Parental smoking and smoking experimentation in childhood increase the risk of being a smoker 20 years later: the Childhood Determinants of Adult Health Study.

AIMS: To examine the long-term effects of childhood smoking experimentation and exposure to parental smoking on adult smoking risk. METHODS: Data were from a 20-year follow-up of 9-15-year-olds who completed questionnaires in the 1985 Australian Schools Health and Fitness Survey (n=6559). The relative risks (RR) of adult current smoking in 2004-05 for childhood exposure to smoking experimentation (never, a few puffs, <10 cigarettes, >10 cigarettes) and parental smoking (none, father, mother, both parents) in 1985, with adjustment for confounders, were estimated by log binomial modelling. Analyses were stratified by age (9-13 and 14-15 years) and sex. FINDINGS: Participation at follow-up was 54% (n=3559). Childhood smoking experimentation increased the risk of being a current smoker particularly for 14-15-year-old experimenters of more than 10 cigarettes [males, RR 2.72, 95% confidence interval (CI) 1.74-4.25; females, RR 6.39, 95% CI 2.85-14.33]. Parental smoking was associated with adult current smoking risk, particularly for 9-13-year-olds with two smoking parents (males, RR 1.53, 95% CI 1.19-1.96; females, RR 1.99, 95% CI 1.52-2.61) and older males with smoking mothers (RR 1.82, 95% CI 1.22-2.73). Parental smoking was not associated with childhood smoking experimentation. CONCLUSIONS: These findings suggest that any childhood smoking experimentation increases the risk of being a smoker 20 years later. As exposure to parental smoking predicted current smoking, parents should be aware of the association between their own smoking behaviour and that of their children.

The large and growing burden of stroke.

Stroke is a disease with impacts ranging from death and disability, to reduced health-related quality of life and depression. To truly understand the burden of this disease we must investigate not only the mortality and prevalence of stroke, but also its incidence within populations. Stroke mortality and incidence declined rapidly during the 1980s and early 1990s; however, this trend appears to have slowed in more recent times. Despite many studies being conducted in Europe, and Australasia, there is a lack of reliable data from developing regions such as Asia and Africa. There are indications that although the mortality rate of stroke in such regions may be less than in developed countries, the simple fact that the populations are large means that the burden of stroke is considerable. Furthermore, as a result of epidemiological transition and rapid urbanization and industrialization many developing regions are exhibiting increased life expectancy, as well as changes in diet and other risk behaviors, such as smoking. This is contributing to a looming epidemic of stroke in these regions, as greater proportions of the population are now at risk of stroke. Fortunately, stroke is largely a preventable disease. The major risk factor for stroke, hypertension, can be controlled using both population-wide approaches, such as changes in the salt content of processed foods, and high-risk individual approaches, such as use of antihypertensive medications. Implementation of effective primary and secondary prevention strategies is likely to have an enormous benefit in reducing the burden of stroke, particularly in developing regions.

Prevalence of depression and use of antidepressant medication at 5-years poststroke in the North East Melbourne Stroke Incidence Study.

BACKGROUND AND PURPOSE: There are few data on the prevalence or treatment of depression from unselected populations long-term poststroke. We assessed the prevalence of depression and antidepressant use at 5-years poststroke in an unselected stroke population. METHODS: Five-year survivors from a prospective community-based stroke incidence study were assessed for depression with the Irritability, Depression and Anxiety Scale. Medications indicated primarily for treatment of depression were recorded. RESULTS: At 5-years poststroke, 441 (45%) of 978 incident cases were alive (mean age=74+/-15 years, 49% female). Seventeen percent of those assessed were depressed. Twenty-two percent with depression were taking an antidepressant medication. Of those taking an antidepressant, 72% were not depressed. CONCLUSIONS: Although nearly one-fifth of survivors were depressed, few were taking antidepressants. Further exploration of this low level of treatment is warranted.

Control of hypertension 5 years after stroke in the North East Melbourne Stroke Incidence Study.

Control of blood pressure after stroke is important for reducing the risk of recurrent stroke. We examined the control of hypertension in a community-based population of 5-year stroke survivors. Cases of first-ever stroke from the North East Melbourne Stroke Incidence Study were interviewed at 5 years poststroke. Blood pressure, history of hypertension, and antihypertensive medications were recorded. Individuals were classified as normotensive (blood pressure < 140/90 mm Hg, no history of hypertension, and no antihypertensive medications), controlled hypertensive (blood pressure < 140/90 mm Hg, history of hypertension, and/or taking antihypertensive medications), uncontrolled hypertensive (blood pressure > or = 140/90 mm Hg, history of hypertension, and/or taking antihypertensive medications), or uninformed hypertensive (blood pressure > or = 140/90 mm Hg, no known history of hypertension, and no antihypertensive medications). At 5 years poststroke, 441 (45%) of 978 first-ever stroke cases were alive. Of these, 305 (69%) had complete data on blood pressure, antihypertensive medication use, and history of hypertension. No statistical differences existed between those with or without these data. Eight-two percent were hypertensive; 63% had controlled hypertension, 30% had uncontrolled hypertension, and 7% were unaware that they were hypertensive. Overall, 67% of individuals classified as uncontrolled or uninformed hypertensive subjects were receiving treatment that was insufficient to achieve target blood pressure levels. Uncontrolled hypertensive subjects were more likely to recall receiving advice to manage their hypertension with medication (P < 0.02) and diet (P < 0.09). Although the majority of hypertensive individuals had controlled hypertension at 5 years poststroke, considerable improvement can be made in the control of hypertension after stroke.

Greater incidence of both fatal and nonfatal strokes in disadvantaged areas: the Northeast Melbourne Stroke Incidence Study.

BACKGROUND AND PURPOSE: Greater stroke mortality has been reported among lower socioeconomic groups. We aimed to determine whether fatal, nonfatal, and overall stroke incidence varied by socioeconomic status. METHODS: All suspected strokes occurring in 22 postcodes (population of 306,631) of Melbourne, Australia, during a 24-month period between 1997 and 1999 were found and assessed. Multiple overlapping sources were used to ascertain cases with standard clinical definitions for stroke. Socioeconomic disadvantage was assigned in 4 bands from least to greatest using an area-based measure developed by the Australian Bureau of Statistics. RESULTS: Overall stroke incidence (number per 100,000 population per year), adjusted to the European population 45 to 84 years of age, increased with increasing socioeconomic disadvantage: 200 (95% CI, 173 to 228); 251 (95% CI, 220 to 282); 309 (95% CI, 274 to 343); and 366 (95% CI, 329 to 403; chi2 for ranks; P<0.0001). Similar incidence patterns were observed for both fatal and nonfatal stroke. Nonfatal stroke contributed most to this incidence pattern: 146 (95% CI, 122 to 169); 181 (95% CI, 155 to 207); 223 (95% CI, 194 to 252); and 280 (95% CI, 247 to 313; chi2 for ranks; P<0.0001). CONCLUSIONS: In this population-based study, both fatal and nonfatal stroke incidence increased with increasing socioeconomic disadvantage. The greater contributor to this incidence pattern was nonfatal stroke incidence. This may have implications for service provision to those least able to afford it. Area-based identification of those most disadvantaged may provide a simple and effective way of targeting regions for stroke prevention strategies.

Long-term outcome in the North East Melbourne Stroke Incidence Study: predictors of quality of life at 5 years after stroke.

BACKGROUND AND PURPOSE: Although much is known about the long-term outcome of stroke patients in terms of mortality and disability, there has been little research on the patient-centered outcome of health-related quality of life (HRQoL). There are limited natural history data on HRQoL beyond 2 years after stroke and no data on those factors present at stroke onset that predict HRQoL beyond 2 years after stroke. For these reasons, we aimed to examine these aspects of HRQoL in an unselected population of stroke patients. METHODS: All cases of first-ever stroke from a prospective community-based stroke incidence study (excluding subarachnoid hemorrhage) were assessed 5 years after stroke. HRQoL was measured with the assessment of quality of life instrument. ANOVA was used to determine baseline predictors of HRQoL. RESULTS: In total, 978 cases were recruited, 45% were male, and the mean age (+/-SD) was 75.5+/-13.8 years. Five years after stroke, 441 (45.1%) were alive and 356 were assessed (80.7%). Those assessed were more often born in Australia and older in age (both P<0.05). Seventy-one survivors (20%) had a very low HRQoL (score < or =0.1). The independent baseline predictors of low HRQoL at 5 years after stroke were increasing age, lower socioeconomic status, and markers of stroke severity. CONCLUSIONS: At 5 years after stroke, we found that a substantial proportion of survivors were suffering from poor HRQoL. As our population ages, the number of strokes and, thus, stroke survivors with poor HRQoL is likely to increase. Therefore, strategies to improve HRQoL should be vigorously pursued.

Sympathetic nervous control of the cerebral circulation in sleep.

Cerebral vessels are extensively innervated by sympathetic nerves arising from superior cervical ganglia, and these nerves might play a protective role during the large arterial pressure surges of active sleep (AS). We studied lambs (n=10) undergoing spontaneous sleep-wake cycles before and after bilateral removal of the superior cervical ganglia (SCGx, n=5) or sham ganglionectomy (n=5). Lambs were instrumented to record cerebral blood flow (CBF, flow probe on the superior sagittal sinus), carotid arterial pressure (P(ca)), intra-cranial pressure (P(ic)), cerebral perfusion pressure (Pcp=Pca-Pic) and cerebral vascular resistance (CVR). Prior to SCGx, CBF (mL min-1) was significantly higher in AS than in Quiet Sleep (QS) and Quiet Wakefulness (QW) (17+/-2, 13+/-3, and 14+/-3 respectively, mean+/-SD, P<0.05). Following SCGx, baseline CBF increased by 34, 31, and 29% respectively (P<0.05). CVR also decreased in all states by approximately 25% (P<0.05). During phasic AS, surges of Pca were associated with transient increases in Pcp, Pic and CBF. Following SCGx, peak CBF and Pic during surges became higher and more prolonged (P<0.05). Our study is the first to reveal that tonic sympathetic nerve activity (SNA) constricts the cerebral circulation and restrains baseline CBF in sleep. SNA is further incremented during arterial pressure surges of AS, limiting rises in CBF and Pic, possibly by opposing vascular distension as well as by constricting resistance vessels. Thus, SNA may protect cerebral microvessels from excessive distension during AS, when large arterial blood pressure surges are common.

Smoking as a crucial independent determinant of stroke.

BACKGROUND: Although smoking is known to be powerful risk factor for other vascular diseases, such as cardiac and peripheral vascular disease, only relatively recently has evidence for the role of smoking in the development of stroke been established. The reasons for this advance lie in the acknowledgement that stroke is a heterogeneous disease, in which its subtypes are associated with different risk factors. Furthermore, improvements in the stringency of epidemiological studies and the greater use of CT scanning have enabled the role of smoking in the development of stroke to be elucidated. SUMMARY OF REVIEW: This is a qualitative examination of high quality epidemiological studies in which the role of smoking and passive smoking, as a risk factor for cerebral infarction, intracerebral haemorrhage and subarachnoid haemorrhage, is examined. In addition, the pathological mechanisms by which smoking or passive smoking may contribute to the development of stroke are reviewed. CONCLUSION: Smoking is a crucial independent determinant of cerebral infarction and subarachnoid haemorrhage, however its role in intracerebral haemorrhage is unclear. Although studies are limited, there is evidence that exposure to passive smoking may also increase the risk of stroke. Smoking appears to be involved in the pathogenesis of stroke via direct injury to the vasculature and also by altering haemodynamic factors within the circulation. Importantly, smoking is modifiable risk factor for stroke. Therefore, the encouragement of smoking cessation may result in a substantial reduction in the incidence of this devastating disease.