Showing papers by "Christopher J. O'Donnell published in 1998"

Fish Consumption and Risk of Sudden Cardiac Death

Abstract: Context.— Dietary fish intake has been associated with a reduced risk of fatal cardiac end points, but not with nonfatal end points. Dietary fish intake may have a selective benefit on fatal arrhythmias and therefore sudden cardiac death. Objective.— To investigate prospectively the association between fish consumption and the risk of sudden cardiac death. Design.— Prospective cohort study. Setting.— The US Physicians’ Health Study. Patients.— A total of 20 551 US male physicians 40 to 84 years of age and free of myocardial infarction, cerebrovascular disease, and cancer at baseline who completed an abbreviated, semiquantitative food frequency questionnaire on fish consumption and were then followed up to 11 years. Main Outcome Measure.— Incidence of sudden cardiac death (death within 1 hour of symptom onset) as ascertained by hospital records and reports of next of kin. Results.— There were 133 sudden deaths over the course of the study. After controlling for age, randomized aspirin and beta carotene assignment, and coronary risk factors, dietary fish intake was associated with a reduced risk of sudden death, with an apparent threshold effect at a consumption level of 1 fish meal per week (P for trend=.03). For men who consumed fish at least once per week, the multivariate relative risk of sudden death was 0.48 (95% confidence interval, 0.240.96; P=.04) compared with men who consumed fish less than monthly. Estimated dietary n-3 fatty acid intake from seafood also was associated with a reduced risk of sudden death but without a significant trend across increasing categories of intake. Neither dietary fish consumption nor n-3 fatty acid intake was associated with a reduced risk of total myocardial infarction, nonsudden cardiac death, or total cardiovascular mortality. However, fish consumption was associated with a significantly reduced risk of total mortality. Conclusion.— These prospective data suggest that consumption of fish at least once per week may reduce the risk of sudden cardiac death in men. JAMA. 1998;279:23-28

Evidence for Association and Genetic Linkage of the Angiotensin-Converting Enzyme Locus With Hypertension and Blood Pressure in Men but Not Women in the Framingham Heart Study

Abstract: Background—There is controversy regarding the association of the angiotensin-converting enzyme deletion-insertion (ACE D/I) polymorphism with systemic hypertension and with blood pressure. We investigated these relations in a large population-based sample of men and women by using association and linkage analyses. Methods and Results—The study sample consisted of 3095 participants in the Framingham Heart Study. Blood pressure measurements were obtained at regular examinations. The ACE D/I polymorphism was identified by using a polymerase chain reaction assay. In logistic regression analysis, the adjusted odds ratios for hypertension among men for the DD and DI genotypes were 1.59 (95% confidence interval [CI], 1.13 to 2.23) and 1.18 (95% CI, 0.87 to 1.62), respectively, versus II (χ2 P=.02). In women, adjusted odds ratios for the DD and DI genotypes were 1.00 (95% CI, 0.70 to 1.44) and 0.78 (95% CI, 0.56 to 1.09), respectively (P=.14). In linear regression analysis, there was an association of the ACE DD ...

Reduced Heart Rate Variability and New-Onset Hypertension Insights Into Pathogenesis of Hypertension: The Framingham Heart Study

Abstract: Heart rate variability (HRV) is a useful noninvasive tool to assess cardiac autonomic function. The purpose of this study was to (1) compare measures of HRV between hypertensive and normotensive subjects and (2) examine the role of HRV as a predictor of new-onset hypertension. The first 2 hours of ambulatory ECG recordings obtained from 931 men and 1111 women attending a routine examination at the Framingham Heart Study were processed for HRV. Three time-domain and 5 frequency-domain variables were studied: standard deviation of normal RR intervals (SDNN), percentage of differences between adjacent normal RR intervals exceeding 50 milliseconds, square root of the mean of squared differences between adjacent normal RR intervals, total power (0.01 to 0.40 Hz), high frequency power (HF, 0.15 to 0.40 Hz), low frequency power (LF, 0.04 to 0.15 Hz), very low frequency power (0.01 to 0.04 Hz), and LF/HF ratio. On cross-sectional analysis, HRV was significantly lower in hypertensive men and women. Among 633 men and 801 women who were normotensive at baseline (systolic blood pressure <140 mm Hg and diastolic blood pressure <90 mm Hg and not receiving antihypertensive treatment), 119 men and 125 women were newly hypertensive at follow-up 4 years later. After adjustment for factors associated with hypertension, multiple logistic regression analysis revealed that LF was associated with incident hypertension in men (odds ratio per SD decrement [OR], 1.38; 95% confidence interval [CI], 1.04 to 1.83) but not in women (OR, 1.12; 95% CI, 0.86 to 1.46). SDNN, HF, and LF/HF were not associated with hypertension in either sex. HRV is reduced in men and women with systemic hypertension. Among normotensive men, lower HRV was associated with greater risk for developing hypertension. These findings are consistent with the hypothesis that autonomic dysregulation is present in the early stage of hypertension.

Heritability of heart rate variability: the Framingham Heart Study.

Abstract: Background —There is evolving evidence that heart rate (HR) is genetically determined. Heart rate variability (HRV) measured by power spectral analysis provides quantitative phenotypic markers of autonomic nervous system activity. Reported determinants of HR and HRV only partially explain their variability in the population. The purpose of this study was to assess the heritability of HR and HRV and estimate the contribution of genetic factors to their variance. Methods and Results —Subjects who underwent ambulatory recordings at a routine examination were eligible; subjects with congestive heart failure, coronary artery disease, diabetes mellitus, and those taking cardioactive medications were excluded. We analyzed high-frequency power, low-frequency power, very low-frequency power, total power, low-frequency/high-frequency ratio, and the standard deviation of normal R-R intervals from 2-hour continuous ECG recordings. Heritability analysis was done by studying correlations between siblings (n=682, in 291 sibships, 517 pairs) and between spouse pairs (n=206 pairs) after adjusting for important covariates. Results from separate models were combined to estimate the components of variance attributable to measured covariates, additive genetic effects (heritability), and household effects. After adjusting for covariates, the correlations were consistently higher among siblings (0.21 to 0.26) compared with spouses (0.01 to 0.19). The measured covariates in general accounted for 13% to 40% of the total phenotypic variance, whereas genetic factors accounted for 13% to 23% of the variation among HR and HRV measures. Conclusions —Heritable factors may explain a substantial proportion of the variance in HR and HRV. These results highlight the contribution of genetic versus environmental factors to autonomic nervous system activity.

Elderly patients receive less aggressive medical and invasive management of unstable angina: potential impact of practice guidelines.

Abstract: Background The Agency for Health Care Policy and Research (AHCPR) released a practice guideline on the diagnosis and management of unstable angina in 1994. Objective To examine practice variation across the age spectrum in the management of patients hospitalized with unstable angina 2 years before release of the AHCPR guideline. Design Retrospective cohort. Setting Urban academic hospital. Patients All nonreferral patients diagnosed as having unstable angina who were hospitalized directly from the emergency department to the intensive care or telemetry unit between October 1, 1991, and September 30, 1992. Measurements Percentage of eligible patients receiving medical treatment concordant with 8 important AHCPR guideline recommendations. Results Half of the 280 patients were older than 66 years; women were older than men on average (70 vs 64 years; P P P P 2 , P Conclusions Older patients were less likely to receive standard therapies for unstable angina before release of the 1994 AHCPR guideline. Patients presenting with congestive heart failure also received care that was more discordant with guideline recommendations. The AHCPR guideline allows identification of patients who receive nonstandard care and, if applied to those patients with the greatest likelihood to benefit, could lead to improved health care delivery.

Electrocardiographic and clinical predictors of acute myocardial infarction in patients with unstable angina pectoris.

Abstract: Among patients with unstable angina pectoris (UAP), those who have non–ST-elevation acute myocardial infarction (AMI) are at higher risk for subsequent adverse events. To determine predictors of AMI in patients with UAP, we studied consecutive nonreferral patients with UAP or AMI admitted from the emergency department to the intensive care or telemetry units of an urban teaching hospital over 1 year. There were 280 study patients (mean age 66 years, 1/3 women); 24% had AMI at presentation, whereas 76% had UAP without evidence of AMI. Thresholds of ≥3 involved leads (odds ratio [OR] 3.3; 95% confidence intervals [CI] 1.6 to 6.9) and ≥0.2 mV (OR 5.1; 95% CI 2.2 to 11.6) of ST depression on the presenting electrocardiogram were strongly associated with AMI. The multivariate predictors of AMI were reported duration of symptoms >4 hours (OR 3.8; 95% CI 1.9 to 7.3), absence of prior revascularization (OR 3.5; 95% CI 1.6 to 7.5), absence of β-blocker use before presentation (OR 2.8; 95% CI 1.3 to 5.8), and presence of new ST depression (OR 2.8; 95% CI 1.4 to 5.7). Using the 4 multivariate predictors, a prediction rule was developed. The percentages of patients with AMI when 0, 1, 2, 3, or 4 characteristics were present, respectively, were 7%, 6%, 24%, 46%, and 83% (p

Isolated Systolic Hypertension: an Important Cardiovascular Risk Factor

Abstract: Hypertension is an established risk factor for cardiovascular disease morbidity and mortality. Randomized trials of antihypertensive therapy have demonstrated the benefits of treating diastolic blood pressure, and recently the value of treating isolated systolic blood pressure has also been established. There is an excess risk of cardiovascular disease in subjects with borderline isolated systolic hypertension. In fact, data from men screened for the Multiple Risk Factor Intervention Trial show that the great majority of excess deaths are in those with high-normal systolic blood pressure or with stage 1 hypertension, i.e., systolic blood pressure 130 to 159 mmHg. Similarly, data from the Framingham Heart Study and the Physicians' Health Study emphasize the importance of mild elevations of systolic blood pressure. As age increases the hemodynamic patterns of blood pressure change due to an increase in large artery stiffness, and borderline isolated systolic hypertension becomes the dominant form of hypertension. These facts make the prevention and control of borderline isolated systolic hypertension a key strategic challenge in the effort to prevent excess mortality attributable to blood pressure levels above normal.

Cardiovascular risks of hypertension: lessons from observational studies.

Abstract: Hypertension is an acknowledged major risk factor for cardiovascular disease and death in both men and women. Despite a historical focus by clinicians on the importance of diastolic blood pressure (DBP) risks, epidemiologic data from numerous large-scale studies have clearly demonstrated that both systolic blood pressure (SBP) and DBP are important determinants of cardiovascular risk. Recent analyses have described notable risks associated with isolated and borderline elevations of SBP, which predominate in the elderly, emphasizing the independent contribution of elevated SBP in determining overall risk. Overviews of large-scale treatment trials show that antihypertensive drug treatment confers a favorable net clinical benefit in patients with diastolic and isolated systolic hypertension, and the magnitude of risk reduction is comparable to that expected from the observational data. However, at any level of SBP or DBP, the absolute magnitude of risk varies widely depending on the burden of coexisting risk factors present. Therefore, it is essential that decisions regarding the urgency, risks and benefits of antihypertensive drug treatments be informed by accurate determinations of overall cardiovascular risk.

Is There a Racial Predisposition to Hypertension

Abstract: Cooper and Kaufman call attention to the difficulty of evaluating racial predisposition to disease.1 They correctly point out that “racial” predisposition to pathology is usually taken to imply the existence of an inborn genetic flaw and that there are inherent weaknesses in efforts to date to infer genetic effects from observed phenotypes. It is indeed hazardous, and very likely erroneous, to draw etiologic inferences from observational investigation of racial differences in the prevalence of hypertension. This difficulty results in part because the “exposure,” ie, race or ethnicity, is an inherent trait that is extremely difficult to measure or even define and in part because the outcome, hypertension, is a complex phenotype. Furthermore, observational studies only provide clues to pathogenesis (implying “guilt by association”) and not definitive evidence. Observational epidemiology has never claimed to provide definitive information on the “cause” of disease, using instead the term “risk factor” to describe the observed relationship. However, arguments regarding the existence or absence of racial or ethnic differences must also consider the large body of human genetic research in rarer Mendelian forms of diseases, some of which have been described as being largely restricted to single racial or ethnic populations. It also seems fair to note that if it were not for the data suggesting a familial aggregation of hypertension, as well as a “racial” vulnerability to development and sequelae of hypertension, there would be little enthusiasm for testing these hypotheses by the more definitive currently available molecular genetic techniques. The best that can be inferred from the evidence for black/white differences in hypertension prevalence or adverse hypertension outcome is that the occurrence of hypertension varies in different subgroups of the population. There is no reason to believe that either blacks or whites are genetically homogeneous. Essential hypertension appears to be a complex …