Hypertension and Target Organ Damage: Don’t Believe Everything You Think!

Raised systolic blood pressure (BP) is a powerful independent risk factor for cardiovascular mortality and death from all causes.1 It is also a major cause of clinical and pre-clinical damage to the heart, brain, retina, kidneys, and arterial blood vessels. Damage to these organs typically manifests as coronary heart disease, heart failure, stroke, other cardiovascular diseases and impaired renal function or endstage kidney failure. The myriad pathophysiological mechanisms associated with the spectrum of target organ damage are shown in Table 1. Although these mechanisms are individually and collectively important, we now know that the magnitude of systolic BP elevation beyond the theoretical minimum risk exposure level and the presence of comorbid risk factors account for most of the observed organ damage and related death and disability. This knowledge has not always been common or without controversy. Half a century ago, most clinicians believed that the rise in systolic BP level with advancing age was a benign physiological response to age-related arterial stiffening. In fact, systolic BP was believed to be normal as long as it did not exceed “100 plus your age.”2 Inherent in this belief was the concept of the BP dividing line above which hypertension and related risk of target organ damage were present, and BP level below that line was considered normal, with the risk of damage considered very low. Thus, a 70-year-old woman with a systolic BP of 170 mm Hg did not need treatment. Objective data from multiple epidemiological studies and hypertension clinical trials have proved these beliefs to be false. Other beliefs proven false include the notion of a benign clinical course in “borderline,” “mild,” or “high-normal” hypertension, especially within the context of multiple comorbid cardiovascular risk factors such as a strong family history of premature CVD, dyslipidemia, cigarette smoking, physical inactivity, poor nutrition, diabetes, obesity, and cardiometabolic syndrome. Similarly, the misconception that left ventricular hypertrophy was an appropriate compensatory physiological response to raised blood pressure has been dispelled by compelling epidemiological data initially gleaned from the Framingham Heart Study.3,4 Another more contemporary belief relates to the burden and severiHypertension and target organ damage: don’t Believe everytHing you tHink!