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As the global population ages, advanced practice nurses (APNs) are increasingly encountering complex chronic health problems in older adults. Among these, Hypertension stands out as a pervasive and significant health concern, contributing substantially to cardiovascular morbidity and mortality. This discussion will delve into the incidence, prevalence, and pathophysiology of hypertension in older adults, extending to the cellular level, and will subsequently educate APNs on comprehensive assessment and tailored care, including the evolving role of genetics and genomics in its management.

Hypertension in Older Adults: Incidence, Prevalence, and Pathophysiology

Hypertension, defined as persistently elevated arterial blood pressure, is a major modifiable risk factor for cardiovascular disease (CVD), stroke, renal failure, and cognitive decline. Its prevalence dramatically increases with age, making it a hallmark condition of older adulthood.

Incidence and Prevalence: Globally, hypertension affects approximately one billion people. In older adults, the prevalence is strikingly high. In high-income countries, over 60% of individuals aged 60 years and older have hypertension, with some estimates reaching 70-80% in those over 75 years. Data from Kenya, like many sub-Saharan African countries, indicates a rising burden of non-communicable diseases (NCDs), with hypertension prevalence among older adults in urban areas often exceeding 50% (e.g., National NCD Survey, Kenya). The incidence also rises steeply with age, reflecting the cumulative effects of lifestyle factors and age-related physiological changes on the cardiovascular system. Unlike younger adults where diastolic hypertension might be more common, isolated systolic hypertension (ISH), defined as systolic blood pressure $\ge$ 140 mmHg and diastolic blood pressure < 90 mmHg, is the predominant form of hypertension in older adults.

Pathophysiology: From Systemic to Cellular Levels:

The pathophysiology of hypertension in older adults is multifactorial, involving a complex interplay of genetic predispositions, lifestyle factors, and age-related physiological changes. At a systemic level, it is characterized by increased peripheral vascular resistance, often due to arterial stiffness, and sometimes by increased cardiac output or fluid retention.

1. Vascular Stiffening (Arteriosclerosis): This is arguably the most significant age-related change contributing to ISH.

   • Systemic: Over time, large elastic arteries (aorta, carotid arteries) undergo structural changes. Elastin fibers in the arterial wall degrade and fragment, while collagen content increases and becomes more cross-linked. This reduces the arteries’ ability to distend and recoil with each heartbeat.
   • Cellular/Molecular: At the cellular level, this involves:
     • Smooth Muscle Cell (SMC) Hypertrophy and Proliferation: Vascular SMCs increase in size and number, contributing to arterial wall thickening.
     • Extracellular Matrix (ECM) Remodeling: Increased deposition of stiff collagen (types I and III) replaces elastic fibers. This process is influenced by inflammatory cytokines (e.g., TNF-$\alpha$, IL-6) and growth factors (e.g., TGF-$\beta$), leading to fibrosis.
     • Reduced Nitric Oxide (NO) Bioavailability: Endothelial dysfunction, common with aging, leads to decreased production or increased degradation of vasodilatory NO. This results from oxidative stress (increased reactive oxygen species, ROS) and decreased activity of endothelial nitric oxide synthase (eNOS).
     • Increased Endothelin-1: This potent vasoconstrictor produced by endothelial cells may be increased in aging vessels.

2. Renin-Angiotensin-Aldosterone System (RAAS) Dysregulation: While older adults often have lower plasma renin activity, the RAAS can still contribute to hypertension, especially in salt-sensitive individuals.