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Examinando por Autor "O’Donnell, Martin"

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  • Publicación
    Acceso abierto
    Anger or emotional upset and heavy physical exertion as triggers of stroke. The INTERSTROKE study
    (European Society of Cardiology, 2022-01-14) Smyth, Andrew; O’Donnell, Martin; Hankey, Graeme J.; Rangarajan, Sumathy; Lopez-Jaramillo, Patricio; Xavier, Denis; Zhang, Hongye; Canavan, Michelle; Damasceno, Albertino; Langhorne, Peter; Avezum, Alvaro; Pogosova, Nana; Oguz, Aytekin; Yusuf, Salim; INTERSTROKE investigators; Masira
    Aims In INTERSTROKE, we explored the association of anger or emotional upset and heavy physical exertion with acute stroke, to determine the importance of triggers in a large, international population. Methods and results INTERSTROKE was a case–control study of first stroke in 32 countries. Using 13 462 cases of acute stroke we adopted a case-crossover approach to determine whether a trigger within 1 hour of symptom onset (case period), vs. the same time on the previous day (control period), was associated with acute stroke. A total of 9.2% (n = 1233) were angry or emotional upset and 5.3% (n = 708) engaged in heavy physical exertion during the case period. Anger or emotional upset in the case period was associated with increased odds of all stroke [odds ratio (OR) 1.37, 99% confidence interval (CI), 1.15–1.64], ischaemic stroke (OR 1.22, 99% CI, 1.00–1.49), and intracerebral haemorrhage (ICH) (OR 2.05, 99% CI 1.40–2.99). Heavy physical exertion in the case period was associated with increased odds of ICH (OR 1.62, 99% CI 1.03–2.55) but not with all stroke or ischaemic stroke. There was no modifying effect by region, prior cardiovascular disease, risk factors, cardiovascular medications, time, or day of symptom onset. Compared with exposure to neither trigger during the control period, the odds of stroke associated with exposure to both triggers were not additive. Conclusion Acute anger or emotional upset was associated with the onset of all stroke, ischaemic stroke, and ICH, while acute heavy physical exertion was associated with ICH only.
  • Publicación
    Acceso abierto
    Anger or emotional upset and heavy physical exertion as triggers of stroke: The INTERSTROKE study
    (2022-01-14) Smyth, Andrew; O’Donnell, Martin; Hankey, Graeme J.; Rangarajan, Sumathy; Lopez-Jaramillo, Patricio; Xavier, Denis; Zhang, Hongye; Canavan, Michelle; Damasceno, Albertino; Langhorne, Peter; Alvaro, Avezum; Pogosova, Nana; Oguz, Aytekin; Yusuf, Salim; INTERSTROKE investigators; Masira
    Aims In INTERSTROKE, we explored the association of anger or emotional upset and heavy physical exertion with acute stroke, to determine the importance of triggers in a large, international population. Methods and results INTERSTROKE was a case–control study of first stroke in 32 countries. Using 13 462 cases of acute stroke we adopted a case-crossover approach to determine whether a trigger within 1 hour of symptom onset (case period), vs. the same time on the previous day (control period), was associated with acute stroke. A total of 9.2% (n = 1233) were angry or emotional upset and 5.3% (n = 708) engaged in heavy physical exertion during the case period. Anger or emotional upset in the case period was associated with increased odds of all stroke [odds ratio (OR) 1.37, 99% confidence interval (CI), 1.15–1.64], ischaemic stroke (OR 1.22, 99% CI, 1.00–1.49), and intracerebral haemorrhage (ICH) (OR 2.05, 99% CI 1.40–2.99). Heavy physical exertion in the case period was associated with increased odds of ICH (OR 1.62, 99% CI 1.03–2.55) but not with all stroke or ischaemic stroke. There was no modifying effect by region, prior cardiovascular disease, risk factors, cardiovascular medications, time, or day of symptom onset. Compared with exposure to neither trigger during the control period, the odds of stroke associated with exposure to both triggers were not additive. Conclusion Acute anger or emotional upset was associated with the onset of all stroke, ischaemic stroke, and ICH, while acute heavy physical exertion was associated with ICH only.
  • Publicación
    Acceso abierto
    Associations of Fish Consumption with Risk of Cardiovascular Disease and Mortality among Individuals with or without Vascular Disease from 58 Countries
    (JAMA Network, 2021-03-08) Mohan, Deepa; Mente, Andrew; Dehghan, Mahshid; Rangarajan, Sumathy; O’Donnell, Martin; Hu, Weihong; Dagenais, Gilles; Wielgosz, Andreas; Lear, Scott; Wei, Li; Diaz, Rafael; Avezum, Alvaro; Lopez-Jaramillo, Patricio; Lanas, Fernando; Swaminathan, Sumathi; Kaur, Manmeet; Vijayakumar, K.; Mohan, Viswanathan; Gupta, Rajeev; Szuba, Andrzej; Iqbal, Romaina; Yusuf, Rita; Mohammadifard, Noushin; Khatib, Rasha; Yusoff, Khalid; Gulec, Sadi; Rosengren, Annika; Yusufali, Afzalhussein; Wentzel-Viljoen, Edelweiss; Chifamba, Jephat; Dans, Antonio; Alhabib, Khalid F.; Yeates, Karen; Teo, Koon; Gerstein, Hertzel C.; Yusuf, Salim; The PURE, ONTARGET, TRANSCEND, and ORIGIN investigators; Masira
    Importance Cohort studies report inconsistent associations between fish consumption, a major source of long-chain ω-3 fatty acids, and risk of cardiovascular disease (CVD) and mortality. Whether the associations vary between those with and those without vascular disease is unknown. Objective To examine whether the associations of fish consumption with risk of CVD or of mortality differ between individuals with and individuals without vascular disease. Design, Setting, and Participants This pooled analysis of individual participant data involved 191 558 individuals from 4 cohort studies—147 645 individuals (139 827 without CVD and 7818 with CVD) from 21 countries in the Prospective Urban Rural Epidemiology (PURE) study and 43 413 patients with vascular disease in 3 prospective studies from 40 countries. Adjusted hazard ratios (HRs) were calculated by multilevel Cox regression separately within each study and then pooled using random-effects meta-analysis. This analysis was conducted from January to June 2020. Exposures Fish consumption was recorded using validated food frequency questionnaires. In 1 of the cohorts with vascular disease, a separate qualitative food frequency questionnaire was used to assess intake of individual types of fish. Main Outcomes and Measures Mortality and major CVD events (including myocardial infarction, stroke, congestive heart failure, or sudden death). Results Overall, 191 558 participants with a mean (SD) age of 54.1 (8.0) years (91 666 [47.9%] male) were included in the present analysis. During 9.1 years of follow-up in PURE, compared with little or no fish intake (≤50 g/mo), an intake of 350 g/wk or more was not associated with risk of major CVD (HR, 0.95; 95% CI, 0.86-1.04) or total mortality (HR, 0.96; 0.88-1.05). By contrast, in the 3 cohorts of patients with vascular disease, the HR for risk of major CVD (HR, 0.84; 95% CI, 0.73-0.96) and total mortality (HR, 0.82; 95% CI, 0.74-0.91) was lowest with intakes of at least 175 g/wk (or approximately 2 servings/wk) compared with 50 g/mo or lower, with no further apparent decrease in HR with consumption of 350 g/wk or higher. Fish with higher amounts of ω-3 fatty acids were strongly associated with a lower risk of CVD (HR, 0.94; 95% CI, 0.92-0.97 per 5-g increment of intake), whereas other fish were neutral (collected in 1 cohort of patients with vascular disease). The association between fish intake and each outcome varied by CVD status, with a lower risk found among patients with vascular disease but not in general populations (for major CVD, I2 = 82.6 [P = .02]; for death, I2 = 90.8 [P = .001]). Conclusions and Relevance Findings of this pooled analysis of 4 cohort studies indicated that a minimal fish intake of 175 g (approximately 2 servings) weekly is associated with lower risk of major CVD and mortality among patients with prior CVD but not in general populations. The consumption of fish (especially oily fish) should be evaluated in randomized trials of clinical outcomes among people with vascular disease.
  • Publicación
    Acceso abierto
    Salt and cardiovascular disease: Insufficient evidence to recommend low sodium intake
    (Oxford Academic, 2020-09-14) O’Donnell, Martin; Mente, Andrew; Alderman, Michael H.; Brady, Adrian J.B.; Diaz, Rafael; Gupta, Rajeev; Lopez-Jaramillo, Patricio; Luft, Friedrich C.; Luscher, Thomas F.; Mancia, Giuseppe; Mann, Johannes F.E.; McCarron, David; McKee, Martin; Messerli, Franz H.; Moore, Lynn L.; Narula, Jagat; Oparil, Suzanne; Packer, Milton; Prabhakaran, Dorairaj; Schutte, Alta; Sliwa, Karen; Staessen, Jan A.; Yancy, Clyde; Yusuf, Salim; Masira
    Several blood pressure guidelines recommend low sodium intake (<2.3 g/day, 100 mmol, 5.8 g/day of salt) for the entire population, on the premise that reductions in sodium intake, irrespective of the levels, will lower blood pressure, and, in turn, reduce cardiovascular disease occurrence. These guidelines have been developed without effective interventions to achieve sustained low sodium intake in free-living individuals, without a feasible method to estimate sodium intake reliably in individuals, and without high-quality evidence that low sodium intake reduces cardiovascular events (compared with moderate intake). In this review, we examine whether the recommendation for low sodium intake, reached by current guideline panels, is supported by robust evidence. Our review provides a counterpoint to the current recommendation for low sodium intake and suggests that a specific low sodium intake target (e.g. <2.3 g/day) for individuals may be unfeasible, of uncertain effect on other dietary factors and of unproven effectiveness in reducing cardiovascular disease. We contend that current evidence, despite methodological limitations, suggests that most of the world’s population consume a moderate range of dietary sodium (2.3–4.6g/day; 1–2 teaspoons of salt) that is not associated with increased cardiovascular risk, and that the risk of cardiovascular disease increases when sodium intakes exceed 5 g/day. While current evidence has limitations, and there are differences of opinion in interpretation of existing evidence, it is reasonable, based upon observational studies, to suggest a population-level mean target of <5 g/day in populations with mean sodium intake of >5 g/day, while awaiting the results of large randomized controlled trials of sodium reduction on incidence of cardiovascular events and mortality.
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