Juan E. Guerra

Intermittent acute aortic regurgitation of a mechanical bileaflet aortic valve prosthesis: diagnosis and clinical implications

Intermittent aortic regurgitation (AR) is an unusual complication after a mechanical prosthetic replacement. We describe a rare case of intermittent dysfunction of a bileaflet mechanical aortic prosthetic valve in a 41-year-old man with a 21 mm Tri-technologies prosthetic valve implanted 4 years before. Transthoracic echocardiography (TTE) before discharge was normal and prosthesis-patient mismatch was ruled out. He was admitted to our hospital because of mild dyspnoea at effort. TTE revealed acute and severe intermittent AR. The patient underwent surgery, during which abnormal proliferation of subvalvular pannus overgrowth on the inflow aspect of the prosthesis was found impeding the normal closure of one of the discs of the prosthesis. The pannus formation was resected, the Tri-technologies prosthetic valve was prophylactic explanted and a 23 mm St Jude Medical bileaflet mechanical prosthesis valve was implanted. We describe the role of TTE and the limitation of the cinefluoroscopy in the diagnosis of Tri-technologies prosthetic dysfunction.

Impaired Myocardial Function in Hypertrophic Cardiomyopathy

Background: Tissue Doppler imaging (TDI) parameters of peak myocardial velocities (S′, E′, and A′) has been employed to assess the regional left ventricular myocardial function. The global function index (GFI) derived from TDI has been recently employed to distinguish the different etiologies of left ventricular hypertrophy. Objective: To analyze whether the GFI or individual TDI parameters of peak myocardial velocities (S′, E′, and A′) allows detecting different degrees of regional myocardial dysfunction in the most frequent forms of hypertrophic cardiomyopathy (HCM). Methods: GFI = (E/E′)/S′ (where E is the peak transmitral flow velocity, E′ is the early diastolic myocardial velocity, and S′ is the peak systolic myocardial velocity) and TDI peak myocardial velocities was measured in the septal and lateral mitral annulus in 101 patients with HCM (mean age 47.5 ± 14 years, 58 women) and in age‐matched group of 30 healthy controls (mean age 46 ± 6 years, 16 women). Results: Forty‐five patients had nonobstructive asymmetric septal HCM, 20 patients had a subaortic gradient ≥ 30 mm Hg, 21 p. had apical HCM, and 15 p. had other forms of HCM (midventricular, symmetric, and biventricular). All patients with HCM exhibited a decrease in early diastolic (E′) and systolic (S′) myocardial velocities, both in the lateral and septal‐mitral annulus border, but more pronounced in septal‐mitral annulus. Septal GFI was higher in HCM patients than in healthy subjects (1.8 (1.1–2.5) and (0.57 (0.31–0.92), respectively, P < 0.001), but no differences were seen when different forms of HCM were compared. Conclusions: In a selected population of patients with HCM and a preserved left ventricular(LV) systolic function, GFI and individual TDI parameters of peak velocity (S′, E′, and A′) and E/E′ ratio were similar in different forms of HCM, indicating that in all patients with HCM there is regional systolic and diastolic myocardial dysfunction, regardless of the location of hypertrophy. (ECHOCARDIOGRAPHY, Volume 26, July 2009)

Speckle tracking echocardiography to assess regional ventricular function in patients with apical hypertrophic cardiomyopathy

AIM To explore regional systolic strain of midwall and endocardial segments using speckle tracking echocardiography in patients with apical hypertrophic cardiomyopathy (HCM). METHODS We prospectively assessed 20 patients (mean age 53 ± 16 years, range: 18-81 years, 10 were male), with apical HCM. We measured global longitudinal peak systolic strain (GLPSS) in the midwall and endocardium of the left ventricle. RESULTS The diastolic thickness of the 4 apical segments was 16.25 ± 2.75 mm. All patients had a normal global systolic function with a fractional shortening of 50% ± 8%. In spite of supernormal left ventricular (LV) systolic function, midwall GLPSS was decreased in all patients, more in the apical (-7.3% ± -8.8%) than in basal segments (-15.5% ± -6.93%), while endocardial GLPPS was significantly greater and reached normal values (apical: -22.8% ± -7.8%, basal: -17.9% ± -7.5%). CONCLUSION This study shows that two-dimensional strain was decreased mainly confined to the mesocardium, while endocardium myocardial deformation was preserved in HCM and allowed to identify subclinical LV dysfunction. This transmural heterogeneity in systolic strain had not been previously described in HCM and could be explained by the distribution of myofibrillar disarray in deep myocardial areas. The clinical application of this novel finding may help further understanding of the pathophysiology of HCM.