Echocardiographic left ventricular hypertrophy in blacks.
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Biomedical subjects
Publications and source records attributed to D D Savage.
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To assess the prevalence, characteristics, and correlates of echocardiographically determined left ventricular hypertrophy (echo LVH) in a free-living population, 510 men and 855 women from the original Framingham cohort (age 59 to 90 years) were studied by M-mode echocardiography. Offspring and offspring spouses (1718 men and 1892 women; age 17 to 75 years) were similarly studied. The severity of echo LVH, as reflected by left ventricular mass indexed to body surface area, ranged from 101 g/m2 (women) and 132 g/m2 (men) to more than 400 g/m2. The prevalence of electrocardiographically assessed LVH increased proportionately with increased echocardiographic left ventricular mass. Women with echocardiographic left ventricular mass indexes exceeding 200 g/m2 were three to four times more likely to have electrocardiographic LVH than men with similar elevations of echocardiographic left ventricular mass index. The prevalence of echo LVH ranged from 6.6% in the younger (offspring study) women to 33% in the older (original cohort) women (8.6% and 23.7%, respectively, for men) and included a spectrum of forms--eccentric-dilated, eccentric-nondilated, concentric, and disproportionate septal thickness--which varied in prevalence in the various age-sex groups. Each of these forms of echo LVH was associated with higher systolic blood pressures at the time of echocardiographic examination and over the previous 30 years when compared with blood pressures of Framingham subjects without echo LVH.
To evaluate the performance of M-mode echocardiography for detection of pressure-overload left ventricular hypertrophy (LVH), we tested the sensitivity of previously defined sex-specific upper limits of normal echo LV measurements in 31 patients with necropsy-proven pressure-overload LVH and determined the prevalence of LVH detected by each echo criterion in 316 employed patients with uncomplicated hypertension, 100 patients with hypertension evaluated in a referral center, and 38 hospital patients with moderate to severe (WHO class 2) hypertension. Echo measurements were LV mass (LVM), LVM index (LVMI), cross-sectional area (CSA), septal and posterior wall thickness (IVST and PWT), LV internal dimension (LVID), and relative wall thickness (RWT). Prevalences of echo LVH were as follows. (Table: see text). Thus, echo criteria based on LVM are more sensitive than other measurements for detection of necropsy-proven pressure-overload LVH and reveal the highest prevalence of LVH in clinical hypertension populations, and the prevalence of LVH in hypertension is highly dependent on the population studied.
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The year 1987 marks the centennial of electrocardiography. As Beamish reminds us, it was the first and foremost technical aid to the cardiologist. During the history of cardiovascular epidemiology, which dates back roughly forty years, electrocardiography has played a central role as a relatively specific marker for coronary and hypertensive heart disease. The lack of sensitivity of electrocardiography and the advent of new technologies such as ultrasonography for assessment of such heart disease in cardiology and cardiovascular epidemiology has raised questions as to whether electrocardiography might be replaced in the next century. Recent developments in computer electrocardiography have rendered suggestions of the decreased importance of electrocardiography premature. Use of computer analysis of electrocardiograms in epidemiologic studies, which dates back less than three decades, has renewed interest in and expanded the role of electrocardiography in cardiology in general and cardiovascular epidemiology in particular. The computer analysis of electrocardiograms has allowed the processing and analysis of large numbers of electrocardiograms in a rapid, efficient, systematic and consistent manner. This has led to new, more sensitive criteria for detection of left ventricular hypertrophy as a discrete variable. In addition, the numerous waveform amplitude and duration measurements by computer have allowed the development of mathematical models to express the likelihood of coronary heart disease (myocardial infarction) and degree of left ventricular hypertrophy (estimates of left ventricular mass) on continuous scales. These developments have contributed substantially to the potential of electrocardiography (and particularly computer electrocardiography) in future studies and clinical applications.(ABSTRACT TRUNCATED AT 250 WORDS)
The cost effectiveness of labetalol and propranolol in the treatment of black adults with mild to moderate hypertension was assessed using published reports from US clinical trials of these agents among such patients. Data from these studies suggest that labetalol and propranolol lower diastolic blood pressure among black hypertensive adults by 11.2 mmHg and 8.4 mmHg, respectively. Results indicate that, for a hypothetical cohort of 1,000 patients on monotherapy, patients treated with labetalol would experience two to seven fewer strokes over a ten-year period, depending upon age and sex, and annual drug costs would be reduced by $190. For stepped care, annual costs would be $205 and $212 lower for those treated initially with labetalol. Labetalol therefore may be more cost effective than propranolol among black adults with mild to moderate hypertension.
Over the past two decades, national hypertension-control programs and policies have focused on early diagnosis and management. Measured by intermediate results--such as percentages of cases now taking medication--these efforts have been markedly successful, especially among black hypertensives. The ultimate measure of success--reduction in hypertension-associated disease and death--must address the one-third excess prevalent among blacks. Biologic and age-specific variables in diagnosis and treatment must be accommodated. Future gains in efficient use of resources and equity in outcome will require use of new technologies and models of targeting.
To assess the relation of echocardiographic left ventricular (LV) mass to reported physical activity, 2 groups of subjects with widely different physical activity levels were evaluated: 50 men with spinal cord injuries and 166 apparently healthy, active men. Multivariate analysis revealed that reported physical activity was a significant independent predictor of LV mass index (LV mass/body surface area) in both injured patients and healthy, active subjects after controlling for age and blood pressure. The relation between LV mass index and physical activity (linear regression) was similar for both groups; LV mass index = 0.00321 (physical activity) + 82.8 and LV mass index = 0.00335 (physical activity) +88.4 for patients and healthy active subjects, respectively. These results suggest that physical activity as assessed by self-report is associated with echocardiographically detectable differences in LV mass in groups with widely divergent physical activity levels. In addition, for each of these groups 1,000 kcal/week of physical activity apparently results in a change of approximately 3 g/m2 in LV mass index. This information may have practical use for correction of LV mass for the effects of physical activity.
The kindling phenomenon was examined in genetically epilepsy-prone (GEPR) and non-epileptic control Sprague-Dawley rats. Kindling stimulations were administered three times a day until each rat had exhibited three Class 5 kindled motor seizures. The mean total number of kindling stimulations required for each experimental group to exhibit three motor seizures of each motor seizure class was determined. The results indicated that the early stage of kindling development was accelerated significantly in both the GEPR-3 and GEPR-9 rats, compared to non-epileptic control rats. Later stages of kindling development were accelerated in GEPR-9 but not GEPR-3 rats. Thus a differential acceleration of kindling development was exhibited by GEPR-3 and GEPR-9 rats. The results suggest the possibility that some brain region(s) involved in the early stages of kindling development may be hyperexcitable in both GEPR-3 and GEPR-9 rats. Other brain region(s) involved with the later stages of kindling development may be more excitable in GEPR-9 rats. These putative alterations may, in part, contribute to the seizure prone state of GEPR rats and the differential seizure responses of GEPR-3 and GEPR-9 rats.
Limbic kindling was examined in genetically epilepsy-prone (GEPR) and non-epileptic control rats. The early stage of kindling development was accelerated in both groups of GEPR rats compared to controls. Later stages of kindling were accelerated in GEPR-9 but not GEPR-3 rats. These results indicate that GEPR rats have an enhanced susceptibility to limbic kindling and suggest that limbic brain alterations may contribute to acceleration of the early stage kindling development in GEPR rats.
Several studies have linked total serum cholesterol concentrations below 200 mg/dl with increased cancer risk, especially among men. Cancer risk appears to be associated primarily with low concentrations of total cholesterol and of low-density lipoprotein cholesterol but not of high-density lipoprotein cholesterol (HDL). It has been suggested that low concentrations of total cholesterol are associated with increased cancer risk indirectly by virtue of their association with low concentrations of carotene and/or retinol. The relationship between serum carotene and cholesterol in a biracial group of 146 first-year college students was investigated. White men and women had similar carotene concentrations. Blacks had higher serum carotene concentrations than whites. There was a significant relationship between carotene concentrations and total cholesterol, which was most evident in men, both black (r = +0.72; P less than 0.01) and white (r = +0.49; P less than 0.01). The correlations for the women were significant, but of lower magnitude than for the men. Significant carotene-HDL relationships were observed among black men (r = 0.31; P less than 0.05) and among women (r = 0.35; P less than 0.05 and r = 0.31; P less than 0.05, black and white, respectively). Furthermore, the women also demonstrated a significant carotene-HDL2 association. The results are consistent with the hypothesis that the association between low serum cholesterol concentrations and cancer may be the result of a relationship between lipoprotein cholesterol concentrations and vitamin A metabolism.
The development of kindling was examined in adult rats exposed to ethanol prenatally. Pregnant Wistar rats were fed a liquid diet containing either 6.7% ethanol or pair fed an isocaloric equivalent. At birth, the litters were cross fostered to surrogate mothers. At 80 days of age, a bipolar electrode was placed either in the right basolateral amygdala or the right angular bundle of entorhinal cortex. Kindling stimulations were administered three times a day until each rat had exhibited three class 5 kindled motor seizures. The total number of kindling stimulations required to exhibit class 1 through class 5 motor seizures was significantly greater in the rats exposed to ethanol prenatally. Further, the retardation in kindling development was due to a slower progression from class 0 to class 1 kindled motor seizures. Progression between other stages was not different between the two groups. Similar results were obtained in both amygdala and angular bundle kindling experiments. Kindling is retarded in a similar fashion by partial destruction of the dentate granule cells of the hippocampal formation. Further, the pattern of dentate granule cell axonal projections to hippocampal CA3 pyramidal neurons is altered in rats exposed to ethanol prenatally. Taken together, these data suggest the possibility that a defect in the neuronal circuitry within the hippocampal formation of fetal alcohol rats may underlie a retardation in their kindling progression. This proposed defect may have functional implications related to learning deficiencies in rats and children exposed to ethanol prenatally.
This report examines the effect of transection of the entorhinal hippocampal projection on amygdaloid kindling. We found that: bilateral knife cuts of entorhinal cortex but not of dorsal neocortex antagonize the development of amygdaloid kindling; and bilateral knife cuts of entorhinal cortex eliminate the seizure-induced decrease in number of muscarinic receptors of dentate granule cells. We suggest the following interpretations of these data: the hippocampal formation circuitry facilitates the development of amygdaloid kindling; and the decline of muscarinic receptors after kindled seizures is due to excessive activation of granule cells by axons from entorhinal cortex, a noncholinergic afferent.
The specific binding of [3H]kainic acid to hippocampal membranes was examined autoradiographically in rats kindled by tetanic stimulation of the amygdala or angular bundle. One day after the last of 3 class 4-5 kindled seizures, the specific binding of [3H]kainic acid in stratum lucidum of area CA3 was 47-61% less than in electrode-implanted unstimulated controls. Specific binding in the inner third of the dentate molecular layer was reduced to a lesser degree. These observations demonstrate that kainic acid receptors are down-regulated by kindling stimulation.
The specific binding of L-[3H]glutamate to hippocampal synaptic membranes was examined in rats kindled by tetanic stimulation of the angular bundle. One day after the last of a minimum of 3 class 4 kindled seizures, the binding of L-[3H]glutamate to a quisqualate-sensitive site (GLU A) was about 40% greater than in electrode-implanted unstimulated controls. Saturation binding data indicated an increase in the maximum density of GLU A binding sites with no change in their affinity for L-glutamate. No such increase was detected 28 days after the last kindled seizure, although the animals were still kindled. Radioligand binding to a site that is much less sensitive to quisqualate (GLU B) was unaffected by kindling stimulation. These observations suggest that an increase in GLU A binding sites could be involved in the induction, but not in the maintenance, of the kindled state.
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To assess the contribution of bias in subject selection to the prevalence of arrhythmias in cases of mitral valve prolapse (MVP), we compared ambulatory arrhythmias in 63 patients with MVP and 28 symptom-matched control subjects. All subjects were in sinus rhythm. Mean 24-hour heart rate of the prolapse population was lower than that of the control group (76 v 82 beats per minute). Mean atrial premature complex (APC) density per 1,000 beats (0.9 v 0.7 for patients with MVP and control subjects, respectively) and mean ventricular premature complex (VPC) density per 1,000 total beats (1.2 v 1.5) did not differ between groups. Small differences between groups in APC and VPC complexity did not reach statistical significance. Our findings suggest that, compared with similarly symptomatic controls, patients with MVP do not have as high an excess prevalence of arrhythmias as previously believed.
The binding of [3H] quinuclidinyl benzilate ( [3H] QNB) to muscarinic cholinergic receptors in dentate gyrus of rat hippocampal formation was analyzed by membrane binding assay and in vitro autoradiography. The destruction of dentate granule cells, either by neonatal irradiation or colchicine injection, resulted in nearly complete elimination of [3H] QNB binding sites in the molecular and granule cell layers. By contrast, neither perforant path transection nor destruction of the septal-hippocampal cholinergic afferents caused a decline of [3H] QNB binding sites. Amygdala kindled seizures resulted in a 30% reduction of [3H] QNB binding sites which was distributed uniformly across the entire molecular and granule cell layers. Thus, most, if not all, of the muscarinic cholinergic receptors present in dentate gyrus appear to reside on the somata and dendritic trees of the dentate granule cells. We propose that this kindled seizure-induced decline of muscarinic receptors represents an endogenous compensatory mechanism designed to stabilize granule cell excitability.