To help determine if coronary angiography can predict the site of a future coronary occlusion that will produce a myocardial infarction, the coronary angiograms of 42 consecutive patients who had undergone coronary angiography both before and up to a month after suffering an acute myocardial infarction were evaluated. Twenty-nine patients had a newly occluded coronary artery. Twenty-five of these 29 patients had at least one artery with a greater than 50% stenosis on the initial angiogram. However, in 19 of 29 (66%) patients, the artery that subsequently occluded had less than a 50% stenosis on the first angiogram, and in 28 of 29 (97%), the stenosis was less than 70%. In every patient, at least some irregularity of the coronary wall was present on the first angiogram at the site of the subsequent coronary obstruction. In only 10 of the 29 (34%) did the infarction occur due to occlusion of the artery that previously contained the most severe stenosis. Furthermore, no correlation existed between the severity of the initial coronary stenosis and the time from the first catheterization until the infarction (r2 = 0.0005, p = NS). These data suggest that assessment of the angiographic severity of coronary stenosis may be inadequate to accurately predict the time or location of a subsequent coronary occlusion that will produce a myocardial infarction. (Circulation 1988;78:1157-1166
The benefit of monitoring blood glucose in indigent women with GDM via the Internet was limited by their infrequent use of the telemedicine system. Although system use was not associated with improved pregnancy outcomes, women in the telemedicine group did experience enhanced feelings of diabetes psychosocial self-efficacy.
Our enhanced telemedicine monitoring system increased system utilization and contact between women with GDM and their healthcare providers but did not impact upon pregnancy outcomes.
To examine the importance of systolic ventricular interdependence on right ventricular function, we used a unique electrically isolated right ventricular free wall preparation. Double-peaked waveforms for right ventricular pressure and pulmonary arterial blood flow occurred over a wide range of pacing intervals between the left and right ventricles. One component of the waveforms could be directly related to right ventricular free wall contraction, whereas the other component was directly related to left ventricular and septal contraction. For left ventricular pressure, the left ventricular component was significantly larger than the right ventricular free wall component (92.7 +/- 3.2 vs. 7.3 +/- 3.2% peak-to-peak value, P less than 0.01). For right ventricular pressure, the left ventricular and septal component was significantly greater than the right ventricular component (63.5 +/- 10.9 vs. 36.5 +/- 10.9% peak-to-peak value, P less than 0.05). Similarly, for pulmonary arterial blood flow, the left ventricular component was significantly greater than the right ventricular component. When right ventricular free wall pacing stopped in diastole, 68 +/- 4% of right ventricular systolic pressure and 80 +/- 4% of pulmonary flow were obtained in the subsequent beat. The results of this study indicate that left ventricular contraction is very important for right ventricular developed pressure and volume outflow.
These results indicate a low perception of risk and cardiovascular knowledge especially among men and inner city residents. Innovative educational strategies are needed to increase risk factor knowledge and awareness among at-risk individuals.
Because of close anatomic association, the pressure and volume in one ventricle can directly influence the pressure and volume in the opposite ventricle. To examine the importance of ventricular interdependence in controlling the circulation, we developed a computer model in which ventricular interdependence could be turned on and off. Left ventricular chamber contractility, as judged by maximal elastance (Emax), was enhanced on the order of 10% as a result of ventricular interaction, whereas right ventricular Emax was affected by as much as 60% under physiological conditions. With increases in systemic vascular resistance, ventricular interaction caused a smaller stroke volume (SV) decrease than with no interaction. For canine data (SV = 21.4 ml), doubling systemic vascular resistance decreased SV by 3.7 without ventricular interdependence, 3.5 with diastolic ventricular interdependence, and 3.3 ml with diastolic and systolic ventricular interdependence. In contrast, with increases in pulmonary vascular resistance, ventricular interaction caused a greater decrease in SV than with no interaction present. Decreasing left ventricular free wall elastance or right ventricular free wall elastance decreased SV. Diastolic ventricular interdependence reduced the SV changes, whereas systolic ventricular interdependence accentuated the SV changes with alterations in right and left ventricular free-wall elastance. The results of the present simulation demonstrate the importance of ventricular interdependence in the observed responses of the right ventricle to volume overload, pressure overload, and ischemia.
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