Accuracy of death certificates for coding coronary heart disease as the cause of death

BACKGROUND: Death certificates are widely used in epidemiologic and clinical investigations and for national statistics. OBJECTIVE: To examine the accuracy of death certificates for coding coronary heart disease as the underlying cause of death. DESIGN: Community-based inception cohort followed since 1948. SETTING: Framingham, Massachusetts. PATIENTS: 2683 deceased Framingham Heart Study participants. MEASUREMENTS: Sensitivity, specificity, and predictive values of the death certificate. The reference standard was cause of death adjudicated by a panel of three physicians. RESULTS: Among 2683 decedents, the death certificate coded coronary heart disease as the underlying cause of death for 942; the physician panel assigned coronary heart disease for 758. The death certificate had a sensitivity of 83.8% (95% CI, 81.1 % to 86.4%), positive predictive value of 67.4% (CI, 64.4% to 70.4%), specificity of 84.1% (CI, 82.4% to 85.7%), and negative predictive value of 92.9% (CI, 91.7% to 94.1%) for coronary heart disease. The death certificate assigned coronary heart disease in 51.2% of 242 deaths (9.0% of total deaths) for which the physician panel could not determine a cause. Compared with the physician panel, the death certificate attributed 24.3% more deaths to coronary heart disease overall and more than twice as many deaths to coronary heart disease in decedents who were at least 85 years of age. When deaths that were assigned unknown cause by the physician panel were excluded, the death certificate still assigned more deaths to coronary heart disease (7.9% overall and 43.1% in the oldest age group). CONCLUSIONS: Coronary heart disease may be overrepresented as a cause of death on death certificates. National mortality statistics, which are based on death certificate data, may overestimate the frequency of coronary heart disease by 7.9% to 24.3% overall and by as much as two-fold in older persons.     

Socioeconomic inequalities in coronary heart disease and stroke mortality among Australian men, 1979-1993

BACKGROUND: During the 1970s in Australia, mortality from coronary heart disease (CHD) and stroke was higher among lower socioeconomic groups and inequalities were widening. This analysis examines subsequent trends in socioeconomic inequalities, with reference to socioeconomic patterns in major cardiovascular risk factors. METHODS: Socioeconomic status was defined by occupation. Age-standardized mortality rates were calculated for men aged 25-64, using death registration data and labour force estimates for 1979-1993. Risk factor data were taken from three cross-sectional population surveys conducted in 1980, 1983 and 1989. RESULTS: Men in manual occupations were at least 35 percent more likely to die from CHD than men in professional occupations and 60 percent more likely to die from stroke. Their 5-year population risk of a coronary event was 30 percent higher. Since 1979, both groups experienced reductions in coronary risk and mortality. CONCLUSIONS: Socioeconomic inequalities in CHD mortality continued to widen during the early 1980s, stabilized thereafter and persisted into the 1990s. Decreases in blood pressure and smoking prevalence contributed most to declines in coronary risk and to socioeconomic differentials.     

Self-efficacy as a marker of cardiac function and predictor of heart failure hospitalization and mortality in patients with stable coronary heart disease: Findings from the Heart and Soul Study.

Objective: The authors sought to evaluate the association of self-efficacy with objective measures of cardiac function, subsequent hospitalization for heart failure (HF), and all-cause mortality. Design: Observational cohort of ambulatory patients with stable CHD. The authors measured self-efficacy using a published, validated, 5-item summative scale, the Sullivan Self-Efficacy to Maintain Function Scale. The authors also performed a cardiac assessment, including an exercise treadmill test with stress echocardiography. Main Outcome Measures: Hospitalizations for HF, as determined by blinded review of medical records, and all-cause mortality, with adjustment for demographics, medical history, medication use, depressive symptoms, and social support. Results: Of the 1,024 predominately male, older CHD patients, 1013 (99%) were available for follow-up, 124 (12%) were hospitalized for HF, and 235 (23%) died during 4.3 years of follow-up. Mean cardiac self-efficacy score was 9.7 (SD 4.5, range 0–20), corresponding to responses between “not at all confident” and “somewhat confident” for ability to maintain function. Lower self-efficacy predicted subsequent HF hospitalization (OR per SD decrease = 1.4, p = .0006), and all-cause mortality (OR per SD decrease = 1.4, p Conclusion: Among patients with CHD, self-efficacy was a reasonable proxy for predicting HF hospitalizations. The increased risk of HF associated with lower baseline self-efficacy was explained by worse cardiac function. These findings indicate that measuring cardiac self-efficacy provides a rapid and potentially useful assessment of cardiac function among outpatients with CHD. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Cardiothoracic ratio and relative heart volume as predictors of coronary heart disease mortality. The Whitehall study 25 year follow-up

Searching for an in vitro model for somatic hypermutation, we have identified an IgM-expressing Burkitt lymphoma line that constitutively diversifies its immunoglobulin V domain at high rate during culture. As in in vivo, the mutations are largely nucleotide substitutions with the pattern of substitutions revealing a component of the human hypermutation program that is preferentially targeted to G/C residues. The substitutions frequently create stop codons with IgM-loss variants also being generated by V domain-specific deletions and duplications. However, in transfectants expressing terminal deoxynucleotidyl transferase, many IgM-loss variants additionally arise through short nontemplated nucleotide insertions into the V (but not C) domain. Thus, antibody hypermutation is likely accompanied by DNA strand breaks scattered within the mutation domain.     

Diastolic dysfunction as a cause of heart failure in the hypertensive patient

A study was undertaken to investigate physical work load, physical capacity, physical strain and perceived health among elderly aides in home-care service. A secondary aim was to compare the work load and strain between the two main types of home-care service available in Sweden today. Work tasks and their distribution among 20 elderly aides (aged 45-65 years), working in open home-care service (clients living in their original flats or houses) and at service apartment houses (clients living in private flats constructed for the elderly and handicapped with service functions) were observed during whole work days. Heart rate and number of steps taken were also measured continuously during the whole work day. Oxygen consumption and work postures for upper arm and back were measured during parts of the work day. The results showed that home-care work is characterised by long periods of standing and walking and that postures potentially harmful for the low back and shoulders occurred frequently. Average physiological strain measured as relative oxygen consumption and heart rate during the work day did not exceed present recommendations. Average physical work load and strain in open home-care service slightly exceeded those in service apartment houses because of more frequent cleaning and walking outdoors. Many aides in this study showed slightly reduced physical capacity, and musculoskeletal problems were common. Many elderly aides in home-care service are probably exposed at work to high risks of overexertion and impaired health as a result of high postural loads in combination with other known important factors, such as time stress and lack of equipment.     

Light chain deposition disease as a cause of renal failure

The objective of the paper is to draw attention to a rare cause of rapidly progressing renal failure which developed in the course of four months as a result of light chain deposition disease. The authors submit two case-histories of the disease assessed by renal biopsy after previous clinical and laboratory suspicion of monoclonal gammapathy. In one patient in the sternal punctate plasmacytoma was diagnosed and in the second case it was not possible to detect any type of monoclonal gammapathy or another possible cause of disease. Renal failure was in both cases irreversible and both patients were enlisted in regular haemodialyzation treatment.     

The Brugada-Brugada syndrome. A contribution to detection of risk patients with reference to sudden heart death without structural heart disease

Infant botulism is caused by intestinal colonization by Clostridium botulinum, C. barati or C. butyricum. Infant botulism has only rarely been reported outside the USA. A 3-month-old boy developed constipation, lethargy, feeding difficulties and descending, severe, symmetric weakness. He was breastfed but had also been fed honey. Supportive care led to complete recovery. The serum was positive for C. botulinum toxin type A-F (mouse toxin neutralization assay). A strain of C. botulinum producing toxin type A and E was identified in the stool. C. botulinum was identified in a jar of honey of the same brand as the honey fed to the patient.     

Nonsustained ventricular tachycardia in severe heart failure. Independent marker of increased mortality due to sudden death. GESICA-GEMA Investigators

BACKGROUND: The goal of the study was to determine the prognostic value of nonsustained ventricular tachycardia (NSVT) in total mortality in severe congestive heart failure (CHF) and in death modes. NSVT is associated with an increased mortality in CHF. However, the predictive value of NSVT as a marker for sudden death or death due to progressive heart failure has not been determined. METHODS AND RESULTS: Five hundred sixteen patients from the GESICA trial (33.4% with NSVT) were initially studied with the results of 24-hour Holter and 2 years of follow-up. Within 2 years, 87 of 173 patients (50.3%) with NSVT and 106 of 343 patients (30.9%) without NSVT died. Relative risk (RR) was 1.69 (95% confidence interval [CI], 1.27 to 2.24; P < .0002), and Cox proportional hazard analysis was 1.62 (95% CI, 1.22 to 2.16; P < .001). Sudden death increased from 8.7% (30 of 343) to 23.7% (41 of 173) in patients with NSVT (RR, 2.77; 95% CI, 1.78 to 4.44; P < .001). Progressive heart failure death was also increased from 17.5% (60 of 343) to 20.8% (36 of 173) (P = .22). Quantitative analysis of 24-hour Holter (first 295 patients) demonstrated that couplets had a similar RR to that of NSVT for both total mortality (RR, 1.81; 95% CI, 1.22 to 2.66; P < .002) and sudden death (RR, 3.37; 95% CI, 1.57 to 7.25; P < .0005). Couplets and/or NSVT (ventricular repetitive beats) were even more predictive for sudden death (RR, 10.1; 95% CI, 1.91 to 52.7; P < .01). CONCLUSIONS: In patients with CHF, NSVT is an independent marker for increased overall mortality rate and sudden death. The absence of NSVT and ventricular repetitive beats in a 24-hour Holter indicates a low probability of sudden death.     

Cutaneous malignant melanoma in Scotland: incidence, survival, and mortality, 1979-94. The Scottish Melanoma Group

OBJECTIVE: To determine the changing incidence of and mortality from cutaneous malignant melanoma in Scotland from 1979 to 1994. DESIGN: Detailed registration of clinical and pathological features, surgical and other treatment, and follow up of all cases of cutaneous malignant melanoma diagnosed from 1979 to 1994 and registered with specialist database for Scotland. SETTING: Scotland. SUBJECTS: 6288 patients with invasive primary cutaneous malignant melanoma diagnosed between 1 January 1979 and 31 December 1994. RESULTS: The annual age standardised incidence of cutaneous malignant melanoma rose significantly from 3.5 to 7.8 per 100,000 per year in men and from 6.8 to 12.3 per 100,000 per year in women (P < 0.001 for both). World standardised rates increased from 2.7 to 6.0 per 100,000 per year in men and 4.6 to 8.50 per 100,000 in women. The incidence of melanoma continued to increase significantly in men of all ages during the study, but the rate stabilised in women after 1986. Mortality from cutaneous malignant melanoma was 1.3 per million per annum in men in 1979, rising to 2.3 per million per annum in 1994 (P < 0.01); it was 2.4 per million per annum in women in 1979, falling to 1.9 per million per annum in 1994 (P = 0.09). The underlying mortality trends showed a continuing rise for men but a downward trend for women that was not significant (P = 0.09). In men, melanoma free survival was 69% at 5 years and 61% at 10 years; in women the corresponding rates were 82% and 75%. Younger patients had higher survival rates, which were not entirely explained by thinner tumours. Over the 15 year period, survival rates improved by 12% overall, only partly owing to thinner tumours. CONCLUSIONS: In Scotland the incidence of melanoma in women has stabilised, while mortality associated with melanoma in women shows a downward trend.     

Role of secondary prevention in congestive heart failure due to coronary artery disease

BACKGROUND: It is unknown whether genetic factors predispose patients to idiopathic pancreatitis. In patients with cystic fibrosis, mutations of the cystic fibrosis transmembrane conductance regulator (CFTR) gene typically cause pulmonary and pancreatic insufficiency while rarely causing pancreatitis. We examined whether idiopathic pancreatitis is associated with CFTR mutations in persons who do not have lung disease of cystic fibrosis. METHODS: We studied 27 patients (mean age at diagnosis, 36 years), 22 of whom were female, who had been referred for an evaluation of idiopathic pancreatitis. DNA was tested for 17 CFTR mutations and for the 5T allele in intron 8 of the CFTR gene. The 5T allele reduces the level of functional CFTR and is associated with an inherited form of infertility in males. Patients with two abnormal CFTR alleles were further evaluated for unrecognized cystic fibrosis-related lung disease, and both base-line and CFTR-mediated ion transport were measured in the nasal mucosa. RESULTS: Ten patients with idiopathic chronic pancreatitis (37 percent) had at least one abnormal CFTR allele. Eight CFTR mutations were detected (prevalence ratio, 11:1; 95 percent confidence interval, 5 to 23; P<0.001). In three patients both alleles were affected (prevalence ratio, 80:1; 95 percent confidence interval, 17 to 379; P<0.001). These three patients did not have lung disease typical of cystic fibrosis on the basis of sweat testing, spirometry, or base-line nasal potential-difference measurements. Nonetheless, each had abnormal nasal cyclic AMP-mediated chloride transport. CONCLUSION: In a group of patients referred for evaluation of idiopathic pancreatitis, there was a strong association between mutations in the CFTR gene and pancreatitis. The abnormal CFTR genotypes in these patients with pancreatitis resemble those associated with male infertility.     

Family history of coronary heart disease is a stronger predictor of coronary heart disease morbidity and mortality than family history of non-insulin dependent diabetes mellitus

The aim of this study was to compare the effect of family history of non-insulin dependent diabetes mellitus (NIDDM) and coronary heart disease (CHD) as risk factors for CHD morbidity and mortality. Altogether, 394 siblings of NIDDM probands and non-diabetic probands, with and without CHD, were followed for 8 years with respect to CHD events in a prospective population-based study. The baseline study was conducted from 1983 to 1985. Age- and sex-adjusted cumulative occurrence of CHD events was higher in the siblings of the probands with CHD and with NIDDM (13.1%; P = 0.037) and in the siblings of the probands with CHD and without NIDDM (15.4%; P = 0.054), compared with the siblings of the probands without NIDDM and without CHD (4.8%). The incidence of fatal CHD events tended to be higher in a group with a family history of NIDDM and CHD, but the trend was not statistically significant. In univariate logistic regression analyses, a family history of CHD was positively associated with cumulative occurrence of CHD events (odds ratio 2.53, P = 0.009), whereas a family history of NIDDM had no significant association (odds ratio 1.39, P = 0.312). After adjustment for age, sex, family history of NIDDM and major cardiovascular risk factors, the association between family history of CHD and cumulative occurrence of CHD events remained significant (odds ratio 2.25, P = 0.048). In conclusion, the present study indicates that a family history of CHD is a stronger predictor of future CHD events than a family history of NIDDM.     

Comparison of mortality from acute myocardial infarction between 1979 and 1992 in a geographically defined stable population

This study documents mortality from acute myocardial infarction (AMI), in hospital and at 1 year, for each of 3 selected 1-year periods in a stable community over a 13-year period beginning in 1979 and continuing into the thrombolytic era, to detect any changes occurring in conjunction with the introduction of new therapies. Every patient with AMI occurring in a geographically defined stable community (Hamilton, Ontario, Canada) in 3 1-year periods (1979 to 1980 [n = 816], 1986 to 1987 [n = 816], and 1991 to 1992 [n = 831]) was identified and clinically characterized by standardized criteria. Subsequent in-hospital and 1-year survival were ascertained prospectively. The 3 cohorts were similar in prognostic factors. Mean age was progressively greater over the study period from 63 years in 1979 to 1980, to 67 years in 1991 to 1992 (p = 0.02). There was no change in in-hospital mortality rates from 1979 to 1980 (17%) and 1986 to 1987 (16%). However, from 1986 to 1987 and 1991 to 1992, in-hospital mortality decreased from 16% to 9% (p < 0.001) and 1-year mortality decreased from 26% to 19% (p < 0.001). For patients who survived the hospital phase of AMI, 1-year mortality did not change and was between 11% and 12% in each of the 3 study periods. From 1986 to 1987 and 1991 to 1992, there was an increase in the use of thrombolytic therapy from 5% to 44% of patients. The acute use of aspirin increased from 30% to 88% and the acute use of beta blockers increased from 19% to 48% of patients. The observed increase in use of these agents could account for half of the actual mortality reduction observed. This prospective population-based survey demonstrates improved in-hospital survival after AMI associated with increased use of established effective therapies between 1987 and 1992. The 1-year mortality of hospital survivors of AMI was unchanged throughout the period of study, remaining at 11% to 12%.     

Long-term prediction of coronary heart disease mortality in two rural Greek populations

In 1960-61 two pooled Greek rural populations totalling 1215 men aged 40-59 years were followed-up for 25 years. A Cox model analysis of fatal coronary events over 15 years showed that serum cholesterol in men aged 40-59 years, cholesterol in men aged 45-64 years, and systolic blood pressure in men aged 50-69 played a predictive role. The coefficient of age became more significant with advancing age and that of cigarette smoking only at 25 years follow-up. The coefficient of cholesterol decreased stepwise and became negative for men aged 50-69; body mass index was without effect in any follow-up of these cohorts. Systolic blood pressure and serum cholesterol increased in these populations by 5.4 mmHg and 23.5 mg.dl-1 (0.61 mmol.l-1), respectively between the years 0 and 10, whereas cigarette consumption decreased minimally. These changes were used to test the predictability of coronary events occurring between years 10 and 25 of follow-up when added to the model containing the factors at entry. Of these changes only systolic blood pressure significantly increased the predictability of coronary deaths. It is concluded that even minor alterations in systolic blood pressure above or below the entry levels can be associated with marked modifications in coronary mortality above or below those occurring naturally in the 15 years after the changes occurred.     

Chronic heart failure in the United States: a manifestation of coronary artery disease

BACKGROUND: Hyperhomocysteinemia occurs in renal failure and may increase the risk for cardiovascular disease, possibly by damaging the endothelium. Folic acid and betaine are required in two separate homocysteine conversion pathways and may therefore lower plasma homocysteine. OBJECTIVE: To study the therapeutic role of betaine and the effect on endothelial function of long-term homocysteine-lowering therapy with folic acid, in peritoneal dialysis (PD) patients. PATIENTS AND DESIGN: Thirty PD patients were randomized to a 12-week treatment with 5 mg folic acid and 4 g betaine daily, or to 5 mg folic acid alone daily. They were then rerandomized to treatment with 1 or 5 mg folic acid daily for 40 weeks. MEASUREMENTS: At baseline and after 52 weeks, endothelial function was assessed by determination of endothelium-dependent vasodilatation and biochemical markers. RESULTS: Plasma total homocysteine (tHcy) was elevated at baseline: 42.6 (5.8) micromol/L. Only 1 patient (3%) had a normal plasma homocysteine (i.e., < or = 15 micromol/L) before therapy. Normalization of plasma homocysteine occurred in 39% of the patients at 12 weeks. Betaine had no additional homocysteine-lowering effect. Plasma tHcy levels were similar during treatment with 1 or 5 mg folic acid daily. Endothelial function was impaired at baseline and had not improved after 52 weeks of treatment. CONCLUSIONS: Peritoneal dialysis patients have hyperhomocysteinemia, which can be normalized with folic acid alone in about 40% of patients. Betaine does not further lower plasma homocysteine. A maintenance dose of 1 or 5 mg folic acid daily results in equivalent plasma homocysteine levels. Long-term reduction in plasma homocysteine did not result in improvement of endothelial function as assessed by our methods.     

Enalapril reduces QTc dispersion in mild congestive heart failure secondary to coronary artery disease

Intranasal administration of protein antigen is an efficient way to induce mucosal tolerance. Suppressive mechanisms that might be involved in this phenomenon include down-regulation of T-helper type-1 (Th1)-mediated processes by Th2 cells. However, since Th2 responses can also be subjected to mucosal tolerance, we wanted to investigate whether suppression of a typical Th1 response, such as a delayed-type hypersensitivity (DTH) reaction by intranasal tolerance induction, was causally related to up-regulation of Th2 responses. We therefore treated mice either systemically or locally with anti-interleukin-4 (IL-4) or anti-IL-10 antibodies before intranasal tolerance induction or before sensitization for DTH to see whether we could prevent or abrogate tolerance. Although the up-regulation of antigen-specific IgE levels in tolerant mice could be prevented by anti-IL-4 treatment, the extent of tolerance as measured by suppression of DTH was not affected. We therefore conclude that up-regulation of Th2 responses observed after intranasal tolerance induction is an additional or consequential rather than a necessary reaction.     

Trends in the incidence of myocardial infarction and in mortality due to coronary heart disease, 1987 to 1994

BACKGROUND AND METHODS: To clarify the determinants of contemporary trends in mortality from coronary heart disease (CHD), we conducted surveillance of hospital admissions for myocardial infarction and of in-hospital and out-of-hospital deaths due to CHD among 35-to-74-year-old residents of four communities of varying size in the United States (a total of 352,481 persons in 1994). Between 1987 and 1994, we estimate that there were 11,869 hospitalizations for myocardial infarction (on the basis of 8572 hospitalizations sampled) and 3407 fatal coronary events (3023 sampled). RESULTS: The largest average annual decrease in mortality due to CHD occurred among white men (change in mortality, -4.7 percent; 95 percent confidence interval, -2.2 to -7.1 percent), followed by white women (-4.5 percent; 95 percent confidence interval, -0.7 to -8.2 percent), black women (-4.1 percent; 95 percent confidence interval, -10.3 to +2.5 percent), and black men (-2.5 percent; 95 percent confidence interval, -6.9 to +2.2 percent). Overall, in-hospital mortality from CHD fell by 5.1 percent per year, whereas out-of-hospital mortality declined by 3.6 percent per year. There was no evidence of a decline in the incidence of hospitalization for a first myocardial infarction among either men or women; in fact, such hospital admissions increased by 7.4 percent per year (95 percent confidence interval for the change, +0.5 to +14.8 percent) among black women and 2.9 percent per year (95 percent confidence interval, -3.6 to +9.9 percent) among black men. Rates of recurrent myocardial infarction decreased, and survival after myocardial infarction improved. CONCLUSIONS: From 1987 to 1994, we observed a stable or slightly increasing incidence of hospitalization for myocardial infarction. Nevertheless, there were significant annual decreases in mortality from CHD. The decline in mortality in the four communities we studied may be due largely to improvements in the treatment and secondary prevention of myocardial infarction.     

Hemochromatosis-associated mortality in the United States from 1979 to 1992: an analysis of Multiple-Cause Mortality Data

BACKGROUND: Hemochromatosis, which can lead to serious chronic diseases resulting from iron overload, has an estimated prevalence of 50 to 80 cases per 10000 persons. However, little population-based information is available on the impact of hemochromatosis on morbidity and mortality. OBJECTIVE: To evaluate trends over 14 years in deaths and medical conditions associated with hemochromatosis in the United States. DESIGN: We searched Multiple-Cause Mortality Files compiled by the National Center for Health Statistics for the years 1979 to 1992 for all records listing hemochromatosis. We used these data to calculate age-adjusted and age-specific mortality rates, identify medical conditions associated with a known diagnosis of hemochromatosis at death, and calculate proportionate mortality ratios for these medical conditions. RESULTS: The listing of hemochromatosis on death certificates increased 60% from 1979 to 1992. Decedents with hemochromatosis were 23, 13, and 5 times more likely to have liver neoplasms, liver disease, and cardiomyopathy, respectively, than were decedents without hemochromatosis. Conversely, decedents with liver neoplasms, liver disease, and cardiomyopathy were 26, 14, and 5 times more likely, respectively, to have hemochromatosis than were decedents without these conditions. Hemochromatosis was 82 times more likely in persons with the combination of liver neoplasms and diabetes and 43 times more likely in those with the combination of liver disease and diabetes than in those without these conditions. CONCLUSIONS: Comparison of the reported prevalence of hemochromatosis among decedents with estimates of prevalence in the general U.S. population suggests that either the penetrance or the recognition of hemochromatosis, or both, is low. Nevertheless, substantial mortality resulting from liver disease, liver neoplasms, cardiomyopathy, and a combination of liver disease and diabetes in patients with hemochromatosis argues for the improved diagnosis and treatment of hemochromatosis in persons with these conditions.