Journal of cardiac failure
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Comparative Study
Treatment with enalapril fails to prevent impaired cardiopulmonary baroreflex control in dogs with left ventricular dysfunction.
That the cardiopulmonary baroreflex control of sympathetic nerve activity is impaired in dogs with left ventricular (LV) dysfunction has been shown previously. This study tested the hypothesis that treatment with the angiotensin-converting enzyme inhibitor enalapril prevents or delays the development of abnormalities of cardiopulmonary baroreflexes in dogs with LV dysfunction. Serial changes in LV volumes and neurohumoral profiles (plasma norepinephrine and renin activity) were assessed in conscious dogs with progressive LV dysfunction due to rapid ventricular pacing. ⋯ Hemodynamic parameters also were comparable in the two groups. Cardiopulmonary baroreflex sensitivity for enalapril-treated dogs was not different from that of untreated paced dogs, and baroreflex gain in both groups was significantly lower than for the nonpaced control dogs (P < .05). Despite adequate converting enzyme blockade, treatment with enalapril failed to prevent the development of attenuated cardiopulmonary baroreflex control of sympathetic nerve activity in dogs with developing LV dysfunction.
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Idiopathic dilated cardiomyopathy is characterized by dilation and impaired contractility of one or both ventricles. Long-term prognosis is poor. Early diagnosis has the potential for substantial reduction of morbidity and mortality. ⋯ Of the relatives examined, 41% had left ventricular abnormalities. These findings provide further evidence for a genetic background of dilated cardiomyopathy. Relatives with left ventricular enlargement may have an early stage and/or latent form of the disease.
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Comparative Study
Evaluation of the dead space/tidal volume ratio in patients with chronic congestive heart failure.
Dead space/tidal volume ratio (VD/VT) evaluation is currently performed in patients with respiratory and cardiac disorders, and includes measurement of arterial CO2 partial pressure (PaCO2). PaCO2 is generally derived from either PETCO2 (end-expiratory CO2 pressure) or PJCO2 (calculated as PJCO2 = 5.5 + 0.9 PETCO2 - 2.1 VT). The applicability of these methods may be questionable in chronic heart failure due to its frequent association with lung dysfunction. ⋯ Measured VD/VTs also strongly correlated with estimated VD/VTs (VD/VT measured = -0.03 + 1.11 VD/VT [estimation 1], r = .90, P < .0001, and VD/VT measured = 0.03 + 0.92 VD/VT [estimation 2], r = .90, P < .0001). However, only at rest and, solely for estimation 1, at submaximal exercise were the slopes and y intercepts of measured versus estimated VD/VT not different from 1 and 0, respectively; in this regard, lung dysfunction was more influential than the severity of cardiac failure. Although PaCO2 strongly correlates with PETCO2 and PJCO2, these measurements may not be reliable for a noninvasive calculation of VD/VT in chronic congestive heart failure.