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Sökning: WFRF:(Dancy Mark)

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1.
  • Ramzy, Ihab S, et al. (författare)
  • Right ventricular stunning in inferior myocardial infarction.
  • 2008
  • Ingår i: International journal of cardiology. - : Elsevier BV. - 1874-1754 .- 0167-5273.
  • Tidskriftsartikel (refereegranskat)abstract
    • AIM: To assess right ventricular (RV) function in patients with inferior myocardial infarction (IMI) and to observe changes following thrombolysis. BACKGROUND: RV dysfunction occurs in 30% of patients with IMI. The extent of such involvement and its potential, recovery has not been determined. METHODS: We studied 30 patients with acute IMI (age 56+/-12 years), on admission, day 7 and day 30 post thrombolysis. No patient had clinical signs of RV failure. RV segmental function was assessed from free wall long axis and global function from filling and ejection velocities. Values were compared with 15 age-matched controls. RESULTS: On admission, RV long axis amplitude, systolic and diastolic velocities were depressed (2.09+/-0.39 vs 2.6+/-0.3 cm, 8.18+/-1.8 vs 10.0+/-2.0 cm/s and 6.9+/-2.7 vs 10.0+/-2.5 cm/s, p<0.01 for all) and global function impaired; reduced Z ratio (0.85+/-0.07 vs 0.9+/-0.04, p<0.01), raised Tei index (0.49+/-0.26 vs 0.3+/-0.1, p<0.001) and prolonged t-IVT (8.16+/-3.9 vs 4.8+/-2 s/m, p<0.01) compared to controls. After thrombolysis, RV long axis amplitude (2.28+/-0.3 cm, p<0.05), systolic velocity (10.0+/-2.7 cm/s, p<0.01), early diastolic velocity (8.3+/-2.16, p<0.05), Z ratio (0.9+/-0.05, p<0.01), Tei index (0.34+/-0.17, p<0.01) and t-IVT (6.2+/-2.7 s/m, p<0.05) all normalised at day 30. Only 4 (13%) patients remained with RV long axis amplitude and one with t-IVT and Tei index values outside the normal 95% CI at day 30. RV inflow diameter and tricuspid regurgitation did not change. CONCLUSION: In IMI, RV segmental and global functions are acutely impaired, and recover in 87% of patients following thrombolysis. In the absence of clear evidence for RV infarction the disturbances in the remaining 13% may represent stunned myocardium that may demonstrate delayed recovery.
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2.
  • Ramzy, Ihab S., et al. (författare)
  • Ventricular endocrine and mechanical function following thrombolysis for acute myocardial infarction
  • 2007
  • Ingår i: International Journal of Cardiology. - : Elsevier BV. - 0167-5273 .- 1874-1754. ; 117:1, s. 51-58
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective The objective of this study was to assess natriuretic peptide release following acute myocardial infarction, and its relationship with ventricular function. Methods A total of 44 patients with acute myocardial infarction were studied; 13 anterior, age (57 Â± 12 years) and 31 inferior, age (58 Â± 12 years). Peptide levels and left ventricular function by echocardiography were assessed at admission and on days 7 and 30 after thrombolysis. Healthy volunteers (n = 21) served as controls. Results Atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) levels rose from admission to day 7 (p = 0.002). While ANP remained elevated at day 30 in both groups, BNP levels fell in patients with anterior myocardial infarction (p = 0.03). Left ventricular fractional shortening was reduced at admission in the two groups (p = 0.01) but returned towards normal in 7 days (p = 0.001) in inferior myocardial infarction and in 30 days in anterior myocardial infarction (p = 0.02). Left ventricular long axis amplitude was universally reduced at admission (p = 0.01) and remained abnormal at day 30 (p = 0.01) in both groups. At day 7, BNP and ANP levels inversely correlated with long axis amplitude of lateral wall in anterior myocardial infarction; (r = âˆ’ 0.7, p = 0.01). BNP correlated inversely with fractional shortening in anterior myocardial infarction (r = âˆ’ 0.7, p = 0.01) at day 30. Conclusion The elevated peptide levels at 7 days post-myocardial infarction correlate with reduced mechanical activity of the adjacent noninfarcted segment. Natriuretic peptides release seem to be related to failure of compensatory hyperdynamic activity of the noninfarcted area rather than directly from the injured myocardial segments.
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