Biomedical subjects
Publications and source records attributed to Michael Bursztyn.
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Cardiovascular events are clustered in the morning hours, after increases in blood pressure and heart rate that accompany awakening and arising. Similar hemodynamic changes occur during the night after nocturnal awakening and getting up. Such changes are common among older patients who have nocturia frequently and rise to urinate. We tested the hypothesis that nocturia may be associated with increased mortality in a population sample of 456 subjects born from 1920 to 1921, examined in 1990, and followed for total mortality until 2002. At baseline, they were questioned about nocturia (> or =2 times at night) as part of a detailed questionnaire and examination. Twelve-year survival was significantly lower (61% vs 72%, p = 0.0206) among subjects reporting nocturia (n = 160, 64% men) compared with those without nocturia (n = 296, 50% men). After accounting for numerous confounders, a proportional hazard model determined the mortality hazard ratio (HR) for nocturia alone to be 0.89 (95% confidence interval [CI] 0.55 to 1.43). The interaction between nocturia and previous coronary heart disease (CHD) was highly significant (p <0.0001), with an interaction variable HR of 2.16 (95% CI 1.01 to 4.61). Survival of patients who had CHD with nocturia (n = 54) versus those without nocturia (n = 65) was 44% versus 66% (p = 0.0201). Among patients with CHD, the mortality HR for nocturia was 2.11 (95% CI 1.16 to 4.00). In conclusion, nocturia is a significant independent predictor of mortality among 70-year-old patients with known CHD and thus warrants special attention.
In humans, intrauterine growth-restricted newborns are prone to develop hypertension as adults. We studied a rat model of pregnancy-induced hypertension associated with intrauterine growth restriction (IUGR) produced by chronic administration of insulin. Fetuses of hyperinsulinemic dams (HDs) were smaller than those of normal dams (5.1+/-0.4 g versus 5.6+/-0.1 g, respectively; P<0.05). At 16 weeks of age, tail-cuff systolic blood pressure was measured, the rats were placed in metabolic cages and euthanized, and the kidneys were examined. Male but not female offspring of HDs (n=9) had higher blood pressure than normal-pregnancy offspring (n=12; 148+/-11 mm Hg versus 118+/-14 mm Hg; P<0.004). In contrast to other models, there was no difference in ours in the number and volume of glomeruli. However, there were significantly greater glomerular, tubulointerstitial, and vascular damage indices in the kidneys of male HD offspring versus controls (2.01+/-0.34 versus 1.08+/-0.16, 1.80+/-0.34 versus 0.76+/-0.12, and 2.13+/-0.81 versus 0.78+/-0.16, respectively; P<0.0001), with similar tubulointerstitial findings in females. Increased expression of collagen type IV, a kidney damage marker indicating fibrosis, was found in the tubulointerstitium. This may be associated with downregulation of bone morphogenetic protein 6, a presumptive antifibrogenic agent, at the end of gestation. In conclusion, male offspring of HDs displayed IUGR and adult hypertension accompanied by several indices of renal fibrosing damage, mainly in the renal tubulointerstitium. Our findings suggest that there is >1 pathway of fetal programming leading from IUGR to development of hypertension in later life.
BACKGROUND: White-coat hypertension and masked hypertension have clinical and prognostic consequences. However, reproducibility of these phenomena is unknown. We examined the reproducibility of the white-coat and masking effects with real-life ambulatory blood pressure monitoring (ABPM). METHODS: In a retrospective analysis of a prospectively assembled ABPM database there were 196 subjects (age 58+/-16 years, 59% female, 73% treated for hypertension) who underwent repeat ABPM for standard clinical indications. White-coat hypertension (or isolated manual uncontrolled hypertension) was defined as normal (<135/85 mmHg) awake blood pressure (BP) and abnormal (>or=140/90 mmHg) manual BP. Masked hypertension (or isolated ambulatory uncontrolled hypertension) was defined as abnormal awake BP with normal manual BP. RESULTS: Treated and untreated subjects had similar distribution among hypertension subgroups; 16% white-coat hypertension (in treated subjects, isolated manual uncontrolled hypertension), 13% masked hypertension (in treated subjects, isolated ambulatory uncontrolled hypertension), 59% uncontrolled hypertension, 12% normal blood pressure (or controlled hypertension). In the second session the prevalence of white-coat and masked hypertension increased. Of 31 subjects with white-coat hypertension in the first session 19 (61%) remained ambulatory normotensive in the second session, while 18 of 25 (72%) masked hypertensive subjects remained ambulatory hypertensive. The reproducibility of the systolic manual-awake blood pressure difference was not inferior to that of other ambulatory variables. In untreated subjects the reproducibility of white-coat hypertension, masked hypertension and the white-coat effect was even better. CONCLUSION: In a real-life ABPM database, we found white-coat hypertension and the masking phenomenon to be reasonably reproducible, as compared to other BP variables.
PURPOSE: The American Heart Association Council on High Blood Pressure Research recently issued recommendations for blood pressure measurement in humans. According to these recommendations, normal 24-hour ambulatory blood pressure is defined as less than 130/80 mm Hg. Concurrently, normal daytime and nighttime blood pressure levels are defined as less than 135/85 mm Hg and less than 120/70 mm Hg, respectively. Our aim was to investigate the intrinsic compatibility of these blood pressure cutoffs in clinical practice. SUBJECTS AND METHODS: We analyzed 4121 consecutive ambulatory blood pressure measurement sessions. Age was 57 +/- 7 years, 53% were female, and 64% and 9% were treated for hypertension and diabetes, respectively. Body mass index was 27 +/- 4 kg/m2, and manual blood pressure was 148 +/- 22/85 +/- 12 mm Hg. Subjects were classified as having normal 24-hour blood pressure if the corresponding value was less than 130/80 mm Hg. Normal awake-sleep blood pressure was diagnosed if awake blood pressure was less than 135/85 mm Hg and sleep blood pressure was less than 120/70 mm Hg. RESULTS: Concordance between the cutoffs was found in 92% of the subjects (kappa = 0.77). Among the 8% of discordant subjects, only 1% were hypertensive applying the 24-hour (but not awake-sleep) blood pressure values, whereas 7% were hypertensive according to awake-sleep but not 24-hour blood pressure values (P <.0001). CONCLUSIONS: In real-life ambulatory blood pressure measurement, a generally good agreement was found between the recently issued ambulatory blood pressure normality suggestions. However, some subjects are classified as hypertensive only according to one of these methods, more often by the awake-sleep cutoff of 135/85 and 120/70 mm Hg. This discordance may be significant in large-scale clinical blood pressure monitoring.
OBJECTIVE: Adrenergic alpha-antagonists have been suggested to confer lesser protection, compared to diuretics, when used as first agents for hypertension. While differences in clinic blood pressure may be partly responsible, this inferiority is unexpected in light of the metabolic advantages of alpha-blockade. The aim of this study was to evaluate the relationship between use of alpha-blockers and blood pressure dipping. METHODS: A database of a 24-h ambulatory monitoring service was cross-sectionally evaluated for associations between antihypertensives and dipping. There were 681 treated subjects during a 3-year period (age 63 +/- 14, 57% female). RESULTS: Overall, 78 of 681 treated hypertensive subjects used alpha-blockers (11%). Nine per cent of dippers and 16% of nondippers were treated with alpha-blockade, odds ratio 2.0. Whereas clinic, 24-h, and awake blood pressures were similar in alpha-blocker users and nonusers, sleep blood pressure was significantly higher in the former group. Furthermore, significantly fewer subjects given alpha-blockers had a controlled sleep blood pressure. Among alpha-blocker nonusers sleep blood pressure was the best controlled category, whereas in alpha-blocker users manual blood pressure had the highest rate of control. Generally, accounting for covariates of alpha-blockade (age, gender, diabetes, total number of medications) did not influence the above-mentioned trends. Finally, a limited negative dose-response relationship between alpha-blockade and dipping magnitude was also noticed. CONCLUSIONS: We found a significant negative association between adrenergic alpha-blockade and the magnitude of sleep-related blood pressure decline. Awaiting results from interventional studies, this may suggest a need to perform ambulatory monitoring in patients given alpha-blocking agents (or at least supine and standing measurements), and may partially clarify the inferiority of doxazosin in the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT).
BACKGROUND: Several studies have suggested that an early increase in renal nitric oxide (NO) production or activity mediates pathophysiologic and morphologic changes in diabetic nephropathy. To evaluate the role of NO in developing diabetic kidney disease, we studied the NO system in streptozotocin (STZ)-induced diabetic rats for a period of 8 weeks. METHODS: Control rats, STZ-induced diabetic rats, and STZ-induced diabetic rats treated with insulin were monitored and sacrificed at 1, 2, and 8 weeks. Urinary cGMP was measured, and the levels and activity of NO synthase (NOS) isoforms in the kidney cortex were determined at specific times by immunoblotting and diaphorase staining. RESULTS: Diabetic rats had increased kidney weight, urinary volume, glucose, sodium and potassium excretion, which was precluded by insulin treatment. Creatinine clearance was increased in the diabetic group and reversed by insulin treatment. Urinary cGMP decreased by 71, 93, and 92% at 1, 2, and 8 weeks of diabetes, respectively, compared with the control animals. Insulin treatment curtailed the urinary cGMP reduction in diabetic animals. Total NOS activity in the renal cortex was reduced by 65, 52, and 44% after 1, 2, and 8 weeks of diabetes, respectively, and returned to normal levels upon insulin treatment. NADPH diaphorase staining of renal cortical slices showed a 77, 63, and 70% decrease in neuronal NOS isoform activity in the macula densa after 1, 2, and 8 weeks of diabetes, respectively, compared with control non-diabetic animals. This reduction was normalized by insulin treatment. Endothelial NOS protein expression in the kidney cortex tended to increase after 1 week of diabetes and its level was elevated significantly after 2 and 8 weeks of diabetes. However, neuronal NOS protein expression in the kidney cortex was reduced by 52% in 2-week diabetic animals, but this reduction was normalized by insulin treatment. CONCLUSIONS: The decreased renal NOS activity during the late phase of diabetes is partially associated with a decrease in neuronal NOS activity and protein expression in kidney macula densa.
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BACKGROUND: The prevalence and implications of masked hypertension are under investigation. The aim of this study was to investigate the clinical characteristics associated with masked hypertension in subjects referred for ambulatory blood pressure (BP) monitoring. METHODS: We analyzed 1494 BP monitoring sessions. A subject was considered to have isolated clinic hypertension if clinic BP was > or =140/90 mmHg and awake BP was <135/85 mmHg. Masked hypertension was diagnosed when clinic BP was <140/90 mmHg and awake BP was > or =135/85 mmHg. RESULTS: Of 1494 individuals, 16% had normal BP, 11% had isolated clinic hypertension, 61% had hypertension, and 11% had masked hypertension. Subjects with masked hypertension were younger and more likely to be male than subjects with isolated clinic hypertension, and their awake heart rate was significantly higher. A negative correlation was found between the awake-clinic systolic BP difference and clinic systolic BP (r = -0.7, P < .0001). The reproducibility of the masking phenomenon was comparable to that of other variables. CONCLUSIONS: In a group of consecutive subjects referred for ambulatory BP monitoring, masked hypertension was found to be as common as isolated clinic hypertension. Masking was correlated with male sex, young age, and higher awake heart rate, thus suggesting a causal relationship with greater daytime physical activity. The linear association of the masking and the white-coat effects to clinic BP suggests that regression toward the mean may partially explain these phenomena.
The objective of this prospective study was to examine the association between serum levels of TNF (tumor-necrosis factor) and IL-6 (interleukin-6) and left ventricular mass in hypertensive patients. Hypertensive patients currently receiving medical therapy were eligible. All subjects underwent echocardiography with measurements of left ventricular (LV) mass and ejection fraction (EF) and had serum levels of TNF and IL-6 measured by ELISA immunoassay. 35 subjects (20F, 15M; mean age 56.4 +/- 10.5 yrs) were studied. 19 patients (54%) had elevated LV mass. Of these patients, 6 (32%) had detectable serum TNF levels and 1 (7%) had detectable IL-6 levels, (p = NS). Hypertensive patients with elevated LV mass do not consistently exhibit elevated cytokine levels when compared to those with normal LV mass.
OBJECTIVE: Blood pressure dipping pattern has clinical and prognostic consequences. However, reproducibility of night-time blood pressure fall during 24-h ambulatory blood pressure monitoring is considered limited. This limited reproducibility is possibly a result of inadequate day-night definitions. We retrospectively examined the reproducibility of blood pressure dipping in clinical practice, applying a method that accounts for sleep-awake states and does not rely on arbitrary day-night definitions. We also examined dipping repeatability in subjects with changing blood pressure. METHODS: Of 962 consecutive ambulatory measurements performed in our unit during a 3-year period, 100 patients (age 60+/-15) had a prior session, and were the subjects of this study. Based on patients' report we defined 'awake blood pressure' as the average of pressure recordings while the subject was awake, including night-time arousals, and 'sleep blood pressure' as the average of pressure recordings while the subject was sleeping, including afternoon naps. RESULTS: We found systolic blood pressure dipping not less reproducible than 24-h, awake- and sleep systolic blood pressure, as evaluated by both Pearson correlations (r=0.52 versus 0.5, 0.5, 0.49, respectively, P < or =0.0002 in all), and Bland-Altman repeatability. In a subgroup of 35 subjects (age 63+/-15) with at least 10 mmHg change in systolic blood pressure between the two sessions, systolic blood pressure dipping remained reproducible (r=0.45, P<0.007). CONCLUSIONS: When interpreted in a way that accounts for sleep-awake pattern, sleep-induced systolic blood pressure dipping in clinical practice is a very reproducible feature of ambulatory blood pressure monitoring, in accordance with its vital prognostic implications.
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