BACKGROUND:Patients with aortic stenosis have a high prevalence of coronary artery disease, but there is little information about the association of coronary artery disease and carotid artery disease.METHODS:The study includes 317 consecutive patients with aortic stenosis, who underwent carotid and coronary angiography during the same catheterization before aortic valve replacement.RESULTS:At univariate analysis, the prevalence of coronary artery disease was associated with (1) presence of carotid artery disease (P < .001); (2) angina pectoris as presentation symptom (P < .001); (3) age more than 65 years (P < .05); and (4) hypertension (P < .05). At multivariate analysis, only carotid artery disease, angina, and age emerged as independent predictors of coronary artery disease. The combination of 2 variables (carotid artery disease, angina) allowed the identification of 4 groups, with decreasing prevalence of coronary artery disease: (1) angina+/carotid artery disease+: 85%; (2) angina-/ carotid artery disease+: 50%; (3) angina+/carotid artery disease-: 41%; (4) angina-/carotid artery disease-: 21% (P < .001).CONCLUSION:In patients with symptomatic aortic stenosis, the presence of significant carotid artery disease is a strong marker of significant coronary artery disease.

The aim of this study was to assess the blood pressure profile of chronic renal failure in comparison with essential hypertension. Thirty hypertensive patients with chronic renal failure due to non-vascular nephropathies were matched by age, sex, and mean 24 h blood pressure, with 30 patients affected by uncomplicated mild-to-moderate essential hypertension. They were studied in an open hospital ward. Diet, meal times, sleep times, and activity schedules were standardized. Noninvasive, automatic, blood pressure recordings were performed for 48 h at sampling intervals of 15 min. The mean 24 h blood pressure almost coincided in the two groups. However, in essential hypertension a mean (+/- SD) nocturnal fall of systolic and diastolic blood pressure was found (12.7 +/- 3.8 and 12.9 +/- 4.8 mm Hg, respectively), while renal patients displayed an average nocturnal increase of 2.7 +/- 8.9 mm Hg and 3.7 +/- 7.8 (P less than .001). The renal patients had also higher heart rates, with a significantly blunted nocturnal fall (4.4 +/- 4.5 beats/min as compared to 9.3 +/- 3.1 beats/min of essential hypertension; P less than .001). Among the renal patients, the day-night blood pressure changes showed no significant correlation with age, creatinine clearance, hematocrit, nocturnal change in heart rate, or day or night mean blood pressure levels. These data suggest that an abnormal day-night pattern of blood pressure is present in chronic renal failure patients independently from external interfering factors. Hence, casual measurements of blood pressure confined to daytime may underestimate a hypertensive condition associated with chronic renal failure.

The purpose of this prospective study was to compare two methods of evaluating antihypertensive treatment efficacy: the traditional sphygmomanometric method and automatic home recording. Thirty hypertensive patients were studied who had been on antihypertensive therapy for at least 3 months. In the first 3 weeks of study their therapy was left unchanged and their diastolic blood pressures, measured with the traditional sphygmomanometer (weekly morning visit in the outpatient clinic; three successive recordings at 5-min intervals; subject seated), were always higher than 95 mmHg. During the following 8 weeks, the physician tried to reduce diastolic blood pressure to not greater than 90 mmHg by changing or increasing the therapy. Before and after any modification in therapy, noninvasive, automatic home, blood pressure monitorings for 24 hours were obtained and analyzed with Halberg's method of single cosinor, but were not made available to the physician until the end of the study. Automatic recordings showed that 18 patients had already had a circadian diastolic mesor less than or equal to 90 mmHg under the original drug regimen. By changing or increasing the therapy, no additional pressure decrease was seen in the home pressure recordings of the whole group of patients, whereas the sphygmomanometric diastolic pressures of 15 patients fell under 90 mmHg. Our study provides additional evidence that casual sphygmomanometric measurements can be misleading when one tries to assess the efficacy of antihypertensive therapy, and a cause of potential overtreatment.

The aim of this study was to assess the possible correlations between casual measurements and automatic monitoring analyzed with the chronobiologic technique in hospitalized hypertensive patients. Forty-three patients (24 men and 19 women) with mild to moderate essential hypertension were studied in an open hospital ward 5 to 7 days after admission. Meal times, sleep times, and visiting hours were standardized. A clinical value of blood pressure was calculated as the arithmetic mean of three sphygmomanometric measurements taken in the morning (patient seated; 5-min interval between measurements). Then, a basal value of blood pressure was considered as the lowest systolic and the lowest diastolic blood pressure among six sphygmomanometric measurements obtained every 5 min (patient supine). Noninvasive, automatic recording of blood pressure was also obtained every 15 min for 24 hours by a quasiportable oscillometric instrument. Blood pressure recordings were analyzed according to the "cosinor" method of Halberg. On average, clinical blood pressure was 160/96 +/- 14/10 mmHg, significantly higher (p less than 0.005) than either basal blood pressure (150/91 +/- 12/8 mmHg) or 24-h recorded blood pressure mesor (144/88 +/- 13/9 mmHg). The differences were not entirely due to diurnal variations, since morning casual measurements were significantly higher than daytime average blood pressure. A chronobiologic assessment of hypertension in hospitalized patients is more representative of true blood pressure behavior, not only because of the multiple recordings but also because of the absence of an alarm reaction that may trigger a pressor response.