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To date, there is no proved medical therapy able to significantly reduce the degenerative process of biologic prosthetic aortic valves. It has recently been suggested that statins may reduce the progression of native aortic valve stenosis. We examined the effect of statin treatment on bioprosthetic aortic valve degeneration and found a beneficial effect of statins in slowing bioprosthetic degeneration.

Background: Left ventricular pseudoaneurysm (LVPA) is a rare entity characterized by a tendency to spontaneous rupture due to its morphology, a lack of myocardial fibers and fibrous tissue delineating the cavity. An early diagnosis is essential in order to guide appropriate therapy., Purpose: To determine the diagnostic accuracy of different imaging techniques, treatment results, and prognosis of patients (pts) with LVPA., Methods: We evaluated the incidence of LVPA during a five-year period. The initial clinical presentation, the etiology of LVPA, time between symptom onset and diagnosis, and use of various non-invasive techniques were studied. Mean follow-up was 15 months., Results: Of 19113 pts admitted to our Institute in a five-year period, LVPA was diagnosed in 11 pts (0.05%) (mean age 51 +/- 3.9 years, 8 men). The diagnosis of LVPA was confirmed by surgery in 4 pts, and by pathology in 2 pts. LVPA was an incidental finding in one asymptomatic pt, it was diagnosed in 6 pts presenting with an acute myocardial infarction (AMI) and in 4 pts presenting with LV failure. The main etiology was coronary artery disease (CAD) (9 pts), with the remaining 2 cases being post-traumatic (thoracic stab wound, surgery). LVPA location was postero-inferior in 6 patients, infero-lateral in 3 patients, and anterior in 2 patients. ECG, X-ray and TTE were performed in all cases. 6 pts had a radionuclide angiography (RNA), 3 pts had a computed tomography (CT) scan and 2 pts had a magnetic resonance imaging (MRI) study. Two-dimensional transthoracic echocardiography (TTE) provided information regarding LVPA dimensions and LV-LVPA flow. Four pts were operated (one died). Of the seven non-operated pts., 5 died., Conclusions: The clinical presentation was variable and non-specific. The most frequent cause of LVPA was MI and the most frequent location was inferior. Echocardiography offered the most reliable information when compared to ventriculography. Because clinical examination, ECG, X-ray data are non-specific for the diagnosis of LVPA, an adequate TTE study performed with a high clinical index of suspicion (especially in pts with inferior MI or thoracic trauma) could facilitate the early diagnosis of LVPA and could be relevant to outcome.

Impaired relaxation is frequently masked by elevated filling pressures, resulting in a pseudonormal flow pattern (E/A >1.0). Because the E/A wave ratio increases as filling pressures rise, it is generally assumed that patients with an E/A ratio of <1.0 (impaired relaxation pattern) have relatively low filling pressures. Nevertheless, patients with an E/A ratio of <1.0 can have as profoundly elevated filling pressures as patients with a pseudonormal or restrictive filling pattern. Because left ventricular (LV) pressure during end-diastole essentially determines atrial afterload, the response of the A-wave velocity to a reduction of atrial afterload by a standardized Valsalva maneuver should allow estimation of LV end-diastolic pressure (LVEDP) regardless of the baseline Doppler flow pattern. This was tested in 20 consecutive patients who were studied by pulse-wave Doppler echocardiography during cardiac catheterization. There was a close correlation between LVEDP and the change in A-wave velocity during the Valsalva maneuver (r = 0.85, SEE 6.7 mm Hg) regardless of the baseline E/A ratio. In patients with a LVEDP of <15 mm Hg the A wave decreased by 21 +/- 15 cm/s. In patients with a LVEDP of >25 mm Hg the A wave increased by 18 +/- 13 cm/s. The change in the E/A ratio during Valsalva correlated fairly with LVEDP (r = -0.72, SEE 8.8 mm Hg), the baseline E/A ratio correlated poorly, and scatter was substantial (r = 0.46, SEE 11.2 mm Hg). Just as elevated filling pressures can mask impaired relaxation, the impaired relaxation pattern can mask the presence of elevated filling pressures. This can be revealed by testing the response of the A wave to the Valsalva maneuver, allowing estimation of LVEDP independent of the baseline E/A ratio.

Background: Left-ventricular pseudohypertrophy reflecting left-ventricular compression was reported in a selected group of patients with cardiac tamponade., Hypothesis: Criteria for the presence of pseudohypertrophy can be established to guide its use as a sign of left-ventricular compression in patients with cardiac tamponade., Methods: Left-ventricular wall thickness, diameters, relative diastolic wall thickness (%) = (posterior wall thickness/end diastolic radius) x 100 and estimated left-ventricular mass were measured in patients with small, moderate and large pericardial effusion, in patients with cardiac tamponade before and after pericardiocentesis (16 patients in each group) and in 30 control subjects with normal echocardiograms., Results: Left-ventricular posterior wall thickness was increased (12 +/- 2 vs. 9 +/- 1 mm, p < 0.001), left-ventricular end-diastolic diameter was reduced (3.9 +/- 0.5 vs. 4.6 +/- 0.3 cm, p < 0.001) and relative left-ventricular diastolic wall thickness was increased (61 +/- 13 vs. 41 +/- 4.5%, p < 0.001) only in patients with cardiac tamponade compared to controls, but not in patients with small, moderate and large effusions, respectively (relative wall thickness: 42 +/- 5, 41 +/- 7 and 44 +/- 7%, p = NS). Mean values of the estimated left-ventricular mass were similar in all groups. Following pericardiocentesis all parameters were normal., Conclusions: Despite normal left-ventricular mass, relative left-ventricular diastolic wall thickness is elevated in patients with cardiac tamponade. In contrast it is normal in patients with various degrees of pericardial effusion supporting its use as a quantitative measure of left-ventricular compression in patients with suspected cardiac tamponade.