Infective endocarditis in hypertrophic cardiomyopathy: A multicenter, prospective, cohort study.

Infective endocarditis (IE) complicating hypertrophic cardiomyopathy (HCM) is a poorly known entity. Although current guidelines do not recommend IE antibiotic prophylaxis (IEAP) in HCM, controversy remains.This study sought to describe the clinical course of a large series of IE HCM and to compare IE in HCM patients with IE patients with and without an indication for IEAP.Data from the GAMES IE registry involving 27 Spanish hospitals were analyzed. From January 2008 to December 2013, 2000 consecutive IE patients were prospectively included in the registry. Eleven IE HCM additional cases from before 2008 were also studied. Clinical, microbiological, and echocardiographic characteristics were analyzed in IE HCM patients (n = 34) and in IE HCM reported in literature (n = 84). Patients with nondevice IE (n = 1807) were classified into 3 groups: group 1, HCM with native-valve IE (n = 26); group 2, patients with IEAP indication (n = 696); group 3, patients with no IEAP indication (n = 1085). IE episode and 1-year follow-up data were gathered.One-year mortality in IE HCM was 42% in our study and 22% in the literature. IE was more frequent, although not exclusive, in obstructive HCM (59% and 74%, respectively). Group 1 exhibited more IE predisposing factors than groups 2 and 3 (62% vs 40% vs 50%, P < 0.01), and more previous dental procedures (23% vs 6% vs 8%, P < 0.01). Furthermore, Group 1 experienced a higher incidence of Streptococcus infections than Group 2 (39% vs 22%, P < 0.01) and similar to Group 3 (39% vs 30%, P = 0.34). Overall mortality was similar among groups (42% vs 36% vs 35%, P = 0.64).IE occurs in HCM patients with and without obstruction. Mortality of IE HCM is high but similar to patients with and without IEAP indication. Predisposing factors, previous dental procedures, and streptococcal infection are higher in IE HCM, suggesting that HCM patients could benefit from IEAP.

The changing face of prosthetic valve endocarditis at a tertiary-care hospital: 1986-2005.

INTRODUCTION AND OBJECTIVES: To investigate changes in the clinical characteristics, etiology and prognosis of prosthetic valve endocarditis at a tertiary-care hospital. METHODS: Retrospective cohort study of all patients diagnosed with prosthetic valve endocarditis using modified Duke criteria between 1986 and 2005. The analysis covered two time periods: January 1986 to December 1995 (P1) and January 1996 to December 2005 (P2). RESULTS: In total, 133 episodes of endocarditis occurred in 122 patients. Of these, 73 (54.9%) were diagnosed in P1 and 60 (45.1%) in P2, with incidences of 2.19% and 2.18%, respectively. The patients' mean age (SD) was 52.6+/-16.6 years in P1 and 66.2+/-11.5 years in P2 (P=.0001). Clinical characteristics were similar in the two study periods. The increase in Enterococcus infection was remarkable (12.5% in P2 vs. 4.9% in P1; relative risk [RR]=2.5; 95% confidence interval [CI], 0.7-9.6), as was the decrease in viridans group Streptococcus infection (12.5% in P2 vs. 31.1% in P1; RR=0.4; 95% CI, 0.2-0.9). Some 90.4% of patients (63/73) underwent surgery in P1, while 68.3% (41/60) underwent surgery in P2. The difference was significant (RR=0.8; 95% CI, 0.6-0.9). The in-hospital mortality rate was 28.8% in P1 and 30% in P2 (RR=1; 95% CI, 0.6-1.7). CONCLUSIONS: Changes in the epidemiology and microbiological etiology of prosthetic valve endocarditis were observed over the 20-year study period. Diagnostic and therapeutic approaches also changed, but mortality remained high.

Consumo de pescado, omega- 3 y factores de riesgo cardiovascular / Fish consumption, omega-3 and cardiovascular risk factores

Uno de los elementos de la dieta mediterránea que presenta claros efectos beneficiosos para la salud cardiovascular es el consumo de pescado. Esos beneficios se deben principalmente en su concentración en ácidos grasos omega-3, cuyo uso como suplemento de la dieta se ha visto generalizado en los últimos años. Aunque no bien conocidos, sus mecanismos de acción incluyen la regulación de moléculas vasoactivas, la inhibición plaquetaria, la reducción de la inflamación y la reducción de los factores de riesgo cardiovascular como la proteina C-reactiva, la homocisteína, los triglicéridos y el colesterol.