title: Dissociation of blood pressure and resistance artery structure: potential clinical implications.
abstract: Essential hypertension (EH) is associated with structural changes in small arteries (SMASCH) in terms of wall thickening and lumen narrowing throughout the entire resistance circulation. This remodelling process occurs early in EH development and is an important contributor to the elevation of vascular resistance. SMASCH also decreases the vasodilatory capability leading to demand-related organ dysfunction (e.g. microvascular angina) and later contributes to organ failure as seen in hypertensive heart and renal failure. In large groups of patients, office blood pressure (BP) precisely predicts strokes and myocardial infarctions, but it is difficult to apply risk prediction equations based on studies of large numbers of patients in individual patients. Office BP may be a rather poor predictor of future cardiovascular events. Adding other risk factors unrelated to BP (SCORE factors) improves risk prediction, and in subgroups with intermediate risk, there may be added value of considering BP-related parameters such as albuminuria or left ventricular hypertrophy. Being directly related to the process of hyper-resistance and dissociated from BP itself, measurements of SMASCH may contribute to risk over and above office BP and other traditional risk parameters. Furthermore, as only antihypertensive treatment regimens resulting in vasodilatation seem to improve SMASCH, this parameter has the potential to guide and improve the management of EH. SMASCH can be assessed, for example, by plethysmography in the forearm or by echocardiography in the heart. These techniques are accurate and reproducible and could constitute part of the diagnostic apparatus for EH patients. This review focuses on methodological issues of SMASCH, haemodynamic consequences, implementation in the clinical setting and suggestions for future research.
authors.affiliation: Department of Cardiology, Aarhus University Hospital, Aarhus, Denmark. klch@mail.dk
authors.forename: Kent L
authors.initials: KL
authors.lastname: Christensen
authors.forename: Niels H
authors.initials: NH
authors.lastname: Buus
mesh_terms: D000818:Animals; D000959:Antihypertensive Agents / Q000627:therapeutic use; D001158:Arteries / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology; D001160:Arterioles / Q000187:drug effects / Q000473:pathology* / Q000503:physiopathology; D015415:Biomarkers; D001794:Blood Pressure / Q000187:drug effects; D006333:Heart Failure / Q000209:etiology / Q000517:prevention & control; D006801:Humans; D006973:Hypertension / Q000175:diagnosis / Q000188:drug therapy / Q000473:pathology* / Q000503:physiopathology; D008833:Microcirculation / Q000187:drug effects; D011379:Prognosis; D051437:Renal Insufficiency / Q000209:etiology / Q000517:prevention & control; D012307:Risk Factors; D014655:Vascular Resistance / Q000187:drug effects; D014661:Vasoconstriction / Q000187:drug effects; D014664:Vasodilation / Q000187:drug effects
chemical_list: D000959:Antihypertensive Agents; D015415:Biomarkers