Temperature, cardiovascular mortality, and the role of hypertension and renin–angiotensin–aldosterone axis in seasonal adversity: a narrative review View Full Text


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Article Info

DATE

2022-05-26

AUTHORS

Harsh Goel, Kashyap Shah, Ashish Kumar, John T. Hippen, Sunil K. Nadar

ABSTRACT

Environmental temperature is now well known to have a U-shaped relationship with cardiovascular (CV) and all-cause mortality. Both heat and cold above and below an optimum temperature, respectively, are associated with adverse outcomes. However, cold in general and moderate cold specifically is predominantly responsible for much of temperature-attributable adversity. Importantly, hypertension—the most important CV risk factor—has seasonal variation such that BP is significantly higher in winter. Besides worsening BP control in established hypertensives, cold-induced BP increase also contributes to long-term BP variability among normotensive and pre-hypertensive patients, also a known CV risk factor. Disappointingly, despite the now well-stablished impact of temperature on BP and on CV mortality separately, direct linkage between seasonal BP change and CV outcomes remains preliminary. Proving or disproving this link is of immense clinical and public health importance because if seasonal BP variation contributes to seasonal adversity, this should be a modifiable risk. Mechanistically, existing evidence strongly suggests a central role of the sympathetic nervous system (SNS), and secondarily, the renin–angiotensin–aldosterone axis (RAAS) in mediating cold-induced BP increase. Though numerous other inflammatory, metabolic, and vascular perturbations likely also contribute, these may also well be secondary to cold-induced SNS/RAAS activation. This review aims to summarize the current evidence linking temperature, BP and CV outcomes. We also examine underlying mechanisms especially in regard to the SNS/RAAS axis, and highlight possible mitigation measures for clinicians. More... »

PAGES

1-13

References to SciGraph publications

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  • 2015-03-20. Blood Pressure Variability: Assessment, Predictive Value, and Potential as a Therapeutic Target in CURRENT HYPERTENSION REPORTS
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  • 2010-03-19. Seasonal variation in metabolic syndrome prevalence in HYPERTENSION RESEARCH
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    30 schema:description Environmental temperature is now well known to have a U-shaped relationship with cardiovascular (CV) and all-cause mortality. Both heat and cold above and below an optimum temperature, respectively, are associated with adverse outcomes. However, cold in general and moderate cold specifically is predominantly responsible for much of temperature-attributable adversity. Importantly, hypertension—the most important CV risk factor—has seasonal variation such that BP is significantly higher in winter. Besides worsening BP control in established hypertensives, cold-induced BP increase also contributes to long-term BP variability among normotensive and pre-hypertensive patients, also a known CV risk factor. Disappointingly, despite the now well-stablished impact of temperature on BP and on CV mortality separately, direct linkage between seasonal BP change and CV outcomes remains preliminary. Proving or disproving this link is of immense clinical and public health importance because if seasonal BP variation contributes to seasonal adversity, this should be a modifiable risk. Mechanistically, existing evidence strongly suggests a central role of the sympathetic nervous system (SNS), and secondarily, the renin–angiotensin–aldosterone axis (RAAS) in mediating cold-induced BP increase. Though numerous other inflammatory, metabolic, and vascular perturbations likely also contribute, these may also well be secondary to cold-induced SNS/RAAS activation. This review aims to summarize the current evidence linking temperature, BP and CV outcomes. We also examine underlying mechanisms especially in regard to the SNS/RAAS axis, and highlight possible mitigation measures for clinicians.
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    38 BP variability
    39 BP variation
    40 CV mortality
    41 CV outcomes
    42 CV risk factors
    43 RAAS activation
    44 activation
    45 adverse outcomes
    46 adversity
    47 aldosterone
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    50 cardiovascular mortality
    51 cause mortality
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    55 cold
    56 control
    57 current evidence
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    80 narrative review
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    86 possible mitigation measures
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