The rationale for performing such diagnostic procedures is well defined. Indeed, the occurrence of end-organ damage has been shown to 1) provide conclusive information on the prognosis of the hypertensive disease, 2) characterise a noticeable fraction of the hypertensive population, 3) be an early marker of the clinical worsening of the high blood pressure state and 4) represent a parameter useful to assess the therapeutic efficacy of a given antihypertensive drug treatment throughout the years.
Although all the above mentioned examinations allow to perform an almost complete diagnostic screening of the hypertensive patient (1), other markers of end organ damage will be available in the near future, such as diastolic dysfunction, cerebral lacunae, impairment of arterial distensibility, endothelial dysfunction, and finally an increase in blood pressure variability and in adrenergic cardiovascular drive.
Assessment of hypertension related end-organ damage might be viewed as an expensive procedure complicating the diagnostic approach of the hypertensive state. This consideration may represent the rationale for the choice made by the American Guidelines issued by the Joint National Committee in its Seventh Report (2) not to regard the search for target organ damage as an essential procedure in the diagnostic approach of the high blood pressure state. The European Guidelines, in contrast, believe that this diagnostic intervention is of crucial relevance for stratifying the cardiovascular risk of the hypertensive patient, thereby allowing the guarantee for a better and more effective therapeutic approach. Indeed it should be emphasised that according to European Guidelines the presence of target organ damage (cardiac hypertrophy or microalbuminuria or carotid atheroma) carries the same cardiovascular risk represented by the presence in the medical history of diabetes mellitus or of 3 or more risk factors. This makes a subject with high-normal blood pressure values (systolic blood pressure between 130 and 139 mmHg or diastolic blood pressure between 85 and 89 mmHg) at “high added risk”, pointing -in practical terms- to a need for prompt and effective therapeutic intervention (1).
Why is detection of hypertension-related target organ damage essential for determining a patient’s prognosis? The reason is a simple one, namely that the presence of cardiac hypertrophy (particularly in the case of the so-called eccentric type) has been shown to be associated with an increased number of fatal and non-fatal cardiovascular events (3). Similar data have been provided for an abnormal increase in carotid wall thickness, which has been recently shown to be linked with an increased chance of developing a myocardial infarction and/or an acute cerebral ischaemic event (4).
During the past few years the interest of investigators and clinicians has been focused on the prognostic relevance of renal dysfunction, given the evidence that the presence of microalbuminuria and/or a slight increase in creatinine is closely related to the future development of coronary heart disease (5-6). It is likely that the pathophysiological link of this relationship is represented by the endothelial dysfunction (7), which, when detected at the level of the renal circulation, is responsible for the occurrence of microalbuminuria which found in the coronary circulation may trigger myocardial ischaemic events.
A further question should be finally addressed. Which evaluation of end-organ damage should be regarded as first choice in daily clinical practice? Although the question still remains unsolved, there are some indications suggesting that microalbuminuria may represent the rational choice. Given the evidence, this procedure 1) is less expensive than others, 2) allows to identify high risk patients and 3) is sufficiently sensitive and reproducible over time that it can be employed in daily clinical practice. Further diagnostic evaluations, represented by the ultrasonographic assessment of left ventricular hypertrophy and carotid wall thickness, will be needed, particularly in patients thought to be at high cardiovascular risk in whom, however, search for renal damage has provided negative results.
The content of this article reflects the personal opinion of the author/s and is not necessarily the official position of the European Society of Cardiology.