Heart and vessels
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Comparative Study
Comparison of hemodynamic data before and after corrective surgery for Down's syndrome and ventricular septal defect.
Left ventricular function and the extent of pulmonary vascular disease were studied in 18 children with Down's syndrome and 20 children without Down's syndrome who underwent corrective surgery for ventricular septal defect (VSD) and severe pulmonary hypertension. This study was conducted between 1985 and 1993. All patients underwent routine cardiac catheterization preoperatively and postoperatively (mean, 11.4 months after surgery). ⋯ Some degree of irreversible pulmonary vascular disease was present after repair of VSD in patients with Down's syndrome. In the Down group, there were no significant changes in left ventricular function after surgery, despite the relief of volume overload. These results suggest that early diagnosis and surgical repair are key elements in the management of patients with Down's syndrome and VSD.
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A 37-year-old female with Marfan's syndrome developed myocardial infarction during a cardiac operation for annuloaortic ectasia and chronic dissecting aneurysm of the aorta. At autopsy, a chronic dissecting aneurysm of the left coronary arterial system (the left main stem, anterior descending branch, first diagonal branch, and circumflex branch) showing a true lumen and a pseudo lumen, which were patent, was found. There was also a hemorrhagic myocardial infarction of the anteroseptal wall and apical portion of the left ventricle.
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To assess atrial contribution to left ventricular (LV) filling in hypertension, we studied, using pulsed Doppler echocardiography, 22 hypertensive patients without apparent LV hypertrophy (LVH), 12 hypertensive patients with LVH, and 24 age-matched normal subjects. From mitral flow velocity waveform, we determined peak velocity of early diastolic filling flow (peak E), peak velocity of late diastolic filling flow (peak A), and the peak A/peak E ratio (peak A/peak E). Peak E decreased in hypertensives without apparent LVH and showed a further decrease in hypertensives with LVH compared with normal subjects (57 +/- 8 [mean +/- SD]; P less than 0.001, 46 +/- 7; P less than 0.0001, vs 65 +/- 10 cm/s). ⋯ In hypertensives, we found no significant correlation between peak A and the wall thickness index (WTI, determined as mean LV wall thickness normalized by LV diastolic dimension), whereas peak E was significantly correlated with WTI (r = -0.65; P less than 0.001). Our findings indicate that atrial contraction can not fully compensate the decrease in early diastolic filling caused by advanced LVH. We conclude that atrial compensation for reduced early diastolic filling is limited in hypertensive patients with advanced left ventricular hypertrophy.
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Clinical investigations focused on finding characteristics of noninvasively obtained measurements of pulmonary blood velocity that can be used to quantitate pulmonary blood flow and/or pulmonary pressure have often yielded results whose imprecision has been attributed to flow pattern variability. To determine flow pattern variability in an in vivo animal model in varying hemodynamic states, main pulmonary artery blood velocity waveforms were recorded in 17 dogs at 2-mm intervals along an anterior to posterior wall-oriented axis using a 20-MHz pulsed Doppler needle probe. Control data were obtained before the animals were subjected to altered flow (atrial level shunts) and pressure (10% O2 inhalation) states. ⋯ Elevated pulmonary blood flow tended to increase the maximum velocities along the anterior wall relative to midline velocities. Neither estimate of cardiac output yielded consistently accurate results (r = 0.77 for model-based method, r = 0.80 for area times central velocity method). Findings of this study, which highlight the dependency of waveform characteristics on sampling site, the large degree of intersubject variability, and the need for large or multiple sample volumes for pulmonary blood flow determination, help clarify inconsistencies observed by clinicians and suggest that future work with animal models will facilitate a greater understanding of the determinants of human pulmonary velocity waveforms.
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A theoretical analysis of the step response in the closed cardiovascular system induced by a sudden shift of the right cardiac output curve predicted that if the relations of the right heart output (COr) and the total systemic capillary flow (CFs) to the systemic venous pressure (Psv) are linear, then the time course of Psv change will become monoexponential with a time constant T given by T = Csv/(Gr + Gs), where Csv is the systemic vein compliance and Gr and Gs are the conductances of the transient COr-Psv and CFs-Psv relationships. A similar prediction was obtained for the time constant T of the pulmonary vein pressure (Ppv) response to the step change in the left cardiac output (COl) curve, pulmonary vein compliance (Cpv) and the conductances of the COl curve, and the pulmonary capillary flow (CFp) curve against Ppv. The actual Psv or Ppv changes following sudden alteration of the COr or COl curve by inflation and deflation of the balloon in the right or left atrium revealed monoexponential time courses. ⋯ A similar linearity of the dynamic CFp-Ppv relationship was suggested from their steady-state curves. The values of Csv calculated from the experimental data were 1.70 +/- 0.12 ml/mmHg/kg body wt in 11 curves and those of Cpv were 0.13 +/- 0.03 ml/mmHg/kg in 15 curves. These results are mostly consistent with those previously reported.