More news about calcium antagonists.
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Antihypertensive Agents↗
Biomedical subjects
M H Alderman
Publications and source records attributed to M H Alderman.
Cancer mortality of Chinese in New York City 1988-1992.
BACKGROUND: This study examines cancer mortality among Chinese migrants in New York City, and compares it with that of residents of China as well as New York City whites. METHOD: Mortality records for 1988-1992 from the New York City Department of Health, and the 1990 US census data for New York City were used for the analysis. Age-specific deaths and the population of urban China reported by the World Health Organization were also used for comparison. Age-adjusted death rates by gender for Chinese and whites in New York City, as well as for Chinese in China were computed using the world standard population. RESULTS: New York Chinese had lower mortality rates for all causes, total cancer, oesophageal and lung cancer deaths than did either New York whites or Chinese in China in both genders. However, they had lower death rates than New York whites, but similar to those in China, for colon cancer in both genders, and breast cancer in females. By contrast, New York Chinese had higher death rates for nasopharyngeal cancer than either New York City whites or Chinese in China. Stomach and liver cancer death rates in New York Chinese fell between those in China and New York City whites. CONCLUSIONS: Cancer mortality rates among Chinese migrants in New York City being the lowest for total cancer and some types of cancers, did not follow the usual pattern of migrants (an intermediate position between rates of native New Yorkers and Chinese in homeland China). However, substantial variations in certain cancer-specific mortality by geography were observed.
Adult↗
Blood pressure J-curve: is it cause or effect?
Clinical trials have demonstrated that antihypertensive therapy leads to the prevention of stroke, consistent with that predicted by epidemiological data. In contrast, in the same studies, the reduction in coronary artery disease events has been substantially less than predicted. Many possible explanations have been proposed to account for this shortfall in the reduction of disease produced by antihypertensive therapy. One suggestion has been that too great a fall in diastolic pressure during treatment actually increases the risk of myocardial infarction. A substantial body of data taken from clinical trials has consistently demonstrated a J-shaped association of diastolic pressure and coronary events. Some studies suggest that this J-shaped association is limited to those with coronary disease, and that the J-phenomenon is the result rather than the cause of atherosclerotic disease of the aorta. A prospective study is underway to resolve this issue. Meanwhile, the cautious physician is advised to seek a moderate decline in diastolic pressure to a level greater than 80 mmHg.
Blood Pressure↗
Is there a link between the circulating renin-angiotensin system and coronary disease? A buoyant view.
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Angiotensin-Converting Enzyme Inhibitors↗
Absolute cardiovascular risk: the basis for deciding to treat.
It has been convincingly demonstrated that a raised blood pressure is a risk factor for cardiovascular disease and that its reduction saves lives. It seems logical to suggest that the whole population's blood pressure distribution should be displaced downwards, since the reduction of blood pressure by only a few millimeters of mercury, if easily and safely achieved, would produce more disease prevention than could be attained by any other conceivable clinical strategy. Physicians already have powerful tools to lower blood pressure in individual patients, but must make challenging decisions as to when and how to use them. Blood pressure level is a reflection of relative risk and one of many risk factors that determine absolute risk. Reduction of blood pressure therefore does not cure cardiovascular disease, but reduces the risk of developing disease. The need for hypotensive therapy should be determined by absolute risk and the opportunity for successful prevention, rather than by a threshold level of blood pressure. The task of the physician is to assist the patient in assessing the balance between the potential for benefit and the burden of intervention, and to provide the best possible care to implement the therapeutic choice that is made.
Antihypertensive Agents↗
Influence of obesity on left ventricular midwall mechanics in arterial hypertension.
The evaluation of the effect of obesity on left ventricular systolic performance may differ in relation to the method used to measure left ventricular function and to the type of study population. Whether obesity worsens left ventricular midwall mechanics in arterial hypertension has never been investigated. Accordingly, we assessed echocardiographic left ventricular midwall shortening-circumferential end-systolic stress relations in 156 normotensive and normal-weight (reference) adults, 94 normotensive and overweight (1985 National Institutes of Health partition values) to obese (body mass index > 30 kg/m2) adults, 263 hypertensive and normal-weight adults, and 224 hypertensive and overweight-to-obese adults. There was an inverse relation of midwall shortening to circumferential end-systolic stress in all groups (all P < .005). Left ventricular performance as a ratio of observed to predicted midwall shortening fell below the fifth percentile in 4 of 94 (4%) of overweight-to-obese normotensive individuals. Eighty-eight of 487 hypertensive subjects (18.1%) exhibited depressed midwall shortening as a percentage of the value predicted from wall stress, with no difference between normal-weight (50 of 263 [19%]) and overweight (38 of 224 [17%]) subjects. Sixty-one normotensive and 131 hypertensive subjects were frankly obese. After adjustment for sex and age, midwall shortening, as either absolute values or a percentage of predicted, was not statistically different among obese, overweight, and normal-weight subjects in both normotensive and hypertensive groups. For each quartile of observed-to-predicted midwall shortening ratio, obese subjects had greater left ventricular end-diastolic volume than normal-weight subjects among both normotensive and, more evidently, hypertensive subjects. A predicted midwall shortening was generated from both wall stress and left ventricular volume with the use of multiple regression analysis. High body mass index, mean blood pressure, aging, and male sex independently predicted low afterload and left ventricular volume-independent midwall left ventricular performance (multiple R = .31, P < .0001). Thus, (1) midwall left ventricular systolic performance in asymptomatic overweight or frankly obese individuals is comparable to that in normal-weight individuals in both the presence and absence of arterial hypertension; (2) however, maintenance of normal life ventricular performance in obese individuals is associated with the use of Starling reserve; and (3) this compensatory mechanism is especially evident when arterial hypertension and obesity coexist.
Adult↗
Renal function during antihypertensive treatment.
To determine the association of renal function and the course of blood pressure in antihypertensive therapy, we studied the changes in serum creatinine as a measure of renal function and in-treatment blood pressure in black and white hypertensive patients. We measured serum creatinine in 2125 mild and moderately hypertensive men during treatment over an average of 5 years. Both unadjusted mean initial and final serum creatinine of 758 blacks (113 and 117 mumol/L respectively) were significantly higher than those of 1367 whites (108 and 107 mumol/L), with a small increase of 4 mumol/L (p < 0.01) for blacks and a fall of 0.9 mumol/L (p > 0.05) for whites. Less than 2% of all patients attained or remained at a final serum creatinine of 177 mumol/L or more. Of this small group (3% blacks, 1.4% whites), 31% had proteinuria at entry. After stratification by in-treatment diastolic blood pressure (< 95 and > or = 95 mm Hg) in each race, mean slopes of reciprocal serum creatinine were estimated, adjusting for age at entry, initial serum creatinine, diastolic pressure, and body-mass index by analysis of covariance. The two adjusted mean slopes did not differ significantly within each race. Multiple regression analysis confirmed that in-treatment diastolic pressure was not independently associated with final serum creatinine. The change in renal function was most likely a reflection of regression towards the mean, and does not support the view that antihypertensive treatment is an important determinant of renal function in mild-to-moderate hypertensive patients. Patients with substantial renal insufficiency may have pre-existing intrinsic renal disease.
Antihypertensive Agents↗
Angina pectoris by Rose questionnaire does not predict cardiovascular disease in treated hypertensive patients.
OBJECTIVE: To determine the predictive value of angina pectoris diagnosed by Rose questionnaire for cardiovascular disease among treated hypertensives. METHODS: The cardiovascular experience of 4093 patients who had no history of cardiovascular disease and had been administered the Rose questionnaire for angina in a worksite treatment program was evaluated. RESULTS: Among 2659 men and 1434 women of similar age (53 versus 54 years), the race distribution was 44 versus 31% whites, 27 versus 41% blacks and 29 versus 28% Hispanics. Overall, the prevalence of angina by Rose questionnaire in women (15%) was twice that in men (7%) in all three races, with Hispanics having the highest (20 versus 10%) prevalence. Those with angina (Rose-plus) and those without (Rose-minus) had similar initial and final blood pressures. In 4.0 years of average follow-up study, the crude incidence rates (per 1000 person-years) of the recorded 120 myocardial infarctions and 35 strokes did not differ significantly between Rose-plus and Rose-minus patients, except for myocardial infarction in Hispanic men (20.5 versus 5.9). When myocardial infarction incidence was adjusted for age within each sex-race subgroup, only Rose-plus Hispanic men had a significantly greater relative risk with Rose-minus as referent (relative risk 3.13, 95% confidence interval 1.31-7.50). Overall, in the Cox proportional hazards regression model, angina by Rose questionnaire was not predictive of myocardial infarction after accounting for other recognized risk factors. CONCLUSIONS: The present data suggest that the Rose questionnaire as a diagnostic tool for angina is not predictive of subsequent clinical events among treated hypertensive patients.
Adult↗
Plasma renin activity and coronary heart disease: are they related?
Both a retrospective and a prospective study of hypertensive patients have detected a significant positive relationship between pretreatment renin and sodium profiles, and the occurrence of coronary artery disease events during treatment. The subgroup of patients with the highest renin-sodium profile, while controlling for other known coronary risk factors as well as pre-existing disease, were significantly more likely to experience a fatal or nonfatal myocardial infarction compared with those with normal or low renin-sodium profiles. A population of almost entirely normotensive subjects failed to show a similar relationship for plasma renin activity alone. In the normotensive patient in whom the plasma renin activity is physiologically linked to blood pressure level, no adverse effect of an elevated plasma renin activity is seen. By contrast, in the hypertensive patient, in whom plasma renin activity should approach zero, there is a direct correlation between the renin-sodium profile and the risk of developing subsequent heart attack.
Coronary Disease↗
Low urinary sodium is associated with greater risk of myocardial infarction among treated hypertensive men.
A sodium-reduced diet is frequently recommended for hypertensive individuals. To determine the relationship of sodium intake to subsequent cardiovascular disease, we assessed the experience of participants in a worksite-based cohort of hypertensive subjects. The 24-hour urinary excretion of sodium (UNaV), potassium, creatinine, and plasma renin activity was measured in 2937 mildly and moderately hypertensive subjects who were unmedicated for at least 3-4 weeks. Morbidity and mortality in these systematically treated subjects were ascertained. Men and women were stratified according to sex-specific quartiles of UNaV. Subjects in these strata were similar in race, cardiovascular status, and pretreatment and intreatment blood pressure. Subjects with lower UNaV were thinner, excreted less potassium, and had higher plasma renin activity. During an average 3.8 years of follow-up, a total of 55 myocardial infarctions occurred. Myocardial infarction and UNaV were inversely associated in the total population and in men but not in women, who sustained only nine events. In men, age- and race-adjusted myocardial infarction incidence in the lowest versus highest UNaV quartile was 11.5 versus 2.5 (relative risk, 4.3, 95% confidence interval, 1.7-10.6). No association was observed between non-cardiovascular disease mortality (n = 11) and UNaV. There was a significant linear trend in proportions of myocardial infarction by UNaV quartile, with a break point after the lowest UNaV quartile.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Isolated diastolic hypertension. A favorable finding among young and middle-aged hypertensive subjects.
To identify pretreatment characteristics associated with subsequent myocardial infarction in young and middle-aged previously untreated hypertensive individuals, we examined the experience of 1560 participants in a work-site hypertension control program who were younger than 60 years. Subjects were categorized by initial blood pressure as having isolated diastolic hypertension (< 160/> or = 90 mm Hg, n = 965) or combined systolic and diastolic hypertension (> or = 160/> or = 90 mm Hg, n = 595). During 4.5 years of follow-up, there were 24 myocardial infarctions, yielding an overall incidence of 3.89 per 1000 person-years. Subjects with systolic/diastolic hypertension were older, had higher cholesterol and blood sugar levels, and included more smokers and people with left ventricular hypertrophy on electrocardiogram than those with isolated diastolic hypertension. Age-adjusted incidence rates for myocardial infarction were 5.20 and 2.21 per 1000 person-years in systolic/diastolic hypertension and isolated diastolic hypertension, respectively, and the relative risk of systolic/diastolic hypertension was 2.31 (95% confidence interval, 1.29-4.15). Among subjects with isolated diastolic hypertension, no myocardial infarction occurred in those with systolic pressure less than 140 mm Hg. Cox regression analysis including other known risk factors showed that pulse pressure, as a continuous variable (hazards ratio, 1.54; 95% confidence interval, 1.08-2.20), and type of hypertension, ie, systolic/diastolic hypertension versus isolated diastolic hypertension (hazards ratio, 2.11; 95% confidence interval, 1.08-4.13), were independently associated with myocardial infarction. These results suggest that young and middle-aged treated hypertensive individuals with normal pretreatment systolic pressure enjoy a more favorable prognosis than do those with systolic elevation.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Differential mortality in New York City (1988-1992). Part One: excess mortality among non-Hispanic blacks.
To determine the distribution of mortality for non-Hispanic blacks and non-Hispanic whites in New York City, death certificates issued in New York City during 1988 through 1992, and the relevant 1990 US census data for New York City, have been examined. Age-adjusted death rates for blacks and whites by gender and cause of death were computed based on the US population in 1940. Also, standard mortality ratios and excess mortality were calculated using the New York City mortality rate as reference. The results showed that New York City blacks had higher age-adjusted death rates than whites regardless of cause, including stroke, AIDS, homicide, and diabetes. The rate for New York City blacks was also higher than the US total for both genders. Using New York City mortality rates as a reference, more than 80% of excess deaths in blacks occurred before age 65. Injury/poisoning was the leading cause of excess death (20.1%) in black males, while in black females, cardiovascular disease was the largest single cause of excess deaths (24.8%). The higher death rates, especially premature death, of blacks in New York City are related to conditions such as violence, substance abuse, and AIDS, for which prevention rather than medical care is the more likely solution, as well as to cardiovascular diseases, where both prevention through behavioral change, and health and medical care, can influence outcome.
Black or African American↗
Differential mortality in New York City (1988-1992). Part Two: excess mortality in the south Bronx.
To display the extent of variations in mortality according to geographic regions in New York City, we have compared mortality in New York City as a whole with that of the South Bronx. Mortality records for 1988 to 1992 and 1990 US census data for New York City were linked. The 471,000 residents of the South Bronx were younger, less educated, and more likely to lack health insurance than other New Yorkers. Using age- and gender-stratified populations and mortality in New York City as standards, age-adjusted death rates and excess mortality in the South Bronx were determined. All-cause mortality in the South Bronx was 26% higher than the city as a whole. Mortality for AIDS, injury and poisoning, drug and alcohol abuse, and cardiovascular diseases were 50% to 100% higher in the South Bronx than in New York City; years of potential life lost before age 65 in the South Bronx were 41.6% and 44.2% higher for men and women, respectively, than in New York City; AIDS accounted for the largest single share of excess premature deaths (21.8%). In summary, inequalities in health status, reflected by higher mortality rates in the South Bronx, are consistent with, and perhaps caused by, lower socioeconomic status and deficient medical care among residents of this inner-city community.
Cause of Death↗
Measures of blood pressure and myocardial infarction in treated hypertensive patients.
OBJECTIVE: To identify entry characteristics associated with subsequent myocardial infarction in treated hypertensive patients. DESIGN: Nested case-control study and cohort study. SETTING AND PATIENTS: The 5730 participants (mean age 53 years; 61% male and 45% Caucasian) were selected from a worksite-based, union-sponsored, systematic hypertension control program from 1973 to 1992. METHODS: In the case-control study myocardial infarction cases were matched by age, sex, year of entry to the program, years of follow-up and previous treatment status (treated or untreated) with non-event subjects. Baseline clinical and biochemical characteristics were analyzed with regard to the outcome of myocardial infarction, using univariate and multivariate analyses, respectively, in case-control and cohort studies. RESULTS: During 5.43 years of follow-up the incidence of myocardial infarction was 6.75/1000 person-years. Univariate analysis indicated that myocardial infarction cases had higher cholesterol level and were more likely to have a previous history of diabetes than controls. The initial systolic blood pressure and pulse pressure of cases were significantly higher than in controls. Logistic regression models indicated that initial pulse pressure, either as a continuous or as a categorical variable, was the only measure of blood pressure independently associated with myocardial infarction after adjustment for other risk factors. Analysis of the experience of the total 5730 as well as 2445 previously untreated patients with a cohort study generated identical results. CONCLUSION: A large pulse pressure difference appears to be the most powerful measure available of initial blood pressure to identify, in advance, those hypertensive patients at greatest risk for a subsequent myocardial infarction.
Blood Glucose↗
Quantifying cardiovascular risk in hypertension.
The facts are that blood pressure is a risk factor for cardiovascular disease and that its reduction saves lives. This has been convincingly demonstrated. The question now is how best to translate that knowledge into practice. Clearly, displacement of the whole community's pressure distribution downward would be of tremendous benefit. A change of only a few mm Hg, if feasible and without cost in health-care terms, would produce more disease prevention than any conceivable clinical strategy. Regrettably, the means to achieve this goal are not available. New tools to improve dietary and behavioral approaches to attaining these goals are desperately needed. For physicians, the immediate issue is how to apply the powerful and varied tools that dramatically lower blood pressure in individual patients. In this clinical setting, blood pressure must be seen for what it is--a reflection of relative risk, a risk factor, and only one of the multiple factors that together determine absolute risk. Blood pressure reduction is not curative (because high blood pressure is not a disease) but rather is a technique to reduce the odds of heart attack, stroke, and renal failure. Hypotensive therapy should therefore be applied when the absolute likelihood for a stroke or heart attack, is great enough to suggest a real chance for benefit by virtue of the reduction of any particular blood pressure level. Therapeutic decisions should weigh the potential for benefit as well as the burden of intervention. The worthy clinician must define those parameters, assist the patient to assess their implications, and finally implement the therapeutic choice that follows, to provide the best possible care.
Cardiovascular Diseases↗
Non-pharmacological treatment of hypertension.
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Alcohol Drinking↗
A new paradigm for blood pressure management.
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Aged↗
Plasma renin activity and ischemic heart disease.
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Humans↗