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Biomedical subjects

H Palmero

Publications and source records attributed to H Palmero.

7 recordsLinked to original sources
PubMed1989

Plasma norepinephrine in Chagas' cardioneuromyopathy: a marker of progressive dysautonomia.

Chronic Chagas' disease produces pathologic changes of the cardiovascular, digestive, and autonomic nervous systems. In an attempt to elucidate the nature of the dysautonomia in patients with Chagas' disease, we measured plasma norepinephrine levels, blood pressure, and heart rate, both supine and standing in 26 patients, and compared these values of patients classified according to three clinical subsets of cardiovascular manifestations with the values of nine normal volunteers and 16 patients with nonchagasic heart failure. Results suggested (1) progressive blockade of the alpha receptor in patients with Chagas' disease who have minimal clinical symptoms (group I) and in those who have ECG alterations without congestive symptoms (group II), as reflected by normal or raised plasma norepinephrine levels without change of diastolic blood pressure during standing, which indicates absent postural reflexes; and (2) blockade associated with partial denervation in patients with Chagas' disease who have class III or IV heart failure (group III), as suggested by a lower supine plasma norepinephrine level and a fall in diastolic blood pressure in the upright position. The findings of reduced plasma norepinephrine levels are in contrast to the elevated plasma norepinephrine levels in patients without Chagas' disease with class III and IV heart failure who have sympathetic hyperactivity.

Adult↗
PubMed1984

Left ventricular wall motion in patients with Chagas's disease.

The effect of early chronic Chagas's disease on the timing and extent of regional left ventricular wall motion was studied with a frame by frame analysis of left ventriculograms in nine patients and compared with those in 19 normal subjects. In all the patients there was hypokinesis or akinesis in the anteroapical region together with delay in the onset of inward movement. Hypokinesis of the proximal inferior segment was also present, but the time of onset of inward motion here was normal. These differences can be explained on the basis of regional asynchrony within the normal left ventricle, where anteroapical wall motion is delayed with respect to that elsewhere. Thus contraction of the diseased anteroapical segment starts against an appreciable pressure and so may be isometric, whereas the affected proximal inferior segment starts contracting earlier against a lower pressure and so is able to shorten. No abnormalities of wall motion were seen during isovolumic relaxation despite segmental involvement, which is a distinctly different finding from that in patients with coronary artery disease. This may be due partly to the absence of incoordinate relaxation in Chagas's disease and partly to myocardial involvement by Chagas's disease in the mid-anterior segment. This is the site of rapid early diastolic wall thinning, which has been put forward as a major mechanism of normal rapid ventricular filling and whose premature activity causes disturbances in regional wall motion before mitral valve opening when relaxation is incoordinate. Thus quantitative analysis of both the timing and amplitude of wall motion indicates fundamental differences between Chagas's disease and coronary artery disease, when a less complex analysis would have shown a similar pattern of segmental dysfunction in both. Since the effect of the same pathological process on wall motion varies with the site of ventricular involvement, the importance of the disturbances seen in Chagas's disease becomes apparent only when the non-uniformity of normal left ventricular structure and function is taken into account.

Angiocardiography↗