Occurrence of bioprosthetic valve thrombosis less than a year after replacement is very uncommon. Here, we describe a case of a 57 year old male, who presented 10 months after receiving a bioprosthetic mitral valve replacement with a two week history of dyspnea on exertion, worsening orthopnea and decreased exercise tolerance. Echocardiography revealed severe mitral regurgitation (MR), thrombosis of the posterior mitral leaflet, left atrial (LA) mural thrombus and a depressed left ventricular ejection fraction of twenty-five percent. Given severe clot burden and decompensated heart failure (New York Heart Association - NYHA class III) repeat sternotomy was done to replace the bioprosthetic mitral valve and remove LA mural thrombus. MR was resolved postoperatively. This brief report further reviews promoting factors, established guidelines and management strategies of bioprosthetic valve thrombosis.

BACKGROUND: Clinically relevant aortic dilatation (>40 mm) and increased cardiovascular risk are common among retired professional American-style football athletes. Among younger athletes, the effect of American-style football participation on aortic size is incompletely understood. We sought to determine changes in aortic root (AR) size and associated cardiovascular phenotypes across the collegiate career. METHODS AND RESULTS: This was a multicenter, longitudinal repeated-measures observational cohort study of athletes across 3 years of elite collegiate American-style football participation. A total of 247 athletes (119 [48%] Black, 126 [51%] White, 2 [1%] Latino; 91 [37%] linemen, 156 [63%] non-linemen) were enrolled as freshmen and studied at pre-and postseason year 1, postseason year 2 (N=140 athletes), and postseason year 3 (N=82 athletes). AR size was measured with transthoracic echo-cardiography. AR diameter increased over the study period from 31.7 (95% CI, 31.4–32.0) to 33.5 mm (95% CI, 33.1–33.8; P<0.001). No athlete developed an AR ≥40 mm. Athletes also demonstrated increased weight (cumulative mean Δ, 5.0 [95% CI, 4.1–6.0] kg, P<0.001), systolic blood pressure (cumulative mean Δ, 10.6 [95% CI, 8.0–13.2] mm Hg, P<0.001), pulse wave velocity (cumulative mean Δ, 0.43 [95% CI, 0.31–0.56] m/s, P<0.001), and left ventricular mass index (cumulative mean Δ, 21.2 [95% CI, 19.2–23.3] g/m2, P<0.001), and decreased E′ velocity (cumulative mean Δ, −2.4 [95%CI, −2.9 to −1.9] cm/s, P<0.001). Adjusting for height, player position, systolic blood pressure, and diastolic blood pressure, higher weight (β=0.030, P=0.003), pulse wave velocity (β=0.215, P=0.02), and left ventricular mass index (β=0.032, P<0.001) and lower E′ (β=−0.082, P=0.001) were associated with increased AR diameter. CONCLUSIONS: Over the collegiate American-style football career, athletes demonstrate progressive AR dilatation associated with cardiac and vascular functional impairment. Future studies delineating aortic outcomes are necessary to determine whether AR dilation is indicative of maladaptive vascular remodeling in this population.

Cardiac sarcoid is an infiltrative, granulomatous disease of the myocardium. It is more prevalent entity than once believed, especially subclinical disease. It affects heart mechanics causing ventricular failure, and disrupts the cardiac electrical system leading to third degree heart block, malignant ventricular arrhythmias, and sudden cardiac death. This makes early diagnosis and treatment of this devastating disease essential. Based on reviewed literature this paper proposes step-wise diagnostic and therapeutic algorithms for patients with suspected cardiac sarcoidoisis who do or do not have prior history of systemic sarcoidosis.