The heart is involved in more than one third of patients with primary (AL) amyloidosis at diagnosis and it is by far the most common cause of death. Rhythm and conduction abnormalities generally represent the terminal event. The aims of this study were to determine the spectrum of Holter abnormalities found in AL amyloidosis and to assess their prognostic significance, particularly in relation to sudden death. Fifty-one patients with AL amyloidosis were included, and all of them had a complete history, physical examination, two-dimensional echocardiography, and 24-hour Holter monitoring. Fifty-five percent of these patients had echographic signs of heart involvement and 23% had heart failure. Complex ventricular arrhythmias were found in 57% of patients, couplets in 29%, and nonsustained ventricular tachycardia in 18%. Overall median survival was 23.4 months. Congestive heart failure, echocardiographic abnormalities, and Holter abnormalities adversely affected survival. The multivariate analysis demonstrated that interventricular septum thickness and couplets were independent predictors of survival. The presence of couplets correlated with sudden death. Holter monitoring may contribute to assessing the prognosis of patients with AL amyloidosis.

To assess the prevalence of an impaired diurnal blood pressure (BP) pattern in a population of both normotensive and hypertensive diabetics, noninvasive ambulatory BP monitoring (SpaceLabs 5200, Redmond, WA) was performed in 96 outpatients with type 2 diabetes (47 normotensives and 48 hypertensives) and in 103 control subjects without diabetes (50 normotensives and 53 hypertensives). Mean 24 h and daytime (06:00 to 22:00) BP and heart rate (HR) were not statistically different in diabetic patients compared to nondiabetic ones. Nighttime (22:00 to 06:00) BP and HR tended to be higher in both normotensive and hypertensive diabetics, although not significantly. Heart rate, diastolic BP (DBP), and especially the nocturnal systolic BP (SBP) decrease, were less marked in both normotensive and hypertensive diabetics, with a consequent increase in rate-pressure. A significant correlation was found between the percent decrease in nighttime SBP and the decrease in orthostatic SBP in casual BP measurements. The analysis of individual recordings allowed us to detect an impaired circadian pattern (the disappearance of the nocturnal BP decrease or a paradoxical BP increase) in 30% of the normotensive and 31% of the hypertensive diabetics (v 6% of the normotensive and 6.4% of the hypertensive nondiabetic subjects). As the absence of a nocturnal BP fall has been associated with the increased prevalence of left ventricular hypertrophy and atherosclerotic cardiovascular disease, its detection by ambulatory monitoring might be of prognostic and therapeutic importance.

The aim of this study was to compare the effects of trandolapril and losartan on plasminogen activator inhibitor type 1 (PAI-1) levels and insulin sensitivity in hypertensive postmenopausal women. We studied 89 hypertensive (diastolic blood pressure >90 and <110 mm Hg) postmenopausal women, aged 51 to 60 years not taking any hormone replacement therapy. Diabetic, obese, and smoking patients were excluded. After a 4-week placebo period, they were randomized to receive 2 mg of oral trandolapril (n=45) or 50 mg of oral losartan (n=44) for 12 weeks according to a double-blind, parallel group design. At the end of the placebo and active treatment periods, blood pressure (BP) was measured, plasma samples were drawn to evaluate PAI-1 antigen levels, and insulin sensitivity was assessed. Both trandolapril and losartan reduced systolic BP (by a mean of 16.9 mm Hg and 15.2 mm Hg, respectively, P < .01 v placebo) and diastolic BP (by a mean of 13.1 mm Hg and 11.9 mm Hg, respectively, P < .01 v placebo) with no difference between the two treatments. The PAI-1 antigen levels were significantly decreased by trandolapril (from 36.9+/-21 ng/dL to 27.2+/-17 ng/dL, P < .05), but not by losartan (from 35.3+/-22 ng/dL to 37.1+/-23 ng/dL, P=not significant). Glucose infusion rate was significantly increased by trandolapril (from 6.67+/-0.56 mg/min/kg to 7.9+/-0.65 mg/min/kg, P < .05), but was not significantly modified by losartan (from 6.7+/-0.47 mg/min/kg to 6.9+/-0.50 mg/min/kg, P= not significant). In the trandolapril group the PAI-1 decrease correlated with glucose infusion rate increase (r=0.36, P=.045) These results provide evidence of different effects of angiotensin converting enzyme inhibitors and AT1 antagonists on fibrinolysis and suggest that the PAI-1 decrease induced by angiotensin converting enzyme inhibitors is related to their action on insulin sensitivity and is not dependent on angiotensin II antagonism but rather on other mechanisms. It remains to be seen whether these findings apply to other patient populations than postmenopausal women.

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