The American journal of cardiology
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This study further defines the mechanism of blood flow during closed-chest compression using transesophageal Doppler echocardiography. Although the echocardiographic demonstration of mitral valve closure during closed-chest compression has been used as evidence of direct cardiac compression, mitral valve closure has also been documented to occur during resuscitation by selectively increasing intrathoracic pressure. Transesophageal Doppler echocardiography was used to assess mitral valve position and flow in 17 adult patients undergoing cardiopulmonary resuscitation with a mechanical piston compression device. ⋯ Left ventricular fractional shortening inversely correlated (r = -0.68; p = 0.02) with the anteroposterior chest diameter, but did not correlate with peak transmitral flow (r = 0.34; p = not significant). It is concluded that the mitral valve closes during the downstroke of chest compression in most adult patients during resuscitation. The absence of a relation between mitral valve flow and left ventricular fractional shortening supports the hypothesis that other factors such as nonuniform increases in intrathoracic pressure cause the mitral valve to open or close during chest compression.
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The renin-angiotensin system (RAS) plays a major role in the control of blood pressure and cardiovascular homeostasis and is involved in the pathogenesis of a number of cardiovascular disorders. The efficacy of angiotensin-converting enzyme (ACE) inhibitors in the treatment of hypertension and congestive heart failure has led to the widespread clinical use of ACE inhibitors in primary or secondary prevention of heart disease. ⋯ Whereas the circulating endocrine RAS appears to be responsible for mediation of acute effects, the tissue RAS seems to be involved in more chronic situations, such as secondary structural changes of the cardiovascular system, and therefore could contribute to the pathogenesis of hypertension as well as other cardiovascular disorders, such as cardiac hypertrophy, coronary artery disease, and atherosclerosis. Several experimental and clinical findings suggest that reversal of cardiovascular structural changes secondary to cardiovascular disease and enhancement of renal sodium excretion by ACE inhibitors are important long-term antihypertensive actions possibly mediated by inhibition of the tissue RAS.
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It is often difficult to predict outcome in hospitalized patients with pericardial effusion. To address this issue, the prognostic value of echocardiography was studied in 187 hospitalized patients diagnosed with pericardial effusions over a 1-year period. The index echocardiogram showed that 11 effusions were large (6%), 39 were moderate (21%), and 137 were small (73%). ⋯ By univariate analysis, each echocardiographic sign was associated with both cardiac tamponade and the combined end point (p less than or equal to 0.01 for comparisons with size and right-sided chamber collapse; p less than or equal to 0.07 for comparisons with IVC plethora). When the data were analyzed with logistic regression modeling, effusion size was the most powerful predictor of outcome (cardiac tamponade: odds ratio 51, 95% confidence interval 3.5-729, p = 0.004; combined end point: odds ratio 78, 95% confidence interval 14-421, p = 0.0001), and neither right-sided chamber collapse nor IVC plethora with blunted response to respiration retained significant associations. It is concluded that echocardiographically determined effusion size is a powerful predictor of outcome in hospitalized patients with pericardial effusion, and that right-sided chamber collapse and IVC plethora with blunted response to respiration add little if any additional prognostic information.