Obstructive nephropathy in the rat: possible roles for the renin-angiotensin system, prostaglandins, and thromboxanes in postobstructive renal function.

Relief of unilateral ureteral obstruction (UUO) of 24 h duration in rats is followed by severe renal vasoconstriction in the postobstructive kidney (POK). The present study examined possible roles of renal prostaglandins (PG) and thromboxanes (TX), as well as the renin-angiotensin system, in this vasoconstriction. Administration of the cyclooxygenase inhibitor indomethacin, which blocks both PG and TX production, failed to improve POK hemodynamics in UUO rats. To explore the possible role of the TX compounds, which include the potent vasoconstrictor thromboxane A2 (TXA2), UUO rats were infused with imidazole, an agent that blocks synthesis of TX, but not of PG. Imidiazole led to two- to threefold increases in the clearance of both inulin and rho-aminohippuric acid by the POK. This effect of imidazole was abolished by indomethacin, suggesting that the amelioration of POK vasoconstriction by imidazole was a result of inhibition of vasoconstrictor TX synthesis (e.g. TXA2), with PG vasodilators (e.g. PGE2 or PG12) still active. Urea, infused in a solution whose osmolality and volume were identical to the imidazole infusion, failed to improve hemodynamics in the POK, making it unlikely that nonspecific effects of volume expansion or osmotic diuresis mediated the beneficial effect of imidazole. Further studies examined the possible role of the renin-angiotensin systems in the vasoconstriction of the POK. UUO rats infused with the angiotensin II antagonist, Saralasin, exhibited no significant improvement in POK function, a finding that might be at least partly attributable to agonist/vasoconstrictor properties of Saralasin. In other experiments, treatment of UUO rats with the angiotensin-converting enzyme blocker SQ 14225 (Captopril), in order to inhibit angiotensin II formation, led to at least twofold increases in the clearance of both inulin and rho-aminohippuric acid in the POK. It is unlikely that Captopril exerted this beneficial effect by potentiating the vasodilator kinins, because the effect was not diminished by administration of either carboxypeptidase B (which destroys the kinins) or Trasylol (which blocks kinin synthesis). Thus, these results suggest that both angiotensin II, as well as metabolites of the PG-TX system, may be important determinants of postobstructive renal hemodynamics in the rat.

Blood pressure as a predictor of cardiovascular events in the elderly: the William Hale Research Program.

This study evaluates the association between blood pressure (BP) and the risk of developing cardiovascular disease (CVD) events in the elderly. The Morton Plant Mease Foundation has followed 4,008 elderly patients >64 years of age for at least 5 years. Systolic and diastolic blood pressure (SBP and DBP) was divided into categories. Cardiovascular disease events were classified as myocardial infarction, stroke, and CVD-related deaths reported from the National Death Index. Cox proportional hazard ratios were used to assess the relationship between BP and CVD events and controlled for weight, gender, smoker, and alcohol use. Ages <75 and >or=75 years were assessed separately. After 11.1 years of follow-up, elevated SBP (P=<0.0001) is strongly associated with developing a future CVD event; the relationship is linear and graded and holds for ages above and below 75 years. The frequency of CVD events was lowest in the SBP <120 mm Hg group. In subjects <75 years of age, DBP elevations were not a significant risk factor for CVD events. (relative risk (RR): DBP 70 to <80 mm Hg=0.92; DBP 80 to <90 mm Hg=0.88; DBP >or=90 mm Hg=1.02.) With subjects >or=75 years of age, a DBP between 80 and 90 is associated with the lowest significant risk for CVD (RR: DBP 70 to <80 mm Hg=0.74; DBP 80 to <90 mm Hg=0.59; DBP >or=90=0.71). In conclusion, these findings support the Joint National Committee on Hypertension recommendations for SBP in the elderly. Further studies are warranted to identify optimal DBP for the elderly at various ages.

Sudden death in cancer patients receiving lithium.

Lithium carbonate may attenuate the incidence and severity of infection associated with cancer chemotherapy but does not appear to improve patient survival. Of 100 patients with small-cell lung cancer receiving an identical regimen of cyclophosphamide, doxorubicin, and vincristine, 40 were assigned to treatment with lithium concurrently. To date, 60 patients have died, including 14 who died suddenly of apparent cardiovascular causes without evident progression of neoplastic disease or concurrent illness. Thirteen of the 14 sudden deaths were among 50 patients with clinical or electrocardiographic evidence of cardiovascular abnormalities before study entry. Among patients with pretreatment cardiovascular abnormalities, lithium administration was associated with a greater risk of sudden death and shorter survival. A strong interaction for risk of death was evident between lithium treatment and the use of bronchodilators. In multivariate analysis, the major predictors of patient survival were the quality of tumor response and treatment with lithium with or without bronchodilators. Lithium treatment is a major risk factor for sudden death in cancer patients with pretreatment cardiovascular changes receiving combination chemotherapy including an anthracycline antibiotic.

Prevalence and mortality rate of congestive heart failure in the United States.

OBJECTIVES: The study was designed to determine the prevalence and mortality rate of congestive heart failure in noninstitutionalized men and women in the U.S. BACKGROUND: Congestive heart failure is a serious condition with significant morbidity and mortality. Earlier epidemiologic descriptions of congestive heart failure were constructed from small surveys, limited data, hospital records or death certificates. No nationally representative data from noninstitutionalized persons have been examined. METHODS: Data collected from the National Health and Nutrition Examination Survey (NHANES-I, 1971 to 1975) were used to determine the prevalence of heart failure on the basis of both self-reporting and a clinical definition. Mortality data were derived from the NHANES-I Epidemiologic Follow-up Study (1982 to 1986). RESULTS: The prevalence of self-reported congestive heart failure approximates 1.1% of the noninstitutionalized U.S. adult population; the prevalence of congestive heart failure based on clinical criteria is 2%. These estimates suggest that between 1 and 2 million adults are affected. Mortality at 10 and 15 years for those persons with congestive heart failure increases in graded fashion with advancing age, with men more likely to die than women. In the group greater than or equal to 55 years old, the 15-year total mortality rate was 39.1% for women and 71.8% for men. CONCLUSIONS: Congestive heart failure is a common problem in the U.S., with significant prevalence and mortality, both of which increase with advancing age. As the population of the U.S. becomes older, the health care impact of congestive heart failure will probably grow.

Role of cytokines in the mechanism of action of amlodipine: the PRAISE Heart Failure Trial. Prospective Randomized Amlodipine Survival Evaluation.

OBJECTIVES: We sought to determine whether the beneficial effects of amlodipine in heart failure may be mediated by a reduction in tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) levels. We postulated that TNF-alpha and IL-6 levels may also have predictive value in patients with congestive heart failure (CHF). BACKGROUND: The molecular mechanism for progression of CHF may involve cytokine overexpression. The effect of amlodipine on cytokine levels in patients with CHF is unknown. METHODS: In the Prospective Randomized Amlodipine Survival Evaluation (PRAISE) trial, we used enzyme-linked immunosorbent assay to measure plasma levels of TNF-alpha in 92 patients and IL-6 in 62 patients in New York Heart Association functional classes III and IV randomized to receive amlodipine (10 mg/day) or placebo. Blood samples were obtained for cytokine measurement at baseline and at 8 and 26 weeks after enrollment. RESULTS: The baseline amlodipine and placebo groups did not differ in demographics and cytokine levels. Mean (+/- SD) plasma levels of TNF-alpha were 5.69 +/- 0.32 pg/ml, and those of IL-6 were 9.23 +/- 1.26 pg/ml at baseline. These levels were elevated 6 and 10 times, respectively, compared with those of normal subjects (p < 0.001). Levels of TNF-alpha did not change significantly over the 26-week period (p = 0.69). However, IL-6 levels were significantly lower at 26 weeks in patients treated with amlodipine versus placebo (p = 0.007 by the Wilcoxon signed-rank test). An adverse event-CHF or death-occurred more commonly in patients with higher IL-6 levels. CONCLUSIONS: Amlodipine lowers plasma IL-6 levels in patients with CHF. The beneficial effect of amlodipine in CHF may be due to a reduction of cytokines such as IL-6.

Weight loss and the heart. Effects of anorexia nervosa and starvation.

Anorexia nervosa is a common psychiatric disorder predominantly affecting young women, associated with significant morbidity and mortality, much involving the cardiovascular system. In contrast, protein-calorie malnutrition, while not strictly analogous to the protein-sparing characteristics often noted in anorexia nervosa, is a problem of global stature. Physiologic consequences of anorexia nervosa include rhythm disturbances, mitral valve prolapse, plus both systolic and diastolic ventricular dysfunction. Diminished exercise capacity occurs in both states, with marked blunting of the heart rate and blood pressure response. Congestive heart failure may appear, especially during refeeding. In addition to the myofibrillar destruction associated with protein-calorie malnutrition, hypophosphatemia, particularly when exacerbated by unrestricted glucose-rich refeedings or hyperalimentation, may be one additional cause of ventricular dysfunction. A high level of suspicion for cardiovascular complications is, therefore, warranted in the evaluation and therapy of weight loss conditions such as starvation and anorexia nervosa.

Adrenomedullin, endothelin, neuropeptide Y, atrial, brain, and C-natriuretic prohormone peptides compared as early heart failure indicators.

OBJECTIVES: The present investigation was designed to determine the best endogenous plasma marker of early congestive heart failure (CHF). METHODS: Forty volunteers with mild CHF (New York Heart Association Class I, n = 12), moderate (Class II, n = 8), or severe (Class III and Class IV, each = n of 5) and 10 age-matched healthy individuals had the simultaneous evaluation of their respective plasma samples by the following radioimmunoassays: atrial natriuretic peptide, ANP; three N-terminal ANP prohormone assays, i.e., proANPs 1-30, 31-67, and 79-98 with the numbers referring to their amino acid (a.a.) sequences in their 126 a.a. prohormone; brain (BNP) and C-natriuretic peptides; N-terminal BNP prohormone; adrenomedullin; neuropeptide Y and endothelin. RESULTS: ProANPs 31-67, 1-30 and 79-98 had 100% (P = 0.01), 83% (P = 0.09) and 50% (P = 0.74) sensitivity in differentiating Class I CHF subjects from healthy subjects. The ANP, BNP, NT-proBNP, CNP, adrenomedullin, neuropeptide Y, and endothelin assays could not differentiate mild CHF subjects from healthy individuals. Logistic regression analysis revealed that only proANP 31-67 significantly (P = 0.0001) discriminated between early CHF (5226 +/- 377 pg/ml) and healthy individuals (1595 +/- 157 pg/ml). The positive and negative predicative values of proANP 31-67 were excellent (100% for each). The peptides measured in these assays were found to be independent markers of CHF with respect to left ventricular ejection fraction. CONCLUSIONS: ProANPs 31-67 is the most sensitive marker in discriminating NYHA Class I CHF subjects from healthy individuals. The ANP, BNP, NT-proBNP, CNP, adrenomedullin, neuropeptide Y and endothelin radioimmunoassays cannot discern mild CHF. These peptides are independent of left ventricular ejection fraction.

The human placenta--a rich source of beta-adrenergic receptors: characterization of the receptors in particulate and solubilized preparations.

A crude particulate fraction of human placenta possesses a high concentration of beta-adrenergic receptors, as determined by (-)-[3H]dihydroalprenolol binding (approximately 240 fmol/mg protein; Kd approximately 2 nM). The sites display all the typical characteristics of beta-adrenergic receptors, including rapid and reversible kinetics, saturability, and appropriate specificity and stereospecificity. Computer modelling of ligand binding data indicate that the binding of (-)-[3H]dihydroalprenolol to these sites conforms closely to the pattern anticipated for interactions of the ligand with a homogeneous class of receptors according to the law of mass action. The rejeptors are readily solubilized with digitonin, retaining their typical beta-adrenergic characteristics. The human placenta is likely to be a particularly useful source of beta-adrenergic receptors for purification because of its high receptor content and its ready availability in substantial quantities.

Atrial natriuretic hormone, vessel dilator, long-acting natriuretic hormone, and kaliuretic hormone decrease the circulating concentrations of CRH, corticotropin, and cortisol.

The present investigation was designed to determine whether atrial natriuretic peptides consisting of amino acids 1-30 (i.e. long-acting natriuretic hormone), 31-67 (vessel dilator), 79-98 (kaliuretic hormone), and 99-126 (atrial natriuretic hormone) of the 126 amino acid atrial natriuretic hormone prohormone decrease CRH, ACTH, and/or cortisol in healthy humans (n = 30). Vessel dilator, kaliuretic hormone, long-acting natriuretic hormone, and atrial natriuretic hormone decreased the circulating concentration of CRH 84%, 74%, 67%, and 62% (P < 0.001 for each), respectively, when infused at 100 ng/kg body weight.min for 60 min. Vessel dilator, kaliuretic hormone, long-acting natriuretic hormone, and atrial natriuretic hormone decreased circulating ACTH concentrations 58%, 80%, 81%, and 70% (P < 0.001) and the circulating concentration of cortisol 73%, 72%, 73%, and 67% (P < 0.001), respectively. The decreases in CRH, ACTH, and cortisol lasted 11/2 to 3 h after cessation of the respective atrial natriuretic peptide infusions. These data, along with the knowledge that cortisol upregulates atrial natriuretic peptides' gene expression and CRH and ACTH stimulate atrial natriuretic peptides' release, suggest that these four atrial natriuretic peptides may be part of an intricate feedback system to help regulate cortisol concentrations via their ability to decrease the circulating concentration of CRH which, in turn, results in a decrease in ACTH and cortisol.

Atrial natriuretic hormone, vessel dilator, long-acting natriuretic hormone, and kaliuretic hormone decrease the circulating concentrations of total and tree T4 and free T3 with reciprocal increase in TSH.

The present investigation was designed to determine whether atrial natriuretic peptides (ANPs) consisting of amino acids 1-30 [i.e. long-acting natriuretic hormone (LANH)], 31-67 (vessel dilator), 79-98 (kaliuretic hormone), and 99-126 (atrial natriuretic hormone [ANH]) of the 126-amino acid ANH prohormone decrease the circulating concentrations of total and free T4 and/or free T3 in healthy humans (n = 30). Vessel dilator, kaliuretic hormone, LANH, and ANH decreased the circulating concentrations of total T4 by 61%, 58%, 47%, and 55% and of free T4 by 60%, 67%, 79%, and 79%, whereas free T3 decreased 72%, 67%, 71%, and 67% (P < 0.05 for each), respectively, when infused at 100 ng/kg BW x min for 60 min. Vessel dilator, kaliuretic hormone, LANH, and ANH simultaneously increased circulating TSH concentrations 4- to 12.5-fold (P < 0.004). The decreases in T4 and T3 with reciprocal increases in TSH lasted 2-3 h after cessation of the respective ANP infusions. The reciprocal increase in TSH with the decreases in T4 and T3 suggests that their modulation of T4 and T3 concentrations occurs in the thyroid rather than in the pituitary or hypothalamus, because TSH would be decreased in the circulation if their inhibitory effects were in either the hypothalamus or pituitary.

Negative feedback of atrial natriuretic peptides.

The present investigation was designed to determine whether atrial natriuretic peptides consisting of amino acids 1-30 [i.e. pro-ANF-(1-30)], 31-67 [i.e. pro-ANF(31-67)], 79-98 [i.e. pro-ANF-(79-98)], and 99-126 [i.e. atrial natriuretic factor (ANF)] of 126-amino acid ANF prohormone have a negative feedback on their own and each others' release. Thirty healthy human subjects were studied with infusion of 100 ng/kg BW.min for 60 min of each of the respective peptides. Pro-ANF-(1-30) decreased the circulating concentrations of pro-ANF-(31-67) and ANF 51% and 89%, respectively. Pro-ANF-(31-67) decreased the circulating concentration of ANF by 55% and the peptides immunologically recognized by the pro-ANF-(1-30) RIA by 58% [this assay recognizes pro-ANF-(1-30) (50%) and pro-ANF-(1-98) (50%)]. Pro-ANF-(79-98) decreased the circulating concentration of ANF by 40%, pro-ANF-(31-67) by 31%, and the peptides recognized by the pro-ANF-(1-30) RIA by 46%. ANF decreased the circulating concentration of pro-ANF-(31-67) by 40% and the peptides recognized by pro-ANF-(1-30) RIA by 38%. Infusion of pro-ANF-(1-30), -(31-67), -(79-98), and -(99-126) also decreased the excretion of the other atrial natriuretic peptides measured in the urine by 32-84%. Infusion of vehicle only did not result in any decrease in these atrial natriuretic peptides in either plasma or urine. These data taken together indicate that each of the respective atrial natriuretic peptides inhibits the release, rather than breakdown, of each other, as increased breakdown would have resulted in their urinary concentrations being increased. This study further indicates that because pro-ANF-(1-98) was decreased in the circulation secondary to pro-ANF-(31-67) and pro-ANF-(79-98) infusions, they inhibit their own release, as they are both derived from pro-ANF-(1-98).

Physical conditioning and left ventricular performance in the elderly: assessment by radionuclide angiocardiography.

In contrast to young persons, normal elderly persons who undergo symptom-limited dynamic exercise demonstrate a decrease in left ventricular (LV) contractile performance characterized by a decrease in LV ejection fraction. To test the hypothesis that physical conditioning can be achieved in older persons and produces improvement in the exercise-induced decrease in LV ejection fraction observed during normal aging, we examined 24 normal elderly persons (mean age 72.0 years) before and after a 12-week program of physical training. The subjects had been screened for evidence of cardiovascular disease including rest and exercise stress electrocardiograms. All subjects underwent rest and exercise upright sitting radionuclide angiocardiography before and after the training program. The subjects achieved cardiovascular training effects as measured by increased functional capacity and decreased double product at one-half the maximum work load attained at the initial stress test. A significant increase occurred after training in the cardiac index response to exercise (p less than 0.02) and in the augmentation of the end-diastolic volume index produced by exercise (p less than 0.05). However, the exercise-induced decrease in LV ejection fraction and increase in LV end-systolic volume index remained unaltered by training. In conclusion, although older persons can achieve overall training effects from a program of physical conditioning, the age-associated differences in LV contractile performance remained unchanged. Our data suggest that deconditioning is not a significant contributor to the decline in LV contractile performance in the elderly.

Effects of kaliuretic peptide on sodium and water excretion in persons with congestive heart failure.

Kaliuretic peptide, a 20-amino acid peptide hormone synthesized in the heart, enhances urine flow twofold, whereas atrial natriuretic peptide (ANP) enhances urine flow four- to 11-fold in healthy persons. The present investigation was designed to (1) determine whether kaliuretic peptide may have beneficial diuretic effects in persons with congestive heart failure (CHF), and (2) compare its beneficial effects with ANP in the treatment of CHF. Kaliuretic peptide (100 ng/kg body weight/min) given intravenously for 60 minutes to subjects with New York Heart Association class III CHF increased urine flow fourfold (p <0.001), which was maximal 212 hours after its infusion was stopped. Kaliuretic peptide enhanced sodium excretion threefold in subjects with CHF (p <0.01). Kaliuretic peptide increased the urinary excretion rate of potassium ion and fractional excretion of potassium 3.5- and twofold (p <0.05), respectively. ANP (same concentration) did not significantly enhance urine flow. ANP enhanced sodium excretion two- to sixfold in half of the CHF subjects, whereas it had no effect on sodium excretion in the other half. ANP did not significantly increase fractional excretion of sodium but did increase fractional excretion of potassium (p <0.05) during the first 20 minutes of its infusion. ANP-infused patients with CHF became hypotensive. None became hypotensive secondary to kaliuretic peptide. These data indicate that the diuretic properties of kaliuretic peptide in persons with CHF, as opposed to those of ANP, are not diminished (but rather are increased) compared with their effects in healthy persons. In patients with CHF, kaliuretic peptide causes a natriuresis-a feature not observed in those without sodium retention.

Evaluation of a QRS scoring system for estimating myocardial infarct size. V. Specificity and method of application of the complete system.

The specificity of a previously developed 57-criteria/32-point QRS scoring system for estimating myocardial infarct (MI) size is evaluated in an extensive control population and the method of application of this system for determining a QRS score from a standard 12-lead electrocardiogram is described. Points are accumulated from Q- and R-wave durations, R- and S-wave amplitudes, R/Q- or R/S-amplitude ratios and the presence of R-wave notching, with each point representing approximately 3% of the left ventricle. The subjects were selected because of the minimal likelihood of their having had myocardial infarcts or other sources of QRS modification. There were 500 consecutively selected normal Caucasian subjects, aged 20 to 69 years, with 50 women and 50 men in each of the 5 decades. Specificity for the 57 individual criteria ranged from 89 to 100%. Fifty-one criteria met the required standard of at least 95% specificity; of the 6 that failed, 3 were successfully modified to achieve this standard and 3 were eliminated. In the resultant 54-criteria/32-point complete system, the total population, as well as both women and men, required more than 3 points to attain at least 95% specificity. Subjects in each of the 5 decades met the specificity standard either at or below the level of more than 3 points. The point score at which 95% or greater specificity was attained for the 10 age/sex subsets varied.(ABSTRACT TRUNCATED AT 250 WORDS)

Kaliuretic peptide and long acting natriuretic peptide as well as atrial natriuretic factor inhibit aldosterone secretion.

The present investigation was designed to determine whether atrial natriuretic peptides consisting of amino acids 1-30 (long acting natriuretic peptide), 31-67 (vessel dilator) and 79-98 (kaliuretic peptide) as well as 99-126 (atrial natriuretic factor (ANF)) of the 126 amino acid ANF prohormone inhibit aldosterone secretion. Thirty healthy human subjects were studied following infusion of 100 ng/kg body weight/min for 60 min of each of the respective peptides. Kaliuretic peptide decreased plasma aldosterone concentration by the greatest amount (6-fold) and plasma aldosterone was still significantly decreased (P < 0.001) three hours after stopping the infusion. In contrast, within 30 min of cessation of the ANF infusion, plasma aldosterone levels had returned to pre-infusion values. Long acting natriuretic peptide also significantly (P < 0.01) decreased plasma aldosterone levels which remained significantly (P < 0.001) decreased 3 h after cessation of infusion. Vessel dilator did not decrease plasma aldosterone levels. Kaliuretic peptide, ANF and long acting natriuretic peptide also decreased (P < 0.01) urinary aldosterone concentrations. None of these peptides changed the plasma potassium concentration. We conclude that two new peptide hormones (long acting natriuretic peptide and kaliuretic peptide) inhibit aldosterone secretion. The length of time that aldosterone secretion is inhibited following kaliuretic peptide and long acting natriuretic peptide infusion is significantly longer (P < 0.001) than following ANF infusion.

Use of multiple radioligands to characterize adenosine receptors in human placenta.

To identify and characterize fully the adenosine receptor of human placenta, particulate preparations of placental parenchyma were examined using several adenosine receptor ligands, [3H]2-chloradenosine ([3H]2-Cl-ADO), [3H]N6-ethylcarboxamideadenosine ([3H]NECA), and [3H]N6-(L-phenylisopropyl)-adenosine ([3H]PIA). Each of the three ligands bound to the particulate preparations with unique binding characteristics. Binding of [3H]PIA characterized a high-affinity low-capacity receptor while the [3H]NECA displayed lower-affinity, higher-capacity binding. Saturation isotherms for [3H]2-Cl-ADO appeared intermediate in terms of affinity and binding capacity. Saturation isotherms of binding data also disclosed displaceable non-receptor binding at high labelled ligand concentrations. Competitive binding studies supported the observation that PIA and NECA bind to sites of high and low affinity, respectively. However, the multicomponent competition curves for [3H]2-Cl-ADO binding suggest binding to the receptors with differential affinity. These studies confirm the presence of adenosine receptors in the human placenta and suggest that these receptors are of both the high-and low-affinity subtypes.

Are sleep complaints an independent risk factor for myocardial infarction?

PURPOSE: To investigate whether subjective sleep complaints are an independent predictor of myocardial infarction (MI) in a community of older adults and to gain clues as to why the association between sleep complaints and incident MI exists. METHODS: Using longitudinal data from the Piedmont study on 2960 adults aged 65 or older who were free of symptomatic heart disease at baseline, we screened 19 potential confounders to determine if any, alone or in combination, could explain the observed relationship between incident MI and sleep complaints. RESULTS: During the three-year follow-up period, there were 152 incident MIs. Restless sleep (incidence density ratio (IDR) = 1.58, 95% confidence interval (CI) = 1.11, 2.24) and trouble falling asleep (IDR = 1.68, 95% CI = 1.09, 2.60) predicted incident MI after adjusting for age, gender, and race. IDRs were not substantially impacted by controlling for smoking, blood pressure, diabetes or obesity. After adjustment for education, number of prescription medicines, self-rated health, and depression score, all IDRs were nullified. In particular, self-rated health and depression were strong independent risk factors for MI. CONCLUSIONS: A subjective sleep complaint increases the likelihood of a first MI in older adults without overt coronary heart disease (CHD) independently of classic coronary risk factors and appears to be a marker for a syndrome of depression and malaise that may have a causal relationship to MI.

Non-Q wave myocardial infarction. Pathophysiology and prognostic implications.

Non-Q wave myocardial infarctions, also known as nontransmural myocardial infarctions or subendocardial myocardial infarctions, have been managed as "mild" coronary events in the past. Substantial evidence now requires modification of this approach. Because of their tendency to be associated with modest cardiac enzyme level elevations, non-Q wave infarcts often result in a favorable early or inhospital prognosis. However, their late complications include recurrent angina, transmural myocardial infarction, and sudden death. Previous myocardial infarction with residual myocardium "at risk" from recurrent ischemia probably bears responsibility for these late complications. Earlier identification of patients at risk and appropriate interventions may improve the long-term prognosis after nontransmural infarcts.

Body composition and source of weight loss after bariatric surgery.

BACKGROUND: Little is known about the composition and source of weight loss after bariatric surgery for morbid obesity. PURPOSE: This study was undertaken to determine changes in weight, body mass index (BMI), lean body weight (LBW), fat weight (FW) and left ventricular cardiac mass (LVM) following vertical banded gastroplasty (VBG). METHODS: After VBG for morbid obesity, 26 women and four men (mean age = 39.1 years) were weighed and had body composition analysis undertaken at intervals. Thirteen patients underwent echocardiography preoperatively and 1 year postoperatively to determine change in LVM and LVM index. RESULTS: Over 12 months there was significant weight loss for all weight parameters examined (p < 0.05). Fat weight loss was most significant; total weight loss and reduction of BMI were significant but less so than fat loss (Wilcoxon's signed ranks test). LBW loss had the smallest contribution to weight loss (p < 0.0001). There was a significant loss of LVM and posterior cardiac wall thickness (p < 0.05). CONCLUSIONS: VBG can lead to loss of lean body weight and left ventricular mass, and more dramatically, fat weight, body weight, and BMI. Cardiac mass and lean body mass are preferentially conserved relative to body fat with weight loss after VBG.

Digitalis use in a retirement community.

Complex medical problems of older patients demand that particular care be taken with their use of digitalis. Although accounting for more than 5% of the top ten prescribed drugs in the United States, studies have suggested that digitalis use might be discontinued in some patients without harm. To assess the potential impact of these observations, a survey was conducted to evaluate the extent of digitalis use in a retirement community in Florida. The community under study consisted of approximately 5600 persons, mean age 72.6 years; 97% were over age 55. The sample of 463 telephone respondents reflected the local census. Digitalis preparations had been taken by 11.4% of the sample, of whom 60% (or 6.9% of the total sample) were currently taking them. Persons taking digitalis tended to be older (P less than .002) and reported worse overall health status than those not taking the drug (P less than .025). Seventeen percent of those who had stopped use of digitalis claimed adverse symptoms or "complications." Of Florida's 10 million population, 23% are over age 60, a proportion increasing yearly. This survey suggests that digitalis use in the elderly is widespread and a potentially important area for investigating management of cardiac problems in the elderly.