Infective Endocarditis Involving the Pulmonary Valve




Pulmonary valve (PV) infective endocarditis (IE) is a rare entity, accounting for 1.5% to 2% of cases of IE. Published data are limited to a few case series and reports. We sought to review the Mayo Clinic experience and describe clinical, echocardiographic, and microbiologic features. We included all patients aged ≥18 years seen from 2000 to 2014 who had a diagnosis of native PV IE and unequivocal echocardiographic involvement of the PV. Nine patients with PV IE were identified. Isolated PV IE was present in 7 (78%) of 9 cases. The median age was 59 years and 22% were women. Three patients had congenital heart disease, 2 had central venous catheters, and 3 had cardiovascular implantable electronic devices. Five patients (56%) received chronic immunosuppressive therapy. Enterococcus faecalis and viridans group streptococci were the most common pathogens, isolated in 22% of cases each. Transthoracic echocardiogram (TTE) and transesophageal echocardiogram (TEE) were done in 6 and 7 patients, respectively. Four patients underwent both procedures. TTE was diagnostic in all cases, but TEE failed to detect PV involvement in 1 patient. Median follow-up was 1.8 years. Five patients (56%) underwent PV replacement. There were no operative deaths. One patient had sudden death during follow-up, unrelated to his PV IE episode. Our results suggest that PV IE is rare but carries significant morbidity. TTE and TEE provide complementary information with TEE providing better visualization of other cardiac structures. Our findings of a high prevalence of immunosuppressive therapy and cardiovascular implantable electronic devices have not been previously reported and deserve further investigation.


Pulmonary valve (PV) infective endocarditis (IE) is a rare entity, accounting for 1.5% to 2% of IE cases. Published literature describing characteristics of patients with PV IE is limited to a few case series and case reports, some published >25 years ago. Reported risk factors include male gender, intravenous drug abuse, central venous catheters, alcoholism, and congenital heart disease (CHD). There is also scarce evidence regarding the yield of transthoracic echocardiogram (TTE) and transesophageal echocardiogram (TEE). We sought to review the Mayo Clinic experience of native PV IE and describe clinical, microbiologic, and echocardiographic features.


Methods


The present study included all patients ≥18 years seen at Mayo Clinic, Rochester, Minnesota, from 2000 to 2014 with a definite diagnosis (by modified Duke criteria ) of IE and unequivocal echocardiographic involvement of the native PV. This study was approved by the Institutional Review Board; only patients who provided research authorization were included.


Mayo Clinic provides primary care to patients from Olmsted County, Minnesota, and also serves as a tertiary referral center for national and international patients. Cases were identified using a free-text search tool of the electronic medical record. The following terms were used individually and in combination: “pulmonary valve,” “pulmonic valve,” and “endocarditis.” Baseline demographic, clinical, and microbiologic data and follow-up information were obtained from the medical records. TTE and TEE images were systemically reviewed by 2 coauthors (W.R.M. and H.M.C.) with special attention to the morphology of the PV, degree of valvular dysfunction, and associated lesions. When >1 echocardiographic study was available, the one closest in time to the diagnosis of IE was selected. Pulmonary regurgitation (PR) severity was graded (trivial, mild, moderate, or severe) according to color and spectral Doppler signals and standard techniques.


Categorical variables are described as counts (%), and continuous variables are presented as medians with ranges in parenthesis. Data were analyzed using JMP for SAS, version 10.0 (Cary, North Carolina).




Results


Nine patients with native PV IE were identified, accounting for 0.8% of all IE cases seen during the study period. Table 1 provides detailed clinical and microbiologic information for each patient. The median age was 59 years (25 to 74) and 22% of affected patients were women; 1/3 of patients had CHD and 22% had a central venous catheter, but none had a history of alcoholism or intravenous drug abuse. Three patients had cardiovascular implantable electronic devices (2 dual-chamber pacemakers and 1 cardiac resynchronization therapy device) with 2 of the 3 having lesions suspicious for vegetation on their device leads at the time of diagnosis. Isolated PV IE was present in 7 of 9 cases (78%); 1 patient had concomitant mitral valve IE and the other patient had tricuspid valve IE. None of the patients had previous documented episodes of IE.



Table 1

Detailed clinical and microbiologic data for native pulmonary valve infective endocarditis cases




























































































































Age Sex CHD Prednisone Rx Comorbidities Potential source +BC Organism Complications Surgery
1 24 M + 0 0 Unknown + Viridans group streptococcus; Actinomyces meyeri Brain abscess 0
2 26 F + 0 0 Unknown 0 VISA; Gemella species Septic PE + (49)
3 63 M + 0 0 Unknown + Streptococcus anginosus Recurrent septic PE 0
4 27 M 0 0 Renal failure/hemodialysis Central venous catheter 0 Presumed coagulase-negative staphylococcus PE with lung infarct + (76)
5 48 F 0 + Myasthenia gravis Temporary pacemaker 0 Viridans group streptococcus None 0
6 59 M 0 + Polyarthritis Unknown + Streptococcus equinus; Streptococcus gallolyticus T5-T6 diskitis; RV failure + (42)
7 68 M 0 + MDS + RPC Unknown 0 Histoplasma capsulatum None + (48)
8 72 M 0 + Rheumatoid arthritis Colonic polyp + Enterococcus faecalis Septic PE; RV failure; ARF + (1875)
9 73 M 0 + Post-renal transplant Urinary tract + Enterococcus faecalis None 0

+ = yes/present; 0 = no/absent; ARF = acute renal failure; + BC = positive blood cultures; CHD = congenital heart disease; F = female; M = male; MDS = myelodysplastic syndrome; PE = pulmonary embolus; RPC = relapsing polychondritis; RV = right ventricle; Rx = therapy; VISA = vancomycin-intermediate Staphylococcus aureus.

Number of days between diagnosis and surgery is shown in parentheses.



Median follow-up was 1.8 years (0.3 to 5.9). Five patients (56%) underwent elective PV replacement—median time interval 49 days (42 to 1,875). No emergent/urgent surgeries were performed. All patients who underwent PV replacement received a bioprosthetic valve. Two patients required additional valvular interventions—1 tricuspid valve repair and 1 tricuspid valve replacement. PV replacement was performed for severe PR in the setting of flail cusp (2 patients), for recurrent pulmonary emboli with associated right-sided cardiac failure (1 patient), for severe PR with moderate-to-severe right ventricular outflow obstruction (1 patient), and for progressive severe right-sided cardiac failure because of PR (1 patient). There were no perioperative deaths. Pathology confirmed PV involvement in all surgical cases. Two patients had morphologic abnormalities of the PV, 1 with cusp fenestrations and 1 with mild fusion of commissures. Signs of active infection were present in 3 of the patients managed surgically: 1 with fungal endocarditis in the setting of previous disseminated histoplasmosis and 2 patients with features of persistent infection and symptomatic right-sided cardiac failure despite antibiotic therapy.


There was 1 late death—a patient with single ventricle who had sudden death 6.1 years after his diagnosis of PV IE. One patient had a second episode of IE 7 years after his initial diagnosis, but there was no involvement of his PV prosthesis by echocardiography.


Echocardiographic features are listed in Table 2 . Figure 1 illustrates the PV IE findings observed in patient 7. Three patients did not have a TTE and 2 patients did not have a TEE at the time of diagnosis. When TTE was performed, it was diagnostic for PV IE in all cases. In 1 patient, TEE findings suggested a right ventricular outflow tract mass/thrombus and subsequent TTE showed valvular rather than subvalvular involvement. TEE imaging provided excellent morphologic assessment of the PV with less thorough evaluation of PR severity (mostly based on color Doppler). Severe PR was present in 56% of patients. In 2 patients, PR severity could not be determined because of paucity of recorded echo-Doppler data. TEE also offered better assessment of other cardiac valves and structures than TTE, particularly when there were abnormalities involving cardiac device leads. Both patients with concomitant non-PV IE involvement had mild structural and functional valve disease.



Table 2

Echocardiographic features of pulmonary valve infective endocarditis and associated findings






























































































TTE TEE Degree of PR Flail cusp Systolic MIG Pulmonary valve mass (mm) Other vegetations
1 + 0 Trivial 0 25 + (7 × 10) 0
2 + + Severe + 104 + (40 × 3) + (VSD)
3 + + Indeterminate 0 8 + (6 × 10) + (mitral valve)
4 0 + Severe + 10 + (16 × 13) + (pacemaker lead)
5 0 + Mild-to-moderate 0 0 + (4 × 4) + (pacemaker lead)
6 + 0 Severe + 0 + (33 × 5) 0
7 + + Severe + 7 + (13 × 15) 0
8 + + Indeterminate + 0 + (24 × 16) + (tricuspid valve)
9 0 +/0 Severe 0 4 + (10 × 10) 0

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Nov 28, 2016 | Posted by in CARDIOLOGY | Comments Off on Infective Endocarditis Involving the Pulmonary Valve

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