Infective endocarditis in French Polynesia: Epidemiology, treatments and outcomes.

BACKGROUND: French Polynesia is a French overseas collectivity in the South Pacific Ocean, where data on infective endocarditis (IE) are lacking. AIMS: To investigate the epidemiology and outcomes of IE in French Polynesia. METHODS: All hospital records from consecutive patients hospitalized in Taaone Hospital, Tahiti, from 2015 to 2018, with an International Classification of Diseases, 10th revision, separation diagnosis of IE (I330), were reviewed retrospectively. RESULTS: From 190 hospital charts reviewed, 105 patients with a final diagnosis of IE, confirmed according to the modified Duke criteria, were included. The median duration of follow-up was 71 days (interquartile range 18-163 days). The mean age was 55±17 years, and there were 68 men (65%). Thirty-five patients (33%) had a history of rheumatic carditis and 43 (41%) had a prosthetic valve. There were 40 (38%) cases of staphylococcal IE, 32 (30%) of streptococcal IE and six (6%) of enterococcal IE. Cardiogenic shock, septic shock and clinically relevant cerebral complications were strongly associated with death from any cause (hazard ratio [HR] 16.85, 95% confidence interval [CI] 5.45-52.05 [P<0.001]; HR 2.62, 95% CI 1.23-5.56 [P=0.01]; and HR 4.14, 95% CI 1.92-8.92 [P<0.001], respectively). Seventy-three patients (69%) had a theoretical indication for surgery, which was performed in 38 patients (36%). Lack of surgery when there was a theoretical indication was significantly associated with death (HR 6.93, 95% CI 3.47-13.83; P<0.0001). CONCLUSIONS: The pattern of IE in French Polynesia differs from Western countries in many ways. Postrheumatic valvular disease remains the main underlying disease, and access to emergency heart surgery is still a challenge.

Rheumatic fever with severe carditis: still prevalent in the South West Pacific.

Rheumatic heart disease (RHD) has a worldwide prevalence of 33 million cases and 270 000 deaths annually, making it the most common acquired heart disease in the world. There is a disparate global burden in developing countries. This case report aims to address the minimal RHD coverage by the international medical community. A Tahitian boy aged 10 years was diagnosed with advanced heart failure secondary to RHD at a local clinic. Previous, subtle symptoms of changes in handwriting and months of fever had gone unrecognised. Following a rapid referral to the nearest tertiary centre in New Zealand, urgent cardiac surgery took place. He returned home facing lifelong anticoagulation. This case highlights the RHD burden in Oceania, the limited access to paediatric cardiac services in countries where the RHD burden is greatest and the need for improved awareness of RHD by healthcare professionals, and the general public, in endemic areas.

Redo aortic root surgery for failure of an aortic homograft is a major technical challenge.

OBJECTIVE: Aortic homografts offer many advantages over prosthetic valves. However, homograft dysfunction due to degeneration or infection may lead to reoperation. Aortic valve replacement in patients who have undergone previous aortic root replacement with an aortic homograft remains a technical challenge. To assess reoperation events a retrospective review was conducted. MATERIALS AND METHODS: From January 2000 to October 2006, 20 consecutive patients (38.8+/-14.9 years old) underwent repeat surgery for aortic homograft failure. RESULTS: Reoperation was performed 7.2+/-3.5 years after implantation of the aortic homograft as a root. Indication was homograft degeneration (n=18 [90%]) and endocarditis (n=2 [10%]). In patients with major homograft wall calcifications or endocarditis, nine aortic root reconstructions were performed (Bentall procedure n=7; homograft implantation n=2). Each homograft was dissected with electrical cauterization and removed 'en-bloc' sparing the coronary buttons. In case of flexible homograft wall, stented prostheses (mechanical n=10, bioprosthesis n=1) were implanted along the homograft annulus. Additional procedures consisted of mitral valve replacements (n=8), tricuspid repairs (n=4), Konno procedure (n=1) and coronary bypass (n=5). Perioperative complications occurred in seven (35%) patients: sternal re-entry accident (n=2); reoperations for mediastinitis (n=1) or bleeding (n=2); renal insufficiency (n=1); total heart block (n=1). No association was found between operative procedures and postoperative complications (Fisher's exact test). Two patients (10%) died from multiorgan failure in the early postoperative period. In total, 94.4% of the survivors remained free from reoperation at 74 months. CONCLUSION: Reoperation on patients with an aortic homograft as a root presents a relatively high perioperative morbidity. The surgical strategy depends on the degree of homograft wall calcification.

Acute severe mitral regurgitation during first attacks of rheumatic fever: clinical spectrum, mechanisms and prognostic factors.

BACKGROUND AND AIM OF THE STUDY: The study aim was to describe the clinical spectrum and mechanism of acute severe mitral regurgitation (MR) observed during first episodes of rheumatic fever (RF), and to identify prognostic factors related to the short-term outcome. METHODS: Since 1990, 44 patients (mean age 9.2 +/- 0.1 years; range: 4-17 years) have been admitted to the authors' institution with severe MR related to a first episode of RF, fulfilling revised Jones' criteria. Twenty-three patients admitted between 1995 and 2002 were included prospectively, and 21 admitted before 1994 were studied retrospectively. RESULTS: Left ventricular end-diastolic and end-systolic dimensions were 51 +/- 2 mm (46 +/- 3 mm/m2 BSA) and 32 +/- 2 mm (28 +/- 2 mm/m2 BSA), respectively; mean fractional shortening of the left ventricle was 39.0 +/- 1.0% (range: 31-52%); Doppler-derived pulmonary arterial systolic pressure (PAPS) was 51 +/- 6 mm (range: 27-90 mm). The mitral valve annulus was enlarged in all patients (mean diameter 31 +/- 2 mm; 27 +/- 4 mm/m2 BSA). MR resulted from prolapse of the anterior mitral valve leaflet (P of AMVL) in 16 patients (36%), and from prolapse of the posterior mitral valve leaflet (P of PMVL) in nine (20%); the other 19 patients (43%) had restrictive motion of the PMVL, with normal motion of the AMVL, resulting in a 'false prolapse' of the AMVL (FP of AMVL). During the six-month interval following the RF episode, mitral valve surgery was required in 11 patients (25%); three patients (7%) died from cardiogenic shock before they could undergo surgery, while the other 30 patients were stabilized under medical treatment. Using univariate analysis, death or mitral valve surgery was associated with PAPS > 50 mm (OR = 1.7, p = 0.04), male gender (OR = 1.88, p = 0.008), clinical signs of congestive heart failure at admission (OR = 2.7, p < 10(-4)), and prolapse of the PMVL (OR = 5.2, p = 0.01). Death occurred, or mitral valve surgery was necessary, in eight patients with P of PMVL (89%), in four with P of AMVL (25%), and in two with FP of AMVL (11%) (p < 0.001). Despite limitations due to co-linearities and small sample size, multivariate analysis identified P of PMVL as the most potent predictor of adverse outcome. The long-term follow up (mean 6.3 years) of patients without P of PMVL, alive and not operated on during the first six-month interval after an RF episode, demonstrated a sharp decrease in the mean severity of MR (from grade 4 to 1.7; range: 1-3). CONCLUSION: In contrast to previous reports of chronic rheumatic MR, acute severe MR due to RF is more frequently related to P of AMVL or P of PMVL, than to FP of AMVL. Patients with P of AMVL or FP of AMVL tend to improve with medical treatment; however, those with P of PMVL carry a poor medical prognosis, and most often require early mitral valve surgery.

Does rheumatic myocarditis really exists? Systematic study with echocardiography and cardiac troponin I blood levels.

AIMS: Revised guidelines for diagnosis of rheumatic fever indicate that rheumatic myocarditis may 'contribute' to the genesis of congestive heart failure. Our objective was to assess non-invasively the presence of non-clinical markers of myocardial involvement in acute rheumatic fever. METHODS: Echocardiography and assessment of cardiac troponin I (cTnI) blood levels were systematically performed in 95 consecutive patients with acute rheumatic fever, who were divided into three groups. Group 1: patients without carditis (n=22); group 2: patients with carditis and without congestive heart failure (n=59); group 3: patients with carditis and congestive heart failure (n=14). RESULTS: Left ventricular ejection fraction was normal in all patients and did not differ between groups (group 1: 0.72+/-0.08, group 2: 0.69+/-0.06, and group 3: 0.66+/-0.07, p=0.09). Left ventricular diameters tend to be larger in group 3, but all patients had severe mitral and/or aortic regurgitation. Mean cTnI was 0.077+/-0.017 ng/ml (normal <0.1 ng/ml), did not differ between groups (p=0.45), and only 13 patients (seven with pericardial effusion) had detectable levels (0.2-0.4 ng/ml). CONCLUSIONS: Our study neither detected cTnI elevations nor echocardiographic abnormalities suggesting significant myocardial involvement during rheumatic fever. Congestive heart failure was always associated to severe valve regurgitation.