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      Circadian Blood Pressure Changes and Cardiac Abnormalities in IgA Nephropathy

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          The absence of diurnal blood pressure rhythm is characteristic of patients with chronic glomerulonephritis already before they develop hypertension. The prognostic importance and possible target organ-damaging effect of the absence are unknown. Simultaneously, 24-hour ambulatory blood pressure monitoring and echocardiographic investigations were done in 12 normotensive and 38 hypertensive IgA nephropathy patients. The hypertensive patients were treated with either angiotensin-converting enzyme inhibitor (ACEI) alone or in combination with a non-dihydropyridine calcium channel blocker. The absence of a night-time blood pressure reduction was frequent in both groups (5/12 vs. 20/38). In the hypertensive patients, blood pressure and left ventricular mass index were higher (124.6 ± 23.3/81.2 ± 15.3 vs. 106.6 ± 33.4/67.4 ± 21.8 mm Hg, p < 0.001, and 124.1 ± 46.2 vs. 89.2 ± 45.6 g/m<sup>2</sup>, p < 0.01). Diastolic left ventricular function was better in normotensive patients, in whom E wave/A wave ratio (E/A) and decelaration time values correlated closely with the diastolic diurnal index (E/A, r = 0.86, p < 0.01; DT, r = –0.70, p < 0.01). In the hypertensive patients, both the left ventricular wall thickness and diastolic function were significantly related to nighttime blood pressure and diurnal index values, but there was no relationship with daytime blood pressure. In conclusion, in IgA nephropathy patients there are mild cardiac abnormalities before they develop hypertension, the abnormalities bearing the closest correlation with the decrease in diurnal blood pressure rhythm. These data suggest the inefficacy of ACEI and calcium channel blockers in treating nighttime hypertension and in reestablishing diurnal rhythm. These phenomena are of great importance in the development of left ventricular hypertrophy and diastolic malfunction.

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          Echocardiographic assessment of left ventricular hypertrophy: comparison to necropsy findings.

          To determine the accuracy of echocardiographic left ventricular (LV) dimension and mass measurements for detection and quantification of LV hypertrophy, results of blindly read antemortem echocardiograms were compared with LV mass measurements made at necropsy in 55 patients. LV mass was calculated using M-mode LV measurements by Penn and American Society of Echocardiography (ASE) conventions and cube function and volume correction formulas in 52 patients. Penn-cube LV mass correlated closely with necropsy LV mass (r = 0.92, p less than 0.001) and overestimated it by only 6%; sensitivity in 18 patients with LV hypertrophy (necropsy LV mass more than 215 g) was 100% (18 of 18 patients) and specificity was 86% (29 of 34 patients). ASE-cube LV mass correlated similarly to necropsy LV mass (r = 0.90, p less than 0.001), but systematically overestimated it (by a mean of 25%); the overestimation could be corrected by the equation: LV mass = 0.80 (ASE-cube LV mass) + 0.6 g. Use of ASE measurements in the volume correction formula systematically underestimated necropsy LV mass (by a mean of 30%). In a subset of 9 patients, 3 of whom had technically inadequate M-mode echocardiograms, 2-dimensional echocardiographic (echo) LV mass by 2 methods was also significantly related to necropsy LV mass (r = 0.68, p less than 0.05 and r = 0.82, p less than 0.01). Among other indexes of LV anatomy, only measurement of myocardial cross-sectional area was acceptably accurate for quantitation of LV mass (r = 0.80, p less than 0.001) or diagnosis of LV hypertrophy (sensitivity = 72%, specificity = 94%).(ABSTRACT TRUNCATED AT 250 WORDS)
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            Clinical relevance of nighttime blood pressure and of daytime blood pressure variability.

            The purpose of this study was to assess whether hypertensive target organ damage is related to average nighttime blood pressure (BP) and to BP variability. Sixty-seven normotensive subjects and 171 borderline, 309 mild, 140 moderate, and 41 severe hypertensive patients were studied with noninvasive ambulatory BP monitoring. Each subject was assigned a target organ damage score of 0 to 5 on the basis of funduscopic changes and degree of left ventricular hypertrophy calculated from electrocardiogram and chest roentgenogram. When the 728 subjects were subdivided into five classes of increasing daytime BP, in each class a significantly higher degree of target organ damage was present in the subjects with higher nighttime diastolic BP. A similar, although nonsignificant, trend was observed in the subjects with higher nighttime systolic BP. In particular, higher nighttime BP levels were accompanied by a more severe degree of left ventricular hypertrophy. As for variability, subjects with higher daytime systolic BP SD, but not with higher daytime diastolic SD, displayed a more severe degree of target organ damage; this was accounted for by a higher degree of retinal abnormalities. The association between target organ damage and systolic BP SD was present both in men and women, while that with nighttime BP was present only in men. No relationship was found between degree of cardiovascular complications and peaks of pressure. These results suggest that a reduced day-night BP difference and an increased daytime BP variability, evaluated as the SD, are associated with a higher degree of hypertensive cardiovascular complications. Whether this BP profile is the cause or the consequence of target organ damage remains to be established.
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              BP as a determinant of cardiac left ventricular muscle mass


                Author and article information

                Am J Nephrol
                American Journal of Nephrology
                S. Karger AG
                October 1999
                26 November 1999
                : 19
                : 5
                : 546-551
                aNephrological Center and Second Department of Medicine, University Medical School of Pécs and bFresenius Dialysis Center, Pécs, Hungary
                13517 Am J Nephrol 1999;19:546–551
                © 1999 S. Karger AG, Basel

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