in only 32 patients (4.7%), a marked difference, reflecting probably the variable definition used in the literature. In the report by Chan et al. presenting 336 patients, whom were transplanted between 1990 and 1995, they reported moderate TR in 27% and severe in 7%, comparable with our findings [2]. Berger et al. found significant TR in 14.1% of 163 HTx patients between 1988 and 2009, during a mean 8.2 years. Significant TR was correlated with the biatrial surgical technique (p < 0.01) and the presence of graft vasculopathy (p < 0.001) [3].
Pathophysiology
There are several mechanisms of post HTx TR. Functional TR is usually caused by annular dilation due to postoperative RV failure due to pre-transplant pulmonary hypertension, RV dysfunction after several rejections, or donor-recipient size-mismatch [4]. On the other hand, structural valve abnormalities caused by torn leaflets, ruptured chordae are due to several surveillance EMB’s in the first year. The risk of EMB related tricuspid valve damage are related to operator experience, patients clinical state, access site, biotome type [5]. Fiorelli et al. followed 417 HTx patients between 1985 and 2010, who underwent in total 3550 EMB (average 8.5/pt) after HTx. Traumatic tricuspid valve injury due to EMB rarely leaded to severe valvular regurgitation and only a minority of patients develop significant clinical symptoms [6]. On the other hand, Alharethi et al. found that flail leaflets were the most common operative finding, suggesting that biopsy-induced trauma is the likely cause of severe TI in these patients [7].
In the report by Tarek et al., orthotopic HTx was performed in 249 patients: 161 by the standard technique versus 88 by the bicaval technique . The incidence of both early and late TR was much lower with bicaval technique. Other variables influencing the prevalence of TR was: 2 or more rejections, total number of EMB’s and severe preoperative pulmonary hypertension [8]. Furthermore, the native and recipient RA diameters were found to be a risk factor for the development of TR. Wartig et al. also found that bicaval orthotopic heart transplantation was the only predictor lower risk of early significant TR (OR = 2.70; 95% CI = 1.68–4.32; p < 0.001).
Clinical Features
TR usually remains asymptomatic for years, despite progressive right atrial and ventricular dilatation and right-sided congestion. However, progressive atrial overload and dilatation results in the long-term atrial arrhythmias (atrial tachycardia’s and atrial fibrillation). The third phase begins when the heart failure symptoms and signs develop. In this phase, physical examination reveals often markedly pulsating and distended jugular veins, progressive hepatomegaly, pulsating liver (“the liver pulse”), liver enzyme abnormalities, liver fibroses and ultimately cardiac cirrhosis. The classical heart failure biomarker is less reliable in the setting of chronic right sided heart failure as a marker of the progression. As shown in Fig. 3.1, the NT-proBNP is chronically 20–25 times the normal value (N < 14) elevated, but escalated very late in the disease course.
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