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Background and Purpose- The importance of weight change for the risk of stroke is not well known. We examined the associations between early- and mid-life weight change and risks of stroke and death during long-term follow-up of healthy men. Methods- We recruited healthy men aged between 40 and 59 years and performed a cardiovascular examination at baseline and again at 7 years. We collected data on weight change since the age of 25 (early-life weight change) and measured weight change from baseline to the visit at 7 years (mid-life weight change). For both weight change periods, participants were divided into the following categories: weight loss, weight gain 0 to 4.9 kg, weight gain 5 to 9.9 kg, and weight gain ≥10 kg. Data on stroke and death were collected up to 35 years, from study visits, hospital records, and the National Cause of Death Registry. We used Cox regression to analyze the associations between weight change during early-life and mid-life and risks of stroke and death. Results- Of the 2014 participants, 2014 (100%) had data on early-life weight change and were followed for a median of 30.1 years, while 1403 had data on mid-life weight change and were followed for a median of 24.6 years. During early-life, compared with those who had weight gain 0 to 4.9 kg, hazard ratio for stroke was 1.46 (95% CI, 1.09-1.95) among those with weight gain 5 to 9.9 kg, 1.39 (95% CI, 1.03-1.87) for those with weight gain ≥10 kg, and 1.46 (95% CI, 0.99-2.11) among those with weight loss. For all-cause death, the hazard ratios were 1.08 (95% CI, 0.92-1.23), 1.14 (95% CI, 0.98-1.33), and 1.29 (95% CI, 1.06-1.56), respectively. During mid-life, there were no significant differences in risk of stroke or death between the groups. Conclusions- Weight increase during early-life, but not mid-life, seems to be associated with increased long-term risk of stroke in healthy men. If these findings can be confirmed, efforts to prevent weight increase should target the younger population.
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Peso Corporal/fisiologia , Acidente Vascular Cerebral/epidemiologia , Tempo , Aumento de Peso/fisiologia , Adulto , Idoso , Humanos , Masculino , Pessoa de Meia-Idade , Obesidade/complicações , Sistema de Registros , Fatores de Risco , Redução de Peso/fisiologiaRESUMO
BACKGROUND: The use of GHB is still widespread with many hospitalised overdose cases. CASE PRESENTATION: A man in his fifties was found unconscious in the street and brought to our Acute Admissions. When first examined he was still unconscious, hypothermic, had snoring respiration and smelled of alcohol. He was otherwise haemodynamically stable. Blood samples showed elevated osmolal and anion gaps. The increase in the osmol gap could be explained by the ethanol level of 210 mg/dL (46 mmol/L), but the reason for the increased anion gap was unknown. Flumazenil and naloxone were administered without effect. As the ethanol concentration alone was unlikely to explain the clinical picture, extended toxicological tests were performed. GHB in plasma was very high (5.0 mmol/L; 520 mg/L) even though the sample was taken almost 4 hours after admission. The GHB concentration (present as an anion) corresponded to the increased anion gap. The patient was comatose for approximately 12 hours, which is unusually long in GHB poisoning. INTERPRETATION: Intoxication with GHB is important to consider in comatose patients where other causes are excluded. Prolonged clinical course may be due to a saturation of the GHB metabolism after a large dose or ingestion of GBL or 1,4-butanediol, both of which are precursors to GHB.
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Overdose de Drogas , Oxibato de Sódio , Equilíbrio Ácido-Base , Coma/induzido quimicamente , Etanol , Humanos , Masculino , Inconsciência/induzido quimicamenteRESUMO
Background and Purpose- Low cardiorespiratory fitness is associated with increased risk of cardiovascular disease. The present study aims to assess whether change of fitness over time has any impact on long-term risk of stroke and death. Methods- We recruited healthy men aged 40 to 59 years in 1972 to 1975, and followed them until 2007. Physical fitness was assessed with a bicycle ECG test at baseline and again at 7 years, by dividing the total exercise work by body weight. Participants were categorized as remained fit, became unfit, remained unfit, or became fit, depending on whether fitness remained or crossed the median values from baseline to the 7-year visit. Outcome data were collected up to 35 years, from study visits, hospital records, and the National Cause of Death Registry. Risks of stroke and death were estimated by Cox regression analyses and expressed as hazard ratios (HRs) with 95% CIs. Results- Of 2014 participants, 1403 were assessed both at baseline and again at 7 years, and were followed for a mean of 23.6 years. Compared with the became unfit group, risk of stroke was 0.85 (0.54-1.36) for the remained unfit, 0.43 (0.28-0.67) for the remained fit, and 0.34 (0.17-0.67) for the became fit group. For all-cause death, risks were 0.99 (0.76-1.29), 0.57 (0.45-0.74), and 0.65 (0.46-0.90), respectively. Among those with high fitness at baseline, the became unfit group had a significantly higher risk of stroke (HR, 2.35; CI, 1.49-3.63) and death (HR, 1.74; CI, 1.35-2.23) than those who remained fit. Among those who had low fitness at baseline, the became fit group had a significantly lower risk of stroke (HR, 0.40; CI, 0.21-0.72) and death (HR, 0.66; CI, 0.50-0.85) than participants in the remained unfit group. Conclusions- Cardiorespiratory fitness at baseline and change in fitness was associated with large changes in long-term risk of stroke and death. These findings support the encouragement of regular exercise as a stroke prevention strategy.
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OBJECTIVE: There is an association between exercise systolic blood pressure (SBP) and cardiovascular disease and mortality. The aim of this study was to investigate this association, with 35 years of follow-up. METHODS: Through 1972-75, 2014 healthy, middle-aged men underwent thorough medical examination and a bicycle exercise test. 1999 participants completed six minutes at 100 W. SBP was measured manually, both before the test and every two minutes during the test. Highest SBP measured during the first six minutes (SBP100W) was used in further analyses. RESULTS: Participants were divided into quartiles (Q) based on their SBP100W; Q1: 100-160 mm Hg (n = 457), Q2: 165-175 mm Hg (n = 508), Q3: 180-195 mm Hg (n = 545) and Q4: 200-275 mm Hg (n = 489). After 35-years follow-up, there was a significant association between exercise SBP at baseline and cardiovascular disease and mortality. In the multivariate analysis adjusting for resting SBP, age, smoking status, total serum cholesterol and family history of coronary heart disease, as well as physical fitness, there is a 1.39-fold (CI: 1.00-1.93, p = 0.05) increased risk of cardiovascular mortality in Q4 compared to Q1. When not adjusting for physical fitness, there is a 1.29-fold (CI: 1.03-1.61, p = 0.02) increase in risk of cardiovascular disease between Q1 and Q4. CONCLUSIONS: The results of this study suggest that the association between exercise SBP at moderate workload and cardiovascular disease and mortality in middle-aged men extends through as long as 35 years and into old ages.
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Pressão Sanguínea/fisiologia , Doenças Cardiovasculares/diagnóstico , Sístole/fisiologia , Adulto , Doenças Cardiovasculares/mortalidade , Seguimentos , Humanos , Masculino , Pessoa de Meia-Idade , Fatores de Risco , Fatores de TempoRESUMO
PURPOSE: The Oslo Ischaemia Study was designed to investigate the prevalence and predictors of silent coronary disease in Norwegian middle-aged men, specifically validating exercise electrocardiography (ECG) findings compared with angiography. The study has been important in investigating long-term predictors of cardiovascular morbidity and mortality, as well as investigating a broad spectrum of epidemiological and public health perspectives. PARTICIPANTS: In 1972-1975, 2014 healthy men, 40-59 years old, were enrolled in the study. Comprehensive clinical examination included an ECG-monitored exercise test at baseline and follow-ups. The cohort has been re-examined four times during 20 years. Linkage to health records and national health registries has ensured complete endpoint registration of morbidity until the end of 2006, and cancer and mortality until the end of 2017. FINDINGS TO DATE: The early study results provided new evidence, as many participants with a positive exercise ECG, but no chest pain ('silent ischaemia'), did not have significant coronary artery stenosis after all. Still, they were over-represented with coronary disease after years of follow-up. Furthermore, participants with the highest physical fitness had lower risk of cardiovascular disease, and the magnitude of blood pressure responses to moderate exercise was shown to influence the risk of cardiovascular disease and mortality. With time, follow-up data allowed the scope of research to expand into other fields of medicine, with the aim of investigating predictors and the importance of lifestyle and risk factors. FUTURE PLANS: Recently, the Oslo Ischaemia Study has been found worthy, as the first scientific study, to be preserved by The National Archives of Norway. All the study material will be digitised, free to use and accessible for all. In 2030, the Oslo Ischaemia Study will be linked to the Norwegian Cause of Death Registry to obtain complete follow-up to death. Thus, a broad spectrum of additional opportunities opens.
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Doença da Artéria Coronariana , Estenose Coronária , Adulto , Eletrocardiografia , Teste de Esforço , Humanos , Isquemia , Masculino , Pessoa de Meia-Idade , Fatores de RiscoRESUMO
There is no consensus on the definition of an exaggerated increase in systolic blood pressure (SBP) during exercise. The aim was to explore a potential threshold for exercise SBP associated with increased risk of coronary heart disease in healthy men using repeated exercise testing. Two thousand fourteen healthy white male employees were recruited into the Oslo Ischemia Study during early 1970s. At follow-up 7 years later, 1392 men were still considered healthy. A bicycle exercise test at 100 W workload was performed at both visits. Cox regression analyses were performed with increasing cutoff levels of peak exercise SBP at 100 W workload (SBP100W) from 160 mm Hg to 200 mm Hg, adjusted for cardiovascular risk factors and physical fitness. Participants with SBP100W below cutoff level at both baseline and first follow-up were compared with participants with SBP100W equal to or above cutoff level at both visits. Compared with participants with SBP100W below all cutoff levels between 165 and 195 mm Hg, coronary heart disease risk was increased among participants with SBP100W equal to or above cutoff at all levels. There was no evidence of a distinct threshold level for coronary heart disease risk, and the relation between SBP100W and coronary heart disease appears linear. When investigating exercise SBP at moderate workload measured at 2 exercise tests in healthy middle-aged white men, there is increasing risk of coronary heart disease with increasing exercise SBP independent of SBP at rest. The association is linear from the low range of exercise SBP, and there is no sign of a distinct threshold level for increased coronary disease risk.
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Pressão Sanguínea/fisiologia , Doença das Coronárias/fisiopatologia , Exercício Físico/fisiologia , Adulto , Teste de Esforço , Humanos , Masculino , Pessoa de Meia-Idade , Fatores de RiscoRESUMO
OBJECTIVE: We investigated the association between exercise SBP at a moderate workload and long-term risk of coronary heart disease (CHD) in men who were healthy when assessed by two bicycle exercise tests 7 years apart. METHODS: During 1972-1975, apparently healthy men (nâ=â1999) were initially enrolled following thorough medical examination and ECG-monitored bicycle exercise test. Participants (nâ=â1392) who were healthy also at a second exercise test 7 years later were included in the present study. They were divided into quartiles, Q1-Q4, according to the highest SBP during the initial 6âmin of the exercise test on a moderate workload of 100âW (SBP100W) at 7 years and followed for up to 28 years. Adjusted Cox regression was used to estimate CHD risk defined as first occurrence of angina pectoris, nonfatal myocardial infarction or CHD mortality. RESULTS: During follow-up, 452 of the 1392 men suffered incident CHD, and unadjusted, there was increased risk of CHD with increasing SBP100âW, with significant differences between Q1-Q4. In the multivariate analysis adjusting for classical coronary risk factors, including SBP at rest, there was increased risk of CHD in Q3 (SBP100âW above 180âmmHg) and Q4 (SBP100âW above 200âmmHg) compared with Q1 (≤160âmmHg, lowest SBP100âW), hazard ratios 1.42 (CI 1.07-1.90) and 1.93 (CI 1.38-2.70), respectively. CONCLUSION: Healthy middle-aged men had increased long-term risk of CHD with exercise SBP above 180âmmHg at moderate workload. The prognostic impact of SBP above 180âmmHg at exercise is independent of classical coronary risk factors and blood pressure at rest.
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Pressão Sanguínea , Doença das Coronárias/epidemiologia , Exercício Físico/fisiologia , Infarto do Miocárdio/epidemiologia , Adulto , Determinação da Pressão Arterial , Eletrocardiografia , Teste de Esforço , Seguimentos , Humanos , Masculino , Pessoa de Meia-Idade , Noruega/epidemiologia , Modelos de Riscos Proporcionais , Fatores de Risco , Carga de TrabalhoRESUMO
Background Physical fitness has been shown to predict cardiovascular death during long-term follow-up. In the present study we aimed to investigate how physical fitness and other cardiovascular risk factors at middle-age influenced the risk of cardiovascular death during the early (0-11 years), intermediate (12-23 years) and late (24-35 years) parts of a 35-year observation period. Methods and results Age-adjusted physical fitness was calculated in 2014 apparently healthy, middle-aged men after maximal bicycle electrocardiogram-tests in 1972-1975 (Survey 1) and 1979-1982 (Survey 2). The men were assessed through 35 years after Survey 1, and 28 years after Survey 2 by Cox proportional hazards models. Low Survey 1 physical fitness was independently associated with increased risks of early and intermediate, but not late, cardiovascular death. Survey 1 to Survey 2 change in physical fitness, age, smoking status, systolic blood pressure and cholesterol impacted cardiovascular death risks in all periods. Family history of coronary heart disease impacted early and intermediate, but not late, cardiovascular death. Conclusions Most classical cardiovascular risk factors were strong predictors of early, intermediate and late cardiovascular death. Physical fitness measured at median age 50 years was independently associated with risk of early cardiovascular death, but the association weakened as time progressed. Change in physical fitness during middle-age impacted cardiovascular death risk in a full lifetime perspective. Thus, our data suggest that physical fitness is a modifiable cardiovascular risk factor with limited duration in contrast to the sustained impact of smoking, blood pressure and cholesterol on cardiovascular mortality.
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Doenças Cardiovasculares/prevenção & controle , Exercício Físico , Estilo de Vida Saudável , Aptidão Física , Comportamento de Redução do Risco , Adulto , Fatores Etários , Doenças Cardiovasculares/diagnóstico , Doenças Cardiovasculares/mortalidade , Nível de Saúde , Voluntários Saudáveis , Humanos , Masculino , Pessoa de Meia-Idade , Noruega/epidemiologia , Prognóstico , Fatores de Proteção , Medição de Risco , Fatores de Risco , Fatores Sexuais , Fatores de TempoRESUMO
Background There are few data on risk factors for stroke during long-term follow-up of healthy individuals. Aims We aimed to investigate the long-term predictive impact on stroke risk of baseline variables including hemodynamic variables measured at rest and during exercise in middle-aged, healthy men. Methods We performed a prospective cohort study of 2014 healthy Norwegian men aged 40-59 years, recruited during the period 1972-1975 and followed until 2007. Participants underwent a comprehensive clinical assessment at baseline, including a bicycle exercise test. Data on stroke, transient ischemic attack, and death were collected on all participants from follow-up visits, medical records, and the National Cause of Death Registry. We used Cox regression for analysis and estimated hazard ratios with 95% confidence intervals, adjusting for traditional risk factors and hemodynamic variables measured at rest and during exercise. Results During 35 years' follow-up, 316 participants (16%) had stroke, of which 287 (91%) were ischemic and 29 (9%) were hemorrhagic. Age (hazard ratio 2.70 per increase in one standard deviation, 95% confidence interval 2.13-3.43), resting systolic blood pressure (hazard ratio 1.24, 95% confidence interval 1.11-1.39), body mass index (hazard ratio 1.14, 95% confidence interval 1.02-1.29), and atrioventricular conduction time (hazard ratio 1.11, 95% confidence interval 1.03-1.19) were significantly associated with long-term risk of stroke, as were maximal systolic blood pressure and heart rate during exercise (hazard ratio 1.28, 95% confidence interval 1.13-1.46, and hazard ratio 0.86, 95% confidence interval 0.74-0.99, respectively). Conclusions Hemodynamic variables at rest and during exercise testing add to the predictive value of clinical variables in healthy, middle-aged men, and should be included in the assessment of long-term risk of stroke, when available.
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Acidente Vascular Cerebral/epidemiologia , Fatores Etários , Pressão Sanguínea , Índice de Massa Corporal , Estudos de Coortes , Frequência Cardíaca , Hemodinâmica , Humanos , Masculino , Pessoa de Meia-Idade , Fatores de RiscoRESUMO
BACKGROUND: Life-threatening bleeding caused by liver injury due to chest compressions is a rare complication in otherwise successful cardiopulmonary resuscitation. Surgical intervention has been suggested to achieve bleeding control; however, reported mortality is high. In this report, we present a brief literature review and a case report in which use of a less invasive strategy was followed by an uneventful recovery. CASE PRESENTATION: A 37-year-old white woman was admitted after out-of-hospital cardiac arrest. Bystander cardiopulmonary resuscitation was immediately performed, followed by advanced cardiopulmonary resuscitation that included tracheal intubation, mechanical chest compressions, and external defibrillation with return of spontaneous circulation. Upon hospital admission, the patient's blood pressure was 94/45 mmHg and her heart rate was 110 beats per minute. Her electrocardiogram showed no signs of ST-segment elevations or Q-wave development. Coronary angiography revealed a proximal thrombotic occlusion of the left anterior descending coronary artery. Successful recanalization, after thrombus aspiration and balloon dilation followed by stent implant, was verified with normalized anterograde flow. Immediately after the patient's arrival in the intensive cardiac care unit, a drop in her blood pressure to 60/30 mmHg and a hemoglobin concentration of 4.5 g/dl were noticed. Transfusion was started, and bedside abdominal ultrasound examination revealed free intraperitoneal fluid. Computed tomography of the abdomen revealed liver injury with active extravasation from the cranial surface of the right lobe and a massive hemoperitoneum. The patient was coagulopathic and acidotic with a body temperature of 33.5 °C. A minimally invasive treatment strategy, including angiography and selective trans-catheter arterial embolization, were performed in combination with percutaneous evacuation of 4.5 L of intraperitoneal blood. After completion of these procedures, the patient was hemodynamically stable. She was weaned off mechanical ventilation 2 days later and made an uneventful recovery. She was discharged to a local hospital on day 13 without neurological disability. CONCLUSIONS: Although rare, bleeding caused by liver injury due to chest compressions can be life-threatening after successful cardiopulmonary resuscitation. Reported mortality is high after surgical intervention, and patients may benefit from less invasive treatment strategies such as those presented in this case report.
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Reanimação Cardiopulmonar/efeitos adversos , Embolização Terapêutica/métodos , Massagem Cardíaca/efeitos adversos , Hemorragia/terapia , Fígado/lesões , Parada Cardíaca Extra-Hospitalar/terapia , Adulto , Angiografia Digital , Feminino , Hemorragia/diagnóstico por imagem , Hemorragia/etiologia , Humanos , Fígado/irrigação sanguínea , Fígado/diagnóstico por imagem , Tomografia Computadorizada por Raios XRESUMO
BACKGROUND: Heart rate reserve (HRR) has been reported to be inversely associated with cardiovascular (CV) disease and death. The impact of physical fitness (PF) on this relationship has not, however, been described in detail. We investigated how different levels of PF influenced the association between HRR and CV death during a 35-year follow-up. METHODS AND RESULTS: HRR and PF were measured in 2014 apparently healthy, middle-aged men during a symptom-limited bicycle exercise test in 1972-75. The men were divided into tertiles (T1-T3) by age-adjusted HRR. Morbidity and mortality data were registered from hospital charts through 2007 and the Norwegian Cause of Death Registry. Adjusted Cox proportional hazard regression models were used to calculate risks. Incidence of CV death was 528 (26%) during median 30 years of follow-up. Men with the lowest HRR had 41% (HR 1.41 [1.14-1.75]) increased risk of CV death compared with the men with the highest. We found a significant interaction between age-adjusted PF and HRR. After stratifying the men by PF, results were statistically significant only among men with the lowest PF, where the men with lowest HRR had a 70% (HR 1.70 [1.12-2.67]) increased risk of CV death compared with the men with the highest. CONCLUSIONS: Low HRR was independently associated with increased risk of CV death in apparently healthy, middle-aged men. The predictive impact of HRR on CV death risk was, however, confined to unfit men.
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Doenças Cardiovasculares/mortalidade , Nível de Saúde , Frequência Cardíaca , Aptidão Física , Adulto , Fatores Etários , Ciclismo , Doenças Cardiovasculares/diagnóstico , Doenças Cardiovasculares/etiologia , Doenças Cardiovasculares/fisiopatologia , Distribuição de Qui-Quadrado , Teste de Esforço/métodos , Seguimentos , Humanos , Incidência , Estimativa de Kaplan-Meier , Masculino , Pessoa de Meia-Idade , Análise Multivariada , Noruega/epidemiologia , Valor Preditivo dos Testes , Prognóstico , Modelos de Riscos Proporcionais , Sistema de Registros , Medição de Risco , Fatores de Risco , Fatores Sexuais , Fatores de TempoRESUMO
BACKGROUND: Chronotropic index is a standardized measure of heart rate (HR) increment during exercise that reflects the combined effects of age, resting HR, and physical fitness. Low chronotropic index has been reported to predict disease and death. We tested whether temporal change in chronotropic index over 7 years influenced risk of cardiovascular death through up to 28 years. METHODS AND RESULTS: Chronotropic index was calculated ([achieved maximal HR-resting HR]/[age-predicted maximal HR-resting HR]) after a symptom-limited bicycle ECG exercise test in 1420 healthy men at 2 examinations 7 years apart, in 1972 and 1979. Events of cardiovascular death were registered by manual scrutiny of all participants' hospital charts and the Norwegian Cause of Death Registry. The participants were divided into quartiles of temporal change in chronotropic index, with quartile one having the most negative value. Cox proportional hazard regression models were used to estimate risks and adjusted for classical cardiovascular risk factors. Incidence of cardiovascular death was 310 (22%) during median of 21 years of follow-up. After multivariable adjustment, and comparison with quartile four (mean +0.11), quartiles one (-0.16), two (-0.04), and three (+0.02) were associated with hazard ratios 1.50 (95% CI 1.10-2.05), 1.10 (0.79-1.53), and 1.04 (0.74-1.45) for cardiovascular death. Results remained robust also after exclusion of 31 participants with exercise ECG-induced signs of coronary ischemia. CONCLUSIONS: Temporal reduction in chronotropic index was associated with increased long-term risk of cardiovascular death and might be a clinically important predictor when assessing risk in healthy individuals over a longer time.
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Doenças Cardiovasculares/fisiopatologia , Previsões , Frequência Cardíaca/fisiologia , Medição de Risco , Adulto , Doenças Cardiovasculares/diagnóstico , Doenças Cardiovasculares/mortalidade , Causas de Morte/tendências , Teste de Esforço , Feminino , Seguimentos , Humanos , Masculino , Pessoa de Meia-Idade , Noruega/epidemiologia , Valor Preditivo dos Testes , Valores de Referência , Estudos Retrospectivos , Fatores de Risco , Taxa de Sobrevida/tendênciasRESUMO
BACKGROUND: Low resting heart rate (HR) has been associated with atrial fibrillation (AF) in athletes. We aimed to study whether low HR at rest or during exercise testing was a predictor of AF in initially healthy middle-aged men. METHODS AND RESULTS: A total of 2014 healthy Norwegian men participated in a prospective cardiovascular survey, including a standardized bicycle exercise test in 1972 to 1975. During ≤35 years of follow-up (53,000 person-years of observation), 270 men developed incident AF, documented by scrutiny of health charts in all Norwegian hospitals. Risk estimation was analyzed with Cox proportional hazard models. Low exercise HR after 6 minutes exercise on the moderate workload of 100 W (HR100W) was a predictor of incident AF. Men with HR100W <100 beats per minute (n=260) were characterized by high physical fitness, low resting and low maximum HR, and they had 1.60-fold AF risk (95% confidence interval, 1.11-2.26) compared with men with HR100W ≥100 beats per minute when adjusted for age, systolic blood pressure, and physical fitness. Additional adjustment for relative heart volume slightly reduced the association. The subgroup of men (n=860) with hypertensive blood pressure measurements at baseline had the highest risk difference between low and high HR100W with hazard ratio 2.08 (1.19-3.45). CONCLUSIONS: Our data indicate that low exercise HR on a moderate workload is a long-term predictor of incident AF in healthy middle-aged men. Elevated baseline blood pressure substantially amplifies this risk. The present results suggest a relationship between increased vagal tone, high stroke volumes and incident AF, and particularly so in physically fit men.
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Fibrilação Atrial/epidemiologia , Frequência Cardíaca , Adulto , Fatores Etários , Pressão Arterial , Fibrilação Atrial/diagnóstico , Fibrilação Atrial/fisiopatologia , Distribuição de Qui-Quadrado , Teste de Esforço , Humanos , Hipertensão/epidemiologia , Hipertensão/fisiopatologia , Incidência , Estimativa de Kaplan-Meier , Masculino , Pessoa de Meia-Idade , Análise Multivariada , Noruega/epidemiologia , Aptidão Física , Valor Preditivo dos Testes , Modelos de Riscos Proporcionais , Estudos Prospectivos , Fatores de Risco , Fatores Sexuais , Volume Sistólico , Fatores de TempoRESUMO
Exercise systolic blood pressure (SBP) predicts coronary heart disease (CHD) in the general population. We tested whether changes in exercise SBP during 7 years predict CHD (including angina pectoris, nonfatal myocardial infarction, and fatal CHD) and mortality over the following 28 years. Peak SBP at 100 W workload (=5.5 METS [metabolic equivalents]; completed by all participants) was measured among 1392 apparently healthy men in 1972-75 and repeated in 1979-82. The men were divided into quartiles (Q1-Q4) of exercise SBP change. Relative risks were calculated using Cox proportional hazard regression adjusting for family history of CHD, age, smoking status, resting SBP, peak SBP at 100 W, total cholesterol at first examination (model 1), and further for physical fitness and change in physical fitness (model 2). The highest quartile, Q4, was associated with a 1.55-fold (95% confidence interval, 1.17-2.03) adjusted (model 1) risk of CHD and a 1.93-fold (1.24-3.02) risk of coronary heart death compared with the lowest, Q1. Q4 had a 1.40-fold (1.06-1.85) risk of CHD and a 1.70-fold (1.08-2.68) risk of coronary heart death using model 2. Q4 was associated with increased risk of cardiovascular death and all-cause death compared with Q1 in model 1, but not in model 2. Our results indicate that an increase in exercise SBP at 100 W over 7 years is independently associated with increased long-term risk of CHD and substantiate our previous finding that high exercise SBP is an important risk factor for CHD in healthy men.